bluuebunny/crossref_metadata_2025_split huggingface dataset:
Radiofrequency catheter ablation of sustained intra-atrial reentrant tachycardia in adult patients. Identification of electrophysiological characteristics and endocardial mapping techniques.
Authors: Chen S A , Chiang C E , Yang C J , Cheng C C , Wu T J , Wang S P , Chiang B N , Chang M S 
Published: June 2012

BACKGROUND
Information about electrophysiological characteristics and radiofrequency ablation of intra-atrial reentrant tachycardia has not been reported before. We proposed that induction and termination of intra-atrial reentrant tachycardia by atrial extrastimuli or rapid atrial pacing and resetting the response pattern by atrial extrastimuli during intra-atrial reentrant tachycardia could ensure the mechanism of reentry and that the earliest site of endocardial activation and concealed entrainment pace mapping with the shortest stimulus-P wave interval could localize a critical area responsible for intra-atrial reentrant tachycardia and radiofrequency ablation.

METHODS AND RESULTS
Seven patients with refractory atrial tachycardia were referred for electrophysiological studies and radiofrequency ablation. Electrophysiological studies and endocardial mapping found (1) 10 atrial foci with atrial tachycardia cycle length of 406 +/- 41 ms; (2) atrial tachycardia had induction and termination by atrial extrastimuli (8 of 10) or rapid atrial pacing (10 of 10); (3) atrial tachycardia had increasing (6 of 10) or mixed (flat and increasing, 4 of 10) resetting response pattern, with resetting interval of 57 +/- 13 ms (14 +/- 4% of atrial tachycardia cycle length); (4) exit sites of atrial tachycardia in right atrial free wall (6 of 10), right atrial septum (3 of 10), and midposterior left atrium (1 of 10); and (5) earliest activation site had timing relative to P wave by -37 +/- 7 ms, and concealed entrainment pace mapping had shortest stimulus-P interval 23 +/- 3 ms. By the endocardial activation pace-mapping technique, radiofrequency energy (8 +/- 1 pulses, 31 +/- 3 W, 101 +/- 11 seconds) successfully eliminated the 10 atrial foci without recurrence (follow-up, 16 +/- 5 months).

CONCLUSIONS
Mechanism of intra-atrial reentrant tachycardia could be confirmed by the electrophysiological characteristics, and radiofrequency ablation energy delivered to a critical area in the atrial reentrant circuit is safe and effective for the treatment of intra-atrial reentrant tachycardia.
Implantation and intermediate-term follow-up of stents in congenital heart disease.
Authors: O'Laughlin M P , Slack M C , Grifka R G , Perry S B , Lock J E , Mullins C E 
Published: June 2012

BACKGROUND
Balloon-expandable stents (Johnson and Johnson Interventional Systems) have been in use for congenital heart disease since late 1989. They have made possible treatment in previously untreatable branch pulmonary artery stenoses and systemic venous stenosis. The purpose of this report is to detail the results and intermediate-term follow-up of stents used for treatment of congenital heart disease.

METHODS AND RESULTS
Eighty-five patients underwent placement of 121 stents in Houston and Boston. Fifty-eight patients had stents put in pulmonary arteries, nine had stents in conduits or outflow tracts, and 21 had stents in venous stenoses or narrowed Fontan anastomoses. (Three patients had stents in two locations.) These stent procedures resulted in gradient reduction from 55.2 +/- 33.3 to 14.2 +/- 13.5 mm Hg in pulmonary arteries, from 41.4 +/- 26.0 to 20.7 +/- 17.0 mm Hg in conduits or outflow tracts, and from 9.8 +/- 6.9 to 2.4 +/- 3.1 mm Hg in venous stenoses or Fontan anastomoses. Diameter of narrowings increased from 4.6 +/- 2.3 to 11.3 +/- 3.2 mm in the pulmonary artery, from 8.8 +/- 3.6 to 12.7 +/- 2.6 in conduits, and from 3.8 +/- 2.9 to 11.3 +/- 2.8 in venous stenoses. Follow-up has shown stent fracture in one patient, restenosis in one, and sudden death in one. Recatheterization has been done in 38 patients an average of 8.6 months after stent installation. Compared with immediately postimplant data, there was no significant change in luminal diameter or pressure gradient. Redilation was performed in 14 patients (17 stents) 1 week to 24 months after implantation (mean, 10.2 months), with a small but significant increase in stenosis diameter.

CONCLUSIONS
We conclude that stent treatment of vascular stenoses in congenital heart disease retains efficacy at medium-term follow-up and offers a much-improved outlook for patients with these lesions.
Growth of the aortic anastomosis, annulus, and root after the arterial switch procedure performed in infancy.
Authors: Hourihan M , Colan S D , Wernovsky G , Maheswari U , Mayer J E , Sanders S P 
Published: June 2012

BACKGROUND
We investigated the size and growth potential of the neoaortic root and aortic anastomosis after the arterial switch operation (ASO) for D-transposition of the great arteries (D-TGA) performed in infants. Circumferential suture lines connecting the great arteries and extensive surgery on the arterial roots to transplant the coronary arteries are essential parts of the ASO. However, little is known about the growth of the aortic anastomosis, the neoaortic root, and the neoaortic annulus after the ASO performed in infancy.

METHODS AND RESULTS
Serial echocardiograms on 50 patients with D-TGA who underwent ASO in infancy at our institution were reviewed, and the size of the aortic anastomosis, the neoaortic root, and the neoaortic annulus were compared with similar structures in a group of 312 control subjects. Before surgery, the native pulmonary root (future neoaortic root) was 1.59 SD larger (P < .001) and the native pulmonary annulus (future neoaortic annulus) was 1.4 SD larger (P < .001) in infants with D-TGA than the aortic root and annulus of control patients. At a mean of 22 months (12 months to 6 1/2 years) after surgery, the diameter of the aorta at the anastomosis was 0.45 SD smaller than the ascending aorta of control subjects (P < .001). The neoaortic root was 2.9 SD larger (P < .001) and the neoaortic annulus was 1.6 SD larger (P < .001) than the comparable structures in the control population. Most important, growth of the aortic anastomosis was commensurate with somatic growth, but the dilation of the neoaortic root appeared to be progressive over time. The neoaortic root was significantly more dilated in patients with a history of pulmonary artery banding (P < .001) and in patients with neoaortic regurgitation (P < .001). The presence of a ventricular septal defect was not significantly related to postoperative neoaortic root size.

CONCLUSIONS
This study underlies the importance of continued acquisition and examination of the data regarding the long-term outcome of the arterial switch operation performed in infancy.
Echocardiographic follow-up of atrial septal defect after catheter closure by double-umbrella device.
Authors: Boutin C , Musewe N N , Smallhorn J F , Dyck J D , Kobayashi T , Benson L N 
Published: June 2012

BACKGROUND
Transcatheter device occlusion of atrial septal defects is an attractive approach, but its efficacy and place in patient management remain to be determined.

METHODS AND RESULTS
To evaluate the medium-term results of atrial septal defect device occlusion and factors influencing residual shunting, transesophageal and transthoracic echocardiograms of 49 patients were reviewed. Transesophageal echocardiograms on 48 patients immediately following surgical closure revealed residual shunting in 2% compared with 91% after device occlusion; this proportion decreased to 53% after a mean follow-up of 10 months. The actuarial analysis suggests a progressive resolution of shunting with time. One patient had residual shunting by transesophageal echocardiography immediately after surgical closure compared with 29 after a mean follow-up of 10 months after device occlusion. Residual shunting was not influenced by (1) dimension, location, or position with relation to the device as assessed by transesophageal echocardiography; (2) location of the defect; or (3) device size relative to the stretched dimension of the defect. In 15 patients, a poor correlation existed between transesophageal and transthoracic echocardiographic findings. Variability in serial transthoracic echocardiographic findings was observed in 14. Right ventricular dimension, heart size, and presence of a murmur at follow-up did not correlate with the presence or size of residual shunting after device occlusion.

CONCLUSIONS
These results suggest that ongoing spontaneous resolution of residual shunting occurs after device insertion. Factors related to the defect or device could not predict eventual resolution of residual shunting. Transthoracic echocardiography in the follow-up of these patients may not be reliable in determining presence of residual shunting.
Natriuretic peptide system in human heart failure.
Authors: Wei C M , Heublein D M , Perrella M A , Lerman A , Rodeheffer R J , McGregor C G , Edwards W D , Schaff H V , Burnett J C 
Published: June 2012

BACKGROUND
Atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-type natriuretic peptide (CNP) are a family of structurally related peptides that participate in the integrated control of renal and cardiovascular function. Previous studies suggest a functional role for these hormonal peptides in cardiorenal regulation in congestive heart failure (CHF).

METHODS AND RESULTS
The present studies were performed in normal subjects (n = 6) and in patients with mild (New York Heart Association [NYHA] class I to II, n = 20) and severe (NYHA class III to IV, n = 20) CHF by use of radioimmunoassay and immunohistochemical staining (IHCS). Plasma ANP was significantly increased in both mild and severe CHF compared with normal subjects. In contrast, plasma BNP was only moderately increased in the severe CHF group, and plasma CNP concentration was unchanged in CHF compared with normal subjects. Atrial tissue concentrations of the natriuretic peptides did not parallel circulating concentrations. ANP predominated in normal atrial tissue, but BNP predominated in CHF. In ventricular tissue, IHCS staining was present for all three peptides in normal ventricular myocardium and was markedly enhanced in CHF.

CONCLUSIONS
These studies support a differential regulation of ANP, BNP, and CNP circulating concentrations and tissue activity in human CHF.
Inhibition of experimental neointimal hyperplasia and thrombosis depends on the type of vascular injury and the site of drug administration.
Authors: Rogers C , Karnovsky M J , Edelman E R 
Published: June 2012

BACKGROUND
Heparin inhibits vascular smooth muscle cell proliferation in tissue culture and limits neointimal hyperplasia after experimental arterial injury but has been ineffective in reducing clinical restenosis. We examined how this discrepancy might reflect suboptimal drug-tissue interactions and/or differences in the vascular response to injury.

METHODS AND RESULTS
Intravenous infusion was compared with local administration of heparin to injured rabbit iliac arteries either from drug-impregnated polymeric controlled release matrices in the perivascular space or from drug-releasing endovascular stents. Occlusive thrombosis, seen in 42% of control stent-bearing arteries, and partial thrombosis were virtually eliminated by heparin delivery from any route. Intimal area 14 days after balloon withdrawal denudation alone was reduced to an equal extent by continuous systemic heparin or by perivascular heparin for the first 3 days. In contrast, endovascular stents produced more exuberant neointimal hyperplasia, the inhibition of which required continuous rather than only early heparin administration. Neither perivascular delivery limited to the first 3 days nor stent-based delivery reduced neointimal hyperplasia as effectively.

CONCLUSIONS
The antiproliferative and antithrombotic effects of heparin differ markedly, depending on the type of arterial injury and the mode of drug administration. Different forms of injury may require different therapies, and complications of arterial intervention such as excessive neointimal hyperplasia and thrombosis may demand alternate therapeutic regimens. Duration, dose, and site of delivery rather than frank resistance to therapy may explain why experimentally effective antiproliferative and antithrombotic agents fail clinically.
Reduced content of connexin43 gap junctions in ventricular myocardium from hypertrophied and ischemic human hearts.
Authors: Peters N S , Green C R , Poole-Wilson P A , Severs N J 
Published: June 2012

BACKGROUND
Gap junctions are a determinant of myocardial conduction. Disturbances of gap-junctional content may account for abnormalities of impulse propagation, contributing to the arrhythmic tendency and mechanical inefficiency of ischemic and hypertrophied myocardium. The aim of this study was to characterize gap junction organization in normal human ventricular myocardium and to establish whether abnormalities exist in myocardium of chronically ischemic and hypertrophied hearts.

METHODS AND RESULTS
Cardiac gap-junctional connexin43 antibodies and confocal microscopy were used in a quantitative immunohistochemical study of surgical myocardial samples to explore the structural basis of electromechanical ventricular dysfunction in chronic ischemic and hypertrophic heart diseases. Normal adult human left ventricular myocardium had a gap-junctional surface area of 0.0051 micron2/micron3 myocyte volume; gap junctions were confined to intercalated disks, of which there was a mean of 11.6 per cell. The right ventricle showed similar gap junction surface area. Left ventricular myocardium from ischemic hearts (distant from any fibrotic scarring), despite normal numbers of intercalated disks per cell, had a reduced gap junction surface area (0.0027 micron2/micron3; P = .02), as did hypertrophied myocardium (0.0031 micron2/micron3; P = .05). The cardiac myocytes in the pathological tissues were larger than normal, and estimated gap-junctional content per cell was reduced in ischemic ventricle (P = .02) compared with normal.

CONCLUSIONS
Gap junctions in normal adult human working ventricular myocardium occupy an area of 0.0051 micron2/micron3 myocyte volume. This surface area is reduced in ventricular myocardium from hearts subject to chronic hypertrophy and ischemia, despite a normal number of intercellular abutments, and this alteration may contribute to abnormal impulse propagation in these hearts.
Regional blood flow, oxidative metabolism, and glucose utilization in patients with recent myocardial infarction.
Authors: Czernin J , Porenta G , Brunken R , Krivokapich J , Chen K , Bennett R , Hage A , Fung C , Tillisch J , Phelps M E 
Published: June 2012

BACKGROUND
Metabolic imaging with positron emission tomography (PET) can detect tissue viability in clinical infarct regions. With appropriate tracer kinetic models and serial PET imaging, regional myocardial blood flow and rates of metabolism can now be quantified in patients with recent myocardial infarctions.

METHODS AND RESULTS
Serial PET imaging with [13N]ammonia, [11C]acetate, and 18F-deoxyglucose was performed in 22 patients with recent infarctions to measure regional blood flow (in milliliters per gram per minute), glucose metabolism (in micromoles per gram per minute), and oxidative metabolism (in clearance rate per minute). Hypoperfused clinical infarct regions were classified as "PET mismatch" if 18F was increased relative to 13N activity or "PET match" if 13N and 18F activities were reduced concordantly. Blood flows differed significantly between normal, mismatch, and match segments (0.83 +/- 0.20, 0.57 +/- 0.20, and 0.32 +/- 0.12 mL.g-1.min-1, respectively). The relation between oxidative metabolism and blood flow was piecewise linear and differed significantly between PET mismatch and PET match. Oxidative metabolism was less severely reduced than blood flow in mismatch regions but but reduced in proportion to blood flow in match regions. There was considerable overlap of blood flows between both types of PET segments.

CONCLUSIONS
Quantification of regional blood flow and substrate metabolism in postinfarction patients revealed alterations in the relation between substrate delivery and consumption demonstrated previously only in invasive animal experiments. The preserved oxidative metabolism in myocardium with PET mismatches may be ascribed to a regional increase in oxygen extraction. Such increase together with preserved glucose utilization may be the prerequisite for survival of ischemically injured myocardium.
Relation of plasma lipoprotein(a) to infarct artery patency in survivors of myocardial infarction.
Authors: Moliterno D J , Lange R A , Meidell R S , Willard J E , Leffert C C , Gerard R D , Boerwinkle E , Hobbs H H , Hillis L D 
Published: June 2012

BACKGROUND
In the minutes to days after myocardial infarction, endogenous lysis of an occlusive coronary arterial thrombus occurs in most subjects. Compared with those in whom thrombolysis does not occur, those with antegrade flow in the infarct artery have improved left ventricular performance, less left ventricular dilatation, and improved survival. This study was performed to assess intrinsic hemostasis and fibrinolysis in survivors of myocardial infarction with or without antegrade perfusion of the infarct artery.

METHODS AND RESULTS
In 105 survivors of infarction (75 men, 30 women; age, 30 to 80 years) not given thrombolytic therapy, coronary angiography revealed a patent (group 1, n = 52) or occluded (group 2, n = 53) infarct artery. Plasma concentrations of plasminogen, fibrinogen, tissue plasminogen activator activity, infarct artery. Plasma concentrations of plasminogen, fibrinogen, tissue plasminogen activator activity, plasminogen activator inhibitor activity, cholesterol, triglycerides, and lipoproteins, including lipoprotein(a) (Lp[a]), were measured in blood procured 23 +/- 13 (mean +/- SD) months after infarction. Groups 1 and 2 were similar in age, sex, race, cardioactive medications, infarct artery, extent of coronary artery disease, and left ventricular performance. Of the plasma constituents assayed, the groups were similar except that Lp(a) averaged 18.5 +/- 21.7 mg/dL in group 1 and 49.1 +/- 44.8 mg/dL in group 2 (P < .001). This difference was evident in both Caucasian (n = 65) (P = .009) and African American (n = 40) (P = .01) subjects.

CONCLUSIONS
Survivors of myocardial infarction who failed to recanalize the infarct artery have higher plasma Lp(a) concentrations than those with a patent infarct artery. Lp(a) may inhibit intrinsic fibrinolysis.
Relation of phasic coronary flow velocity profile to clinical and hemodynamic characteristics of patients with aortic valve disease.
Authors: Hongo M , Goto T , Watanabe N , Nakatsuka T , Tanaka M , Kinoshita O , Yamada H , Okubo S , Sekiguchi M 
Published: June 2012

BACKGROUND
Our objective was to assess phasic coronary blood flow and velocity characteristics of the proximal portion of the left anterior descending artery and to evaluate their relation to the clinical and hemodynamic manifestations in patients with aortic valve disease.

METHODS AND RESULTS
We examined 26 patients with chronic aortic regurgitation (AR), 12 patients with predominant aortic stenosis (AS), and 11 control subjects using an intravascular Doppler catheter with spectral analysis. Angiographic assessment of AR identified 10 patients with mild regurgitation and 16 with severe regurgitation. The resting systolic coronary flow velocity-time integral (VTI) was significantly higher and the diastolic VTI was slightly but significantly higher in patients with severe regurgitation than in those with mild regurgitation (11.8 +/- 4.2 vs 4.1 +/- 1.1 cm, P < .001; 18.5 +/- 5.8 vs 13.2 +/- 3.2 cm, P < .05) and control subjects (4.0 +/- 1.0 cm, P < .001 and 13.3 +/- 3.6 cm, P < .05), respectively. Patients with AS had a slightly lower resting systolic VTI (3.8 +/- 1.4 cm) and a higher diastolic VTI (14.6 +/- 3.7 cm) than control subjects. Resting coronary blood flow was greater in patients with aortic valve disease than in control subjects. There was a significant correlation between the ratio of the resting systolic to diastolic VTI (S/D ratio) and the ratio of the aortic systolic to diastolic pressure (r = .75, P < .001) in patients with AR. The S/D ratio was inversely correlated with left ventricular systolic pressure (r = -.92, P < .001) and positively correlated with the ratio of the aortic systolic to diastolic pressure (r = .68, P < .05) in patients with AS.

CONCLUSIONS
Our results indicate that hemodynamic changes related to aortic valve disease contribute to alterations in the resting phasic coronary blood flow and velocity profiles observed in these patients.
Streptokinase induces intravascular release of platelet-activating factor in patients with acute myocardial infarction and stimulates its synthesis by cultured human endothelial cells.
Authors: Montrucchio G , Bergerone S , Bussolino F , Alloatti G , Silvestro L , Lupia E , Cravetto A , Di Leo M , Emanuelli G , Camussi G 
Published: June 2012

BACKGROUND
Reocclusion of a successfully recanalized infarct-related artery may account for failure of thrombolytic therapy. Evidence suggests that the intravascular activation of platelets may limit the response to this treatment. The aim of the present study was to investigate whether platelet-activating factor (PAF), an ether lipid mediator with multiple potent biological activities, is synthesized during therapy with thrombolytic agents. Two sets of experiments were performed: (1) we extracted and quantified PAF in blood of patients with acute myocardial infarction treated or untreated with streptokinase (SK), and (2) since the endothelium/platelet interaction is thought to be at the basis of vascular reocclusion, we studied whether cultured human endothelial cells synthesize PAF after stimulation with SK or plasmin.

METHODS AND RESULTS
PAF was extracted from blood samples immediately after acidification to destroy the acid-labile PAF-acetylhydrolase in 25 patients with acute myocardial infarction treated (group A, n = 14) and untreated (group B, n = 11) with intravenous infusion of SK. PAF was detected in 10 of 14 patients of group A and none of group B. PAF began to be detectable 60 to 90 minutes after SK infusion and disappeared from the circulation within 120 to 180 minutes. Percent variation of platelet count over basal values correlated negatively with the amount of PAF present in the circulation at 90 minutes (r = -.719; P < .001) and at 120 minutes (r = -.652; P < .001). Cultured human umbilical cord vein-derived endothelial cells (ECs) synthesized PAF in a dose-dependent manner in response to SK and plasmin, with a synthesis that peaked at 15 minutes and persisted up to 30 minutes for SK and 2 hours for plasmin. PAF extracted from blood samples or from ECs was quantified by bioassay performed after purification by thin-layer chromatography and high-performance liquid chromatography (HPLC). PAF-bioactive material was characterized as PAF with physicochemical and enzymatic treatments, HPLC-tandem mass spectrometry, and specific PAF-receptor antagonists.

CONCLUSIONS
The observation that PAF was detectable in the blood of patients of group A only after treatment with SK and was not detectable in patients with a comparable infarct not treated with SK (group B) suggested that SK stimulates the synthesis of this mediator either directly or via plasmin generation. Indeed, cultured human ECs synthesize PAF after stimulation with both SK and plasmin. PAF production by ECs may promote platelet activation and interaction of these cells as well as of circulating leukocytes with endothelium. These events may limit the beneficial effects of thrombolytic therapy.