摘要:

Background Sudden death (SD) and acute myocardial infarction (AMI) are the main complications limiting long-term survival after heart transplantation (HT). They are unpredictable and, at present, unpreventable. Platelet aggregation (PA) has recently emerged as a significant prognostic indicator in nontransplanted coronary disease patients. The main purpose of the present study was to evaluate to what extent PA could predict SD and AMI in long-term survivors of HT independently of serum lipid levels.36%) or low (<36%) ADP-induced platelet aggregation was 4.3 (95% confidence interval, 1.9 to 9.5, P=.0001).Conclusions This study provides the first demonstration of an association between increased platelet aggregation and subsequent SD or AMI in HT recipients. It suggests that platelets and thrombosis also are implicated in the pathogenesis of AMI and SD in HT recipients. Identification of a safe and effective antiplatelet therapy should be actively pursued. (Circulation. 1994;89:2590-2594.)

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

Background Supply of sulfhydryl groups with the administration of N-acetylcysteine (NAC) has been reported to reverse tolerance to nitroglycerin but not to isosorbide dinitrate (ISDN). Lack of interaction between NAC and ISDN was suggested as an explanation for these findings. The present study was therefore designed to further evaluate this hypothesis. For this purpose, we compared the hemodynamic and hormonal effects of ISDN when given alone and in combination with NAC.Methods and Results We performed a randomized, crossover design evaluation of the hemodynamic and hormonal effects of ISDN and ISDN+NAC in 14 patients with chronic congestive heart failure due to left ventricular systolic dysfunction. The findings of this study demonstrated a substantial NAC-mediated potentiation of ISDN effect on mean right atrial pressure (-11+-21% versus -38+-27%, -17+-20% versus -34+-27%, and -7+-20% versus -25+-26% at 2, 3, and 4 hours, respectively; all P<.05), mean pulmonary artery wedge pressure (-18+-16% versus -33+-14%, -15+-25% versus -33+-19%, -14+-22% versus -25+-22%, and -16+-16% versus -26+-16% at 2, 3, 4, and 5 hours, respectively; all P<.05), mean pulmonary artery pressure (-8+-11% versus -20+-15% at 3 hours, P<.05), and cardiac output (an increase of 2+-16% versus 25+-20% at 4 hours, P<.05). Although there were no significant changes in serum catecholamine levels and plasma renin concentration with both regimens, ISDN+NAC resulted in a greater fall in plasma levels of atrial natriuretic peptide (296+-251 pg/mL after ISDN versus 202+-118 pg/mL after ISDN+NAC, P<.05).Conclusions The results of this study provide strong evidence for the existence of an interaction between thiols and ISDN and further support the role of sulfhydryl groups in the activation and therapeutic action of organic nitrates. The discrepancy between the results of this study demonstrating NAC-induced potentiation of ISDN effects and a previous study showing failure to reverse ISDN tolerance with NAC may suggest that ISDN-NAC interaction requires normal intracellular levels of sulfhydryl groups and does not occur after intracellular sulfhydryl group depletion. (Circulation. 1994;89:2595-2600.)

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

Background Studies indicate that centrally mediated rhythms in sympathetic tone play a prominent role in diurnal cardiovascular variability. Recent evidence from heart transplant recipients, in whom blood pressure does not decline during sleep despite normal variability in plasma norepinephrine, however, suggests that afferent cardiac nervous traffic is necessary for the generation of diurnal variability. This implies that in the presence of an innervated heart excluded from the systemic circulation, blood pressure would still decrease during sleep. To assess this hypothesis, we studied 24-hour blood pressure, heart rate, and neuroendocrine variability in patients with biventricular assist devices in whom the retained native hearts had ceased to pump.Methods and Results Eight patients were free of medication and were studied every 3 hours. Pump rates and output were kept constant throughout the study. Blood pressure showed a significant decline during sleep, as did norepinephrine and epinephrine (all P<.05). Atrial natriuretic factor showed a significant increase around midnight (P<.01). Significantly elevated levels were found for all hormones studied except for aldosterone and endothelin.Conclusions Our results suggest that diurnal variations in cardiac function or in catecholamine levels (indicative of sympathetic activity) as found in cardiac transplant recipients alone are not responsible or sufficient for producing a nocturnal drop in blood pressure. The presence of an innervated heart appears crucial in this respect. This could be of importance for the understanding of circadian cardiovascular pathophysiology. (Circulation. 1994;89:2601-2604.)

