Slow-release nifedipine versus placebo in the treatment of arterial hypertension. A double blind ergometric evaluation of cardiac workload

The effects of slow-release nifedipine on blood pressure and cardiac workload have been studied during bicycle exercise testing in a randomized, double blind trial in 20 patients with mild to moderate hypertension. After a fortnight's wash-out, patients were allocated to either slow-release nifedipine (20 mg twice daily) or placebo for a 2-month period. At baseline and at the end of treatment blood pressure and heart rate were measured at rest and during ergometric exercise; cardiac workload was calculated as the product of systolic blood pressure by heart rate. Significant decreases in blood pressure at rest and in cardiac workload on exercise were demonstrated at the end of nifedipine treatment. The reduction of cardiac workload was mainly due to the lower baseline values of resting blood pressure. Heart rate showed a reduction of its increase during ergometric exercise at the end of nifedipine treatment as compared to baseline, likely due to an improvement in stroke volume.     

Changes in plasma catecholamine concentrations in patients with coronary heart disease during pacing and physical exercise

To study the difference in sympathetic activity during pacing the right atrium or during physical exercise in patients with coronary heart disease, we investigated circulating plasma catecholamine concentrations in the coronary sinus and brachial artery radioenzymatically in 11 male patients with well documented coronary artery disease. Heart rate was increased stepwise 20 beats/min from 90 beats/min up to 150 beats/min by pacing the right atrium and physical exercise was performed by increasing work load stepwise by 25 from 25 up to 100 W on an ergometric bicycle. Plasma noradrenaline and adrenaline concentrations were increased significantly only during physical exercise. In addition, there was an increase in arterial-coronary sinus noradrenaline difference during graded physical exercise, whereas no further release of noradrenaline from the myocardium occurred during pacing. An enhanced cardiac sympathetic tone in patients with coronary heart disease is discussed. It is suggested that atrial pacing is not an adequate stimulus evoking an overall increase of cardiac and peripheral sympathetic tone.     

Exercise technetium 99m sestamibi single-photon emission computed tomography late after coronary artery bypass surgery: Long-term follow-up

Background and hypothesis: The prognostic value of exercise technetium 99m sestamibi single-photon emission computed tomography (SPECT) imaging in patients with previous bypass surgery is unknown. The aim of our study was to assess the prognostic information obtained with exercise scintigraphy performed for routine follow-up or reappearance of symptoms. Methods: We studied 75 patients referred to our Center at a mean of 38 ± 53 months from the revascularization procedure and prospectively followed them for 38 ± 24 months. Results: Fifteen patients (20%) had events at follow-up: there were 4 cardiac deaths, 3 nonfatal acute myocardial infarctions, 8 late revascularization procedures (4 percutaneous transluminal angioplasty and 4 repeat bypass surgery). Univariate analysis identified a history of typical angina (p = 0.001), a clinically positive ergometric test (p = 0.009), peak exercise heart rate (p = 0.0003), percentage of maximal predicted heart rate (p = 0.0001), peak exercise double product (p = 0.048), therapy during exercise (p = 0.003), scintigraphic summed reversibility score (i.e., the summation of the segmental differences between stress and rest) (p = 0.014), as significant predictors of events. Three multivariate models were built, with clinical variables (Model 1, chi square 15.97), ergometric variables (Model 2, chi square 19.66), and with scintigraphic variables added to clinical/ergometric variables (Model 3, chi square 31.13). The scintigraphic variable selected in the model as significant predictor of events was the summed reversibility score (p = 0.008). Conclusions: Exercise sestamibi SPECT scintigraphy provides optimal prognostic information after clinical and ergometric parameters in patients with previous bypass surgery.     

Left ventricular mass and blood pressure during ergometric exercise in primary hypertension

