bluuebunny/crossref_metadata_2025_split huggingface dataset:
Pulmonary Edema
Authors: FISHMAN ALFRED P. 
Published: June 2012

The pathogenesis of clinical pulmonary edema is considered in the light of recent physiologic and anatomic insights. Pulmonary edema is depicted as a persistent imbalance between the forces that move water into the extravascular spaces and the biologic devices for its removal. In the normal lung, intricate anatomic arrangements coupled with elaborate physiologic mechanisms maintain the gas-exchanging surfaces moist and free of excess protein. A transient excess of water in the interstitial space is associated with an increase in lymphatic flow. Should the excess rate of formation persist or increase, pulmonary edema may become manifest clinically, first as interstitial edema and then as alveolar and airway edema. The distribution of edema within the lung may be nonuniform, often favoring the central portions early in its genesis but later redistributing under the influence of gravity. A critical limitation in anatomic design is imposed by the narrow channels through which lymph passes out of the thorax into systemic veins. Accordingly, the pulmonary lymphatic system, which seems better suited to return proteins than water to the systemic circulation, may become a limiting factor in relieving pulmonary edema in states of unremitting water movement into the extravascular spaces.
The anatomic and physiologic principles are then applied to current clinical enigmas, such as "shock lung," high-altitude pulmonary edema, and the edema that follows an overdose of narcotic agents, such as heroin. In "shock lung" after severe systemic hypotension, nonuniform pulmonary hypoperfusion is identified as the critical pathogenetic factor in the pulmonary edema that occurs during recovery, i.e. after systemic blood pressures have been restored to normal by large transfusions. The corresponding etiologic role for high-altitude pulmonary edema is attributed to anatomic variations in precapillary resistances in the lungs during a burst of severe pulmonary hypertension. The situation is more complicated for the pulmonary edema that follows narcotic overdosage since not only may the medication elicit severe respiratory depression, arterial hypoxemia, respiratory acidosis, and their sequelae–left ventricular failure, leakage of minute pulmonary vessels, and impaired lymphatic drainage–but the self-administered medication may be contaminated with substances that may, per se, cause minute pulmonary vessels to leak.
Clinical and Anatomic Implications of Intraventricular Conduction Blocks in Acute Myocardial Infarction
Authors: SCHEINMAN M. , BRENMAN B. 
Published: June 2012

The electrocardiogram in 480 patients with acute myocardial infarction showed right bundle-branch block (RBBB) with normal QRS axis in 18 patients (3.7%), left bundle-branch block (LBBB) in 31 (8%), RBBB and left anterior hemiblock (LAH) in 23 (4.8%), RBBB and left posterior hemiblock (LPH) in four (1%), LAH alone in 20 (4%), LPH in one (0.2%), and no evidence of intraventricular conduction (I-V) disturbance in 383 (80%). Eighteen of the 97 patients with I-V block showed 1° A-V block, and seven of the 18 (39%) showed abrupt progression to high-grade A-V block, while only six of 79 (8%) without 1° A-V block showed similar progression.
Cause of death in patients with I-V block was cardiac failure and/or shock in 92%; only three instances of primary asystole occurred. The incidence of complete heart block was higher in the I-V disease group (15%) than in the group without block (5%), but not significantly. Patients with LAH or RBBB and LAH usually had occlusion of the left anterior descending artery with extensive septal infarction, while patients with RBBB or LBBB had a more variable pattern of vessel involvement. Presence of I-V block in patients with acute myocardial infarction implies a hectic clinical course with poor prognosis, but does not justify prophylactic temporary transvenous intracardiac pacing except perhaps in the subgroup with associated 1° A-V block.
Serial Determination of Plasma Catecholamines in Myocardial Infarction
Authors: VIDEBAEK JØRGEN , CHRISTENSEN NIELS JUEL , STERNDORFF BENT 
Published: June 2012

