索他洛尔治疗心房颤动的临床评价

目的观察索他洛尔对心房颤动的治疗效果及其对QT间期、血压、心率的影响.方法 59例初发或复发的心房颤动患者入院接受索他洛尔复律治疗.结果治疗后59例中有38例（64.4%）转复为窦性心律,其中12例（31.6%）随访期间复发,治愈率44.1%;5例（8%）因严重心动过缓、房室传导阻滞而停药;16例（27.1%）治疗4周无效而停药,换用胺碘酮治疗或电复律. 治疗后心率明显减慢,收缩压、舒张压显著下降,QTc无明显变化.结论索他洛尔是治疗心房颤动的安全有效药物.     

关于乙胺碘呋酮的临床应用体会

乙胺碘呋酮(胺碘酮)属于抗快速心律失常药物,按药物对动作电位的主要效应分类的第三类,它可以使有效不应期延长,但不减慢激动的传导。本类药物还有溴苄胺和索他洛尔。另外,胺碘酮对血管平滑肌有特异性松弛作用,能扩张冠状动脉和外周动脉,降低冠脉循环阻力和外周血管阻力,且通过α和β肾上腺素能受体的非竞争性抑制而降低儿茶酚胺的交感兴奋作用,故有降压作用,可用于高血压病的治疗。对心脏可减慢静息和运动时的心率,对心肌氧利用率虽无影响,但有抑制交感兴奋作用,而有效的缓解心绞痛。目前,胺碘酮已广泛应用于临床,并成为颇受注视的药物,本…     

运动疗法在心脏术后康复中的作用

目的：探讨运动疗法在心脏术后康复中的作用。方法：21例心脏手术后患者均接受功率自行车或／和跑台训练为主的康复训练，并采用常规心电运动试验对康复训练前后的各项指标进行比较。结果：运动训练后，运动时间和最大运动负荷显著增加，安静时，心率、血压（包括收缩压和舒张压）、心率－血压乘积均显著下降（P＜0．05，P＜0．01），安静时心电图最大ST段压低明显改善（P＜0．01）；同等负荷量运动时，心率、血压、心率－血压乘积及运动诱发的最ST段压低与安静状态时有相似的改变(P＜0．05，P＜0．01）。结论：心脏术后的康复训练有助于增加体能，减轻心肌缺血，增加心肌储备功能，从而改善了患者的生活质量。     

索他洛尔治疗心律失常疗效观察

应用索他洛尔治疗房、室性心律失常59例。用药前、后分别测血压、心率、心电图QTc、24小时动态心电图及肝、肾功能等血生化指标。结果房性心律失常者有效率为60%,室性心律失常者有效率为87.2%,总有效率78.0%。用药过程中仅有心率减慢、QTc延长及早期收缩压下降。索他洛尔治疗房、室性心律失常安全、有效,剂量以160mg/d为宜。     

索他洛尔对重症心肌炎合并恶性心律失常的影响

目的 探讨索他洛尔对重症心肌炎合并恶性心律失常(MVA)的影响.方法 将59例患者分为索他洛尔组39例及对照组20例,分别监测血压、心率、心电图、QTc、24 h动态心电图,观察各阶段MVA发生率.结果 索他洛尔对室性心律失常的总有效率87.2％,用药过程中仅有心率减慢、QTc延长及早期收缩力下降.结论 索他洛尔能有效降低重症心肌炎合并MVA的发生率.     

索他洛尔对重症心肌炎合并恶性心律失常的影响

目的：探讨索他洛尔对重症心肌炎合并恶性心律失常（MVA）的影响。方法：将59例患者分为索他洛尔组39例及对照组20例,分别监测血压、心率、心电图、QTc、24 h动态心电图,观察各阶段MVA发生率。结果：索他洛尔对室性心律失常的总有效率87.2%,用药过程中仅有心率减慢、QTc延长及早期收缩力下降。结论：索他洛尔能有效降低重症心肌炎合并MVA的发生率。     

胺碘酮对室性心律失常患者QTc离散度的影响及临床意义

受国际多中心心律失常抑制试验 (CAST)的影响 , 类抗心律失常药物的应用受到限制 ,近年来 类抗心律失常药物 (如胺碘酮、索他洛尔 )临床应用逐渐增多。本文观察了胺碘酮对室性心律失常的疗效及近期致心律失常作用 ,测量了用药前后QTc离散度 (QTcd)的变化 ,以探讨二者之间的关系。1　对象与方法1.1　患者选择　入选患者具备下述条件 :1具有器质性心脏病的基础 ;2经动态心电图检查为 L own分级 级以上的室性期前收缩或非持续性室速 ;3具有轻中度的心功能不全 (心功能 ～ 级 ) ;4常规心电图检查剔除束支阻滞、频发室性期前收缩二联律或…     

胺碘酮治疗室性心律失常的疗效与QT间期的关系——附100例报告

目的:探讨胺碘酮治疗室性心律失常时QT间期与疗效的相关性.方法:100例室性心律失常患者予胺碘酮(负荷量600 mg/d治疗7日,再给予400 mg/d治疗7日,其后用200 mg/d治疗2周,继以100～200 mg/d治疗4个月)治疗,观察患者治疗后QT间期延长与抗心律失常有效率的关系及其不良反应.结果:胺碘酮治疗室性心律失常有效率高达95%,其维持量小(100～200 mg/d),且无明显不良反应.治疗后QT间期延长者较QT间期不延长者效果好.对负荷期末QT间期不延长者,延长其用药负荷期后部分患者可取得满意疗效.结论:胺碘酮用于治疗室性心律失常时,QT间期延长者较不延长者疗效好.     

曲美他嗪对心肌梗死患者运动耐量的影响

为探讨曲美他嗪对心肌梗死患者运动耐量的影响，将127例心肌梗死患者机分为治疗组(64例)和对照组(63例)，比较两组治疗前后运动耐量。结果表明，治疗前两组运动耐量、运动诱发心绞痛或收缩压下降≥10mmHg的比率无明显差异(P&;gt;0．05)；治疗3个月后，治疗组的运动量、运动时间，最大心率、心率血压乘积均明显高于对照组(P&;lt;0．05)，运动诱发的心绞痛或收缩压下降≥10mmHg的比例明显低于后者(P&;lt;0．05)。提示曲美他嗪能显著提高心肌梗死患者的运动耐量。     

运动疗法在心脏术后患者中的作用

目的探讨运动疗法在心脏术后康复中的作用.方法21例心脏手术后患者均接受功率自行车或/和跑台训练为主的康复训练,并采用常规心电运动试验对康复训练前后的各项指标进行比较.结果运动训练后,运动时间和最大运动负荷显著增加,安静时,心率、血压(包括收缩压和舒张压)、心率-血压乘积均显著下降(P<0.05,P<0.01),安静时心电图最大ST段压低明显改善(P<0.01);同等负荷量运动时,心率、血压、心率-血压乘积及运动诱发的最大ST段压低与安静状态时有相似的改变(P<0.05,P<0.01).结论心脏术后的康复训练有助于增加体能,减轻心肌缺血,增加心肌储备功能,从而改善了患者的生活质量.     

Effects of Sotalol on the Circadian Rhythmicity of Heart Rate and QT Intervals With a Noninvasive Index of Reverse-Use Dependency

BACKGROUND: The effects of sotalol on the 24-hour profile of the QT interval relative to that of the heart rate (HR) may be helpful in determining the time course of the drug's action in controlling cardiac arhythmias. This has not been previously determined. Thus, the objective of the current study was to evaluate the influence of the drug on the circadian rhythmicity of HR and QT intervals from Holter recordings in ambulatory patients. Reverse-use dependency (RUD) of sotalol was also studied noninvasively from Holter recordings. METHODS AND RESULTS: Holter recordings of 18 patients with ventricular arrhythmias were analyzed before and after 3-7 days of treatment with sotalol. We developed and used a signal processing system. A new noninvasive index to evaluate RUD was defined and applied to sotalol as a test agent. Sotalol significantly reduced HR from 76.9 +/- 3.2 to 60.0 +/- 1.1 (P <.001). The mean QT interval increased from 393 +/- 11 ms to 489 +/- 9 ms, whereas the mean normalized QT (QTc) interval increased from 415 +/- 5 ms to 487 +/- 5 ms (P <.001) during the drug treatment. Circadian rhythmicity of RR interval was abolished, but the circadian rhythms of the QT and QTc intervals were maintained during continuous treatment with sotalol. This finding is in contrast to amiodarone, which abolished the circadian rhythmicity of QTc interval while maintaining that of RR interval. RUD index was increased from 0.13 +/- 0.08 to 0.24 +/- 0.10 (P <.001) after sotalol, consistent with increased RUD with sotalol. CONCLUSIONS: The effects of sotalol on the circadian rhythmicity of HR and QTc interval are dissociated. They are in direct contrast to those reported for amiodarone, a difference that may be of clinical significance. The RUD index introduced here provides a noninvasive parameter for comparing short-term as well as long-term effects of class III antiarrhythmic drugs on RUD.     

Atrioventricular Interval Optimization and Exercise Tolerance

Modern pacemakers offer many programming options regarding the AV interval including the ability to vary AV intervals depending on whether atrial activity is paced or spontaneous and to shorten AV intervals with increasing rates. To determine if optimization of these features improves exercise tolerance, 14 patients with intact sinus node function and AV block treated with dual chamber pacemakers were enrolled in a randomized double-blind crossover trial. Doppler echocardiographic measurements of cardiac index and mitral flow were assessed over a range of programmable AV intervals at rest to determine each patient's optimal AV interval. Eleven patients completed serial graded exercise tests with spiroergometry after randomly programming the AV interval three ways in a crossover manner: fixed AV interval = 150 ms without rate adaptation (150/Fixed), fixed AVinterval = 150 ms with rate adaptation (150/R), or optimized AV interval with rate adaptive AV interval shortening (optimized/R). Exercise capacity was determined by maximum oxygen uptake. Ten men and four women, age 64 +/- 8 years, were enrolled. At rest, optimization of the AVintervalimproved the cardiac index by 21% (P < 0.001) and mitral flow by 13.4% (P < 0.001) when compared to least-favorable AV intervals. During exercise, no differences in maximum heart rates were noted. Maximum oxygen uptake was increased in both groups with rate adaptive AVinterval shortening when compared tofixed AVinterval without rate adaptation: 13.9% (adjusted P < 0.04) and 14.6% (adjusted P < 0.02) in optimized/R and 150/R, respectively. No differences were noted between optimized/R and 150/R. In conclusion, rate adaptive AV interval shortening improved exercise tolerance independent of changes in heart rate. However, optimization of the AV interval with Doppler echocardiography at rest did not further improve exercise capacity.     

Effects of Sotalol on His-Purkinje Conduction and Refractoriness in Humans

BACKGROUND: The effects of sotalol on refractoriness in human ventricular and atrial muscles have been well established, but the drug's effect on the electrical properties of the His-Purkinje system in humans is not known, especially whether sotalol's effect is due solely to its action on prolonging repolarization or in combination with its beta-blocking properties. We studied the electrophysiologic effects of intravenous sotalol and propranolol in patients undergoing electrophysiologic studies of cardiac arrhythmias. METHODS AND RESULTS: We studied 22 patients (19 men, 3 women; mean age, 60 +/- 6 years) who had coronary artery disease and assessable anterograde, retrograde, or both, His-Purkinje system function. Fifteen patients underwent electrophysiologic studies before and after intravenous sotalol (1.5 mg/kg), and 7 patients underwent electrophysiologic studies before and after intravenous propranolol (0.15 mg/kg). Both sotalol and propranolol had no significant effect on the H-V interval, but sotalol significantly increased ventricular refractoriness and His-Purkinje refractoriness, both in anterograde and retrograde conduction, whereas propranolol did not, Sotalol's effect on His-Purkinge refractoriness also caused atrioventricular block distal to the His bundle during atrial pacing at a moderately fast rate. Sotalol was not effective in preventing bundle branch re-entry tachycardia, nevertheless, it increased cycle length of bundle branch re-entry tachycardia by increasing refractoriness. CONCLUSIONS: Sotalol increased His-Purkinje refractoriness in humans but had no effect on His-Purkinje conduction. The drug must be used judiciously in patients with a diseased His-Purkinje system because it may cause atrioventricular block distal to His at fast heart rates. Sotalol had no effect on macrore-entry utilizing bundle branches.     

Different Effects of Amiodarone and Quinidine on the Homogeneity of Myocardial Refractoriness in Patients With Intraventricular Conduction Delay

BACKGROUND: Increases in QT and JT dispersion have been suggested as indicative of a proarrhythmic potential as a result of heterogeneity in myocardial refractoriness, the reduction of which by antiarrhythmic agents might be associated with a beneficial effect on the development of serious ventricular arrhythmias. METHODS: To test the hypothesis that amiodarone reduces the heter-ogeneity of ventricular refractoriness to a significantly greater extent than quinidine in patients with intraventricular conduction defects under treatment for ventricular arrhythmias, the corrected and uncorrected QT and JT intervals and dispersions from 12-lead surface electrocardiograms were determined in 120 patients with intraventricular conduction defects with cardiac arrhythmias before and during treatment with amiodarone (n = 60) and quinidine (n = 60). RESULTS: Amiodarone increased QT from 403 +/- 50 ms to 459 +/- 47 ms (P <.001), with a similar increase in the corrected QT interval (QTc) (P <.001). Amiodarone reduced QT dispersion by 40% (P <.001), whereas quinidine increased by 18% (P <.001). The net effects of both drugs were similar for OTc. Amiodarone, but not quinidine, reduced heart rate significantly; amiodarone had no effect on the QRS; but quinidine increased if (P <.001). Quinidine as well as amiodarone increased the JT and JTc intervals significantly, but the effect of quinidine was qualitatively less striking. Amiodarone decreased the JT dispersion by 33% (P <.001) and JTc dispersion by 37% (P <.001). On the other hand, quinidine increased the corresponding values for JT and JTc by 18% (P <.001) and 21% (P <.001), respectively. The overall data on QT and JT dispersion indicate an improvement in the homogeneity of myocardial refractoriness with amiodarone treatment and the converse with quinidine treatment; this observation is consistent with a lower proarrhythmic propensity and mortality with amiodarone than with quinidine. Quinidine increased the QRS interval more than amiodarone, and the data indicate that in patients with intraventricular conduction defects, the monitoring of the JT interval might more accurately reflect changes in myocardial repolarization. CONCLUSIONS: Amiodarone and quinidine both increased the corrected and uncorrected QT and JT intervals; amiodarone decreased and quinidine increased the dispersion of these intervals, and these results suggested an improvement in the homogeneity of myocardial refractoriness as a result of amiodarone treatment and the converse as a result of quinidine treatment. Quinidine increased the QTS interval more than amiodarone, and the data indicate that in patients with intraventricular conduction defects, the monitoring of the JT interval might more accurately reflect changes in myocardial repolarization.     

Sotalol Is More Powerful Than Propranolol in Suppressing Complex Ventricular Arrhythmias

BACKGROUND: Sotalol has combined type II and type III antiarrhythmic properties. Although the beta-blocking action of sotalol is thought to contribute to its antiarrhythmic actions, few data are available from direct comparative clinical trials with pure beta-blocking drugs. METHODS AND RESULTS: In this double-blind, randomized, multicenter, placebo-controlled, parallel study, we have compared the antiarrhythmic efficacy and safety of treatment with sotalol vs propranolol in 181 patients with organic heart disease and frequent (>30 ventricular premature complexes [VPCs]/h) repetitive ventricular premature complexes. Eighty-seven were randomized to receive sotalol and 94 received propranolol. The demographic and clinical characteristics of the two groups were identical, and the majority of patients had coronary artery disease or hypertensive heart disease. Most patients had a long-standing history (>5 years) of ventricular arrhythmias and, in a significant proportion, antiarrhythmic therapy with other drugs had failed in the past. After withdrawal of all antiarrhythmic drugs and 1 week of placebo, qualified patients were randomized to sotalol (320 mg/day) or propranolol (120 mg/day). patients not achieving adequate response were given higher doses of sotalol (640 mg/day) or propranolol (240 mg/day)At baseline, both groups had comparable frequency of total VPCs/hour (274/h and 255/h for sotalol and propranolol groups, respectively) which was reduced to 71 VPCs/h and 109/VPCs/h, respectively, at the end of phase 1. At final evaluation there was a significantly greater response to sotalol as demonstrated by 80% reduction in VPCs/hour with sotalol compared with only 50% reduction noted in the propranolol group. Adequate therapeutic response was also achieved in a significantly greater percentage of patients on sotalol compared with propranolol (56% vs 29%, P =.02). Sotalol was also superior to propranolol in suppressing the VT events/day during phase 1 (89% vs 78% reduction in VT events/day, P <.05). Sotalol was more effective than propranolol in all subgroups and in patients with heart rate <75 beats per minute. CONCLUSIONS: Sotalol is more powerful than propranolol in suppressing ventricular arrhythmias documented on Holter recordings. The superiority of sotalol appears to be related to its combined class II and class III antiarrhythmic actions.     

Frequency-dependent Cardiac Electrophysiologic Effects of Tedisamil: Comparison With Quinidine and Sotalol

BACKGROUND: Tedisamil is a potent bradycardiac/antiischemic drug known to lengthen cadiac repolarization by blocking various potassium channels. Recent in vivo experiments revealed that it is an antiarrhythmic agent. It was therefore of interest to compare the cellular electrophysiologic effects of tedisamil with those of quinidine and sotalol in isolated cardiac preparations. METHODS AND RESULTS: The conventional microelectrode technique was applied in isolated dog cardiac Purkinje and ventricular muscle fibers and in rabbit left atrial muscle. Tedisamil (1 μM) and sotalol (30 μM) lengthened, while quinidine (10 μM) shortened action potential duration in dog Purkinje fibers. The phase 1 repolarization was delayed by tedisamil and quinidine and not changed by sotalol. In dog ventricular muscle and in rabbit atrial muscle, all three drugs studied lengthened repolarization. In dog Purkinje fiber, tedisamil and sotalol lengthened action potential duration more at slow than at high stimulation frequency (reverse use-dependence). In dog ventricular muscle fibers, the effect of the drugs was not clearly frequency dependent. In rabbit atrial muscle fibers, the quinidine-evoked repolarization lengthening was most pronounced at intermediate cycle lengths (500-1000 ms). Tedisamil and quinidine but not sotalol depressed the maximal rate of depolarization (V(max)), which depended on the stimulation frequency (use-dependence). The nature of the use-dependent V(max) block differed between quinidine and tedisamil. Quinidine decreased V(max) at a relatively wide range of stimulation frequencies whle tedisamil. Quinidine decreased V(max) at a relatively wide range of stimulation frequencies while tedisamil decreased V(max) largely at high rate of stimulation. Tedisamil and quiinidine prevented or decreased the pinacidil-evoked action potential shortening in dog ventricular muscle, suggesting block of the ATP-dependent potassium channels (I(KATP)), while with sotalol such effect was not observed. CONCLUSIONS: Although tedisamil, quinidine, and sotalol are known to lengthen the QT interval, their cellular electrophysiologic effects substantially differ. Tedisamil lengthens repolarization and prevents pinacidil-evoked action potential duration shortening, suggesting I(K(ATP)) blockade. Its effect on the V(max) is limited mostly to fast heart rate. These electrophysiologic effects of tedisamil resemble those of chronic amiodarone treatment.     

Abnorme Verkürzung der linksventrikul?ren Diastolendauer unter k?rperlicher Belastung bei Patienten mit dilatativer Kardiomyopathie

BACKGROUND AND PURPOSE: Cardiac performance can be characterized in terms of the relative duration of systole and diastole. In pediatric patients with dilated cardiomyopathy (DCM), a disproportionate shortening of left ventricular diastole was observed. The present study was intended to reproduce these findings in an adult patient group and to evaluate exercise-related changes of both time intervals. PATIENTS AND METHODS: Exercise radionuclide angiography was used in 61 patients with DCM NYHA (New York Heart Association) stage II-III. The phases of the cardiac cycle were derived from a radionuclide time-activity curve with high temporal resolution. The control group consisted of 26 patients referred for ventricular function assessment with radionuclide angiography before cardiotoxic cancer treatment. RESULTS: When the duration of systole was expressed as the product of systolic time and heart rate, DCM patients exhibited a significant increase in left ventricular systolic time at rest (23.9 vs. 21.5 s/min; p = 0.006) and during peak exercise (29.2 vs. 26.7 s/min; p = 0.01). The prolongation of left ventricular systole at peak exercise was evident, although the peak heart rate was significantly lower in the patient group than in the control group (118 vs. 127/min; p = 0.04). In DCM patients the diastolic time loss per beat was further quantified using a regression equation obtained from the healthy control group. A significant shortening of left ventricular diastolic time was confirmed during peak exercise. Furthermore, a progressive loss in diastolic time per beat from rest to peak exercise was noted. CONCLUSION: Cardiac cycle abnormalities of patients with DCM are characterized by a prolongation of left ventricular systole and an abnormal shortening of left ventricular diastole. The systolic-diastolic mismatch is accentuated during exercise and has the potential to impair the cardiac reserve in these patients by restricting ventricular filling and perfusion.     

The Ventricular Paced QT Interval—The Effects of Rate and Exercise

Changes in the QT and QTc intervals in 19 patients were studied at a ventricular paced rate difference of 50 beats/min. In all patients the measured QT interval shortened as the pacing rate was increased, from a mean value of 441 ms to 380 ms (p < 0.001), but when correct ed for heart rate the QTc- lengthened from a mean value of 518 ms to 575 ms. In 11 patients the QT in terval was measured at rest and immediately following exercise sufficient to increase the atrial rate by approximately 50 beats/min at identical ventricular paced rates. In all patients exercise-induced QT interval shortening from a mean value of 433 ms to 399 ms (p < 0.001). These results show first that Bazett's formula is unsuitable for correction of QT interval changes induced by ventricular pacing, and second that heart rate and changes in sympathetic tone independently influence the duration of the QT interval. It is suggested that these resuits are relevant to the design of physiological pacemakers in which the duration of the QT interval influences the discharge frequency of the pacemaker and to the consideration of ventricular pacing for the treatment of abnormal repolarization syndromes. (PACE, Vol. 5, May-June, 1982)     

Efficacy, safety, hemodynamic effects, and pharmacokinetics of high-dose moricizine during short- and long-term therapy

Moricizine, 15 mg/kg, was given to 10 patients with frequent ventricular ectopic depolarizations, eight of whom had previously been treated unsuccessfully with antiarrhythmic drugs. A single-blind inpatient study was followed by therapy for up to 6 months. Two patients developed aggravation of arrhythmia during inpatient therapy. Of the eight patients who completed the inpatient study, seven achieved greater than or equal to 80% suppression of total ventricular ectopic depolarizations (P less than 0.001). During inpatient therapy the mean of the individual patients' suppression of total ventricular ectopic depolarizations was 87.9%, paired ventricular beats 99.3%, nonsustained ventricular tachycardia 99.6%, and premature atrial contractions 89.0%. Suppression was maintained during long-term therapy. The PR interval increased 27% (P less than 0.001), QRS interval increased 10% (P less than 0.0001), QTc increased 1% (P not significant), and JTc decreased 2% (P not significant). Heart rate, blood pressure, and left ventricular performance at rest and exercise were unchanged by moricizine. Moricizine half-life was 9.2 +/- 3.4 hours. Plasma levels of moricizine decreased after 10 days of therapy, suggesting induction of metabolic enzyme systems.     

Prolongation of the QT interval in heart failure occurs at low but not at high heart rates

Abnormal left ventricular structure and function as in, for example, left ventricular hypertrophy or chronic heart failure, is associated with sudden cardiac death and, when the ejection fraction is depressed, with prolongation of the QT interval. The dependence on heart rate of QT interval prolongation in these conditions, and the relationship of any abnormalities either to deranged autonomic nervous system function or to an adverse prognosis, has not been well studied. We therefore investigated (1) the dependence on heart rate of the QT interval, and (2) the relationship between both QT interval and the QT/heart rate slope and markers of adverse prognosis in these two conditions. The QT interval was measured at rest and during exercise in 34 subjects with heart failure, 16 subjects with left ventricular hypertrophy and 16 age-matched controls with normal left ventricular structure and function. QTc (corrected QT) intervals at rest were significantly longer in heart failure patients (471+/-10 ms) than in controls (421+/-6 ms) or in subjects with hypertrophy (420+/-6 ms) (P<0.05). At peak exercise, despite the attainment of similar heart rates, the QT intervals no longer differed from each other, being 281+/-7 ms for controls, 296+/-11 ms in hypertrophy and 303+/-10 ms in heart failure (no significant difference). The QT/heart rate slope was significantly increased in heart failure [2.3+/-0.1 ms.(beats/min)(-1)] compared with controls [1.55+/-0.06 ms.(beats/min)(-1)] and hypertrophy [1. 66+/-0.1 ms.(beats/min)(-1)] (P<0.001). In left ventricular hypertrophy, despite animal data suggesting that QT interval prolongation should occur, no abnormalities were found in QT intervals at rest or during exercise. The QT/heart rate slope did not relate to any markers for an adverse prognosis, except that of prolongation of QT interval. Long QT intervals were associated principally with impairment of left ventricular systolic function. Our data emphasize the dynamic nature of the QT interval abnormalities found in heart failure.