The pathophysiology of left ventricular hypertrophy (LVH) in hypertensive patients is still an intriguing point. The lack of a close relationship between LVH and systolic or diastolic blood pressure at rest, previously observed by other investigators, was confirmed in our group of 45 patients with uncomplicated primary hypertension. The strength of correlation between echocardiographic left ventricular mass (LVMe) and blood pressure, expressed as incremental area (IA = total area under the curve--basal area), however, increased during bicycle exercise testing (r = 0.33, p less than 0.05 for diastolic blood pressure; r = 0.39, p less than 0.01 for systolic blood pressure; r = 0.41, p less than 0.01 for mean arterial pressure). Other echocardiographic parameters of myocardial mass such as LVM index (LVMI) and septal thickness (ST) were also significantly correlated with blood pressure during exercise. These results suggest either that blood pressure during exercise is a better index of the cardiac workload than resting blood pressure or that the pathogenesis of cardiac hypertrophy involves an enhanced reactivity to adrenergic drive, particularly stimulated during ergometric exercise. Increased blood pressure alone, however, only partly accounts (about 20%) for the increase in myocardial mass in hypertensive patients; other factors, therefore, need to be further investigated for a better understanding of the pathophysiology of left ventricular hypertrophy.     

Value of an ergometric test for the assessment of cardiac failure

Cardiac failure is usually defined according to clinical and haemodynamic criteria at rest although these patients are mainly symptomatic on effort. Is it possible to substitute or associate a more "objective" method to the NYHA functional classification such as exercise stress testing? If so, is there a correlation between these two types of classification and resting haemodynamic data; have they any predictive value of the patient's exercise capacity? Twenty two patients with severe cardiac failure (Class III or IV of the NYHA), 18 men and 4 women with a mean age of 58 years, underwent a triangular exercise stress test on a bicycle ergometer to 80 p. 100 or more of their theoretical maximal heart rate. The ergometric parameters chosen for the study were the maximal oxygen consumption or its value when limited by symptoms, the maximal work with respect to weight, the total duration of exercise and the percentage increase in systolic blood pressure. The haemodynamic parameters chosen were pulmonary capillary pressure, systolic index, ejection fraction and the velocity of circumferential fibre shortening. No correlation was found between the NYHA functional class and exercise capacity. A dissociated correlation was observed between exercise capacity and resting haemodynamic data. The best correlation was between systolic index and exercise capacity (work performed corrected for body weight, r = 0.70, p less than 0.01; oxygen consumption, r = 0.60, p less than 0.01). After one month of treatment with a vasodilator (Prazosin) in 10 patients, the duration of exercise increased by 2.2 +/- 0.5 min.(ABSTRACT TRUNCATED AT 250 WORDS)     

Hemodynamic basis of the reduced oxygen uptake relative to work rate during incremental exercise in patients with chronic heart failure

BACKGROUND: The ratio of the increase in oxygen uptake to the increase in work rate (DeltaVO2/DeltaWR) during incremental exercise is reduced in patients with severe chronic heart failure (CHF). However, the pathophysiological basis of the reduced O2 uptake relative to work rate has not been elucidated. METHODS: To elucidate the hemodynamic basis of the reduced ratio of DeltaVO2/DeltaWR during exercise in severe CHF, 48 patients with CHF (15 patients in class I, 21 in class II and 12 in class III) performed maximal ergometer exercise with respiratory gas analysis. Cardiac output and systemic O2 extraction were measured at 1-min intervals during exercise. RESULTS: Both peak VO2 and peak cardiac output decreased as the severity of CHF advanced. Patients in class III showed significantly reduced DeltaVO2/DeltaWR than those in class I (8.2+/-0.9 vs. 9.8+/-1.5 ml/min/W, P<0.01). Cardiac output at rest was significantly lower, and O2 extraction at rest was significantly higher in class III than class I. The ratio of the increase in cardiac output to the increase in work rate (DeltaCO/DeltaWR) was significantly lower in class III than class I (42.5+/-14.5 vs. 60.6+/-10.3 ml/min/W), and the ratio of the increase in O2 extraction to the increase in work rate (DeltaO2 extraction/DeltaWR) was significantly higher in class III than class I (0.45+/-0.13 vs. 0.34+/-0.08%/W). The DeltaVO2/DeltaWR was significantly correlated with the DeltaCO/DeltaWR (r=0.67, P<0.01), and the DeltaCO/DeltaWR was inversely correlated with DeltaO2 extraction/DeltaWR (r=-0.65, P<0.01). CONCLUSIONS: Decreased O2 supply due to reduced cardiac output was not fully compensated by the increased O2 extraction. Reduced ratio of DeltaVO2/DeltaWR in advanced CHF reflected the severely attenuated cardiac output response to exercise.     

Effect of tricyclic antidepressive agents on hemodynamics and plasms norepinephrine level in man during rest and exertion]

The effects of i.v. injected antidepressants Imipramine (Tofranil, Geigy) and Dimetacrine (Istonil, Siegfried) on cardiavascular functions were investigated in 18 patients at diagnostic cardiac catheterization. 4 patients were additionally studied during ergometric exercise before and 45 min. after application of both thymoleptica. Determinations of noradrenaline plasma concentrations were carried out in 8 patients. The results show of 25 mg (= 22,1 mg free base) Imipramine or 33.5 mg (= 21.4 mg free base) Dimetacrine did not induce significant changes in heart rate and cardiac index. 2. Already 15 min. after application of both drugs a clear increase in left ventricular end-diastolic pressure (LVEP) was observed. Maximal increase in LVEP - in mean, 26% after Imipramine (p less than 0.0005) and 40% after Dimetacrine (p less than 0.05) - was reached 30-45 min, after injection. 3. A simultaneous increase in mean systemic arterial pressure was related to a marked increase in noradrenaline plasma concentration in all 8 investigated patients. 4. After application of tricyclic antidepressant a larger increase in pulmonary arterial enddiastolic pressure was observed during ergometric exercise.     

Cardiac output-O2 uptake relation during incremental exercise in patients with previous myocardial infarction.

BACKGROUND. The cardiac output-O2 uptake (VO2) relation, which is thought to be linear and predictable in normal humans, has not been clarified in cardiac patients. We evaluated the relation between cardiac output and VO2 during the incremental exercise test in patients with previous myocardial infarction. METHODS AND RESULTS. Twenty-two patients (age, 58.1 +/- 8.0 years) with previous myocardial infarction performed a symptom-limited exercise test on a cycle ergometer. VO2 was calculated from the expired gas analysis, and cardiac output was measured by a computerized cadmium telluride detector every 10 seconds during exercise. The ratio of increase in VO2 to the increase in work rate (delta VO2/delta WR) below and above the anaerobic threshold (AT) was 11.1 +/- 3.6 and 11.1 +/- 2.9 ml/min/W, respectively, showing no significant difference. However, the ratio of increase in cardiac output to increase in work rate (delta CO/delta WR) below the AT was 50.1 +/- 26.6 ml/min/W and was significantly decreased to 11.8 +/- 25.3 ml/min/W above the AT (p = 0.0002). The decreased delta CO/delta WR above the AT primarily would be due to silent myocardial ischemia produced by exercise, as there was the presence of 201Tl redistribution in 15 of 16 patients in whom myocardial 201Tl scintigraphy with dipyridamole or exercise stress testing was evaluated. delta CO/delta VO2, which has been reported to be approximately 5.5 in normal subjects, was only 4.4 +/- 2.6 at work rates below the AT and was decreased to 1.1 +/- 2.3 at work rates above the AT. CONCLUSIONS. The relation between cardiac output and VO2 during exercise in patients with previous myocardial infarction differs profoundly from that reported in normal subjects. These findings must be considered when we noninvasively estimate the change in cardiac output during exercise by obtaining VO2 in patients with coronary artery disease.     

Haemodynamic changes during graded exercise in patients with diabetic autonomic neuropathy

Summary Haemodynamic variables were measured during supine rest and during ergometer cycle exercise at two work loads (50 W and 100 W) in normal subjects (n = 7), in insulin-dependent diabetic subjects without neuropathy (n = 8), in insulin-dependent diabetic subjects with slight autonomic neuropathy (decreased beat-to-beat variation in heart rate, which is considered due to a cardiac parasympathetic defect; n = 8), and in insulin-dependent diabetic subjects with severe autonomic neuropathy, including orthostatic hypotension (n = 7). Compared with normal subjects, cardiac stroke volume was lower in the diabetic subjects with autonomic neuropathy, both at rest and during exercise (p < 0.025), whereas intermediate values were found in the diabetic subjects without neuropathy. The increase in cardiac output in response to exercise was smaller (p < 0.05) in both diabetic groups with autonomic neuropathy compared with the normal and diabetic subjects without autonomic neuropathy. The increase in hepato-splanchnic vascular resistance was smaller in the diabetic subjects with severe autonomic neuropathy than in the normal subjects and the diabetic subjects without autonomic neuropathy (p < 0.025), whereas intermediate values were found in the diabetic subjects with slight autonomic neuropathy. We conclude that, in diabetic patients with severe autonomic neuropathy, the responses of the heart and the splanchnic resistance vessels to exercise are impaired. While sympathetic neuropathy may be responsible for impaired function of splanchnic resistance vessels, both cardiac sympathetic neuropathy and diabetic cardiomyopathy may be involved in the impaired cardiac response to exercise in diabetic subjects with autonomic neuropathy.     

Respiration as a reliable physiological sensor for controlling cardiac pacing rate.

A study was carried out to determine whether variations in the respiration rate during physical exercise could be used as a physiological variable in controlling the rate of an implanted pacemaker. The relation between respiration rate and heart rate was significantly correlated in 73 patients (19 with normal lung function, four with restrictive pulmonary disease, and 50 with obstructive airways disease) during repeated calibrated ergometric tests; no significant differences were found between the subgroups. An external computerised programmable system with algorithm control activated by a radio frequency system was used to vary the cardiac stimulation rate in relation to respiration rate in 11 patients implanted with ventricular inhibited pacemakers. In addition, a prototype programmable pacemaker dependent on respiration rate was implanted in two patients. Maximum values of oxygen uptake, minute ventilation, and work time were increased during the exercise stress tests when the variable cardiac pacing rate was used. Thus respiration rate appears to be a valid and stable physiological variable for controlling the cardiac stimulation rate in order to improve cardiac output in patients dependent on pacemakers.     

Prolonged recovery of cardiac output after maximal exercise in patients with chronic heart failure

OBJECTIVES: The aim of this study was to characterize the kinetics of cardiac output during recovery from maximal exercise in patients with chronic heart failure (CHF). BACKGROUND: Recent studies have shown that oxygen uptake kinetics during recovery from exercise are delayed in patients with CHF. However, the kinetics of cardiac output during recovery from maximal exercise in CHF has not been examined. METHODS: Thirty patients with CHF performed maximal upright ergometer exercise with respiratory gas analysis. Kinetics of oxygen uptake (VO2) and carbon dioxide output (VCO2) during recovery were characterized by T1/2, the time to reach 50% of the peak values. Cardiac output was measured at 1-min intervals during exercise and recovery. Kinetics of cardiac output during recovery were characterized by the ratios of cardiac output during the first 4 min of recovery to cardiac output at peak exercise. Overshoot of cardiac output was defined as a further increase in cardiac output at 1 min of recovery above the cardiac output at peak exercise. RESULTS: Both T1/2 VO2 and T1/2 VCO2 increased as CHF worsened. The ratios of cardiac output during recovery to cardiac output at peak exercise were significantly correlated with T1/2 VO2 (r = 0.47 to 0.62, p < 0.05) and T1/2 VCO2 (r = 0.40 to 0.70, p < 0.05). There was a negative correlation between cardiac index at peak exercise and both T1/2 VO2 (r = -0.65, p < 0.001) and T1/2 VCO2 (r = -0.60, p < 0.001). Overshoot of cardiac output was recognized in 11 of 30 patients. Cardiac index at peak exercise was significantly lower in patients with overshoot (4.5 +/- 0.9 L/min/m2) than in those without overshoot (6.1 +/- 2.1 L/min/m2, p < 0.05). However, because of a continued increase in cardiac output at 1 min of recovery in patients with overshoot, there were no differences in cardiac index after the first minute of recovery. Heart rate at peak exercise and recovery of heart rate did not differ between these groups. Overshoot of cardiac output was caused by a rebound increase in stroke volume which was due to a reduction in systemic vascular resistance. CONCLUSIONS: Prolonged kinetics of VO2 or VCO2 during recovery from maximal exercise represent impairment of circulatory response to exercise and delayed recovery of cardiac output after exercise. Overshoot of cardiac output at 1 min of recovery was characteristic of severe CHF with poor cardiac output response to exercise.     

Behavior of central venous blood temperature in short duration and repeated stress--possibilities for temperature controlled frequency-adapted pacemaker stimulation

Although an exercise-induced increase in blood temperature has been well-known for some time, there was still some doubt whether the change in central venous blood temperature with short-lasting and repetitive physical exercise can be measured and utilized by a temperature controlled pacing system. We studied the central venous blood temperature with short-lasting and repetitive exercise in ten healthy young volunteers and in ten pacemaker patients. The blood temperature was measured intracardially while they walked upstairs. A height of 20 m was covered within 100 +/- 5 s. An oxygen uptake of 27 ml/min/kg was calculated for this level of exercise. After walking upstairs once, the volunteers had an increase in central venous blood temperature of 0.3 degrees C and the pacemaker patients of 0.37 degrees C. After walking upstairs three times, the volunteers had an overall rise in blood temperature of 0.67 degrees C and the pacemaker patients of 0.86 degrees C. Thus, the central venous blood temperature shows a pronounced, measurable increase with short-lasting exercise as well. However, the rises in blood temperature accumulate with repetitive exercise, as the duration of exercise (100 s) when walking upstairs once is not sufficient for a new level of temperature to be reached according to the level of exercise. Thus, a temperature controlled pacing system should take these complex changes into consideration.     

Improvement of physical performance and aerobic capacity mediated by a novel 4--week ambulatory cardiac rehabilitation program

During a 4-week ambulatory cardiac rehabilitation program, 262 patients with coronary artery disease (CAD), 235 men and 27 women, 53.6 +/- 10.2 years, performed 30.5 +/- 2.9 exercise units. Before and after the rehabilitation program exercise, capacity was assessed by bicycle ergometry. There was a significant (p < 0.001) increase in the maximum exercise capacity at the end of the program (105.3 +/- 32.3 vs. 121.9 +/- 37.3 W). Physical work capacity on the 2.0 mmol lactate level improved (p < 0.001) from 72.2 +/- 23.5 to 86.4 +/- 25.8 W, on the 2.5 mmol/l level (p < 0.001) from 83.5 +/- 23.2 to 97.4 +/- 26.4 W, and on the 3.0 mmol/l level (p < 0.001) from 93.1 +/- 23.0 to 106.6 +/- 26.1 W. Despite enhanced performance, heart rate remained unaltered on the 2.0, 2.5, and 3.0 mmol/l lactate level. Furthermore, ergometric performance on predefined heart rate levels was significantly (p < 0.001) increased: 85/min: from 56.0 +/- 24.1 to 65.8 +/- 24.5 W, 90/min: from 62.0 +/- 27.3 to 71.2 +/- 26 W; 95/min: from 67.2 +/- 26.4 to 77.5 +/- 27.6 W; 100/min: from 71.1 +/- 29.6 to 80.6 +/- 28.1 W; 105/min: from 69.8 +/- 26.2 to 81.9 +/- 28.2 W and 110/min: from 73.6 +/- 28.9 to 90.4 +/- 29.4 W. The results demonstrate that physical performance in patients with CAD was improved by our novel ambulatory cardiac rehabilitation program. This improvement included an increase in maximum as well as endurance work capacity; furthermore, this increase was accompanied by a decrease in resting and exercise heart rates. The results demonstrate an absolute increase of physical performance, more importantly an increase of physical performance at defined lactate levels in the presence of unchanged heart rates mediated by the rehabilitation program. Thus, this increase was independent of motivational factors in the patients and/or the investigators during the re-exercise test. On the contrary, our data demonstrate that it is based on an improvement of aerobic endurance capacity associated with a therapeutically beneficial significant decrease of heart rate for a defined workload. The effects were independent of pharmacological influences (e.g., beta-receptor antagonists). These findings are of clinical importance with respect to reduction of myocardial oxygen consumption in patients with CAD.     

30 d头低位卧床期间体育锻炼对立位耐力、运动耐力和心率变异性的影响

目的:观察和比较30 d -6°头低位卧床期间下肢肌力训练和自行车功量计训练对立位耐力、最大运动时间、体质量以及心率变异性（HRV）的影响,旨在进一步明确体育锻炼方法对失重所致心血管失调的对抗效果,为制定我国载人航天飞行时航天员失重对抗方案提供实验依据。方法:15名男性健康被试者,随机分为对照组、下肢肌力训练组和自行车功量计训练组3组,每组5人。对照组仅-6°头低位卧床30 d,不进行任何处理,下肢肌力训练组和自行车功量计训练组在30 d卧床期间分别进行下肢肌力训练和自行车功量计训练。实验前后测量立位耐力、最大运动时间,实验期间测量体质量及HRV。结果:卧床30 d,对照组的立位耐力较卧床前显著降低（P<0.01）,而下肢肌力训练组和自行车功量计训练组的立位耐力较卧床前有所降低,但未达到显著水平。卧床第30 d,对照组和下肢肌力训练组的最大运动时间较卧床前显著降低（P<0.05）,而自行车功量计训练组较卧床前无明显变化,且较对照组和下肢肌力训练组显著升高（P<0.05）。卧床期间,对照组体质量较卧床前有降低趋势,下肢肌力训练组有升高趋势,自行车功量计训练组无明显变化;卧床第10 d,下肢肌力训练组体质量较对照组显著增加（P<0.05）。HRV分析发现,卧床期间对照组归一化低频（LFn）、低频功率与高频功率的比值（LF/HF）较卧床前有升高趋势,归一化高频（HFn）有降低趋势,两锻炼组上述指标变化与对照组相似。结论:30 d头低位卧床可引起立位耐力和运动耐力显著降低,心血管自主神经调节均衡性发生改变。下肢肌力训练在一定程度上能够提高模拟失重后的立位耐力,而自行车功量计训练可提高模拟失重后的立位耐力和运动耐力。     

Effects of cold exposure on submaximal exercise performance and adrenergic activation in patients with congestive heart failure and the effects of beta-adrenergic blockade (carvedilol or metoprolol)

Patients with congestive heart failure (CHF) exhibit a decrease in maximal exercise capacity in response to a cold environment. The aim of this study was to further investigate the impact of cold exposure on submaximal exercise capacity, systemic adrenergic drive, and the effects of long-term beta-adrenergic blockade on these parameters. Thirty-three patients with CHF, with exercise limited by dyspnea and left ventricular ejection fraction of 26 +/- 4%, were randomized to receive metoprolol or carvedilol for 6 months. The observations were compared with 12 age-matched healthy volunteers. Maximal exercise performance with gas exchange analyses were assessed using a ramp protocol, and endurance capacity was measured using 2 constant-load exercise tests performed randomly at 20 degrees C and -8 degrees C. Healthy volunteers increased their submaximal exercise time by 20% (1,353 +/- 455 [20 degrees C] vs 1,635 +/- 475 seconds [-8 degrees C]; p <0.05), whereas patients with CHF exhibited a 21% decrease in exercise time (1,182 +/- 549 [20 degrees C] vs 931 +/- 524 seconds [-8 degrees C]; p <0.05) at -8 degrees C. Beta blockers increased submaximal exercise duration at 20 degrees C (+261 +/- 617 seconds; p <0.05) and -8 degrees C (+374 +/- 729 seconds; p <0.05). Norepinephrine increased to a greater extent at 4 minutes and at the time of exhaustion (at -8 degrees C) only in patients with CHF. Beta-adrenergic blockade caused no significant decrease in plasma norepinephrine levels. Patients with symptomatic CHF exhibited a significant decrease in submaximal exercise time in response to moderate cold exposure. Beta-blocker therapy with either metoprolol or carvedilol significantly increases submaximal exercise time and attenuates the impact of cold exposure on functional capacity.     

Exercise intolerance due to sustained atrial bigeminy with short coupling interval

Atrial bigeminy is a supraventricular arrhythmia rarely associated with severe symptoms. We report the case of a 22-year-old woman with no prior cardiac disease presenting with exercise intolerance since several months. No apparent heart disease other than a spontaneous conducted atrial bigeminy with a short coupling interval was found. At bicycle ergometric testing, symptoms occurred, because of an inadequate increase in pulse rate, due to sustained atrial bigeminy. At electrophysiological study, an ectopic atrial focus at the right atrial septum was successfully ablated.     

Nonischemic changes in right ventricular function on exercise. Do normal volunteers differ from patients with normal coronary arteries?

Factors other than ischemia may alter right ventricular function both at rest and on exercise. Normal volunteers differ from cardiac patients with normal coronary arteries with regard to their left ventricular response to exercise. This study examined changes in right ventricular function on exercise in 21 normal volunteers and 13 patients with normal coronary arteries, using first-pass radionuclide angiography. There were large ranges of right ventricular ejection fraction in the two groups, both at rest and on exercise. Resting right ventricular ejection fraction was 40.2 +/- 10.6% (mean +/- SD) in the volunteers and 38.6 +/- 9.7% in the patients, p = not significant, and on exercise rose significantly in both groups to 46.1 +/- 9.9% and 45.8 +/- 9.7%, respectively. The difference between the groups was not significant. In both groups some subjects with high resting values showed large decreases in ejection fraction on exercise, and there were significant negative correlations between resting ejection fraction and the change on exercise, r = -0.59 (p less than 0.01) in volunteers, and r = -0.66 (p less than 0.05) in patients. Older volunteers tended to have lower rest and exercise ejection fractions, but there was no difference between normotensive and hypertensive patients in their rest or exercise values. In conclusion, changes in right ventricular function on exercise are similar in normal volunteers and in patients with normal coronary arteries. Some subjects show decreases in right ventricular ejection fraction on exercise which do not appear to be related to ischemia.     

Exercise cardiac output is maintained with advancing age in healthy human subjects: cardiac dilatation and increased stroke volume compensate for a diminished heart rate

To assess the effect of age on cardiac volumes and function in the absence of overt or occult coronary disease, we performed serial gated blood pool scans at rest and during progressive upright bicycle exercise to exhaustion in 61 participants in the Baltimore Longitudinal Study of Aging. The subjects ranged in age from 25 to 79 years and were free of cardiac disease according to their histories and results of physical, resting and stress electrocardiographic, and stress thallium scintigraphic examinations. Absolute left ventricular volumes were obtained at each workload. There were no age-related changes in cardiac output, end-diastolic or end-systolic volumes, or ejection fraction at rest. During vigorous exercise (125 W), cardiac output was not related to age (cardiac output [1/min] = 16.02 + 0.03 [age]; r = .12, p = .46). However, there was an age-related increase in end-diastolic volume (end-diastolic volume [ml] = 86.30 + 1.48 [age]; r = .47, p = .003) and stroke volume (stroke volume [ml] = 85.52 + 0.80 [age]; r = .37, p = .02), and an age-related decrease in heart rate (heart rate [beats/min] = 184.66 - 0.70 [age]; r = -.50, p = .002). The dependence of the age-related increase in stroke volume on diastolic filling was emphasized by the fact that at this high workload end-systolic volume was higher (end-systolic volume [ml] = 3.09 + 0.65 [age]; r = .45, p = .003) and ejection fraction lower (ejection fraction = 88.48 - 0.18 [age]; r = -.33, p = .04) with increasing age. These findings indicate that although aging does not limit cardiac output per se in healthy community-dwelling subjects, the hemodynamic profile accompanying exercise is altered by age and can be explained by an age-related diminution in the cardiovascular response to beta-adrenergic stimulation.     

Limitations of regional myocardial thallium clearance for identification of disease in individual coronary arteries

The purpose of this study was to critically evaluate the usefulness of postexercise regional myocardial thallium-201 clearance for identifying disease in individual coronary arteries. Exercise and redistribution planar imaging studies were performed in 114 subjects, including 19 normal volunteers and 95 patients undergoing cardiac catheterization (70 with and 25 without greater than or equal to 50% narrowing in one or more coronary arteries). Thallium clearance was measured from predefined myocardial regions corresponding to the left anterior descending, left circumflex and right coronary arteries and was expressed as the percent decrease in activity at 4 h, assuming monoexponential clearance. In regions perfused by a normal or insignificantly diseased coronary artery, mean 4 h clearance was 58.9 +/- 9.4% for normal volunteers, 43.1 +/- 15.5% for catheterized patients without coronary artery disease and 36.3 +/- 24.9% for catheterized patients with coronary artery disease (p less than 0.001 patients with coronary artery disease versus normal volunteers). Clearance from normal regions was significantly associated with two measures of exercise performance: percent of predicted maximal heart rate achieved (r = 0.49) and exercise duration (r = 0.35). In regions perfused by a stenotic coronary artery, mean clearance was lower (31.1 +/- 19.8%) but was not significantly different from that in normal regions in the same patients. Clearance from diseased regions was also associated with maximal exercise heart rate (r = 0.28) and exercise duration (r = 0.41), but not with percent coronary artery stenosis (r = 0.02). After taking exercise performance into account, the number of diseased vessels or the presence or absence of disease in a given vessel had little influence on regional thallium clearance. Although measurement of regional post-exercise thallium clearance may help to identify stenotic coronary arteries in selected patients, variability related to exercise performance and other physiologic and technical factors greatly limits the clinical usefulness of absolute thallium clearance measurements.