ISSN:0009-7322    

出版商:OVID    

年代:1995

数据来源: OVID

ISSN:0009-7322    

出版商:OVID    

年代:1995

数据来源: OVID

ISSN:0009-7322    

出版商:OVID    

年代:1995

数据来源: OVID

ISSN:0009-7322    

出版商:OVID    

年代:1995

数据来源: OVID

ISSN:0009-7322    

出版商:OVID    

年代:1995

数据来源: OVID

ISSN:0009-7322    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

Background The use of warfarin anticoagulation for several weeks before cardioversion results in a 90% reduction in the incidence of cardioversion-related thromboembolism. The mechanism of this benefit, however, is unknown; it has been widely attributed to organization and adherence of atrial thrombi, a finding observed among pathological studies of patients with rheumatic valvular disease.Methods and Results Serial transesophageal echocardiography was performed in 14 patients with nonrheumatic atrial fibrillation after identification of atrial thrombi on initial transesophageal study. All patients received warfarin anticoagulation and were followed clinically for signs of thromboembolism. Eighteen atrial thrombi were identified on initial transesophageal study, including 14 thrombi confined to the left atrial appendage, 2 in the body of the left atrium, 1 in the right atrial appendage, and 1 in the body of the right atrium. Thrombus size varied from 5 to 20 mm, and 6 were considered mobile. After a median of 4 weeks of warfarin, 16 of 18 atrial thrombi (89%; 95% CI, 73% to 100%) had completely resolved on transesophageal echocardiographic study. In addition, no new thrombi were identified on follow-up study, and no patient had a clinical thromboembolic event between studies.Conclusions These data strongly support the hypothesis that among patients with nonrheumatic atrial fibrillation, the mechanism of clinical benefit with 3 to 4 weeks of warfarin before cardioversion is related to thrombus resolution and prevention of new thrombus formation rather than thrombus organization. (Circulation. 1995;92:156-159.)

ISSN:0009-7322    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

Background Little is known about the characteristics of the inwardly rectifying K sup + channel (I sub K1) and the influence of preexisting heart disease on the channel properties in the human heart.Methods and Results We studied the characteristics of cardiac I sub K1 in freshly isolated adult human atrial and ventricular myocytes by using the patch-clamp technique. Specimens were obtained from the atria and ventricles of 48 patients undergoing cardiac surgery or transplantation and from four explanted donor hearts. The action potential in ventricular myocytes exhibited a longer duration (391.4+-30.2 milliseconds at 90% repolarization, n=10) than in atrium (289.4+-23.0 milliseconds, n=18, P<.001) and had a fast late repolarization phase (phase 3). The final phase of repolarization in ventricle was frequency independent. Whole-cell IK1in ventricle exhibited greater slope conductance (84.0+-7.9 nS at the reversal potential, EK; n=27) than in atrium (9.7+-1.2 nS at EK; n=8, P<.001). The steady-state current-voltage (I-V) relation in ventricular IK1demonstrated inward rectification with a region of negative slope. This negative slope region was not prominent in atrial IK1. The macroscopic currents were blocked by Ba2+ and Cs sup +. The channel characteristics in ventricular myocytes from patients with congestive heart failure after idiopathic dilated cardiomyopathy (DCM) exhibited distinct properties compared with those from patients with ischemic cardiomyopathy (ICM). The action potential in ventricular myocytes from patients with DCM had a longer duration (490.8+-24.5 milliseconds, n=11) compared with that for ICM (420.6+-29.6 milliseconds, n=11, P<.01) and had a slow repolarization phase (phase 3) with a low resting membrane potential. The whole-cell current slope conductance for DCM was smaller (41.2+-9.0 nS at EK, n=7) than that for ICM (80.7+-17.0 nS, n=6, P<.05). In single-channel recordings from cell-attached patches, ventricular IK1channels had characteristics similar to those of atrial IK1; channel openings occurred in long-lasting bursts with similar conductance and gating kinetics. In contrast, the percent of patches in which IK1channels were found was 34.7% (25 of 72) of patches in atrium and 88.6% (31 of 35) of patches in ventricle. Single IK1channel activity for DCM exhibited frequent long-lasting bursts separated by brief interburst intervals at every holding voltage with the open probability displaying little voltage sensitivity ((approximately) 0.6). Channel activity was observed in 56.2% (18 of 32) of patches for DCM and 77.4% (24 of 31) of patches for ICM. Similar results were obtained from atrial IK1channels for DCM. In addition, channel characteristics were not significantly different between ICM and explanted donor hearts (donors). IK1channels in cat and guinea pig had characteristics virtually similar to those of humans, with the exception of lower open probability than that in humans.Conclusions These results suggest that the electrophysiological characteristics of human atrial and ventricular I sub K1 channels were similar to those of other mammalian hearts, with the possible exception that the channel open probability in humans may be higher, that the whole-cell I sub K1 density is higher in human ventricle than in atrium, and that IK1channels in patients with DCM exhibited electrophysiological properties distinct from IK1channels found in patients with ICM and in donors. (Circulation. 1995;92:164-174.)

ISSN:0009-7322    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

Background It has been proposed that aldosterone exerts direct effects on heart function, most notably on the development of myocardial fibrosis during ventricular hypertrophy in rat. Initial events in aldosterone action entail its binding to mineralocorticoid receptor (MR). Because MR displays similar affinities for aldosterone and glucocorticoids, the in vivo aldosterone selectivity of MR requires the presence of an enzyme, 11 beta -hydroxysteroid dehydrogenase (11-HSD), which metabolizes glucocorticoids into inactive derivatives. Although evidence exists for the presence of MR in rodent heart, no data are available for humans; moreover, the existence of cardiac 11-HSD is controversial.Methods and Results The heart samples used originated from tissue removed during cardiac surgery in nontransplant patients or from endocavitary biopsies done for the follow-up of heart transplantation. The expression of MR was examined at the mRNA and protein level by in situ hybridization with cRNA probes specific for human MR mRNA and by immunodetection with two specific anti-MR antibodies. 11-HSD catalytic activity was determined by measurement of the metabolic rate of tritiated corticosteroids by cardiac samples. In nontransplanted hearts, an in situ hybridization signal equivalent to that found in the whole kidney was present on cardiomyocytes. Specific immunolabeling of cardiomyocytes with anti-MR antibodies demonstrated the presence of the MR protein. Cardiac 11-HSD activity was detected (243+-26 fmol x 30 min sup -1 x mg protein sup -1) and was dependent on the cofactor NAD, not NADP, suggesting that it corresponds to the form of the enzyme specifically responsible for MR protection. In transplanted hearts that presented severe alterations, MR immunodetection was weaker and irregular, with no specific hybridization signal.Conclusions Our results demonstrate that MR is coexpressed with 11-HSD in human heart, which thus possesses the cellular machinery required for direct aldosterone action. (Circulation. 1995;92:175-182.)

ISSN:0009-7322    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

Background Bradykinin causes endothelium-dependent vasodilation of isolated human coronary arteries in vitro. However, the effect of bradykinin on vasomotion of human coronary arteries in vivo has not been studied. The aim of this study was to examine whether bradykinin-induced vasodilation is altered at the atherosclerotic or spastic site of human coronary arteries in vivo.Methods and Results The effect of bradykinin on vasomotion of epicardial coronary arteries was evaluated in 8 patients with normal coronary arteries (control group), 14 patients with organic coronary stenosis (coronary artery disease (CAD) group), and 8 patients with vasospastic angina (VSA group). Changes in the diameter of epicardial coronary artery were assessed by quantitative coronary arteriography. Intracoronary administration of bradykinin at graded doses (60, 200, and 600 ng) dilated epicardial coronary arteries without altering arterial pressure or heart rate in all patients of either group. In the control group, vasomotor responses of the site where acetylcholine caused dilation were compared with the responses of the site where acetylcholine caused constriction. The magnitudes of bradykinin-induced dilation at the site with acetylcholine-induced dilation (mean+-SD: 6+-6%, 11+-9%, and 15+-9%) were comparable to that (3+-6%, 8+-8%, and 13+-9%) at the site with acetylcholine-induced constriction. In the CAD group, vasomotor responses of the stenotic site (% diameter stenosis, 15% to 50%) and nonstenotic site were examined. The bradykinin-induced dilation at the stenotic site (0+-4%, 3+-8%, and 5+-9%) was significantly less (P<.01) than at the nonstenotic site (3+-4%, 8+-6%, and 16+-11%) and in the control group. Coronary vasodilation with nitrate at the stenotic site (20+-11%) was comparable to that at the nonstenotic site (22+-16%) and in the control group (21+-10%). In the VSA group, vasomotor responses of the site with acetylcholine-induced spasm and the site without spasm were examined. The bradykinin-induced vasodilation at the spastic site (5+-5%, 16+-15%, and 33+-17%) was comparable to that at the nonspastic site (4+-8%, 12+-14%, and 21+-9%). Nitrate-induced dilation was comparable at the spastic site (51+-19%) and the nonspastic site (32+-13%). The ratio of bradykinin-induced vasodilation to nitrate-induced vasodilation at the spastic site was comparable to the control group.Conclusions These results suggest that bradykinin causes vasodilation of human epicardial coronary arteries in vivo and that bradykinin-induced endothelium-dependent vasodilation is impaired at the stenotic site but is preserved at the angiographically normal site where endothelium-dependent vasodilation by acetylcholine is impaired and at the spastic site. (Circulation. 1995;92:183-189.)

ISSN:0009-7322    

出版商:OVID    

年代:1995

数据来源: OVID