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

Background Functional capacity and quality of life are subjectively improved after cardiac transplantation. However, the objective improvement in exercise tolerance after transplantation has been disappointing. The extent to which allograft diastolic dysfunction contributes to this exercise intolerance has not been defined.Methods and Results Thirty cardiac transplant recipients between 3 and 16 months after transplantation and 30 age-matched normal control subjects underwent maximal symptom-limited graded upright bicycle exercise testing with simultaneous radionuclide angiography, invasive hemodynamic monitoring, and breath-by-breath gas analysis. Mean blood pressure was higher in the transplant group at supine rest (112.1 versus 97.7 mm Hg), normalized with upright posture, and became lower than normal at peak exercise (121.1 versus 133.2 mm Hg). Systolic function as measured by ejection fraction was normal in both groups. However, the cardiac transplant recipients had significantly lower exercise tolerance, achieving a mean maximal work rate of 390 kilopond-meters per minute (kpm/min), compared with 825 kpm/min in the normal subjects. Peak oxygen consumption was 12.3 mL x min sup -1 x kg sup -1 in the transplant group, 46% lower than the normal group's value of 22.9 mL x min sup -1 x kg sup -1. The transplant patients had a resting tachycardia (94 beats per minute) and a 79% reduction in exercise heart rate reserve compared with normal. Despite this chronotropic incompetence, stroke index response to exercise was consistently lower after transplantation, accounting for a 41% reduction in cardiac index at maximal exercise. The lower stroke index was accompanied by a 32% lower end-diastolic volume index at rest and a 14% lower end-diastolic volume index at peak exercise. Despite the smaller ventricular volumes after transplantation, pulmonary capillary wedge pressure was 35% higher than normal at supine rest and 50% higher at maximal exercise. Right atrial and mean pulmonary arterial pressures were similarly elevated. The ratio of pulmonary capillary wedge pressure to end-diastolic volume index was significantly higher during the postural change and exercise, suggesting allograft diastolic dysfunction. Arteriovenous oxygen difference was similar between groups at rest and with submaximal exercise but was 24% lower at maximal exercise in the transplant group, suggesting an abnormality in peripheral oxygen uptake or utilization.Conclusions Exercise tolerance is severely limited during the first 16 months after cardiac transplantation despite preservation of allograft left ventricular systolic function. This intolerance is due to an inadequate cardiac index response from a combination of chronotropic incompetence and diastolic dysfunction limiting the appropriate compensatory use of the Starling mechanism. In addition, there is a peripheral abnormality in oxygen transport or utilization that may partially reflect the effects of deconditioning. (Circulation. 1994;89:2605-2615.)

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

Background There is increasing recognition of myocardial angiotensin-converting enzyme, which is induced with the development of left ventricular hypertrophy (LVH). The potential physiological significance of subsequent increased angiotensin I to II conversion in the presence of LVH is unclear but has been postulated to cause abnormal Ca2+ handling and secondary diastolic dysfunction. Accordingly, we hypothesized that acute angiotensin-converting enzyme inhibition would result in decreased production of angiotensin II and improved active (Ca2+ -dependent) relaxation in patients with hypertensive LVH.Methods and Results Intracoronary (IC) enalaprilat was administered to 25 patients with and without LVH secondary to essential hypertension. Indexes of diastolic and systolic LV function were determined from pressure (micromanometer)-volume (conductance) analysis at steady state and with occlusion of the inferior vena cava. Patients were divided into those receiving high-(5.0 mg, n=15) and low-dose (1.5 mg, n=10) IC enalaprilat during a 30-minute infusion at 1 mL/min. The high-dose patients were further divided along the median normalized LV wall thickness of 0.671 cm/m2. The time constant of isovolumic relaxation (TauL0.671 cm/m2(TauL, 56+-2 versus 44+-2 and 45+-2 milliseconds, respectively, P<.01 by ANOVA) and shortened only in this patient group (Tau sub L, 49+-3 versus 46+-2 and 43+-2 milliseconds, respectively, P<.01 versus baseline and other groups by ANOVA). The improvement in TauLwas directly proportional to the degree of LVH (r=.92, P<.001). Although there was a decrease in LV end-diastolic pressure (23+-2 to 15+-1 mm Hg, P<.01) and volume (86+-8 to 67+-9 mL/m2, P<.05) in those patients with a reduction in TauL, this is due to movement down a similar diastolic pressure-volume relation with no change in chamber elastic stiffness (0.023+-0.002 to 0.025+-0.004 mL sup -1, P=NS).Conclusions Intracoronary enalaprilat resulted in an improvement in active (Ca sup 2+ -dependent) relaxation in those patients with more severe hypertensive LVH. The improvement in active relaxation was directly proportional to the severity of LVH. These results support the hypothesis that the cardiac renin-angiotensin system is an important determinant of active diastolic function in hypertensive LVH. (Circulation. 1994;89:2616-2625.)

