prompt_front: Now, answer the following question based on the text below, only give me the answer and do not output any other words.

Question: Who is responsible for carrying out the functions assigned under the act?

Read the following text and answer briefly.

Context 1: Bare Acts Live
Himachal Pradesh Town and Country Planning Act, 1977
Himachal Pradesh Town And Country Planning Rules, 1978
3  Form of Notice 
4  Manner of publication of notice 
5  Manner of publication of Regional Plan 
6  Notice of Modifications in Regional Plan 
7  Manner of publication of existing land-use map 
8  Manner of publication of approved Interim Development Plan 
9  Manner of publication of draft development plan 
10  Manner of publication of approved development plan 
11  Intention of development undertaken on behalf of Union or State Government 
12  Form of application for permission for development of land by others 
13  Form of permission 
14  Manner of communication of order under sub-section (4) of Section 31 
16  Notice by owner to purchase interest in land 
17  Manner of communication of revocation and modification permission to development 
20  Preparation of town development scheme 
21  Acquisition of land 
22  Mode of levy 
23  Power to borrow money 
24  Terms and conditions subject to which loans may be raised by the Special area Development Authority 
1  Short title, extent, commencement and application 
3  Director and other officers 
4  Establishment of regions 
5  Director to prepare regional plan 
6  Survey 
7  Contents of regional plan 
8  Preparation of regional plan 
9  Finalisation of regional plan 
10  Restriction on use of land or development thereof 
11  Exclusion from claims of amount in certain cases 
12  Review of regional plan 
13  Planning area 
14  Director to prepare development plans 
15  Existing land use maps 
16  Freezing of land use 
17  Interim development plans 
18  Development plan 
19  Publication of draft development plan 
20  Sanction of development plans 
21  Director to prepare sectoral plan 
22  Contents of sectoral plan 
23  Provisions of sections 19 and 20 to apply to sectoral plan 
24  Review of development plan and sectoral plan 
25  Director to control land use 
26  Conformity with development plan 
27  Prohibition of development without permission 
28  Development undertaken on behalf of Union or State Government 
29  Development by local authority or by any authority constituted under this Act 
30  Application for permission for development by others 
30A  Exemption from development permission in rural areas falling within Planning or Special Area 
30B  Exemption in respect of development of certain lands or buildings 
31  Grant or refusal of permission 
34  Lapse of permission 
35  Obligation to acquire land 
36  Deletion of reservation of designated land from draft or final development plan 
37  Power of revocation and modification or permission to development 
38  Penalty for unauthorised development or for use otherwise than in conformity with development plan 
39  Power to require removal of unauthorised development 
40  Establishment of Town and Country Development Authority 
41  Incorporation of Town and Country Development Authority 
42  Constitution of Town and Country Development Authority 
42A  Constitution of Town and Country Development Authority for the Capital Town of Himachal Pradesh 
43  Term of office of Chairman and other members 
44  Resignation of members and filling of casual vacancy 
45  Remuneration of Chairman 
46  Leave of absence and appointment etc  of acting Chairman 
47  Meeting of Town and Country Development Authority 
48  Chief Executive Officer 
49  Other officers and servants 
50  Conditions of service of Chief Executive Officer and other officers and servants 
51  Town development schemes 
53  Power to revise the development schemes 
54  Power of State Government to give Directions 
55  Restriction on land use and development 
56  Lapse of scheme 
57  Town development scheme public purpose 
58  Acquisition of land for Town and Country Development Authority 
59  Developments 
60  Disposal of land, buildings and other development works 
61  Development charges 
63  Fund of Town and Country Development Authority 
64  Annual budget 
66  Constitution of special areas 
67  Special area Development Authority 
68  Incorporation of Special Area Development Authority 
70  Functions 
71  Powers 
72  Fund of Special Area Development Authority 
73  Annual estimates 
74  Power of State Government of supervision and control 
76  Power of Government to review plans etc  for ensuring conformity 
78  Dissolution of authorities 
79  Right of entry 
80  Jurisdiction of Court 
82  Member and officers to be public servants 
83  Suit and other proceedings 
84  Vacancy not to invalidate proceedings 
85  Member to continue till successor enters upon office 
86  Interpretation of regional plan etc 
87  Powers to moke rules 
89  Power to lay the rules and regulations 
The Himachal Pradesh Town and Country Planning Act, 1977
(as amended by Amendment Act No  22 of 1983)
Amended by Act No  8 of 2009
Act published in the Rajpatra, Extraordinary, dated the 30th September, 1977 vide Law Department Notification No  LLR-D(6)5/77, dated the 22nd September, 1977 
An Act to make provision for planning and development and use of land; to make better provision for the preparation of development plans and sectoral plans with a view to ensuring that town planning schemes are made in a proper manner and their execution is made effective; to constitute the Town and Country and Development Authority for proper implementation of town and country development plan; to provide for the development and administration of special areas through the Special Area Development Authority; to make provision for the compulsory acquisition of land required for the purpose of the development plans and for purposes connected with the matters aforesaid 
Be it enacted by the Himachal Pradesh Legislative Assembly in the Twenty-eighth Year of the Republic of India as follows:-
1  Short title, extent, commencement and application  - (1) This Act may be called the Himachal Pradesh Town and Country Planning Act, 1977 
(3) It shall come into force on such date as the State Government may, by notification, appoint and different dates may be appointed for different areas and for different provisions of this Act 
(4) Nothing in this Act shall apply to-
(a) lands comprised within a cantonment under the Cantonments Act, 1924; (2 of 1924) 
(b) lands owned, hired or requisitioned by the Central Government for the purpose of naval, military and air force works;
(c) lands under the control of railway administration for the purpose of construction and maintenance of works under Chapter III of the Indian Railways Act, 1890; (9 of 1890) and
(d) lands owned by any department of the Central Government where operational constructions are going on 
(a) "agriculture" includes horticulture, farming, raising of annual or periodical crops, fruits, vegetables, flowers, grass, fodder, trees or any kind of cultivation of soil, the reserving of land for fodder, grazing or thatching areas, breeding and keeping of livestock including cattle, horses, donkeys, mules, pigs, breeding of fish and keeping of bees, and the use of land ancillary to the farming of land, but does not include-
(i) keeping of cattle purely for the purpose of milking and selling the milk and milk products,
(ii) a garden which is an appendage of buildings, and the expression "agricultural" shall be construed accordingly;
(b) "amenity" includes roads and streets, water and electric supply, open spaces, parks, recreational area, natural feature, playgrounds, street lighting, drainage, sewerage and other utilities, services and conveniences;
(c) "building" includes any structure or erection, or part of a structure or erection, which is intended to be used for residential, industrial, commercial or other purposes, whether in actual use or not;
(d) "building operation" includes-
(i) erection or re-erection of a building or any part thereof,
(ii) roofing or re-roofing of any part of building or an open space,
(iii) any material alteration or enlargement of a building,
(iv) any such alteration of a building as is likely to alter its drainage or sanitary arrangements, or materially affect its security,
(v) the construction of a door opening on any street or land not belonging to the owner;
(e) "commercial use" means the use of any land or building or part thereof for the purpose of carrying on any trade, business or profession, or sale or exchange of goods of any type whatsoever and includes running of with a view to make profit hospitals, nursing homes, infirmaries, educational institutions, hostels, restaurants and boarding houses not being attached to any educational institutions, sarais and also includes the use of any land or building for storage of goods or as buildings for storage of goods or as an office whether attached to an industry or otherwise;
(f) "court" means the principal civil court of original jurisdiction in the district;
(g) "development" with its grammatical variations means the carrying out of a building, engineering, mining or other operations in, on, over or under land, or the making of any material change in any building or land or in the use of either, and includes sub-division of any land;
(h) "development plan" means interim development plan or development plan prepared under this Act;
(i) "director" means the Director of Town and Country Planning appointed under this Act;
(j) "existing land use map� means a map indicating the use to which lands in any specified area are put at the time of preparing the map, and includes the register prepared, with the map giving details of land-use;
(k) "land" includes benefits to arise out of land and things attached to the earth or permanently fastened to anything attached to the earth;
(l) "member" means a member of a Town and Country Development Authority or a Special Area Development Authority, as the case may be, and includes a Chairman thereof;
(m) "occupier" includes-
(i) a tenant,
(ii) an owner in occupation of or otherwise using his land,
(iii) a rent free tenant,
(iv) a licensee, and
(v) any person liable to pay to the owner, damages for the use and occupation of the land;
(n) "owner" includes a mortgagee in possession, a person who for the time being is receiving or is entitled to receive, or has received, the rent or premium for any land whether on his own account or on behalf of or for the further benefit of any other person or as an agent, trustee, guardian or receiver for any other person or for religious or charitable institutions or who would receive the rent or be entitled to receive the rent or premium if the land were to be let and includes a head of a Government department, General Manager of a Railway and the Chief Executive Officer, by whatever name designated, or a local authority, statutory authority, company, corporation or undertaking in respect of properties under their control;
(o) "planning area" means any area declared to be planning area under this Act;
(p) "region" means any area established to be a region under this Act;
(q) "regional plan" means a plan for the region prepared under this Act and approved by the State Government;
(r) "sector" means any sector of a planning area for which, under the development plan, a detailed sectoral plan is prepared;
(s) "slum area" means any predominantly residential area, where the dwellings which by reason of dilapidation, over-crowding, faulty arrangement of design, lack of ventilation, light or sanitary facilities or any combination of these factors are detrimental to safety, health or moral and which is defined by a development plan as a slum area;
(t) "special area" means a special area designated as such under section 66;
(u) "Special Area Development Authority� means an authority constituted under section 67;
(v) "Town Development Scheme" means a scheme prepared for the implementation of the provisions of a development plan by the Town and Country Development Authority; and
(w) "Town and Country Development Authority" means an authority established under section 40 
Director of Town and Country Planning
3  Director and other officers  - (1) After the commencement of this Act the State Government shall, by notification in the Official Gazette, appoint an officer for the purpose of carrying out functions assigned to him under this Act, as the Director of Town and Country Planning for the State and may appoint such other categories of officers as it may deem fit 
(2) The Director shall exercise such powers and perform such duties as are conferred or imposed upon him by or under this Act and the officers appointed to assist the Director shall, within such area as the State Government may specify, exercise such powers and perform such duties conferred and imposed on the Director by or under this Act as the State Government may, by special or general order, direct 
(3) The officers appointed to assist the Director shall be subordinate to him and shall work under his guidance, supervision and control 
4  Establishment of regions  - (1) The State Government may, by notification,-
(a) declare any area in the State to be a region for the purposes of this Act;
(b) define the limits of such area; and
(c) specify the name by which such region shall be known 
(2) The State Government may, by notification, alter the name of any such region and on such alteration, any reference in any law or instrument or other document to the region shall be deemed to be a reference to the region as re-named unless expressly otherwise provided or the context so requires 
(3) The State Government may, by notification,-
(a) alter the limits of a region so as to include therein or exclude therefrom Such area as may be specified in the notification;
(b) amalgamate two or more regions so as to form one region;
(c) divide any region into two or more region; or
(d) declare that the whole or part of the area comprising a region shall cease to be a region or part thereof 
5  Director to prepare regional plan  - Subject to the provisions of this Act and the rules made thereunder, it shall be the duty of the Director-
(i) to carry out a survey of the regions;
(ii) to prepare an existing land use map; and
(iii) to prepare a regional plan 
6  Survey  - (1) The Director shall, with a view to prepare the existing land use map, and other maps as are necessary for the purpose of regional plan,-
(a) carry out such surveys as may be necessary;
(b) obtain from any department of Government and any local authority such maps, survey reports and land records as may be necessary for the purpose 
(2) It shall be the duty of every Government department and local authority to furnish, as soon as may be possible, maps, reports and record, as may be required by the Director 
7  Contents of regional plan  - The regional plan shall indicate the manner in which land in the region should be used, the phasing of development, the net work of communications and transport, the proposals for conservation and development of natural resources, and in particular-
(a) allocation of land to such purposes as residential, industrial; agricultural or as forests or for mineral exploitation;
(b) reservation of open spaces for recreational purposes, gardens, tree belts, and animal sanctuaries;
(c) access or development of transport and communication facilities such as roads, railways, water ways, and the allocation and development of airports;
(d) requirements and suggestions for development of public utilities such as water supply, drainage and electricity;
(e) allocation of areas to be developed as "Special Areas� wherein new towns, townships, large industrial estates or any other type of large development projects may be established;
(f) landscaping and the preservation of areas in their natural state,
(g) measures relating to the prevention of erosion, including rejuvenation of forest areas;
(h) proposals relating to irrigation, water supply or flood control works 
8  Preparation of regional plan  - (1) After preparation of the existing land use map, the Director shall cause to be prepared a draft regional plan and publish it by making a copy thereof available for inspection and publishing a notice in such form and manner as may be prescribed inviting objections and suggestions from any person with respect to the draft plan before such date as may be specified in the notice, such date not being earlier than sixty days from the publication of the notice  Such notice shall specify in regard to the draft plan the following particulars, namely-
(a) the existing land use map and the narrative report thereon;
(b) a narrative report supported by necessary map and charts explaining the provisions of the draft plan;
(c) a note indicating the priorities assigned to works included in the draft plan and the phasing of the programme of development as such;
(d) a notice on the role being assigned to different departments of Government, the Town and Country Development Authorities; the Special Area Development Authorities, and the Local Authorities in the enforcement and implementation of draft plan 
(2) The Director shall consider all the objections and suggestions received by him within the period specified in the notice under sub-section (1) and shall, after giving a reasonable opportunity to all persons affected thereby of being heard, prepare the regional plan containing such modifications, if any, as he considers necessary and submit it to the State Government for approval together with all connected documents, plans, maps and charts 
9  Finalisation of regional plan  - (1) The State Government may approve the draft regional plan submitted under section 8 with or without modification or reject or return the same to the Director for reconsideration 
(2) Immediately after the draft regional plan is approved under sub-section (1) the State Government shall publish in such manner, as may be prescribed, a notice stating that the regional plan has been approved and mentioning a place where a copy of the plan may be inspected at all reasonable hours and shall specify therein a date on which the regional plan shall come into operation:
Provided that where the State Government approves the draft regional plan with modifications, it shall not be published, unless the State Government having published such modifications in the Official Gazette along with a notice inviting objections and suggestions thereon, within a period of not less than thirty days from the date of publication of such notice have considered the objections and suggestions after giving a reasonable opportunity of being heard to persons affected thereby 
10  Restriction on use of land or development thereof  - (1) Notwithstanding anything contained in any other law for the time being in force, on or after the date of publication of the draft regional plan, no person, authority, department of Government or any other person shall change the use of land for any purpose other than agriculture, or carry out any development in respect of any land contrary to the provisions of the draft plan, without the prior approval of the Director or any officer next to him authorised by the Director, in this behalf 
(2) Notwithstanding anything contained in any law for the time being in force, the permission referred to in sub-section (1) shall not be granted otherwise than in conformity with the provision of the draft or final plan and no permission, if granted, shall be construed to confer any legal right whatsoever on the person seeking the permission 
(3) If any work is carried out in contravention of the provisions of this section, the Municipal Corporation or Municipal Committee within its local area, and the Collector in area outside such local areas, may cause such work to be removed or demolished at the cost of the defaulter, which shall be recovered from him in the same manner as an arrear of land revenue:
Provided that no action shall be taken under this sub-section unless the person concerned is given a reasonable opportunity of being heard and a notice calling upon him to remove or demolish the work within a time specified therein 
(4) Any person aggrieved by the order of the Municipal Corporation, Municipal Committee or Collector, as the case may be, calling upon to remove or demolish the work may prefer an appeal to the Director within fifteen days of the receipt of the notice under sub-section (3) and the order of the Director in such appeal shall be final 
11  Exclusion from claims of amount in certain cases  - Where the regional plan assigns a particular land use to a certain areas and any land situate therein is already put to such use, subject to substantially similar restrictions in force under any other law which was in force on the date on which restrictions were imposed by or under this Act and if amount in respect of such restrictions have already been paid under any such other law which was in force for the time being in respect of the property or any right or interest therein to the claimant, or any predecessor in interest of the claimant, the owner shall not be entitled to any further amount on account of injury or damage caused to his rights by reasons of the restrictions placed on the use of the land under the provisions of this Act 
12  Review of regional plan  - (1) The Director may, on his own motion or if so required by the State Government, at any time after a regional plan has come into operation, undertake the review and evaluation of the regional plan and make such modification in it as may be justified by the circumstances 
(2) The foregoing provisions of this Chapter shall, so far as they can be made applicable, apply to the modifications under sub-section (1) as these provisions apply in relation to the preparation, publication and approval of a regional plan 
Planning Area and Development Plans
13  Planning area  - (1) The State Government may, by notification, constitute planning areas for the purposes of this Act and define the limits thereof 
(2) The State Government may, by notification -
(a) alter the limits of a planning area so as to include therein or excluse therefrom such area as may be specified in the notification;
(b) amalgamate two or more planning areas so as to constitute one planning area;
(c) divide any planning area into two or more planning areas;
(d) declare that the whole or part of the area constituting the planning area shall cease to be a planning area or part thereof 
14  Director to prepare development plans  - Subject to the provisions of this Act and the rules made thereunder, the Director shall-
(a) prepare an existing land use map;
(b) prepare an interim development plan;
(c) prepare a development plan;
(d) prepare a sectoral plan;
(e) carry such surveys and inspections and obtain such pertinent reports from government departments, local authorities and public institutions as may be necessary for the preparation of the plans;
(f) perform such duties and functions as are supplemental, incidental, and consequential to any of the foregoing functions or as may be assigned by the State Government for the purpose of carrying out the provisions of this Act 
15  Existing land use maps  - (1 )The Director shall carryout the survey and prepare an existing land use map and, forthwith publish the same in such manner as may be prescribed together with public notice of the preparation of the map and of the place or places where the copies may be inspected, inviting objections and suggestions in writing from any person with respect thereto within thirty days from the date of publication of such notice 
(2) After the expiry of the period specified in the notice published under sub-section (1), the Director may, after allowing a reasonable opportunity of being heard to all such persons who have filed the objections or suggestions, make such modifications therein as may be considered desirable 
(3) As soon as may be after the map is adopted with or without modifications the Director shall publish a public notice of the adoption of the map and the place or places where the copies of the same may be inspected 
(4) A copy of the notice shall also be published in the Official Gazette and it shall be conclusive evidence of the fact that the map has been duly prepared and adopted 
16  Freezing of land use  - On the publication of the existing land use map under section 15-
(a) no person shall institute or change the use of any land or carry out any development of land for any purpose other than that indicated in the existing land use map without the permission in writing of the Director;
Provided that the Director shall not refuse permission if the change is for the purpose of agriculture;
(b) no local authority or any officer or other authority shall, not withstanding anything contained in any other law for the time being in force, grant permission for the change in use of land otherwise than as indicated in the existing land use map without the permission in writing of the Director;
[(c) no Registrar or the Sub-Registrar, appointed under the Indian Registration Act, 1908, shall, in any planning area constituted under section 13, register any deed or document of transfer of any sub-division of land by way of sale, gift, exchange, lease or mortgage with possession, unless the sub-division of land is duly approved by the Director, subject to such rules as may be framed in this behalf by the State Government:]
Provided that the Registrar or the Sub-Registrar may register any transfer,-
(i) where the land is owned by a person and the transfer is made without involving any further divisions;
(ii) where the partition/sub-division of land is made in a Joint Hindu Family;
(iii) where the lease is made in relation to a part or whole of a building;
(iv) where the mortgage is made for procuring the loans for construction or improvements over the land either from the Government or from any other financial institution constituted or established under any law for the time being in force or recognised by the State Government 
17  Interim development plans  - As soon as may be, after the declaration of a planning area, the Director shall, within such time as may be necessary, prepare, after consultation with local authorities concerned, if any, and submit to the State Government an interim development plan for the planning area or any of its parts and such other area or areas contiguous or adjacent to the planning areas as the State Government may direct to be included in the interim development plan 
(2) The interim development plan shall-
(a) indicate broadly the land use proposed in the planning area;
(b) allocate broadly areas or sector of land for-
(i) residential, industrial, commercial or agricultural purposes,
(ii) open spaces, parks and gardens, green belts, zoological gardens and play-grounds,
(iii) public institutions and offices,
(iv) such special purposes as the Director may deem fit;
(c) lay down the pattern of National and State Highways connecting the planning area with the rest of the region, ring roads, arterial roads and the major roads within the planning areas;
(d) provide for the location of airports, railway stations, bus termini and indicate the proposed extension and development of railways and canals;
(e) make proposals for general land scaping and preservation of natural areas;
(f) project the requirement of the planning area of such amenities and utilities as water, drainage, electricity and suggest their fulfilment;
(g) propose broad based regulations for sectoral development, by way of guide-lines, within each sector of the location, height, size of buildings and structures, open spaces, court-yards and the use to which such buildings and structures and land may be put;
(h) lay down the board-based traffic circulation patterns in a city;
(i) suggest architectural control features, elevation and frontage of buildings and structures;
(j) indicate measures for flood control, prevention of air and water pollution, disposal of garbage and general environmental control 
(3) Subject to provisions of the rules made under this Act for regulating the form and contents of the interim development plan any such plan shall include such maps and such descriptive matter as may be necessary to explain and illustrate the proposals in the interim development plan 
(4) As soon as may be, after the submission of the interim development plan, under sub-section (1) the State Government may either approve the interim development plan or may approve it with such modification as it may consider necessary 
(5) The State Government shall publish the interim development plan as approved under sub-section (4) in the Official Gazette  The interim development plan shall come into operation from the date of its publication in the Official Gazette and shall be binding on all local authorities functioning within the planning areas 
18  Development plan  - A development plan shall -
(a) indicate broadly the land use proposed in the planning areas;
(b) allocate broadly areas or sector of land for,-
(c) lay down the pattern of National and State Highways connecting the planning area with the rest of the region, ring roads, arterial roads, and the major roads within the planning area;
(d) provide for the location of airports, railway stations, bus termini and indicate the proposed extension and development of railways;
(g) propose broad-based regulations for sectoral development, by way of guide-line, within each sector of the location, height, size of buildings and structures, open spaces, court-yards and the use to which such buildings and structures and land may be put;
(h) lay down the broad-based traffic circulation patterns in a city;
19  Publication of draft development plan  - (1) The Director shall forthwith publish the draft development plan prepared under section 18 in such manner as may be prescribed together with a notice of the preparation of the draft development plan and the place or places where the copies may be inspected, inviting objections and suggestions in writing from any person with respect thereto, within thirty days from the date of publication of such notice Such notice shall specify in regard to the draff development plan the following particulars, namely:-
(i) the existing land use maps;
(ii) a narrative report, supported by maps and charts, explaining the provisions of the draft development plan;
(iii) the phasing of implementation of the draft development plan as suggested by the Director,
(iv) the provisions for enforcing the draft development plan and stating the manner in which permission to development may be obtained;
(v) an approximate estimate of the cost of land acquisition for public purposes and the cost of works involved in the implementation of the plan 
(2) The Director shall, not later than ninety days after the date of expiry of the notice period under sub-section (1), consider all the objections and suggestions as may be received within the period specified in the notice under sub-section (1)and shall, after giving reasonable opportunity to all persons affected thereby of being heard, make such modifications in the draft development plans as he may consider necessary, and submit, not later than six months after the publication of the draft development plan, the plan so modified, to the State Government for approval together with all connected documents, plans, maps and charts 
20  Sanction of development plans  - (1) As soon as may be after the submission of the development plan under section 19 the State Government may either approve the development plan or may approve it with such modifications as it may consider necessary or may return it to the Director to modify the same or to prepare a fresh plan in accordance with such directions as it may issue in this behalf 
(2) Where the State Government approves the development plan with modifications, the State Government shall, by a notice, published in the Official Gazette, invite objections and suggestions in respect of such modifications within a period of not less than thirty days from the date of publication of the notice in the Official Gazette 
(3) After considering objections and suggestions and after giving a hearing to the persons desirous of being heard the State Government may confirm the modification in the development plan 
(4) The State Government shall publish the development plan as approved, under the foregoing provisions in the Official Gazette and shall along with the plan publish a public notice, in such manner as may be prescribed, of the approval of the development plan and the place or places where the copies of the approved development plan may be inspected 
(5) The development plan shall come into operation from the date of publication thereof in the Official Gazette and as from such date shall be binding on all Development Authorities constituted under this Act and all local authorities functioning within the planning area 
(6) After the coming into operation of the development plan, the interim development plan shall stand modified or altered to the extent the proposals in the development plan are at variance with the interim development plan 
Sectoral Plan
21  Director to prepare sectoral plan  - The Director may, on his own motion, at any time after the publication of the development plan, or thereafter if so required by the State Government shall, within six months of such requisition, prepare a sectoral plan 
22  Contents of sectoral plan  - (1) The sectoral plan shall enlarge the details of land use as indicated in the development plan and shall -
(a) indicate the land liable to acquisition for public purpose or the purposes of the Union Government, the State Government, the Town and Country Development Authority, the Special Area Development Authority, the local authority or any other authority established by or under any enactment for the time being in force 
Provided that no land shall be so designated unless the acquisition proceedings are likely to be completed within ten years of the preparation of the plan;
(b) define in detail and provide for areas reserved for agriculture, public and semi-public open spaces, parks, playgrounds, gardens, recreational areas, green belts and natural reserves;
(c) allocate in detail areas or sectors for residential, commercial, industrial, agricultural and other purposes;
(d) define and provide for the complete road and street pattern for the present and in the future and indicate the traffic circulation;
(e) lay down in detail the projected road and street improvement;
(f) indicate and provide for areas reserved for public buildings, institutions and civic developments;
(g) assess, make projections for and provide for the future requirements of amenities, services and utilities such as municipal, transport, electricity, water and drainage;
(h) prescribe in detail the sectoral regulations for each sector, with a view to facilitating on individual layout and regulating the location, height, number of storeys and the size of buildings and other structures, the size of the court-yards, courts and other open spaces and the use of the buildings, structures and land;
(i) define areas which have been badly laid out or areas which have developed so as to form slums, and provide for their proper development and/or relocation;
(j) designate areas for future development and expansion;
(k) indicate the phasing of the programme of development 
(2) The sectoral plan may and if possible shall, indicate -
(a) control over architectural features; elevation and frontage of buildings and structures; and
(b) the details of development of specific areas for housing, shopping centres, industrial areas, educational and cultural institutions and civic centres 
23  Provisions of sections 19 and 20 to apply to sectoral plan  - The provisions of sections 19 and 20 shall apply for the preparation, publication, approval and operation of sectoral plan as they apply in respect of the development plan 
24  Review of development plan and sectoral plan  - The Director may on his own motion or if so required by the State Government shall, at any time after the sectoral plan has come into operation, undertake a review and evaluation of the development plan and sectoral plan 