By the use of a precise and sensitive double-isotope derivative technic, plasma catecholamine concentration was measured at 2-hour intervals in 10 patients during the first 48 hours of myocardial infarction.
Plasma catecholamine concentration was elevated in most patients, but to an extremely variable degree. In each patient, however, the values were rather stable during the study period. High levels of plasma catecholamines were correlated to the clinical state of the patients. Patients who received antiarrhythmic treatment on admission to the hospital had higher values than untreated patients. There was no temporal correlation between plasma catecholamine concentration and ventricular arrhythmias. In contrast to the plasma catecholamine level, the heterotopic ventricular activity declined spontaneously in the untreated patients within the study period.
It is emphasized that the plasma catecholamine concentration in patients with acute myocardial infarction is considerably lower than the level necessary to produce arrhythmias in experimental myocardial infarction.
Pathology of Angina Pectoris
Authors: VLODAVER ZEEV , NEUFELD HENRY N. , EDWARDS JESSE E. 
Published: June 2012

Among the wide variety of causes of angina pectoris, two major categories may be recognized: the anatomic, causing arterial obstruction, and the functional.
The anatomic causes may be divided according to anatomic sites as follows: (1) the major coronary arterial trunks and their epicardial branches, (2) the coronary ostia at the aorta, and (3) the intramyocardial "small" arteries. The major coronary arteries are by far the most common sites for anatomic lesions. Atherosclerosis in its various anatomic manifestations is responsible for about 90% of the cases of angina. Commonly, hypertension and, less commonly, valvular disease are associated. The balance of cases of angina result from various states given below. Nonatheromatous diseases of the major coronary arteries include embolism, primary dissecting aneurysm of a coronary artery, arteritis, and anomalous communication of a coronary artery. Coronary ostial narrowing results from various diseases of the aorta including atherosclerosis, saccular and dissecting aneurysm, inflammation, and calcification of the aorta in relation to origin of a coronary artery. Lesions causing obstruction of the intramyocardial arteries are commonly part of systemic diseases such as hematologic, embolic, metabolic, and degenerative.
Functional causes of angina pectoris include aortic valvular disease and functionally related conditions, thyroid disease, and pulmonary hypertension.
Echocardiography in the Diagnosis of Ebstein's Anomaly of the Tricuspid Valve
Authors: LUNDSTRÖM NILS-RUNE 
Published: June 2012

Nineteen patients aged between 4 days and 40 years with Ebstein's anomaly of the tricuspid valve have been examined with echocardiography. The diagnosis was verified with angiocardiography in all but one patient. The results at echocardiography are compared with those found in some other patients where an echo from the anterior tricuspid leaflet could be obtained (atrial septal defect, total anomalous pulmonary venous return, pulmonary hypertension, and one patient with congenital tricuspid stenosis).
An echo from the anterior tricuspid leaflet could be obtained in all patients with Ebstein's anomaly. This echo had an abnormal pattern of movement with an abnormally anterior position during the entire diastole. A late tricuspid opening was found in most patients. A late tricuspid closure compared with the time of mitral closure was a constant finding. It is suggested that this late tricuspid closure is mainly caused by mechanical factors related to the abnormal, large anterior tricuspid leaflet. The abnormal pattern of movement of the echo from the anterior tricuspid leaflet with a late tricuspid closure has not been found in any other patient examined.
Nonrheumatic Subvalvular Mitral Regurgitation
Authors: CAVES PHILIP K. , SUTTON GEORGE C. , PANETH MATTHIAS 
Published: June 2012

Thirty-three patients are reported with nonrheumatic mitral regurgitation due to rupture or stretching of the chordae tendinaeae or papillary muscles. Nineteen (58%) had no definite predisposing etiological factors (average age 59 years). Six (19%) had a previous myocardial infarction. It is proposed that rupture or stretching of the chordae resulted from degenerative or ischemic changes in the chordae and/or papillary muscles. Six young patients had ruptured chordae from other causes. Two patients had myocardial infarction resulting in rupture of the posteromedial papillary muscle.
Characteristic clinical findings included progressive dyspnea of sudden onset, sinus rhythm, systolic thrill, accentuated pulmonary valve closure sound, third heart sound, and widely propagated pansystolic murmur. The electrocardiogram frequently showed inferolateral ischemic changes. Plain chest radiographs usually showed a normal-sized heart and left atrium in patients in sinus rhythm. At cardiac catheterization a characteristic high V wave in the pulmonary artery wedge pressure was seen in 88% of patients. The left ventricular end-diastolic pressure was highest in the six postinfarct patients in whom the ejection fraction was significantly low.
Vein Graft Surgery for Coronary Artery Disease
Authors: SHELDON WILLIAM C. , RINCON GUSTAVO , EFFLER DONALD B. , PROUDFIT WILLIAM L. , SONES F. MASON 
Published: June 2012

One thousand patients were operated upon with vein graft techniques for severe coronary artery obstructions between May 1967 and July 1970, with a hospital mortality rate of 4% and a 5.6% incidence of angiographically confirmed in-hospital myocardial infarctions. Postoperative angiograms, performed in 619 of the survivors, revealed patency of one or more vein grafts in 84.2% of patients, and 82.5% of all grafts were patent in studies performed 1 to 49 months after surgery.
The hospital survivors were followed for 22 to 60 months; only three patients were lost to follow-up. The survival curve for this group of patients was compared with that of another group of 469 patients who also had severe coronary artery disease and were potential surgical candidates, but were studied in an earlier period and did not have surgical treatment. The annual rate of attrition for each of the four years of follow-up in the surgical group averaged 4.8% per year (2.5% per year excluding hospital mortality), and 9.3% per year in the nonsurgical group. Remission of symptoms correlated closely with the completeness of revascularization.
Myocardial revascularization with vein graft techniques can be accomplished successfully and with low risk in the majority of properly selected patients, resulting in a significant improvement in symptoms, as well as in long-term survival.
Lesions Observed in Arterial Autogenous Vein Grafts
Authors: JONES MICHAEL , CONKLE DAVID M. , FERRANS VICTOR J. , ROBERTS WILLIAM C. , LEVINE FREDERICK H. , MELVIN DAVID B. , STINSON EDWARD B. 
Published: June 2012

Autogenous vein grafts used for canine femoral and aortocoronary arterial bypasses were evaluated from 2 to 365 days postoperatively. Femoral grafts showed focal endothelial disruption, mural fibrin deposition, and medial edema with inflammatory infiltrates during the first week; loss of medial smooth muscle cells and focal subendothelial lesions with intact endothelium by 2 weeks; and diffuse subendothelial lesions by 12 weeks, Coronary grafts studied at 6, 9, and 12 months had medial fibrosis and extensive intimal proliferation causing up to 90% luminal narrowing. Extension of the intimal process into the coronary artery distal to the bypass graft also compromised the arterial lumen. Coronary grafts obtained from humans dying 17 and 57 days after graft insertion revealed a similar subendothelial proliferation.
Electron microscopy showed that the subendothelial lesions were composed of mature smooth muscle cells and collagen primarily oriented parallel to the axis of blood flow. Recurrent endothelial cell damage, followed by mural fibrin deposition and organization, appears to be the cause of the subendothelial proliferative lesions.
Valve Replacement for Bacterial and Fungal Endocarditis
Authors: UTLEY JOE R. , MILLS JOHN , HUTCHINSON JOHN C. , EDMUNDS L. HENRY , SANDERSON RICHARD G. , ROE BENSON B. 
Published: June 2012

Twenty-eight of 143 patients treated for infective endocarditis had replacement of one or more cardiac valves within six months after the diagnosis was made. Twenty-two patients (16%) with bacterial endocarditis had operation, and six died in hospital. All six patients with fungal endocarditis required vale replacement, and one died in hospital. Uncontrolled or progressive heart failure was the indication for operation in all patients with bacterial endocarditis. When severe heart failure was present, 5 of 11 patients with bacterial endocarditis died in hospital, and only 1 of 3 patients with associated bacteremia survived. If blood cultures were sterile, the duration of preoperative antibiotic therapy did not correlate with hospital survival. None of the patients with bacterial endocarditis developed prosthetic infections, but two developed paravalvular leak.
Massive emboli or persistent mycotic septicemia were the indications for valve replacement in patients with fungal endocarditis. Viable organisms were cultured from the excised valves in all of these patients in spite of preoperative amphotericin B for 30 to 140 days and negative blood cultures. Excision of the infected valve cured the infection in all patients.
Five patients died 6 weeks to 36 months after operation. At the present time 16 patients remain alive 14 to 47 months after operation. Six of nine drug addicts are alive 15 to 27 months postoperatively.
Arrival of Excitation at the Right Ventricular Apical Endocardium in Wolff-Parkinson-White Syndrome Type B
Authors: BEFELER BENJAMIN , CASTELLANOS AGUSTIN , CASTILLO CESAR A. , AGHA ABDUL S. , VAGUEIRO M. CELESTE , MYERBURG ROBERT J. 
Published: June 2012

His bundle and bipolar right ventricular apex (RVA) and right ventricular outflow tract (RVOT) catheter electrograms taken from sites 1 mm apart were recorded simultaneously with various surface leads in two patients with Wolff-Parkinson-White syndrome (WPW) type B. In "fusion" beats the presence of a normal H-RVA interval indicated that the apex of the right ventricle was activated by the impulse emerging from the right branch. On the other hand, a shorter-than-normal H-RVA interval implied that the RVA was depolarized by the activation front propagating from the pre-excited site. When this occurred, the V-RVA intervals gave a rough estimate of conduction time from pre-excited area to RVA. The values obtained (40 and 50 msec, respectively) were shorter than in two other patients with WPW type A.
The arrival of excitation patterns in the right ventricular endocardium were similar in WPW type B and in beats produced by RVA stimulation but differed markedly from that of left anterior hemiblock even when the surface electrocardiographic leads showed abnormal left axis deviation in all instances. This resemblance between ventricular complexes attributed to WPW type B and those resulting from stimulation of an inferior (apical) site suggests, but does not prove, that the impulses propagated from an equivalent region of the right ventricle. These simultaneously recorded His bundle and right ventricular endocardial electrograms during electrical stimulation of the heart have increased our knowledge of Wolff-Parkinson-White syndrome.
Sleep and Ventricular Premature Beats
Authors: LOWN BERNARD , TYKOCINSKI MARK , GARFEIN ANDRE , BROOKS PHILLIP 
Published: June 2012

Sixty-nine 24-hour electrocardiographic monitoring sessions were conducted in 54 ambulatory subjects. Thirty-one had coronary heart disease (CHD); 11 had miscellaneous heart ailments; and 12 were free of any heart disease. Monitoring was accomplished with a miniaturized cassette recorder and ventricular premature beats (VPBs) were analyzed as to incidence and grade. The occurrence of VPBs during sleep hours was compared to the awake state.
In 22 patients, the incidence of VPBs was reduced by at least 50% during sleep. An additional 13 patients showed a reduction of 25 to 50%. If patients free of ectopic activity during 24-hour monitoring sessions are excluded from analysis, then in 35 of 45 patients, or in 78%, sleep was associated with a lowered occurrence of ventricular extrasystoles. During sleep the VPB grade was likewise lowered. Thus the mean grade for 45 patients changed from 2.75 while awake to 1.78 while asleep. It is of interest that in a number of these patients, trials of various antiarrhythmic drugs were less effective than sleep in reducing the incidence and grade of VPBs. It is concluded that treatment of sporadically occurring ventricular ectopic activity in some patients may require attention to the neurophysiologic trigger rather than the cardiac target.
Left Ventricular Pressure-Volume Relationships During Myocardial Ischemia in Man
Authors: McCANS JOHN L. , PARKER JOHN O. 
Published: June 2012

It has been shown in man that myocardial ischemia, whether precipitated by exercise or pacing-induced tachycardia, is associated with abnormalities of left ventricular end-diastolic pressure. There has been controversy as to whether this relationship is due to decreased myocardial compliance or to an increase in left ventricular volume as a manifestation of left ventricular failure. Simultaneous measurements of left ventricular pressure and left ventricular volume using ultrasonic techniques were carried out in five normal subjects and 21 patients with coronary artery disease. In the normal subjects a decrease in left ventricular end-diastolic pressure during pacing was associated with a decrease in left ventricular end-diastolic volume, and during interruption of pacing, pressures and volumes returned to normal. In nine patients with coronary artery disease who did not develop angina, a similar response was seen. In 12 patients with coronary artery disease who developed angina during pacing, the reduction in left ventricular end-diastolic volume during pacing was less marked than the other groups and during periods of interruption the increase in diastolic pressure to 26 mm Hg was accompanied by an increase in left ventricular end-diastolic volume to 24% above control values. The end-systolic volume showed a similar increase during myocardial ischemia.
These data suggest that the changes in left ventricular filling pressure seen during myocardial ischemia are related to increase in left ventricular volume but do not exclude the possibility that there may be accompanying changes in left ventricular diastolic compliance.
Left Ventricular Function and Coronary Artery Anatomy Before and After Myocardial Infarction
Authors: STEWART DOUGLAS K. , HAMILTON GLEN W. , MURRAY JOHN A. , KENNEDY J. WARD 
Published: June 2012

Six patients underwent cardiac catheterization before and after occurrence of a myocardial infarction. Results from the two procedures allowed the quantitation of changes in coronary artery anatomy and left ventricular performance associated with myocardial infarction.
Left ventricular biplane or single plane angiography and selective coronary angiography were used to evaluate coronary artery anatomy, left ventricular end diastolic pressure (LVEDP), left ventricular end diastolic volume (LVEDV), end systolic volume (LVESV), and systolic ejection fraction (SEF) under resting conditions.
Four patients had developed occlusion of the artery supplying the area of infarction. In five cases new or progressive contraction abnormalities occurred. One patient had no change in contraction pattern or SEF. Systolic ejection fraction fell in three patients, with no change in LVEDV. In two patients LVEDV rose and SEF fell.
These data demonstrate that a wide spectrum of functional abnormalities is associated with myocardial infarction. Infarction was always associated with significant coronary artery stenosis, but not necessarily associated with occlusion. The SEF and contractile pattern were the indicators of left ventricular dysfunction which most frequently deteriorated.
Late Postoperative Conduction Disturbances After Repair of Ventricular Septal Defect and Tetralogy of Fallot
Authors: GODMAN M. J. , ROBERTS N. K. , IZUKAWA T. 
Published: June 2012

His bundle electrograms were recorded in five children who developed complete heart block (CHB) five months to five years after cardiac surgery. In four children who had an electrocardiographic pattern of right bundle branch block and left axis deviation (RBBB and LAD) preceding the appearance of CHB, the site of block was distal to the area generating the His potential. The fifth child, who had an electrocardiographic pattern of RBBB with normal axis prior to the development of CHB, had block occurring proximal to the area generating His potential. All five children had had transient CHB in the immediate postoperative period.
In an additional 17 postoperative patients, His bundle recordings were obtained during sinus rhythm. Five out of ten patients with RBBB and LAD on the electrocardiogram and one patient with LBBB had H-V interval prolongation, a recording suggesting incomplete bilateral bundle branch block or trifascicular block. Six patients with RBBB only on the electrocardiogram had normal H-V intervals. All the patients with H-V interval prolongation had had CHB transiently in the immediate postoperative period.
This study suggests that patients with an electrocardiographic pattern of RBBB and LAD who have had transient CHB postoperatively may have, more extensive residual damage to the conduction system than suspected on the basis of the surface electrocardiogram alone and because of the risk of late recurrence of CHB should be given a guarded prognosis.
Deterioration of Myocardial Function Following Aorto-Coronary Bypass Operation
Authors: SHEPHERD RICHARD L. , ITSCOITZ SAMUEL B. , GLANCY D. LUKE , STINSON EDWARD B. , REIS ROBERT L. , OLINGER GORDON N. , CLARK CHESTER E. , EPSTEIN STEPHEN E. 
Published: June 2012

Twenty-two patients underwent cardiac catheterization before and an average of five months after aorto-coronary bypass operation (ACBO). Two groups were examined: 10 patients with all grafts patent, and 12 patients with one or more grafts occluded. All patients improved symptomatically, regardless of graft patency. However, in the occluded group, left ventricular end-diastolic pressure (LVEDP) increased (4.4 ± 2.2 mm Hg,
P
< 0.05), stroke volume index fell (9.8 ± 3.1 ml/m
2
,
P
< 0.05), ejection fraction decreased (10 ± 4%,
P
< 0.05), and left ventricular stroke work index fell (12 ± 3 g-m/m
2
,
P
< 0.01).

Qualitative analysis of segmental left ventricular contractility was performed. Of 28 segments supplied by patent grafts, six improved and nine deteriorated. Of 22 segments supplied by occluded grafts, none improved and eight deteriorated. Frequently no angiographically demonstrable basis for the segmental deterioration was evident.
We concluded that while ACBO may appreciably benefit severely symptomatic patients, our results do not substantiate the claim that ACBO should be recommended when the primary surgical goal is preservation or enhancement of myocardial function.