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

Background The association between alcohol and blood pressure (BP) may be related to the temporal sequencing of alcohol use and BP measurement. We investigated the effects of single and repeated intakes of alcohol on 24-hour BP.Methods and Results Fourteen male habitual drinkers with essential hypertension were placed sequentially on a 4-day control phase: a nonalcoholic drink with the same calories as alcohol was given at dinner (5 pm to 6 pm) and a 7-day drinking phase: alcohol (ethanol, 1 mL/kg) was given at dinner under standardized conditions. Ambulatory BP measurements were performed on day 3 of the control phase and on days 1 and 7 of the alcohol phase. The average 24-hour systolic and diastolic BPs on day 1 were significantly lower than those in the control phase and on day 7. Between 6 pm and midnight, both systolic and diastolic BPs on days 1 and 7 (121+-2/73+-1 and 126+-4/75+-2 mm Hg, respectively) were significantly lower than those in the control phase (139+-4/83+-2 mm Hg). Between midnight and 8 am (6 to 14 hours after the last drink), both systolic and diastolic BPs on day 7 (138+-4/83+-2 mm Hg) were significantly higher than those in the control phase (131+-4/79+-2 mm Hg) and day 1 (129+-3/77+-1 mm Hg). Between 8 am and 3 pm, BPs showed no difference among the three phases.Conclusions A single intake of alcohol has a depressor effect on BP that lasts for several hours after drinking, while repeated intakes for 7 days have both depressor and pressor effects according to the differences in time intervals after the last drink. This study suggests that the chronic effects of alcohol on BP might be overestimated when based on casual BP measurements alone. (Circulation. 1994;89:2626-2633.)

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

Background Obesity is associated with an increased incidence of cardiovascular complications, but the underlying mechanism is unknown. In experimental animals, overfeeding is associated with sympathetic activation, and there is evidence that adrenergic mechanisms contribute to cardiovascular complications.Methods and Results We recorded resting postganglionic sympathetic nerve discharge (using intraneural microelectrodes) to skeletal muscle blood vessels in 37 healthy subjects covering a broad spectrum of percent body fat. To assess potential functional consequences of sympathetic nerve discharge, we simultaneously measured calf vascular resistance and energy expenditure. The resting rate of sympathetic nerve discharge to skeletal muscle was directly correlated with body mass index (r=.67, P<.0001) and percent body fat (r=.64, P<.0001). In addition to body fat, muscle sympathetic nerve activity was correlated with age (r=.40, P<.02), plasma insulin concentration (r=.34, P<.04), and plasma lactate concentration (r=.35, P<.04). Together, these four covariates accounted for 58% of the variance of muscle sympathetic nerve activity (P<.0001). The rate of sympathetic nerve discharge to calf blood vessels was directly correlated with calf vascular resistance (r=.40, P<.02) but did not predict energy expenditure (r=.22, P=.19).Conclusions In healthy humans, body fat is a major determinant of the resting rate of muscle sympathetic nerve discharge. Overweight-associated sympathetic activation could represent one potential mechanism contributing to the increased incidence of cardiovascular complications in overweight subjects. (Circulation. 1994;89:2634-2640.)

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

Background Recent development of a prototype single-lead unipolar transvenous defibrillator offers the possibility of device implantation with the ease of a permanent pacemaker. Lowering defibrillation energy requirements would allow for a further reduction in defibrillator generator size and enhance the feasibility of pacemaker-like placement. However, if achieving a lower defibrillation energy requires placing additional intracardiac leads, the potential advantage of a smaller generator may be offset by the disadvantages of a more complex lead system. The purpose of this study was to compare defibrillation energy requirements of a single-lead unipolar defibrillator with a three-electrode system employing an additional lead in the coronary sinus..4). Using either defibrillation system, all patients were successfully defibrillated by <24 J and over half of patients by <10 J.Conclusions A unipolar transvenous biphasic defibrillation system is an effective means of treating ventricular fibrillation. The added complexity of additional leads is not offset by any significant improvement in defibrillation efficacy or energy requirements. Given the simplicity and effectiveness of a single-lead system coupled with a small generator, placement of defibrillation systems may now approach the ease of pacemaker implantation. (Circulation. 1994;89:2641-2644.)