(2) The foregoing provisions of sections 19, 20 and 23 shall, so far as may be apply to the modification under sub-section (1) as those provisions apply in relation to the preparation, publication and approval of a development plan or a sectoral plan 
Control of Development And Use of Land
25  Director to control land use  - The overall control of development and the use of land in the planning area shall, as from the date of publication in the Official Gazette of a notification by the State Government, vest in the Director 
26  Conformity with development plan  - (1) After coming into force of the development plan, the use and development of land shall conform to the provisions of the development plan:
Provided that the Director may, at his discretion, permit the continued use of land for the purpose for which it was being used at the time of the coming into Operation of the development plan 
Provided further that such permission shall not be granted for a period exceeding seven years from the date of coming into operation of the development plan 
27  Prohibition of development without permission  - After coming into operation of the development plan, no person shall change the use of any land or carry out any development of land without the permission in writing of the Director 
Provided that no such permission shall be necessary -
(a) for carrying out works for the maintenance, repair or alteration of any building which does not materially alter the external appearance of the building;
(b) for carrying out work for the improvement or maintenance of a highway, road or public street by the Union or State Government or an authority established under this Act or by a local authority having jurisdiction, provided that such maintenance or improvement does not change the road alignment contrary to the provisions of the development plan;
(c) for the purpose of inspecting, repairing or renewing any drain, sewers, mains, pipes, cables, telephone or other apparatus including the breaking open of any street or other land for that purpose;
(d) for the excavation or soil shaping in the interest of agriculture;
(e) for restoration of land to its normal use where land has been used temporarily for any other purposes 
(f) for use for any purpose incidental to the use of building for human habitation, or any other building or land attached to such buildings;
(g) for the construction of a road intended to give access to land solely for agricultural purposes
28  Development undertaken on behalf of Union or State Government  - (1) When the Union Government or the State Government intends to carry out development of any land for the purpose of its departments or offices or authorities, the officer-in-charge thereof shall inform in writing to the Director the intention of the Government to do so, giving full particulars thereof, accompanied by such documents and plans as may be prescribed at least thirty days before undertaking such development 
(2) Where the Director raises any objection to the proposed development on the ground that the development is not in conformity with the provisions of the development plan, the officer shall,-
(i) make necessary modification in the proposals for development to meet the objections raised by the Director, or
(ii) submit the proposal for development together with the objections raised by the Director to the State Government for decision:
Provided that where no modification is proposed by the Director within thirty days of the receipt of the proposed plan by the Government, the plan will be presumed to have been approved 
(3) The State Government, on receipt of the proposals for development together with the objections of the Director shall, approve the proposals with or without modifications or direct the officer to make such modifications in the proposals as it considers necessary in the circumstances 
(4) The decision of the State Government under sub-section (3) shall be final and binding 
29  Development by local authority or by any authority constituted under this Act  - Where a local authority or any authority specially constituted under this Act intends to carry out development on any land for the purpose of that authority, the procedure applicable to the Union or State Government, under section 28 shall, mutatis' mutandis, apply in respect of such authority 
30  Application for permission for development by others  - (1) Any person, not being the Union Government, State Government, a local authority or a special authority constituted under this Act intending to carry out any development on any land, shall make an application in writing to the Director for permission, in such form and containing such particulars and accompanied by such documents as may be prescribed 
(2) Such application shall also be accompanied by such fee as may be prescribed 
[30A  Exemption from development permission in rural areas falling within Planning or Special Area  - (1) Any person who owns land in rural areas, falling within Planning or Special Areas wherein neither Interim Development Plan nor Development Plan has been notified, shall be exempted from permission under this Act for the following development activities up to the limits as may be prescribed: -
(i) Residential activities such as farm-houses and residential houses up to three storeys, cattle shed, toilet, septic tank, kitchen, store, parking shed or garage and rain shelter;
(ii) Commercial activities such as basic commercial activities like shops of general merchandise, cobbler, barber, tailoring, fruit, vegetable, tea or sweet, eating places and dhabas, chemist and farm produce sale depot;
(iii) Service Industries such as cottage or house-hold, service industries like carpentry, knitting, weaving, blacksmith, goldsmith, atta-chakki with capacity up to five horse-power, water mill, agriculture equipments or machinery repair, electrical, electronic and house-hold appliances;
(iv) Public amenities such as public amenities like panchayat offices, schools, mahila mandals, yuvak mandals, community halls, post offices, dispensaries and clinics (including health, veterinary and Indian System of Medicines) information technology kiosks, patwar khanas, guard huts, anganwaries, electricity and telephone installations and connections, roads and paths, ropeways, water tanks, rain harvesting tanks, overhead or underground water tan 
Context 3: Do you know the difference between V T  and T V?
Like any exclusive club, heart disease has its own jargon, understandable only by other members of the club, particularly by cardiac care providers  For example, I remember lying in my CCU bed (that’s the Coronary Intensive Care Unit), trying to memorize the letters LAD (that’s the Left Anterior Descending, the large coronary artery whose 99% blockage had caused my MI (myocardial infarction – in my case, the so-called ‘widowmaker’ heart attack) 
To help others needing simultaneous translation of this new lingo in your research or in your own medical records, here’s a helpful list of some of the most common acronyms/terms you’ll likely find around the cardiac ward 
NOTE from CAROLYN: This entire patient-friendly, jargon-free glossary (all 8,000 words!) is also part of my book “A Woman’s Guide to Living with Heart Disease“ (Johns Hopkins University Press, November 2017) 
AA – Anti-arrhythmic: Drugs used to treat patients who have irregular heart rhythms 
Ablation – See Cardiac Ablation 
ACE Inhibitor – Angiotension Converting Enzyme inhibitor: A drug that lowers blood pressure by interfering with the breakdown of a protein-like substance involved in regulating blood pressure 
ACS – Acute Coronary Syndrome: An emergency condition brought on by sudden reduced blood flow to the heart  The first sign of acute coronary syndrome can be sudden stopping of your heart (cardiac arrest) 
AED – Automatic External Defibrillator: A portable defibrillator for use during a cardiac emergency; it can be used on patients experiencing sudden cardiac arrest by applying a brief electroshock to the heart through electrodes placed on the chest 
AF or Afib – Atrial Fibrillation: An irregular and often rapid heart rate that can cause poor blood flow to the body  Afib symptoms include heart palpitations, shortness of breath, weakness or fainting  Episodes of atrial fibrillation can come and go, or you may have chronic atrial fibrillation 
AFL – Atrial Flutter: A type of arrhythmia where the upper chambers of the heart (the atria) beat very fast, causing the walls of the lower chambers (the ventricles) to beat inefficiently as well 
A-HCM – Apical Hypertrophic Cardiomyopathy: Also called Yamaguchi Syndrome or Yamaguchi Hypertrophy, a non-obstructive form of cardiomyopathy (a disease of the heart muscle that leads to generalized deterioration of the muscle and its pumping ability) in which a portion of the heart muscle is hypertrophied (thickened) without any obvious cause although there may be a genetic link  It was first described in individuals of Japanese descent 
AI – Aortic Insufficiency: A heart valve disease in which the aortic valve does not close tightly, leading to the backward flow of blood from the aorta (the largest blood vessel) into the left ventricle (a chamber of the heart) 
AIVR – Accelerated Idioventricular Rhythm: Ventricular rhythm whose rate is greater than 49 beats/min but less than 100 beats/min, usually benign  (Ventricles are the two main chambers of the heart, left and right) 
Angina (stable) – A condition marked by distressing symptoms typically between neck and navel that come on with exertion and go away with rest, caused by an inadequate blood supply to the heart muscle typically because of narrowed coronary arteries feeding the heart muscle  Also known as Angina Pectoris  Unstable angina (UA) occurs when fatty deposits (plaques) in a blood vessel rupture or a blood clot forms, blocking or reducing flow through a narrowed artery, suddenly and severely decreasing blood flow to the heart muscle  Unstable angina is not relieved by rest; it’s dangerous and requires emergency medical attention 
Antiplatelet drugs – Medications that block the formation of blood clots by preventing the clumping of platelets (examples: Plavix, Effient, Brillinta, Ticlid, etc)  Heart patients, especially those with implanted stents after PCI, are often prescribed dual antiplatelet therapy (DAPT) which includes one of these prescribed meds along with daily low-dose aspirin 
Aorta – The main artery of the body, carrying blood from the left side of the heart to the arteries of all limbs and organs except the lungs 
Aortic Stenosis: A disease of the heart valves in which the opening of the aortic valve is narrowed  Also called AS 
Aortic valve – One of four valves in the heart, this valve allows blood from the left ventricle to be pumped up (ejected) into the aorta, but prevents blood from returning to the heart once it’s in the aorta 
AP – Apical Pulse: A central pulse located at the apex (pointy bottom) of the heart 
Apex – the lowest (pointy) tip of the heart that points downward at the base, forming what almost looks like a rounded point 
Apical Hypertrophic Cardiomyopathy (A-HCM): Also called Yamaguchi Syndrome or Yamaguchi Hypertrophy, a non-obstructive form of cardiomyopathy (a disease of the heart muscle that leads to generalized deterioration of the muscle and its pumping ability) in which a portion of the heart muscle is hypertrophied (thickened) without any obvious cause  There may be a genetic link  It was first described in people of Japanese descent 
Arrhythmia – A condition in which the heart beats with an irregular or abnormal rhythm 
AS – Aortic Stenosis: A disease of the heart valves in which the opening of the aortic valve is narrowed 
ASD – Atrial Septal Defect: See Septal Defect 
Atrial Flutter – A heart rhythm problem (arrhythmia) originating from the right atrium, most often involving a large circuit that travels around the area of the tricuspid valve (between the right atrium and the right ventricle (this is called typical atrial flutter)  Less commonly, atrial flutter can also result from circuits in other areas of the right or left atrium that cause the heart to beat fast (called atypical atrial flutter) 
Atrial Septum, the membrane that separates the left and the right upper chambers of the heart (the atria) 
Atrium – A chamber of the heart that receives blood from the veins and forces it into a ventricle or ventricles  Plural: atria 
AV – Atrioventricular: A group of cells in the heart located between the upper two chambers (the atria) and the lower two chambers (the ventricles) that regulate the electrical current that passes through it to the ventricles  Also Atrioventricular Block: An interruption or disturbance of the electrical signal between the heart’s upper two chambers (the atria) and lower two chambers (the ventricles)  Also Aortic valve: The valve that regulates blood flow from the heart into the aorta 
AVNRT – Atrioventricular Nodal Re-entry Tachycardia: a heart rhythm problem that happens when there’s an electrical short circuit in the centre of the heart, one of the most common types of SVT, most often seen in people in their twenties and thirties, and more common in women than in men 
BAV – Bicuspid Aortic Valve: The most common malformation of the heart valves in which the aortic valve has only two cusps instead of three 
BB – Beta Blocker: A blood pressure-lowering drug that limits the activity of epinephrine, a hormone that increases blood pressure 
BBB – Bundle Branch Block: – A condition in which parts of the heart’s conduction system are defective and unable to normally conduct the electrical signal, causing an irregular heart rhythm (arrhythmia) 
BMI – Body mass index: A number that doctors use to determine if you’re overweight  BMI is calculated using a formula of weight in kilograms divided by height in meters squared (BMI =W [kg]/H [m2])  Better yet, just click here to figure out your own BMI 
BNP blood test – BNP (B-type Natriuretic Peptide) is a substance secreted from the ventricles or lower chambers of the heart in response to changes in pressure that happen when heart failure develops and/or worsens  The level of BNP in the blood increases when heart failure symptoms worsen, and decreases when the heart failure condition is stable 
BP – Blood Pressure: The force or pressure exerted by the heart in pumping blood; the pressure of blood in the arteries  See also hypertension 
BrS – Brugada Syndrome: Brugada syndrome is a genetic heart disease that is characterized by distinctively abnormal electrocardiogram (EKG/ECG) findings and an increased risk of sudden cardiac arrest 
CAA – Coronary artery anomaly: A congenital defect in one or more of the coronary arteries of the heart 
CABG – Coronary Artery Bypass Graft: A surgical procedure that reroutes blood flow around a diseased or blocked blood vessel that supplies blood to the heart by grafting either a piece of vein harvested from the leg or the artery from under the breastbone 
CA – Coronary Artery: The arteries arising from the aorta that arch down over the top of the heart and divide into branches  They provide blood to the heart muscle 
CAD – Coronary Artery Disease: A narrowing of the arteries that supply blood to the heart  The condition results from a plaque rupture/blood clot or spasm and greatly increases the risk of a heart attack 
Cardiac Ablation – A procedure performed by an Electrophysiologist (EP) – a cardiologist with specialized training in treating heart rhythm problems – that typically uses catheters — long, flexible tubes inserted through a vein in the groin and threaded to the heart — to correct structural problems in the heart that cause an arrhythmia  Cardiac ablation works by scarring or destroying the tissue in your heart that triggers an abnormal heart rhythm 
Cardiac Arrest – Also known as Sudden Cardiac Arrest: The stopping of the heartbeat, usually because of interference with the electrical signal that regulates each heartbeat (often associated with coronary heart disease)  Can lead to Sudden Cardiac Death 
Cardiac Catheterization – An invasive procedure in which a catheter is inserted through a blood vessel in the wrist/arm or groin with x-ray guidance  This procedure can help provide information about blood supply through the coronary arteries, blood pressure, blood flow throughout the chambers of the heart, collection of blood samples, and x-rays of the heart’s ventricles or arteries  It’s typically performed in the cath lab during angiography 
Cardiac Resynchronization Therapy (CRT) also called bi-ventricular pacemaker: an electronic pacing device that’s surgically implanted in the chest to treat the delay in heart ventricle contractions that occur in some people with heart failure 
Cardiac Tamponade – Pressure on the heart that occurs when blood or fluid builds up in the space between the heart muscle (myocardium) and the outer covering sac of the heart (pericardium)  Also called Tamponade 
Cardiomyopathy – a chronic disease of the heart muscle (myocardium), in which the muscle is abnormally enlarged, thickened, and/or stiffened 
Cardioversion – A medical procedure in which an abnormally fast heart rate (tachycardia) or cardiac arrhythmia like atrial fibrillation is converted to a normal rhythm using electricity or drugs  Synchronized electrical cardioversion uses a therapeutic dose of electric current to the heart at a specific moment in the cardiac cycle  Chemical cardioversion uses medications to convert to normal rhythm 
Cath lab – the room in the hospital/medical clinic where cardiac catheterization procedures take place (for example, when a stent is implanted into a blocked coronary artery) 
CCB – Calcium Channel Blocker: A drug that lowers blood pressure by regulating calcium-related electrical activity in the heart 
CDS – Cardiac Depression Scale: A scale that can help assess the effects of depression occurring as a result of a heart disease diagnosis 
CHF – Heart Failure (also called Congestive Heart Failure): A condition in which the heart cannot pump all the blood returning to it, leading to a backup of blood in the vessels and an accumulation of fluid in the body’s tissues, including the lungs 
CM – Cardiomyopathy: A disease of the heart muscle that leads to generalized deterioration of the muscle and its pumping ability 
CO – Cardiac Output: The amount of blood the heart pumps through the circulatory system in one minute 
Collateral arteries – These extra coronary blood vessels are sometimes able to bypass a blockage in an artery in order to supply enough oxygenated blood to enable the heart muscle to survive when in danger of being damaged because of blockage(s) 
Collateral arteries – Blood vessels that provide an alternative arterial supply of blood to an area of the heart that’s in danger of being deprived of oxygenated blood because of one or more blocked arteries 
Congenital heart defect – one of about 35 different types of heart conditions that happen when the heart or the blood vessels near the heart don’t develop normally before a baby is born (in about 1% of live births)  Because of medical advances that treat babies born with heart defects, there are now for the first time more adults with congenital heart disease than children 
Congestive heart failure (CHF) – a chronic progressive condition that affects the pumping power of your heart muscle  Often referred to simply as heart failure, CHF specifically refers to the stage in which fluid builds up around the heart and causes it to pump inefficiently 
COPD – Chronic Obstructive Pulmonary Disease: A lung disease defined by persistently poor airflow as a result of breakdown of lung tissue (known as emphysema) and dysfunction of the small airways Often associated with smoking, it typically worsens over time 
Coronary Microvascular Disease – A heart condition that causes impaired blood flow to the heart muscle through the small vessels of the heart  Also called Microvascular Disease or Small Vessel Disease 
Coronary Reactivity Test – An angiography procedure specifically designed to examine the blood vessels in the heart and how they respond to different medications  Physicians use these images to distinguish different types of blood vessel reactivity dysfunction (such as Coronary Microvascular Disease) 
Costochondritis– the cause of severe chest pain, but NOT heart-related; it’s an inflammation of the cartilage that connects a rib to the breastbone 
Coumadin – A drug taken to prevent the blood from clotting and to treat blood clots  Coumadin is believed to reduce the risk of blood clots causing strokes or heart attacks  See also Warfarin 
Cox Maze procedure – A complex “cut-and-sew” surgical procedure done to treat atrial fibrillation through a complicated set of incisions made in a maze-like pattern on the left and right atria (the upper chambers of the heart) to permanently interrupt the abnormal electrical signals that are causing the irregular heartbeats of Afib  See also: Mini-Maze 
CP – Chest Pain (may also be felt as squeezing, pressure, fullness, pressure, heaviness, burning or tightness in the chest) 
CPR – Cardiopulmonary Resuscitation: An emergency procedure in which the heart and lungs are made to work by manually compressing the chest overlying the heart and forcing air into the lungs, used to maintain circulation when the heart stops pumping during Cardiac Arrest  Current guidelines suggest hands-only CPR  See also AED 
CQ10 – Co-enzyme Q10: A dietary supplement sometimes recommended for heart patients taking statin drugs 
CRP – C-reactive protein: A byproduct of inflammation, produce by the liver, found in the blood in some cases of acute inflammation 
CRT – Cardiac Resynchronization Therapy also called bi-ventricular pacemaker: an electronic pacing device that’s surgically implanted in the chest to treat the delay in heart ventricle contractions that occur in some people with heart failure 
CT – Computed tomography (CT or CAT scan): An x-ray technique that uses a computer to create cross-sectional images of the body 
CTA – Computerized Tomographic Angiogram: An imaging test to look at the arteries that supply the heart muscle with blood  Unlike a traditional coronary angiogram, CT angiograms don’t use a catheter threaded through your blood vessels to your heart but instead rely on a powerful X-ray machine to produce images of your heart and heart vessels 
CV – Coronary Vein: One of the veins of the heart that drain blood from the heart’s muscular tissue and empty into the right atrium 
CV – Cardiovascular: Pertaining to the heart and blood vessels that make up the circulatory system 
DBP – Diastolic blood pressure: The lowest blood pressure measured in the arteries  It occurs when the heart muscle is relaxed between beats 
DCM – Dilated Cardiomyopathy: A disease of the heart muscle, primarily affecting the heart’s main pumping chamber (left ventricle)  The left ventricle becomes enlarged (dilated) and can’t pump blood to your body with as much force as a healthy heart can 
DDI – Drug-drug interaction: A situation in which a medication affects the activity of another medication when both are administered together 
DIL – Diltiazem: A calcium channel blocker drug that acts as a vasodilator; used in the treatment of angina pectoris, hypertension, and supraventricular tachycardia 
Diuretic – A class of drugs used to lower blood pressure  Also known as “water pills” 
Dobutamine stress echocardiography: This is a form of a stress echocardiogram diagnostic test  But instead of exercising on a treadmill or exercise bike to stress the heart, the stress is obtained by giving a drug that stimulates the heart and makes it “think” it’s exercising  The test is used to evaluate your heart and valve function if you are unable to exercise  It is also used to determine how well your heart tolerates activity, and your likelihood of having coronary artery disease (blocked arteries), and it can evaluate the effectiveness of your cardiac treatment plan  See also TTE and Stress Echocardiogram 
Dressler’s syndrome – Happens to a small number of people three to four weeks after a heart attack  The heart muscle that died during the attack sets the immune system in motion, calling on lymphocytes, one of the white blood cells, to infiltrate the coverings of the heart (pericardium) and the lungs (pleura)  It also starts generating antibodies, which attack those two coverings  Chest pain (CP) is the predominant symptom; treated with anti-inflammatory drugs 
Dual Antiplatelet Therapy – Medications that block the formation of blood clots by preventing the clumping of platelets (examples Plavix, Effient, Brillinta, Ticlid, etc ) are often prescribed along with aspirin as part of what’s known as dual antiplatelet therapy, especially to patients who have undergone PCI and stent implantation 
DVT – Deep Vein Thrombosis: A blood clot in a deep vein in the calf 
ECG / EKG – Electrocardiogram: A test in which several electronic sensors are placed on the body to monitor electrical activity associated with the heartbeat 
Ectopic beats – small changes in an otherwise normal heartbeat that lead to extra or skipped heartbeats, often occurring without a clear cause, most often harmless 
EF – Ejection Fraction: A measurement of blood that is pumped out of a filled ventricle  The normal rate is 50-60% 
EKG/ECG – Electrocardiogram: A test in which several electronic sensors are placed on the body to monitor electrical activity associated with the heartbeat 
Endothelium: A single-cell layer of flat endothelial cells lining the closed internal spaces of the body such as the inside of blood vessels  Endothelial dysfunction affects the ability of these cells to help dilate blood vessels, control inflammation or prevent blood clots  The endothelium is associated with most forms of cardiovascular disease, such as hypertension, coronary artery disease, chronic heart failure, peripheral vascular disease, diabetes, chronic kidney failure, and severe viral infections 
Enhanced External Counterpulsation – EECP is an FDA-approved non-invasive, non-drug treatment for angina  It works by promoting the development of collateral coronary arteries  The therapy is widely used in prominent heart clinics such as the Cleveland Clinic, Mayo Clinic and Johns Hopkins – especially for patients who are not good candidates for invasive procedures such as bypass surgery, angioplasty or stenting 
EP – Electrophysiologist: A cardiologist who has additional training in diagnosing/treating heart rhythm disorders 
EPS – Electrophysiology Study: A test that uses cardiac catheterization to study patients who have arrhythmias (abnormal hear rhythm)  An electrical current stimulates the heart in an effort to provoke an arrhythmia, which is immediately treated with medications  EPS is used primarily to identify the origin of the arrhythmia and to test the effectiveness of medications used to treat abnormal heart rhythms 
EVH – Endoscopic Vessel Harvesting: To create the bypass graft during CABG open heart surgery, a surgeon will remove or “harvest” healthy blood vessels from another part of the body, often from the patient’s leg or arm  This vessel becomes a graft, with one end attaching to a blood source above and the other end below the blocked area  See CABG 
Exercise stress test – An exercise test (walking/running on a treadmill or pedalling a stationary bike) to make your heart work harder and beat faster  An EKG is recorded while you exercise to monitor any abnormal changes in your heart under stress, with or without the aid of drugs to enhance this assessment  See also: MIBI, Echocardiogram, Nuclear Stress Test 
Familial hypercholesterolemia (FH) – A genetic predisposition to dangerously high cholesterol levels  FH is an inherited disorder that can lead to aggressive and premature cardiovascular disease, including problems like heart attacks, strokes, or narrowing of the heart valves 
Femoral Artery: a major artery in your groin/upper thigh area, through which a thin catheter is inserted, eventually making its way into the heart during angioplasty to implant a stent; currently the most widely used angioplasty approach in the United States, but many other countries now prefer the Radial Artery access in the wrist 
FFR – Fractional Flow Reserve: A test used during coronary catheterization (angiogram) to measure pressure differences across a coronary artery stenosis (narrowing or blockage) defined as as the pressure behind a blockage relative to the pressure before the blockage 
HC – High Cholesterol: When fatty deposits build up in your coronary arteries 
HCTZ – Hydrochlorothiazide: A drug used to lower blood pressure; it acts by inhibiting the kidneys’ ability to retain water  Used to be called “water pills” 
Heart Failure – a chronic progressive condition that affects the pumping power of your heart muscle  Sometimes called Congestive Heart Failure (CHF) 
Holter Monitor – A portable monitoring device that patients wear for recording heartbeats over a period of 24 hours or more 
HTN – Hypertension: High blood pressure, the force of blood pushing against the walls of arteries as it flows through them 
Hypokinesia – Decreased heart wall motion during each heartbeat, associated with cardiomyopathy, heart failure, or heart attack  Hypokinesia can involve small areas of the heart (segmental) or entire sections of heart muscle (global)  Also called hypokinesis 
ICD – Implantable Cardioverter Defibrillator: A surgically implanted electronic device to treat life-threatening heartbeat irregularities 
IHD – Ischemic Heart Disease: heart problems caused by narrowing of the coronary arteries, causing a decreased blood supply to the heart muscle  Also called coronary artery disease and coronary heart disease 
INR – International Normalized Ratio: A laboratory test measure of blood coagulation, often used as a standard for monitoring the effects of the anti-coagulant drug, warfarin (coumadin) 
IST – Inappropriate sinus tachycardia: A heart condition seen most often in young women, in which a person’s resting heart rate is abnormally high (greater than 100 bpm), their heart rate increases rapidly with minimal exertion, and this rapid heart rate is accompanied by symptoms of palpitations, fatigue, and/or exercise intolerance 
Interventional cardiologist – A cardiologist who is trained to perform invasive heart procedures like angiography, angioplasty, percutaneous coronary intervention (PCI), implanting stents, etc 
IVS – Interventricular Septum: The stout wall that separates the lower chambers (the ventricles) of the heart from one another 
IVUS – Intravascular Ultrasound: A form of echocardiography performed during cardiac catheterization in which a transducer (a device that can act as a transmitter (sender) and receiver of ultrasound information) is threaded into the heart blood vessels via a catheter; it’s used to provide detailed information about the blockage inside the blood vessels 
LAD – Left Anterior Descending coronary artery: One of the heart’s coronary artery branches from the left main coronary artery which supplies blood to the left ventricle 
LAFB – Left Anterior Fascicular Block: A cardiac condition,distinguished from Left Bundle Branch Block because only the anterior half of the left bundle branch is defective and more common than left posterior fascicular block 
LAHB – Left Anterior Hemiblock: The Left Bundle Branch divides into two major branches – the anterior and the posterior fascicles  Occasionally, a block can occur in one of these fascicles 
Left Circumflex Artery – The artery carries oxygenated blood from the heart to the body; it’s a branch of the Left Main Coronary Artery after the latter runs its course in between the aorta and the Main Pulmonary Artery 
Left Main Coronary Artery – The artery that branches from the aorta to supply oxygenated blood to the heart via the Left Anterior Descending Artery (LAD) and the Left Circumflex Artery 
Lipids – fat-like substances found in your blood and body tissues; a lipid panel is a blood test that measures the level of specific lipids in blood to help assess your risk of cardiovascular disease, measuring four types of lipids: total cholesterol, HDL cholesterol, LDL cholesterol, and triglycerides 
Lipoprotein-a or Lp(a) – molecules made of proteins and fat, carrying cholesterol and similar substances through the blood  A high level of Lp(a) is considered a risk factor for heart disease; detectable via a blood test 
Long QT syndrome (LQTS): A heart rhythm disorder that can potentially cause fast, chaotic heartbeats that may trigger a sudden fainting spell or seizure  In some cases, the heart may beat erratically for so long that it can cause sudden death 
LV – Left Ventricle – One of four chambers (two atria and two ventricles) in the human heart, it receives oxygenated blood from the left atrium via the mitral valve, and pumps it into the aorta via the aortic valve 
LVAD – Left ventricular assist device: A mechanical device that can be placed outside the body or implanted inside the body  An LVAD does not replace the heart – it “assists” or “helps” it pump oxygen-rich blood from the left ventricle to the rest of the body, usually as a bridge to heart transplant 
LVH – Left Ventricular Hypertrophy: A thickening of the myocardium (muscle) of the Left Ventricle (LV) of the heart  
Lumen – The hollow area within a tube, such as a blood vessel 
Main Pulmonary Artery – Carries oxygen-depleted blood from the heart to the lungs 
MIBI – Nuclear Stress Test/Cardiac Perfusion Scan/Sestamibi: tests that are used to assess the blood flow to the heart muscle (myocardium) when it is stressed by exercise or medication, and to find out what areas of the myocardium have decreased blood flow due to coronary artery disease  This is done by injecting a tiny amount of radionuclide like thallium or technetium (chemicals which release a type of radioactivity called gamma rays) into a vein in the arm or hand 
Microvascular disease – a heart condition that causes impaired blood flow to the heart muscle through the small blood vessels of the heart  Symptoms mimic those of a heart attack  Also called Coronary Microvascular Disease or Small Vessel Disease  I live with this diagnosis and have written more about it here, here and here 
Mini-Maze – a surgical procedure to treat atrial fibrillation, less invasive than what’s called the Cox Maze III procedure (a “cut-and-sew” procedure), and performed on a beating heart without opening the chest 
Mitral Valve: One of four valves in the heart, the structure that controls blood flow between the heart’s left atrium (upper chamber) and left ventricle (lower chamber)  The mitral valve has two flaps (cusps)  See also MV and/or Valves 
Mitral valve prolapse: a condition in which the two valve flaps of the mitral valve don’t close smoothly or evenly, but instead bulge (prolapse) upward into the left atrium; also known as click-murmur syndrome, Barlow’s syndrome or floppy valve syndrome 
MR – Mitral regurgitation: (also mitral insufficiency or mitral incompetence) a heart condition in which the mitral valve does not close properly when the heart pumps out blood  It’s the abnormal leaking of blood from the left ventricle, through the mitral valve and into the left atrium when the left ventricle contracts 
MRI – Magnetic Resonance Imaging: A technique that produces images of the heart and other body structures by measuring the response of certain elements (such as hydrogen) in the body to a magnetic field  An MRI can produce detailed pictures of the heart and its various structures without the need to inject a dye 
MS – Mitral Stenosis: A narrowing of the mitral valve, which controls blood flow from the heart’s upper left chamber (the left atrium) to its lower left chamber (the left ventricle)  May result from an inherited (congenital) problem or from rheumatic fever 
MUGA – Multiple-Gated Acquisition Scanning: A non-invasive nuclear test that uses a radioactive isotope called technetium to evaluate the functioning of the heart’s ventricles 
Murmur – Noises superimposed on normal heart sounds  They are caused by congenital defects or damaged heart valves that do not close properly and allow blood to leak back into the originating chamber 
MV – Mitral Valve: The structure that controls blood flow between the heart’s left atrium (upper chamber) and left ventricle (lower chamber) 
Myocardial Infarction (MI, heart attack) – The damage or death of an area of the heart muscle (myocardium) resulting from a blocked blood supply to the area  The affected tissue dies, injuring the heart



ground_truth: The Director of Town and Country Planning is responsible for carrying out the functions assigned under the act.

prompt_front: Now, answer the following question based on the text below, only give me the answer and do not output any other words.

Question: What is the effect of the proximity of superconductivity on the Kondo effect?

Read the following text and answer briefly.

Context 2: \section{Introduction}
\label{sec:Intro}

The exchange interactions control the magnetic order and properties of a vast number of materials
\cite{White2006Dec}
and lead to many fascinating phenomena, such as various types of the Kondo effect 
\cite{Kondo,NozieresBlandin,Pustilnik_Glazman} 
Double quantum dots (DQDs), and in general multi-impurity systems, constitute
a convenient and controllable playground,
where nearly as much different exchange mechanisms compete with each other to
shape the ground state of the system 
\emph{Local exchange} between the spin of a quantum dot (QD)
and the spin of conduction band electrons gives rise to the
Kondo effect \cite{Kondo,Hewson_book}  
\emph{Direct exchange} arriving with an additional side-coupled QD may destroy it or lead to the 
two-stage Kondo screening \cite{Pustilnik_Glazman,Cornaglia,Granger,ZitkoBonca,ZitkoPRB2010,Ferreira} 
In a geometry where the two QDs contact the same lead, conduction band electrons 
mediate the \emph{RKKY exchange} \cite{RK,K,Y}  The RKKY interaction competes
with the Kondo effect and leads to the quantum phase transition of a still debated nature
\cite{Doniach,Jones,Affleck,Bork,Neel,KondoRKKYexp,Hans,Hans2,Fabian} 
Moreover, in DQDs coupled in series also \emph{superexchange} can alter the Kondo physics significantly
\cite{Zitko_2QDEx,Sela} 

Recently, hybrid quantum devices, in which the interplay between various magnetic correlations
with superconductivity (SC) plays an important role, have become an important direction of research
\cite{hybridQDs,SCspintronics}  In particular, chains of magnetic atoms on SC surface have proven 
to contain self-organized Majorana quasi-particles and exotic spin textures
\cite{Braunecker,Klinovaja,Vazifeh,Yazdani},
while hybrid DQD structures have been used to split the Cooper pairs coherently into two entangled 
electrons propagating to separated normal leads \cite{CPS1,CPS2,CPS4,CPS5,CPS9} 
The latter is possible due to non-local (\emph{crossed}) Andreev reflections (CARs),
in which each electron of a Cooper pair tunnels into different QD, and
subsequently to attached lead  Such processes give rise to an exchange mechanism \cite{Yao},
that we henceforth refer to as \emph{the CAR exchange}, which can greatly modify
the low-temperature transport behavior of correlated hybrid nanostructures 

The CAR exchange may be seen as RKKY-like interaction between
two nearby impurities on SC surface \cite{Yao} 
The effect can be understood as a consequence
of spin-dependent hybridization of the Yu-Shiba-Rusinov (YSR)
states \cite{Yu,Shiba,Rusinov} in SC contact,
caused both by the overlap of their wave functions
and their coupling to Cooper-pair condensate 
This process is the most effective when the YSR states 
are close to the middle of the SC gap, {\it e g } in the YSR-screened phase \cite{YSRscreening} 
The mechanism presented here is essentially the same,
yet in the considered regime can be understood
perturbatively without referring to YSR states,
as a consequence of the non-local pairing induced by SC electrode  
In particular, the presence of YSR bound states close to the Fermi level 
is not necessary for significant consequences for the Kondo physics, 
as long as some inter-dot pairing is present  


The proximity of SC induces pairing in QDs \cite{RozhkovArovas,Buitelaar} 
and tends to suppress the Kondo effect if the superconducting energy gap $2\Delta$ 
becomes larger than the relevant Kondo temperature $T_K$ 
\cite{Buitelaar2002Dec,adatomsSC,Kondo_vs_SC1,Kondo_vs_SC2,Zitko_Kondo-Andreev,Zitko_S-QD-N,IW_Sau,YSRscreening} 
Moreover, the strength of SC pairing can greatly affect the Kondo physics in the sub-gap transport regime:
For QDs attached to SC and normal contacts, it can enhance the Kondo effect
\cite{DomanskiIW,KWIW,part1}, while
for DQD-based Cooper pair splitters, it tends to suppress both the $\mathrm{SU}(2)$ and $\mathrm{SU}(4)$ Kondo effects \cite{IW_Kacper} 
Our main result is that the non-local pairing induced by superconducting 
proximity effect, which gives rise to CAR exchange, can be the sole cause of the Kondo screening 
Moreover, relatively small values of coupling to SC, $\GS{}\ll U$, are sufficient for the effect to occur 
This is in contrast to the DQD system considered in Ref ~\cite{part1},
where only one of the quantum dots is proximized, such that 
CAR exchange cannot arise,
and the Kondo physics becomes qualitatively
affected only for $\GS{}\sim U/2$ %


\begin{figure}[bt]
\centering
\includegraphics[width=1\linewidth]{Fig1 png}
\caption{
		 (a) Schematic of the considered system  Left/right (L/R) lead
		 is coupled to the first quantum dot (QD1), while superconductor
		 is attached to both QD1 and QD2 
		 (b)-(d) illustrate an example of direct spin exchange:
		 spin-up electron from the initial state (b) hops to the other QD (c) and spin-down electron 
		 hops back (d)  Note, that the final state is in fact the same singlet state, 
		 only with opposite sign 
		 (e)-(g) show an example of process contributing to crossed Andreev reflection (CAR) exchange 
		 A Cooper pair from SC approaches DQD (e) and two singlets of the same charge 
		 are formed (f), before the Cooper pair is re-emitted (g) 
		 (h)-(j) present an example of RKKY process: an electron scattered off
		 one QD (h) mediates the spin exchange towards the other (i), before it is finally scattered
		 off there, too (j) 
		 }
\label{fig:system}
\end{figure}


In this paper we discuss the CAR-induced Kondo screening in a setup comprising T-shaped DQD
with normal and superconducting contacts, see \fig{system}(a) 
We note that despite quite generic character of CAR exchange,
and its presence in systems containing at least two localized electrons
coupled close to each other to the same SC bath,
to best of our knowledge CAR-induced screening
has hardly been identified in previous studies
\cite{CPS1,CPS2,CPS4,CPS5,CPS9,IW_Kacper,IW_Sau,Zitko_Josephson,Zitko_S2QD,Martinek2017} 
In the system proposed here [\fig{system}(a)], its presence is evident 
Moreover, CAR exchange magnitude can be directly related to the relevant energy scales, such as the Kondo 
temperature, which provides a fingerprint for quantitative experimental verification of our predictions  

The paper is organized as follows  In \Sec{model} we describe the considered system 
and present the model we use to study it  In \Sec{scales} the relevant energy scales are estimated
to make the discussion of main results concerning CAR-induced Kondo effect in \Sec{main} more clear  
Finally, the influence of effects neglected in \Sec{main} are presented in the following sections,
including CAR exchange interplay with RKKY interaction (\Sec{RKKY}), particle-hole asymmetry (\Sec{asym}),
couplings asymmetry (\Sec{x}) and reduced efficiency of CAR coupling (\Sec{coef})  In summary,
the effects discussed in \Sec{main} remain qualitatively valid in all these cases 
The paper is concluded in \Sec{conclusions} 


\section{Model}
\label{sec:model}

The schematic of the considered system is depicted in \fig{system}(a) 
It contains two QDs attached to a common SC lead 
Only one of them (QD1) is directly attached to the left (L) and right (R) normal leads,
while the other dot (QD2) remains coupled only through QD1 
The SC is modeled by the BCS Hamiltonian, 
$H_{\mathrm{S}}=\sum_{\mathbf{k}\sigma}\xi_{\mathbf{k}}a_{\mathbf{k}\sigma}^{\dag}a_{\mathbf{k}\sigma}-\Delta\sum_{\mathbf{k}}(a^\dag_{\mathbf{k}\uparrow}a_{-\mathbf{k}\downarrow}^{\dag}+a_{-\mathbf{k}\downarrow}a_{\mathbf{k}\uparrow})$,
with energy dispersion $\xi_{\mathbf{k}}$, energy gap $2\Delta>0$ and $a_{\mathbf{k}\sigma}$ annihilation operator 
of electron possessing spin $\sigma$ and momentum $\mathbf{k}$  The coupling between
SC and QDs is described by the hopping Hamiltonian 
$H_{\mathrm{TS}}=\sum_{i\mathbf{k}\sigma}v_{\mathrm{S}i}(d^\dagger_{i\sigma}a^{}_{\mathbf{k}\sigma}+h c )$,
with $d^\dagger_{i\sigma}$ creating a spin-$\sigma$ electron at QD$i$  The matrix element 
$v_{\mathrm{S}i}$ and the normalized density of states of SC in normal state, $\rho_{\rm S}$, 
contribute to the coupling of QD$i$ to SC electrode as $\GS{i} = \pi \rho_{\rm S} |v_{{\rm S}i}|^2$  
We focus on the sub-gap regime, therefore, we integrate out SC degrees of freedom lying outside the energy gap \cite{RozhkovArovas} 
This gives rise to the following effective Hamiltonian,
$H_{\mathrm{eff}}=H_{\mathrm{SDQD}}+H_{\rm L}+H_{\rm R}+H_{\rm T}$, 
where 
\begin{eqnarray}
H_{\rm SDQD} 	& = & 
				\sum_{i\sigma} \varepsilon_{i} n_{i\sigma} 
				+\sum_{i} U n_{i\uparrow} n_{i\downarrow} 
				+U' (n_1-1)(n_2-1) 
				\nonumber\\
				&+&\sum_\sigma t(d^\dagger_{1\sigma}d^{}_{2\sigma} + h c ) 
				+J \vec{S}_1\vec{S}_2
				\nonumber\\
				&+&\sum_{i} \!\!\left[ \Gamma_{{\rm S}i} (d^\dagger_{i\uparrow} d^\dagger_{i\downarrow} \!+\! h c )
				+\Gamma_{\rm SX} (d^\dagger_{i\uparrow} d^\dagger_{\bar{i}\downarrow} \!+\! h c ) \right]
	\label{H_DQD} 
\end{eqnarray}
is the Hamiltonian of the SC-proximized DQD
\cite{IW_Kacper,Walldorf2018Feb}, with QD$i$ energy level $\varepsilon_i$,
inter-site (intra-site) Coulomb interactions $U'$ ($U$),
inter-dot hopping $t$, and CAR coupling $\GS{\rm X}$ 
$n_{i\sigma}=d^\dagger_{i\sigma}d^{}_{i\sigma}$ denotes the electron number operator 
at QD$i$, $n_i=n_\uparrow+n_\downarrow$, and $\bar{i}\equiv 3-i$  
Our model is strictly valid in the regime where $\Delta$ is the largest 
energy scale  Nevertheless, all discussed phenomena are
present in a full model for energies smaller than SC gap 
Moreover, by eliminating other consequences of the presence of SC lead,
our model pinpoints the fact that the non-local pairing is 
sufficient for the occurrence of the CAR exchange 
The presence of out-gap states shall result mainly in additional broadening of DQD energy levels,
changing the relevant Kondo temperatures 
We note that the procedure of integrating out out-gap states neglects the 
RKKY interaction mediated by SC lead and other possible indirect exchange mechanisms%
 \footnote{
 Note, that by RKKY interaction we mean only such an effective exchange, 
 which arises due to multiple scattering of a single electron or hole, see \fig{system}(h)-(j) 
 Other mechanisms leading to the total indirect exchange are considered separately 
 In particular, in the large gap limit, exchange described in Ref ~\cite{Yao} is in fact reduced to
 the CAR exchange, and additional antiferromagnetic contribution would arise for finite gap 
 }  
To compensate for this,
we explicitly include the Heisenberg term $ J \vec{S}_1\vec{S}_2$ in
$H_{\rm SDQD}$, with $\vec{S}_i$ denoting the spin operator of QD$i$
and a Heisenberg coupling $J$ substituting the genuine RKKY exchange 

The normal leads are treated as reservoirs of noninteracting electrons,
$H_{r}=\sum_{\mathbf{k}\sigma}\varepsilon_{r\mathbf{k}}c^\dagger_{r\mathbf{k}\sigma}c^{}_{r\mathbf{k}\sigma}$,
where $c^{}_{r\mathbf{k}\sigma}$ annihilates an electron of spin 
$\sigma$ and momentum $\mathbf{k}$ in lead $r$ ($r={\rm L,R}$) with the corresponding energy $\varepsilon_{r\mathbf{k}\sigma}$ 
The tunneling Hamiltonian reads,
$H_{\rm T} = \sum_{r\mathbf{k}\sigma} v_{r} (d^\dagger_{1\sigma}c^{}_{r\mathbf{k}\sigma} + h c )$,
giving rise to coupling between lead $r$ and QD$i$ of strength $\Gamma_r = \pi \rho_r |v_r|^2$,
with $\rho_r$ the normalized density of states of lead $r$ and $v_r$ the 
local hopping matrix element, assumed momentum-independent 
We consider a wide-band limit, assuming constant $\Gamma_r=\Gamma/2$
within the cutoff $\pm D = \pm 2U$ around the Fermi level  

For thorough analysis of the CAR exchange mechanism and its consequences
for transport, we determine the linear conductance between the two normal leads from
\begin{equation}
G = \frac{2e^2}{h} \pi \Gamma \int \left[ -\frac{\partial f_T}{\partial\omega} \right] \mathcal{A}(\omega) {\rm d} \omega ,
\label{G}
\end{equation}
where $f_T$ is the Fermi function at temperature $T$,
while $\mathcal{A}(\omega)$ denotes the normalized local spectral density 
of QD1 \cite{fn1} 
Henceforth, unless we state otherwise, we assume a maximal CAR coupling, 
$\GS{\rm X} = \sqrt{\GS{1}\GS{2}}$ \cite{IW_Kacper,Walldorf2018Feb},
$\GS{1}=\GS{2}=\GS{}$ and consider DQD tuned to the particle-hole symmetry point, 
$\varepsilon_1=\varepsilon_2=-U/2$  However, these assumptions are not crucial for the results presented
here, as discussed in Secs ~\ref{sec:asym}-\ref{sec:coef} 

\section{Estimation of relevant energy scales}
\label{sec:scales}

Since we analyze a relatively complex system, let us build up the understanding of its behavior starting
from the case of a QD between two normal-metallic leads, which can be obtained in our 
model by setting $t=\GS{}=J=U'=0$  Then, the conductance as a function of temperature, $G(T)$, grows
below the Kondo temperature $T_K$ and reaches maximum for $T\to 0$, $G(T\!=\!0)=G_{\rm max}$ 
At particle-hole symmetry point, the unitary transmission is achieved, $G_{\rm max}= G_0 = 2e^2/h$;
see short-dashed line in \fig{G-T}(a) 
An experimentally relevant definition of $T_K$ is that at $T=T_K$ 
$G(T)=G_{\rm max}/2$  $T_K$ is exponentially small in 
the local exchange $J_0 = 8\Gamma / (\pi \rho U)$, and is approximated by
$T_K \approx D \exp[-1/(\rho J_0)]$ \cite{Hewson_book} 

The presence of a second side-coupled QD, $t,U'>0$, significantly enriches the physics of the system 
by introducing direct exchange between QDs, see \fig{system}(b-d) 
In general, effective inter-dot exchange can be defined as energy difference between 
the triplet and singlet states of isolated DQD, 
$J^{\mathrm{eff}} = E_{S=1} - E_{\rm GS}$  Unless $U$ becomes very large, superexchange can be neglected
\cite{Zitko_2QDEx} and $J^{\mathrm{eff}}$ is determined by \emph{direct exchange}, $J^{\mathrm{eff}}\approx 4t^2/(U-U')>0$ 
When the hopping $t$ is tuned small \cite{CPS1}, one can expect $J^{\mathrm{eff}}\lesssim T_K$, which 
implies the two-stage Kondo screening \cite{Pustilnik_Glazman,Cornaglia} 
Then, for $T \ll T_K$, the local spectral density of QD1 serves as a band of width $\sim T_K$ for QD2 
The spin of an electron occupying QD2 
experiences the Kondo screening below the associated Kondo temperature
\begin{equation}
T^* = a T_K \exp(- b T_K / J_{\rm eff})
\label{Tstar}
\end{equation}
with $a$ and $b$ constants of order of unity \cite{Pustilnik_Glazman,Cornaglia} 
This is reflected in conductance, which drops to $0$ with lowering $T$, maintaining characteristic 
Fermi-liquid 
$G\sim T^2$ dependence \cite{Cornaglia}; see the curves indicated with squares 
in \fig{G-T}(a)  Similarly to $T_K$, experimentally relevant definition of $T^*$ is that 
$G(T\!=\!T^*) = G_{\rm max}/2$  Even at the particle-hole 
symmetry point $G_{\rm max} < G_0$, because the single-QD strong-coupling fixed point 
is unstable in the presence of QD2 and $G(T)$ does not achieve $G_0$ exactly,
before it starts to decrease 


The proximity of SC gives rise to two further exchange mechanisms that
determine the system's behavior  First of all, the (conventional)
\emph{RKKY interaction} appears, $J \sim \GS{}^2$ \cite{RK,K,Y}  
Moreover, the \emph{CAR exchange} emerges as a consequence of finite $\GS{}$ \cite{Yao}  
It can be understood on the basis 
of perturbation theory as follows  DQD in the inter-dot singlet state may absorb
and re-emit a Cooper pair approaching from SC; see \fig{system}(e)-(g)  As a second-order
process, it reduces the energy of the singlet, which is the ground state of isolated DQD 
A similar process is not possible in the triplet state due to spin conservation 
Therefore, the singlet-triplet energy splitting $J^{\mathrm{eff}}$ is increased (or generated for $t=J=0$)  
More precisely, the leading ($2$nd-order in $t$ and $\GS{}$) terms
in the total exchange are 
\begin{equation}
J^{\mathrm{eff}} 	\approx 	J + \frac{4t^2}{U-U'+\frac{3}{4}J} + \frac{4\GS{}^2}{U+U'+\frac{3}{4}J} 
\label{Jeff}
\end{equation}
Using this estimation, one can predict $T^*$ for finite $\GS{}$, $t$ and $J$ with \eq{Tstar} 
Apparently, from three contributions corresponding to:
(i) RKKY interaction, (ii) direct exchange and (iii) CAR exchange, only the first may bear a negative (ferromagnetic) sign 
The two other contributions always have an anti-ferromagnetic nature 
More accurate expression for $J^{\mathrm{eff}}$ is derived in Appendix~\ref{sec:downfolding}
[see \eq{A_J}] by the Hamiltonian down-folding procedure  The relevant terms differ 
by factors important only for large $\GS{}/U$  
Finally, it seems worth stressing that normal leads are not necessary for CAR exchange to occur 
At least one of them is inevitable for the Kondo screening though, and two symmetrically coupled 
normal leads allow for measurement of the normal conductance 


It is also noteworthy that inter-dot Coulomb interactions
decrease the energy of intermediate states contributing to direct exchange 
[\fig{system}(c)], while increasing the energy of intermediate
states causing the CAR exchange [\fig{system}(f)] 
This results in different dependence of corresponding terms in \eq{Jeff} on $U'$ 
As can be seen in \figs{G-T}(b) and \ref{fig:G-T}(c), it has a significant effect 
on the actual values of $T^*$ 

\begin{figure}
\includegraphics[width=1\linewidth]{Fig2 pdf}
\caption{(a) Linear conductance $G$ as function of $T$ calculated for 
		 $\varepsilon_1=\varepsilon_2=-U/2$, $\Gamma=U/5$, $U'=U/10$ and different situations, 
		 as indicated  The quantity $\xi\equiv\sqrt{\GS{}^2+t^2}$ is fixed 
		 for different curves drawn with the same dashing style 
		 Note the logarithmic scale on both axes 
		 %
		 (b) Points show $T^*/T_K$ calculated by NRG from curves in subfigure (a)  
		 Lines present the fit to \eq{Tstar} with $J^{\mathrm{eff}}$ obtained from \eq{Jeff} 
		 %
		 (c) The same as (b), only for $U'=0$ 
		 %
		 (d) and (e) show the residual conductance $G_{\mathrm{min}} \equiv G(T \!=\! 0)$ as a function of
		 $\GS{}$ for $t=0$ (denoted "CAR") and $t=\GS{}$ (denoted "Both")  
		 Dotted line is a guide for eyes  $U'=U/10$ in (b) and (d) and $U'=0$ in (c) and (e) 
		}
\label{fig:G-T}
\end{figure}

\section{CAR exchange and Kondo effect}
\label{sec:main}

To verify \eqs{Tstar}-(\ref{Jeff}) we calculate $G$ using
accurate full density matrix numerical renormalization group (NRG) technique \cite{WilsonNRG,Weichselbaum,FlexibleDMNRG,fn2} 
We compare $U'=0$ case with experimentally relevant value $U'=U/10$ \cite{Keller2013Dec} 
While for two close adatoms on SC surface RKKY interactions may lead to prominent consequences
\cite{Klinovaja}, the conventional ({\it i e } non-CAR) contribution should 
vanish rapidly when the inter-impurity distance $r$ exceeds a few lattice constants \cite{RKKYrange,SC_RKKY}  
Meanwhile, the CAR exchange may remain significant for $r$ of the order
of coherence length of the SC contact \cite{Yao}  Therefore, we first neglect the conventional RKKY coupling and analyze its consequences in Sec ~\ref{sec:RKKY} 

The main results are presented in \fig{G-T}(a), showing the temperature dependence of $G$
for different circumstances  
For reference, results for $\GS{}=0$ are shown, exhibiting 
the two-stage Kondo effect caused by \emph{direct} exchange mechanism 
As can be seen in \figs{G-T}(b) and \ref{fig:G-T}(c), an excellent agreement of $T^*$ found from NRG calculations and \eq{Tstar} 
is obtained with $a=0 42$ and $b=1 51$, the same for both $U'=0$ and $U'=U/10$  Note, 
however, that $J^{\mathrm{eff}}$ is different in these cases, cf  \eq{Jeff},
and $U'$ leads to increase of $T^*$ 

Furthermore, for $t=0$ and $\GS{}>0$ the two-stage Kondo effect caused solely by the \emph{CAR
exchange} is present; see \fig{G-T}(a) 
Experimentally, this situation
corresponds to a distance between the two QDs smaller than the superconducting coherence length,
but large enough for the exponentially suppressed direct hopping to be negligible 
While intuitively one could expect pairing to compete with any kind of magnetic ordering,
the Kondo screening induced by CAR exchange is a beautiful example of a superconductivity
in fact leading to magnetic order, namely the formation of the Kondo singlet 
This CAR-exchange-mediated Kondo screening is our main finding 
For such screening, \eq{Tstar} is still fulfilled with very similar 
parameters, $a=0 37$ ($a=0 35$) and $b=1 51$ ($b=1 50$) for $U'=0$ ($U'=U/10$),
correspondingly; see \figs{G-T}(b-c) 
Moreover, as follows from \eq{Jeff}, $U'$ reduces CAR exchange, and therefore diminishes $T^*$ 
For the same values of $J^{\mathrm{eff}}$, the dependence of $G(T)$ for $t=0$ and $\GS{}>0$ is hardly different 
from the one for $\GS{}=0$ and $t>0$ for $T\geq T^*$ (results not shown) 
However, $G(T)$ saturates at residual value $G_{\mathrm{min}}$ as $T\to 0$ only for finite
$\GS{}$, which at particle-hole symmetry makes $G_{\mathrm{min}}$
the hallmark of SC proximity and the corresponding CAR exchange processes 
From numerical results, one can estimate it as
\begin{equation}
G_{\mathrm{min}} = \frac{e^2}{h} \cdot c \, \frac{\GS{}^2}{U^2} 
	\qquad {\scriptstyle (\GS{1}=\GS{2}=\GS{})} ,
\label{Gmin}
\end{equation}
with $c\approx 2 25$, barely depending on $U'$ and getting smaller for $t>0$  
This is illustrated in \figs{G-T}(d-e), where the dotted line corresponds to \eq{Gmin} with $c=2 25$  

Lastly, in \fig{G-T}(a) we also present the curves obtained for $t=\GS{}$ chosen such, 
that the quantity $\xi=\sqrt{t^2+\GS{}^2}$ remains the same 
in all the cases 
This is to illustrate what happens when \emph{both} (direct and CAR) exchange interactions are
present  \fig{G-T}(c) clearly shows that $T^*$ remains practically unaltered for $U'=0$ 
The comparison with \fig{G-T}(b) proves that in this case it practically does not depend 
on $U'$  The enhancement of direct exchange is compensated by the decrease of the CAR one  
On the contrary, $G_{\mathrm{min}}$ decreases for larger $t$ below the estimation given by Eq ~(\ref{Gmin}), 
as can be seen in \figs{G-T}(d-e)  

While analyzing the results concerning $G_{\mathrm{min}}(\GS{})$ plotted in \figs{G-T}(d-e) 
one needs to keep in mind that $G_{\mathrm{min}}$ is obtained at deeply cryogenic conditions  To illustrate
this better, $G(\GS{})$ obtained for $t=0$ and $T=10^{-6}U$ is plotted with solid line 
in \fig{3}  Clearly, for weak $\GS{}$ the system exhibits rather conventional (single-stage)
Kondo effect with $G=G_{\mathrm{max}}\approx 2e^2/h$, while QD2 is effectively decoupled ($G_{\mathrm{max}}<2e^2/h$
in the proximity of SC lead \cite{KWIW})  Only for larger values of $\GS{}$
the CAR exchange is strong enough, such that $T^*>T$ and the dependence $G(\GS{})$ continuously 
approaches the $T=0$ limit estimated by \eq{Gmin} and presented in \figs{G-T}(d-e) 

\section{CAR-RKKY competition}
\label{sec:RKKY}

\begin{figure}
\includegraphics[width=0 98\linewidth]{Fig3 pdf}
\caption{Linear conductance $G$ vs  $\GS{}$ calculated
		 for $t=0$, $\Gamma=U/5$, $U'=U/10$, finite $T=10^{-6}U$
		 and different values of RKKY coupling $J$, as indicated  
		 Inset shows QD1 spectral function $\mathcal{A}(\omega)$ as a function of energy $\omega$
		 for points on $J=-0 1U$ curve, indicated with corresponding symbols 
		}
\label{fig:3}
\end{figure}

Let us now discuss the effects introduced by the conventional RKKY interaction 
We choose $t=0$ for the sake of simplicity and
analyze a wide range of $\GS{}$, starting from the case of anti-ferromagnetic 
RKKY interaction ($J>0$)  Large $J>0$ leads to the formation of a molecular singlet in the 
nanostructure  This suppresses the conductance, unless $\GS{}$ becomes of the order of $U/2$, 
when the excited states of DQD are all close to the ground state  This is illustrated 
by double-dotted line in \fig{3} 
Smaller value of $J>0$ causes less dramatic consequences, namely it just increases $J^{\mathrm{eff}}$ according
to \eq{Jeff}, leading to enhancement of $T^*$, cf  \eq{Tstar}  This is presented with
dot-dashed line in \fig{3} 

The situation changes qualitatively for ferromagnetic RKKY coupling, $J<0$ 
Then, RKKY exchange and CAR exchange have opposite signs and compete with each other 
Depending on their magnitudes and temperature, one
of the following scenarios may happen 

For $J^{\mathrm{eff}} > 0$, {\it i e } large enough $\GS{}$, and $T<T^*$, the system is in the 
singlet state due to the two-stage Kondo screening of DQD spins  $G(T\!=\!0)$ is reduced 
to $G_{\mathrm{min}}$, which tends to increase for large negative $J$; see dashed lines in \fig{3}  
In the inset to \fig{3}, the spectral density of QD1 representative for this regime is plotted 
as curve indicated by triangle  It corresponds to a point on the $J=-0 1U$ curve in the main 
plot, also indicated by triangle  The dip in $\mathcal{A}(\omega)$ has width of order of $T^*$ 

For finite $T$, there is always a range of sufficiently small $|J^{\mathrm{eff}}|$, where QD2 becomes effectively
decoupled, and, provided $T<T_K$, $G$ reaches $G_{\mathrm{max}}$ due to conventional Kondo effect 
at QD1  This is the case for sufficiently small $\GS{}$ for $J=0$ or $J=-0 01U$, and in the narrow
range of $\GS{}$ around the point indicated by a circle in \fig{3} for $J=-0 1U$ (for $J=0 01U$, 
the considered $T$ is close to $T^*$ and $G$ does not reach $G_{\rm max}$)  The conventional Kondo effect manifests itself with 
a characteristic peak in $\mathcal{A}(\omega)$, as illustrated in the inset in \fig{3} with line denoted by circle 

Finally, large enough $J^{\mathrm{eff}} < 0$ and low $T$, give rise to an effective ferromagnetic coupling of DQDs 
spins into triplet state  Consequently, the underscreened Kondo effect occurs 
\cite{Mattis,NozieresBlandin} for weak $\GS{}$ and, {\it e g }, $J=-0 1U$; 
see the point indicated by square in \fig{3} 
This leads to $G=G_{\mathrm{max}}$ and a peak in $\mathcal{A}(\omega)$, whose shape is significantly different from the
Kondo peak, cf  the curve denoted by square in the inset in \fig{3}  



\section{Effects of detuning from the particle-hole symmetry point}
\label{sec:asym}

\begin{figure}
\includegraphics[width=0 98\linewidth]{Fig4 pdf}
\caption{
         (a) Linear conductance between the normal leads $G$ as a function of temperature $T$
         for parameters corresponding to \fig{G-T}(a) with $\xi=U/10$, and additional curves for finite 
         detuning from particle-hole symmetry point, $\delta_1=-\delta_2$, 
         and two values of $\xi=\sqrt{t^2+\GS{}^2}$, as indicated in the figure 
         (b) $G_{\mathrm{min}} \equiv G(T \!=\! 0)$ as a function of QD1 detuning $\delta_1$ for different
         exchange mechanisms, $\xi=U/10$ and $\delta_2=\pm\delta_1$ (as indicated) 
		}
\label{fig:asym}
\end{figure}

At PHS $G_{\mathrm{min}}=G(T \!=\! 0)=0$ in the absence of superconducting lead, making $G_{\mathrm{min}} > 0$ a hallmark
of SC-induced two-stage Kondo effect  However, outside of PHS point $G_{\mathrm{min}} > 0$ even in the case of 
the two-stage Kondo effect caused by the direct exchange  
Exact PHS conditions are hardly possible in real systems, and the fine-tuning of the QD energy
levels to PHS point is limited to some finite accuracy 
Therefore, there may appear a question, if the results obtained at PHS are of any importance for the
realistic setups  As we show below --- they are,
in a reasonable range of detunings $\delta_i=\varepsilon_i +U/2$ 

In \fig{asym}(a) we present the $G(T)$ dependence in and outside the PHS, corresponding to 
parameters of \fig{G-T}(a)  
Clearly, for considered small values of $\delta_1=\delta_2=\delta$, 
$G_{\mathrm{min}}<10^{-3}e^2/h$ for direct exchange only, while $G_{\mathrm{min}}$ in the presence of a superconductor is 
significantly increased and close to the PHS value  Furthermore, for $|\delta_1| \sim |\delta_2| 
\sim \delta$, the residual conductance caused by the lack of PHS, $G_{\mathrm{min}} \approx e^2/h \cdot (\delta/U)^2$,
which is a rapidly decreasing function in the vicinity of PHS point, as illustrated in \fig{asym}(b)
with lines denoted by a square  Evidently, in the regime $|\delta_i| < 0 01U$ the residual conductance
caused by SC is orders of magnitude larger, leading to the plateau in $G_{\mathrm{min}}(\delta_1)$ dependence,
visible in \fig{asym}(b) 
Taking into account that the realistic values of $U$ in the semiconductor quantum dots are rather 
large, this condition seems to be realizable by fine-tuning of QD gate voltages 

Lastly, let us point out that while in the presence of only one exchange mechanism, \emph{CAR} or
\emph{direct}, $G_{\mathrm{min}}(\delta_1)$ dependencies depicted in \fig{asym}(b) are symmetrical with respect
to sign change of $\delta_1$, for \emph{both} exchange mechanisms the dependence is non-symmetric  

\section{Effects of asymmetry of couplings to superconductor}
\label{sec:x}

\begin{figure}
\includegraphics[width=0 98\linewidth]{Fig5 pdf}
\caption{
		 (a) Linear conductance between the normal leads, $G$, as a function of temperature, $T$,
		 for parameters corresponding to \fig{G-T}(a) with $\xi=U/10$, for different values 
		 of asymmetry coefficient $x$ [see \eq{xGS}], in the presence of \emph{CAR} exchange only 
		 %
		 (b) The second-stage Kondo temperature $T^*$ normalized by $T_K$ as a function of $x$, 
		 calculated with the aid of NRG (points) and a fit to \eq{Tstar} (lines) 
		 with $J^{\mathrm{eff}}$ from \eq{Jeff} 
		 %
		 (c) The zero-temperature conductance $G_{\mathrm{min}}$ as a function of QD1 coupling to SC lead, $\GS{1}$,
		 compiled from data obtained at different circumstances (as indicated in the legend)
		 for different $x$  Dotted line corresponds to \eq{Gmin2} with $c=2 25$ 
		}
\label{fig:x}
\end{figure}

Similarly to PHS, the ideal symmetry in the coupling between respective QDs and SC lead is hardly possible
in experimental reality  As shown below, it does not introduce any qualitatively new features 
On the other hand, it decreases the second stage Kondo temperature, which is already small, therefore,
quantitative estimation of this decrease may be important for potential experimental approaches 
To analyze the effects of $\GS{1}\neq\GS{2}$, we introduce the asymmetry parameter $x$ and extend
the definition of $\GS{}$,
\beq
x = \frac{\GS{1}-\GS{2}}{\GS{1}+\GS{2}}, \quad \GS{} = \frac{\GS{1}+\GS{2}}{2} 
\label{xGS}
 \end{equation} 
Note, that even for a fixed $\GS{}$, the actual CAR coupling $\GS{\rm X}=\GS{}\sqrt{1-x^2}$ decreases
with increasing $|x|$, which is a main mechanism leading to a decrease of $T^*$ outside the $x=0$ point
visible in \figs{x}(a) and (b)  To illustrate this, the curves corresponding to \emph{both} exchange
mechanisms were calculated using $x$-dependent $t=\GS{\rm X}$ instead of $t=\xi/\sqrt{2}$  
Therefore, $\xi$ was generalized for $x\neq 0$ by setting $\xi=\sqrt{t^2(1-x^2)^{-1}+\GS{}^2}$ 
Clearly, in \fig{x}(b) the curves for different exchange mechanisms are very similar and differ mainly 
by a constant factor, resulting from different influence of $U'$; see \Sec{scales}  
The magnitude of $T^*$ changes is quite large, exceeding an order of magnitude for $x=\pm 0 5$ 
and $\xi=U/20$  Moreover, $T^* \to 0$ for $x\to\pm 1$  Consequently, for strongly asymmetric
devices one cannot hope to observe the second stage of Kondo screening 

A careful observer can note that the $T^*(x)$ dependency is not symmetrical; note for example different 
$T^*$ for $x=\pm 0 5$ in \fig{x}(a)  This is caused by the dependence of the first stage Kondo temperature
$T_K$ on $\GS{1}$ \cite{part1,DomanskiIW},
\beq
\widetilde{T}_K(\GS{1}) = T_K \cdot \exp\!\left( \frac{\pi}{2} \frac{\GS{1}^2}{\Gamma U}\right) 
 \end{equation} 
Here, $T_K$ is, as earlier, defined in the absence of SC, while $\widetilde{T}_K$ is a function 
of $\GS{1}$, such that $G(\widetilde{T}_K) = G_{\rm max}(\GS{1})/2$ in the absence of QD2  
As $\widetilde{T}_K$ grows for increasing $\GS{1}$ (or $x$), $T^*$ decreases according to \eq{Tstar}  
Its $\GS{}$ dependence can be accounted for by small changes in the coefficients $a$ and $b$ in \eq{Tstar}, 
as long as $x$ is kept constant  

To close the discussion of $T^*(x)$ dependence let us point out, that in \eq{A_J} 
there appears a correction to \eq{Jeff} for $x\neq 0$  However, it is very small due to additional
factor $\GS{}^2/U^2$ in the leading order  Its influence on curves plotted in \fig{x}(b) is hardly visible 

In turn, let us examine the $x$ dependence of the $T=0$ conductance $G_{\mathrm{min}}$  As can be seen 
in \fig{x}(a), it monotonically increases with $x$, as it crosses $x=0$ point  In fact, \eq{Gmin}
can be generalized to
\beq
G_{\mathrm{min}} = \frac{e^2}{h} \cdot c \, \frac{\GS{1}^2}{U^2} ,
\label{Gmin2}
 \end{equation} 
with $c\approx 2 25$ (indicated by a dotted line in \fig{x}(c))  Note that $G_{\mathrm{min}}$ is proportional to 
$\GS{1}^2=(x+1)^2 \GS{}^2$, instead of simply $\GS{}$, cf  \eq{Gmin}  The values of $G_{\mathrm{min}}$ obtained
from all analyzed $G(T)$ dependencies for different $x$ have been compiled in \fig{x}(c) 
It is evident, that \eq{Gmin2} is approximately fulfilled for all the considered cases 

Finally, it seems noteworthy that the normal-lead coupling asymmetry, 
$\Gamma_{\rm L}\neq \Gamma_{\rm R}$, is irrelevant for the results except for a constant factor
diminishing the conductance $G$ \cite{KWIWJB-asym} 



\section{The role of CAR efficiency}
\label{sec:coef}

\begin{figure}[tb]
\includegraphics[width=0 98\linewidth]{Fig6 pdf}
\caption{Linear conductance between the normal leads
		 $G$ as a function of coupling to SC lead, $\GS{}$, for indicated values of RKKY exchange $J$
		 and the efficiency of CAR processes reduced by factor (a) $\mathcal{C}=0 9$ and (b) $\mathcal{C}=0 5$ 
		 Other parameters as in \fig{3} 
		 Insets: QD1 local spectral density $\mathcal{A}(\omega)$ as a function of energy $\omega$
		 for points on $J=-0 1U$ curve, indicated with corresponding symbols 
		} 
\label{fig:C}
\end{figure}

Up to this point we assumed $\GS{\rm X} = \sqrt{\GS{1}\GS{2}}$, which is valid when the two 
quantum dots are much closer to each other than the coherence length in the superconductor 
This does not have to be the case in real setups, yet relaxing this assumption does not 
introduce qualitative changes  Nevertheless, the model cannot be extended to inter-dot 
distances much larger than the coherence length, where $\GS{\rm X}\to 0$ 

To quantitatively analyze the consequences of less effective Andreev coupling we define the 
CAR efficiency as $\mathcal{C} \equiv \GS{\rm X} / \sqrt{\GS{1}\GS{2}}$ and analyze $\mathcal{C} < 1$
in the wide range of $\GS{1}=\GS{2}=\GS{}$ and other parameters corresponding to \fig{3}  
The results are presented in \fig{C} 

Clearly, decreasing $\mathcal{C}$ from $\mathcal{C}=1$ causes diminishing of $\GS{\rm X}$, and consequently of CAR 
exchange  For a change as small as $\mathcal{C}=0 9$, the consequences reduce to some shift of the 
conventional Kondo regime, compare \fig{C}(a) with \fig{3}  Stronger suppression of CAR may, 
however, increase the SC coupling necessary to observe the second stage of Kondo screening caused
by CAR outside the experimentally achievable range, see \fig{C}(b)  Moreover, the reduced $T^*$
leads to narrowing of the related local spectral density dip, while the
increased critical $\GS{}$ necessary for the observation of the second stage of screening leads to the
shallowing of the dip  This is visible especially in the inset in \fig{C}(b) 


\section{Conclusions}
\label{sec:conclusions}

The CAR exchange mechanism is present in any system comprising at least
two QDs or magnetic impurities coupled to the same superconducting contact
in a way allowing for crossed Andreev reflections 
In the considered setup, comprised of two quantum dots in a T-shaped geometry 
with respect to normal leads and proximized by superconductor,
it leads to the two-stage Kondo
screening even in the absence of other exchange mechanisms 
This CAR induced exchange screening is characterized by a residual 
low-temperature conductance at particle-hole symmetric case 
We have also shown that the competition between CAR exchange and RKKY
interaction may result in completely different Kondo screening scenarios 

The presented results bring further insight into the low-temperature
behavior of hybrid coupled quantum dot systems, which hopefully could be verified
with the present-day experimental techniques 
Moreover, non-local pairing is present also in bulk systems such as non-$s$-wave superconductors 
The question if an analogue of discussed CAR exchange may play a role there
seems intriguing in the context of tendencies of many strongly correlated materials
to possess superconducting and anti-ferromagnetic phases 


\begin{acknowledgments}
This work was supported by the National Science Centre in Poland through project no 
2015/19/N/ST3/01030 
We thank J  Barna\'{s} and T  Maier for valuable discussions 
\end{acknowledgments}








ground_truth: It tends to suppress the Kondo effect.

prompt_front: Now, answer the following question based on the text below, only give me the answer and do not output any other words.

Question: What is the purpose of an ICD?

Read the following text and answer briefly.

Context 3: 
Myocardium – The muscular tissue of the heart 
New Wall-Motion Abnormalities – Results seen on an echocardiogram test report (see NWMA, below) 
Nitroglycerin – A medicine that helps relax and dilate arteries; often used to treat cardiac chest pain (angina)  Also called NTG or GTN 
NSR – Normal Sinus Rhythm: The characteristic rhythm of the healthy human heart  NSR is considered to be present if the heart rate is in the normal range, the P waves are normal on the EKG/ECG, and the rate does not vary significantly 
NSTEMI – Non-ST-segment-elevation myocardial infarction: The milder form of the two main types of heart attack  An NSTEMI heart attack does not produce an ST-segment elevation seen on an electrocardiogram test (EKG)  See also STEMI 
Nuclear Stress Test – A diagnostic test that usually involves two exercise stress tests, one while you’re exercising on a treadmill/stationary bike or with medication that stresses your heart, and another set while you’re at rest  A nuclear stress test is used to gather information about how well your heart works during physical activity and at rest  See also: Exercise stress test, Nuclear perfusion test, MIBI 
Open heart surgery – Any surgery in which the chest is opened and surgery is done on the heart muscle, valves, coronary arteries, or other parts of the heart (such as the aorta)  See also CABG 
Pacemaker – A surgically implanted electronic device that helps regulate the heartbeat 
PAD – Peripheral Artery Disease: A common circulatory problem in which narrowed arteries reduce blood flow to the limbs, usually to the legs  Symptoms include leg pain when walking (called intermittent claudication) 
PAF – Paroxysmal Atrial Fibrillation: Atrial fibrillation that lasts from a few seconds to days, then stops on its own  See also Atrial Fibrillation 
Palpitations – A noticeably rapid, strong, or irregular heartbeat due to agitation, exertion or illness 
Paroxysmal Atrial Fibrillation – An unusual heart arrhythmia of unknown origin, at one time believed to be associated with an unusual sensitivity to alcohol consumption 
PDA – patent ductus arteriosus: A persistent opening between two major blood vessels leading from the heart  The opening is called ductus arteriosus and is a normal part of a baby’s circulatory system before birth that usually closes shortly after birth  But when it remains open, it’s called a patent ductus arteriosus  If it’s small, it may never need treatment, but a large PDA left untreated can allow poorly oxygenated blood to flow in the wrong direction, weakening the heart muscle and causing heart failure or other complications 
Pericardium: two thin layers of a sac-like tissue that surround the heart, hold it in place and help it work 
PET – Positron Emission Tomography: A non-invasive scanning technique that uses small amounts of radioactive positrons (positively charged particles) to visualize body function and metabolism  In cardiology, PET scans are used to evaluate heart muscle function in patients with coronary artery disease or cardiomyopathy 
PFO – Patent Forman Ovale: An opening between the left and right atria (the upper chambers) of the heart  Everyone has a PFO before birth, but in 1 out of every 3 or 4 people, the opening does not close naturally as it should after birth 
Plaque – A deposit of fatty (and other) substances in the inner lining of the artery wall; it is characteristic of atherosclerosis 
POTS – Postural Orthostatic Tachycardia Syndrome: A disorder that causes an increased heart rate when a person stands upright 
PPCM – Post-partum cardiomyopathy: A form of cardiomyopathy that causes heart failure toward the end of pregnancy or in the months after delivery, in the absence of any other cause of heart failure 
Preeclampsia – a late-pregnancy complication identified by spikes in blood pressure, protein in the urine, possible vision problems  Women who experience pregnancy complications like preeclampsia are at significantly higher risk for heart disease 
Prinzmetal’s Variant Angina – Chest pain caused by a spasm in a coronary artery that supplies blood to the heart muscle 
PSVT – Paroxysmal Supraventricular Tachycardia: – An occasional rapid heart rate (150-250 beats per minute) that is caused by events triggered in areas above the heart’s lower chambers (the ventricles)  “Paroxysmal” means from time to time  See also supraventricular tachycardia (SVT) 
Pulmonary Valve: One of the four valves in the heart, located between the pulmonary artery and the right ventricle of the heart, moves blood toward the lungs and keeps it from sloshing back into the heart 
PV – Pulmonary Vein: A vein carrying oxygenated blood from the lungs to the left atrium of the heart 
PVC – Premature Ventricular Contraction: An early or extra heartbeat that happens when the heart’s lower chambers (the ventricles) contract too soon, out of sequence with the normal heartbeat  In the absence of any underlying heart disease, PVCs do not generally indicate a problem with electrical stability, and are usually benign 
RA – Right Atrium: The right upper chamber of the heart  The right atrium receives de-oxygenated blood from the body through the vena cava and pumps it into the right ventricle which then sends it to the lungs to be oxygenated 
Radial Artery: the artery in the wrist where a thin catheter is inserted through the body’s network of arteries in the arm and eventually into the heart during a procedure to implant a stent  Doctors may also call this transradial access, the transradial approach, or transradial angioplasty  Because it’s associated with fewer complications, this is increasingly considered the default access approach in most countries, except in the U S  where the traditional Femoral Artery (groin) approach is still the most popular access 
RBBB – Right Bundle Branch Block: A delay or obstruction along the pathway that electrical impulses travel to make your heart beat  The delay or blockage occurs on the pathway that sends electrical impulses to the right side of your heart  See also Left Bundle Branch Block 
RCA – Right Coronary Artery: An artery that supplies blood to the right side of the heart 
Restenosis – The re-closing or re-narrowing of an artery after an interventional procedure such as angioplasty or stent placement  Sometimes called “stent failure” 
RHD – Rheumatic Heart Disease: Permanent damage to the valves of the heart caused especially by repeated attacks of rheumatic fever 
RM – Right Main coronary artery: A blood vessel that supplies oxygenated blood to the walls of the heart’s ventricles and the right atrium 
RV – Right Ventricle: The lower right chamber of the heart that receives de-oxygenated blood from the right atrium and pumps it under low pressure into the lungs via the pulmonary artery 
SA – Sinus node: The “natural” pacemaker of the heart  The node is a group of specialized cells in the top of the right atrium which produces the electrical impulses that travel down to eventually reach the ventricular muscle, causing the heart to contract 
SB – Sinus Bradycardia: Abnormally slow heartbeat 
SBP – Systolic Blood Pressure: The highest blood pressure measured in the arteries  It occurs when the heart contracts with each heartbeat  Example: the first number in 120/80 
SCAD – Spontaneous Coronary Artery Dissection: A rare emergency condition that occurs when a tear forms in one of the blood vessels in the heart, causing a heart attack, abnormalities in heart rhythm and/or sudden death  SCAD tends to strike young healthy women with few if any cardiac risk factors 
SD – Septal defect: A hole in the wall of the heart separating the atria (two upper chambers of the heart) or in the wall of the heart separating the ventricles (two lower chambers) 
Sestamibi stress test – See MIBI 
Short QT intervals (SQT): An abnormal heart rhythm where the heart muscle takes a shorter time to recharge between beats  It can cause a variety of complications from fainting and dizziness to sudden cardiac arrest 
Sick Sinus Syndrome (also known as sinus node dysfunction) is caused by an electrical problem in the heart; a group of related heart conditions that can affect how the heart beats, most commonly in older adults, although it can be diagnosed in people of any age  “Sick sinus” refers to the sinoatrial node (see below)  In people with sick sinus syndrome, the SA node does not function normally 
Sinoatrial node (SA): also commonly called the sinus node; it’s a small bundle of neurons situated in the upper part of the wall of the right atrium (the right upper chamber of the heart)  The heart’s electrical impulses are generated there  It’s the normal natural pacemaker of the heart and is responsible for the initiation of each heartbeat 
Spontaneous Coronary Artery Dissection (SCAD) – A rare emergency condition that occurs when a tear forms in one of the blood vessels in the heart, causing a heart attack, abnormalities in heart rhythm and/or sudden death  SCAD tends to strike young healthy women with few if any cardiac risk factors 
SSS – Sick Sinus Syndrome: The failure of the sinus node to regulate the heart’s rhythm 
ST – Sinus Tachycardia: A heart rhythm with elevated rate of impulses originating from the sinoatrial node, defined as greater than 100 beats per minute (bpm) in an average adult  The normal heart rate in the average adult ranges from 60–100 bpm  Also called sinus tach or sinus tachy 
Statins – Any of a class of drugs that lower the levels of low-density lipoproteins (LDL) – the ‘bad’ cholesterol in the blood – by inhibiting the activity of an enzyme involved in the production of cholesterol in the liver  Examples of brand name statins: Lipitor, Crestor, Zocor, Mevacor, Levachol, Lescol, etc  Also available as a cheaper generic form of the drug 
STEMI – ST-elevation heart attack (myocardial infarction)  The more severe form of the two main types of heart attack  A STEMI produces a characteristic elevation in the ST segment on an electrocardiogram (EKG)  The elevated ST segment is how this type of heart attack got its name  See also NSTEMI 
Stent – An implantable device made of expandable, metal mesh (looks a bit like a tiny chicken wire tube) that is placed (by using a balloon catheter) at the site of a narrowing coronary artery during an angioplasty procedure  The stent is then expanded when the balloon fills, the balloon is removed, and the stent is left in place to help keep the artery open  TRIVIA ALERT: the coronary stent was named after Charles Stent (1807-1885), an English dentist who invented a compound to produce dentures and other things like skin grafts and hollow tubes (essentially what a metal coronary stent is)  His real claim to fame occurred when he suggested using his material to coat underwater trans-Atlantic cable, which had broken several times as a result of corrosion by seawater  You’re welcome 
Stint – a common spelling mistake when what you really mean is the word “stent” (see above) 
Stress Echocardiography – A standard echocardiogram test that’s performed while the person exercises on a treadmill or stationary bicycle  This test can be used to visualize the motion of the heart’s walls and pumping action when the heart is stressed, possibly revealing a lack of blood flow that isn’t always apparent on other heart tests  The echocardiogram is performed just before and just after the exercise part of the procedure  See also TTE 
Sudden Cardiac Arrest – The stopping of the heartbeat, usually because of interference with the electrical signal (often associated with coronary heart disease)  Can lead to Sudden Cardiac Death 
Takotsubo Cardiomyopathy – A heart condition that can mimic a heart attack  Sometimes called Broken Heart Syndrome, it is not a heart attack, but it feels just like one, with common symptoms like severe chest pain and shortness of breath  It sometimes follows a severe emotional stress  Over 90% of reported cases are in women ages 58 to 75  Also referred to as Broken Heart Syndrome, stress cardiomyopathy, stress-induced cardiomyopathy or apical ballooning syndrome 
TAVR – Transcatheter aortic valve replacement: A minimally invasive procedure to repair a damaged or diseased aortic valve  A catheter is inserted into an artery in the groin and threaded to the heart  A balloon at the end of the catheter, with a replacement valve folded around it, delivers the new valve to take the place of the old  Also called TAVI (Transcatheter aortic valve implantation) 
Tetralogy of Fallot – A rare condition caused by a combination of four heart defects that are present at birth, affecting the structure of the heart and causing oxygen-poor blood to flow out of the heart and into the rest of the body  Infants and children with Tetralogy of Fallot usually have blue-tinged skin because their blood doesn’t carry enough oxygen  Often diagnosed in infancy, but sometimes not until later in life depending on severity 
Tg – Triglycerides: The most common fatty substance found in the blood; normally stored as an energy source in fat tissue  High triglyceride levels may thicken the blood and make a person more susceptible to clot formation  High triglyceride levels tend to accompany high cholesterol levels and other risk factors for heart disease, such as obesity 
TIA – Transient Ischemic Attack: A stroke-like event that lasts only for a short time and is caused by a temporarily blocked blood vessel 
TEE – Transesophageal echocardiogram: This test involves an ultrasound transducer inserted down the throat into the esophagus in order to take clear images of the heart structures without the interference of the lungs and chest 
Treadmill Stress Test – See Exercise Stress Test 
troponin – a type of cardiac enzyme found in heart muscle, and released into the blood when there is damage to the heart (for example, during a heart attack)  A positive blood test that shows elevated troponin is the preferred test for a suspected heart attack because it is more specific for heart injury than other blood tests, especially the newer high sensitivity troponin tests (hs-cTnT) 
TTE – Transthoracic Echocardiogram: This is the standard echocardiogram, a painless test similar to X-ray, but without the radiation, using a hand-held device called a transducer placed on the chest to transmit high frequency sound waves (ultrasound)  These sound waves bounce off the heart structures, producing images and sounds that can be used by the doctor to detect heart damage and disease 
TV – Tricuspid Valve: One of four one-way valves in the heart, a structure that controls blood flow from the heart’s upper right chamber (the right atrium) into the lower right chamber (the right ventricle) 
UA or USA – Unstable Angina: Chest pain that occurs when diseased blood vessels restrict blood flow to the heart; symptoms are not relieved by rest; considered a dangerous and emergency crisis requiring immediate medical help 
Valves: Your heart has four one-way valves that keep blood flowing in the right direction  Blood enters the heart first through the tricuspid valve, and next goes through the pulmonary valve (sometimes called the pulmonic valve) on its way to the lungs  Then the blood returning from the lungs passes through the mitral (bicuspid) valve and leaves the heart through the aortic valve 
Vasodilator: A drug that causes dilation (widening) of blood vessels 
Vasospasm: A blood vessel spasm that causes sudden constriction, reducing its diameter and blood flow to the heart muscle  See also Prinzmetal’s Variant Angina 
VB – Ventricular Bigeminy: A heart rhythm condition in which the heart experiences two beats of the pulse in rapid succession 
Vena Cava – a large vein that carryies de-oxygenated blood into the heart  There are two in humans, the inferior vena cava (carrying blood from the lower body) and the superior vena cava (carrying blood from the head, arms, and upper body) 
Ventricle – each of the two main chambers of the heart, left and right 
VF – Ventricular Fibrillation: A condition in which the ventricles (two lower chambers of the heart) contract in a rapid, unsynchronized fashion  When fibrillation occurs, the ventricles cannot pump blood throughout the body  Most sudden cardiac deaths are caused by VF or ventricular tachycardia (VT) 
VLDL – Very Low Density Lipoprotein: Molecules made up of mostly triglycerides, cholesterol and proteins  VLDL, also known as the “very bad” cholesterol, carries cholesterol from the liver to organs and tissues in the body  It may lead to low density lipoproteins (LDL), associated with higher heart disease risks  VLDL levels are tricky to measure routinely, and are usually estimated as a percentage of your triglyceride levels  By reducing triglycerides, you are usually also reducing your VLDL levels 
Warfarin – A drug taken to prevent the blood from clotting and to treat blood clots  Warfarin is believed to reduce the risk of blood clots causing strokes or heart attacks  Also known as Coumadin 
Widowmaker heart attack – The type of heart attack I survived, since you asked  A nickname doctors use to describe a severely blocked left main coronary artery or proximal left anterior descending coronary artery of the heart  This term is used because if the artery gets abruptly and completely blocked, it can cause a massive heart attack that will likely lead to sudden cardiac death  Please note the gender imbalance here: despite the number of women like me who do experience this type of cardiac event, doctors are not calling this the widowermaker, after all 
WPW – Wolff-Parkinson-White Syndrome: A condition in which an extra electrical pathway connects the atria (two upper chambers) and the ventricles (two lower chambers)  It may cause a rapid heartbeat 
NOTE FROM CAROLYN: I was very happy when we were able to include this entire glossary in my book, “A Woman’s Guide to Living with Heart Disease“ (Johns Hopkins University Press, 2017) 
Are we missing any important heart acronyms/terms from this list? Let me know!
Please can someone explain something for me  I am a 53 yr old woman and generally fit and healthy  Had 2 ECG’s due to a one off dizzy spell during a stressful time dealing with my fathers terminal diagnosis  The 2nd ECG request did give me concern as i did not know why i had to have one  On 24/01/19 at my doctors appointment she explained that on 3 the leads it showed inverted T waves  And she explained that it may suggest angina  I was so shocked  Wasn’t expecting that  She gave me a GNT (nitroglycerin) spray in case I do get pain and take 75Mg of aspirin  I’m now waiting for a Cardiology referral 
I am so stressed and consumed by what might be wrong  My maternal grandmother had angina and valve issues  Her 3 brothers all had double bypasses  Could I have inherited this? I am not overweight at 63kg and 5 ft 9  I walk 20-25 miles a week at work and general walking here and there  I started HRT (patches evorol 25 -50) in July as menopause pain was making me feel like I was 90 and was getting me down 
I am worried so much now and analysing every ache/ twinge I get  I feel like a hypochondriac at the moment  I’m worried what will happen at the cardiologist and what the test will entail and tell me  I am waiting on cholesterol test which I had on 25/01/19  Can I have inverted T waves and be fine  Please help I am so scared and crying far too much 
Hello Colleen – the first thing is: please take a big deep breath before you read another word here! I’m not a physician so of course cannot comment on your specific case, but I can tell you generally that the definition of “angina” (as this glossary lists above) is “distressing symptoms”, typically chest pain that gets worse with exertion, and goes away with rest  That’s classic stable angina… typically caused by something that’s reducing blood flow to the heart muscle (causing the chest pain of angina) 
A family history that might make a difference for you personally is only in what’s called your ‘first degree’ relatives: for example, if your mother or sister were diagnosed with heart disease before age 65, or if your Dad or brother were diagnosed before age 55, then doctors would consider that you have a family history as a risk factor for heart disease  There’s little if any scientific evidence that a grandparent or uncle’s heart disease history has any effect on your own risk 
It is a very good thing that you’re having further tests and a referral to a cardiologist, if only to ease your mind  There are many reasons for inverted T-waves, ranging from cardiac issues to completely benign conditions  One way of looking at this is choosing to believe that seeing a cardiologist will ease your mind one way or the other – so this is something to look forward to, not dread  If the cardiologist spots something suspicious, a treatment plan will be created  If not, you can wave goodbye and go back to happily living your life 
Try thinking of this cardiology appointment just as you would if your car were making some frightening noises and you were bringing it to your mechanic for a check up  You could work yourself into a complete state worrying ahead of time if the car trouble is going to be serious, or you could look at this appointment as the solution – at last! – to figuring out what’s wrong so the mechanic can recommend the next step 
Thank you for this list of so many definitions provided in plain English  what a valuable resource this is  THANK YOU, I have been looking for translations FOR PATIENTS not med school graduates– like this for three years 
My family doctor had me wear a 24 hr EKG  After reading the results, she has scheduled a scope to look inside my heart by a specialist  Completely forgoing a stress test  Said I have major changes in the EKG, what type of changes could they be looking at? Had LAD STENT INSERTED 7 YRS AGO – WHAT COULD THEY BE LOOKING FOR?
This is a great wealth of information, Carolyn! I looked and did not see my diagnosis, which is aortic stenosis  I looked under aortic as well as stenosis  Did I just miss it somehow?
I learned some new information, I am a bit familiar now, but not when I had my MI, it was like learning a new language  But, my favorite part was seeing SCAD on this list! Thank you 
Thanks and welcome! I was thinking of editing that SCAD definition actually: I suspect that that it isn’t so much that SCAD is “rare”, but it’s more that it’s “rarely correctly diagnosed” 
I totally agree that SCAD is not as rare as I believed for many years  Once awareness is spread to all medical staff, I believe many lives will be saved  Hoping for a brighter future for all SCAD patients 
I hope so too, Cathy  Perhaps when more SCAD studies (like Mayo Clinic’s) are published and read by more and more MDs, it will no longer be “rarely correctly diagnosed” 
It’s great to see IST on here  I was diagnosed with it 9 years ago and the lack of awareness is frustrating 
What a great resource for heart patients and their families!
Thanks so much, Ashley  I recently updated my original 2011 list after the world-famous Cleveland Clinic tweeted their glossary recently and I noticed that their list had a few glaring omissions (like SCAD and Brugada Syndrome) so this made me wonder what my list might be missing, too  Let me know if there’s anything else you think should be included, okay?
How is your health these days? How are you feeling?
New for me too  I have just been diagnosed with A-HCM: Apical Hypertrophic Cardiomyopathy 
I’ll add that one to my list, Kathleen – thanks!
Just saw this, Carolyn, and you’ve compiled a great resource  One note on A-HCM: Present thinking is that it’s due to a genetic modification  Runs in families though sometimes occurs spontaneously  I have not as yet done genetic testing, though it’s been offered 
Thanks Kathleen – like many cardiac diagnoses, it sounds like a moving target… Good luck to you!
This list is great  I’ve just been diagnosed and am utterly overwhelmed  Even in the WomenHeart online support community, I often have no clue most days what others are talking about with all these initials about their heart tests and specific disease  This is VERY helpful, thank you SO MUCH  Love your website which has been a godsend since my diagnosis 



ground_truth: Implantable Cardioverter Defibrillator (ICD) is a surgically implanted electronic device to treat life-threatening heartbeat irregularities.