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

Background Recent reports suggest that adenosine, in addition to terminating supraventricular tachycardia involving the atrioventricular (AV) node, may have antiarrhythmic effects on atrial tachycardia. The electrophysiological effects of adenosine on supraventricular tissue include shortening of action potential duration in atrial myocytes mediated by the potassium current, IKACh,Ado; shortening of action potential duration and hyperpolarization in sinus node cells; and antiadrenergic electrophysiological effects resulting from inhibition of adenylyl cyclase. We therefore hypothesized that the response of atrial tachycardia to adenosine would be mechanism specific, with termination of atrial tachycardia due to sinus node reentry or cAMP-mediated triggered activity, transient suppression of automatic atrial tachycardia, and an absence of antiarrhythmic effect on tachycardia due to intra-atrial reentry.Methods and Results Adenosine (mean+-SD, 143+-54 micrograms/kg IV) was administered to 27 patients (55+-19 years) in atrial tachycardia whose mechanism was confirmed by electrophysiological study. Adenosine terminated sinus node reentrant tachycardia in 6 of 6 patients and terminated atrial tachycardia due to triggered activity in the 1 patient in whom it was identified. Adenosine transiently suppressed automatic atrial tachycardia in 7 of 7 patients and had no effect in 13 patients with intra-atrial reentrant tachycardia, including 8 patients with atrial flutter.Conclusions These findings demonstrate that adenosine's effects on atrial tachycardia are mechanism specific and can be used to differentiate between reentrant tachycardia confined to the region of the sinus node or atria and between nonreentrant atrial tachycardia due to either triggered activity or automaticity. (Circulation. 1994;89:2645-2654).

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

Background Accessory pathways (APs) exhibiting "Mahaim fiber" physiology (antegrade conduction only, long conduction time, and decremental properties) often connect the lateral right atrium to the right bundle branch (right atriofascicular pathways). Potentials from these pathways have not been recorded previously. The purpose of this study was to determine whether AP activation potentials could be recorded from right atriofascicular APs and to determine whether these potentials could be used to localize a site for catheter ablation.Methods and Results Of 26 consecutive patients referred for catheter ablation of an AP producing a preexcited (antidromic) atrioventricular (AV) reentrant tachycardia having a left bundle branch block pattern with short ventriculoatrial and long AV intervals, 23 (88.5%) were found to have a right atriofascicular AP. During antidromic AV reentrant tachycardia, (1) right atrial extrastimuli (that did not penetrate the AV node) advanced the timing of the next QRS complex, indicating that the AP was connected to the right atrium; (2) earliest antegrade ventricular activation was recorded at the apical right ventricular free wall; and (3) ventricular activation was preceded by activation of the distal right bundle branch, indicating a fascicular insertion or a ventricular insertion close to the terminus of the right bundle branch. A single, discrete, high-frequency AP potential was recorded at the lateral, anterolateral, or posterolateral tricuspid annulus in 22 of the 23 patients 63+-12 milliseconds after the local atrial potential and 83+-23 milliseconds before the local ventricular potential during sinus rhythm. The AP potential was also recorded at sites along the right ventricular free wall between the tricuspid annulus and the site of earliest ventricular activation at the apical region. Programmed atrial stimulation and adenosine each produced prolongation of AP conduction time because of an increase in the A-AP interval and Wenckebach block proximal to the AP potential. Radiofrequency current applied at a site recording the AP potential (tricuspid annulus in 19 patients and right ventricular free wall in 3 patients) eliminated AP conduction in all 22 patients. Tachycardia has not recurred in any patient during 18+-13 months of follow-up. AP conduction was absent in all 9 patients who had a follow-up electrophysiological study 3.8+-1.7 months after ablation.Conclusions Right atriofascicular APs consist of two components. The proximal component is located at the lateral, anterolateral, or posterolateral tricuspid annulus, does not generate an AP potential recordable by catheter electrodes, and is responsible for the decremental conduction properties. The "distal" component extends from the tricuspid annulus to the distal right bundle branch at the apical right ventricular free wall and generates a large, high-frequency AP potential that accurately identifies a site for ablation. (Circulation. 1994;89:2655-2666.)

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID