Biomedical subjects

S Adamopoulos

Publications and source records attributed to S Adamopoulos.

At least 37 records · Page 2Linked to original sources

PubMed1995

Circadian pattern of heart rate variability in chronic heart failure patients. Effects of physical training.

The effect of physical training on the circadian pattern of heart rate variability (recorded over 24 h in relation to both time and frequency) was assessed in 12 chronic heart failure patients randomized, in a cross-over design, to 8 weeks training or detraining, and compared with 12 age-matched normals. Training improved heart rate variability indices: all R-R interval 5 min standard deviations increased by 17.6%, the root mean square of the differences of successive R-R intervals by 34.9%, the percentage difference between adjacent normal R-R intervals > 50 ms by 112.5%, total power by 58.3%, high frequency by 128.5% and low frequency by 65.0%. Compared with controls, circadian variations in autonomic parameters were maintained in chronic heart failure. Training-induced changes were observed at different time intervals throughout the day: the highest values were at 0100 h-0700 h (detraining: low frequency 361 +/- 83 ms2, high frequency 126 +/- 47 ms2; training: low frequency 535 +/- 202 ms2, high frequency 227 +/- 115 ms2, P < 0.01) and the lowest at 1300 h-1900 h (detraining: low frequency 91 +/- 23 ms2, high frequency 39 +/- 14 ms2; training: low frequency 154 +/- 42 ms2, high frequency 133 +/- 67 ms2, P < 0.05). In chronic heart failure, training maintains and improves circadian variations in heart rate variability measures.

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PubMed1995

Rat skeletal muscle metabolism in experimental heart failure: effects of physical training.

Skeletal muscle metabolic abnormalities exist in chronic heart failure. The influence of physical training on muscle metabolism after myocardial infarction was studied in a rat model. 31P magnetic resonance spectroscopy and enzyme assays were performed in Wistar rats 12 weeks after coronary artery ligation. Infarcted rats were allocated randomly to either 6 weeks of training or non-training. Spectra were collected from the calf muscles during sciatic nerve stimulation at 2 Hz. Fibre typing and enzymatic assays were performed on the muscles of the contralateral non stimulated leg. Post-mortem rats were also divided into severe and moderate heart failure according to the lung weight per body weight. At 200 g twitch tension, phosphocreatine and pH were found to be significantly lower in the non-trained severe heart failure group compared with the other groups. Phosphocreatine recovery half-time was significantly longer in the non-trained group with severe heart failure and correlated with the citrate synthase activity in the muscle. The training did not induce a change in the enzyme activities in the infarcted animals with moderate heart failure but did correct the lower citrate synthase activity in the non-trained severe heart failure animals. This normalization of muscle metabolism was achieved by training without any change in calf muscle mass, making atrophy unlikely to be the sole cause of the metabolic changes in heart failure. Training in rats with severe heart failure can reverse the abnormalities of skeletal muscle metabolism, implicating decreased physical activity in the aetiology of these changes.

3-Hydroxyacyl CoA Dehydrogenases↗

PubMed1994

Load dependence of changes in forearm and peripheral vascular resistance after acute leg exercise in man.

1. It is known that acute exercise is often followed by a reduction in arterial blood pressure. Little is known about the time course of the recovery of the blood pressure or the influence of the intensity of the exercise on this response. Controversy exists, in particular, concerning the changes in peripheral resistance that occur during this period. 2. Eight normal volunteers performed, in random order on separate days, voluntary upright bicycle exercise of three different intensities (maximal, moderate and minimal load) and, on another day, a control period of sitting on a bicycle. They were monitored for 60 min after each test. 3. Diastolic pressure fell after maximal exercise at 5 min (-15.45 mmHg) and 60 min (-9.45 mmHg), compared with the control day. Systolic and mean pressure also fell (non-significantly) after 45 min; heart rate was significantly elevated for the whole hour of recovery (at 60 min, +7.23 beats min-1). No changes in post-exercise blood pressure and heart rate were observed on the days of moderate and minimal exercises. 4. An increase in cardiac index was observed after maximal exercise compared with control (at 60 min, 2.6 +/- 0.3 vs. 1.9 +/- 0.2 l min-1 m-2). This was entirely accounted for by the persistent increase in heart rate, with no significant alteration in stroke volume after exercise on any day.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1994

Abnormal autonomic control of the cardiovascular system in syndrome X.

Anomalies of autonomic control of the coronary circulation may play a role in the development of syndrome X (angina pectoris, ischemic-appearing results on exercise test, and normal coronary arteriograms). Twenty-six patients with syndrome X and 20 healthy sex- and age-matched control subjects were studied by means of analysis of heart rate variability during 24-hour Holter monitoring. Spectral and nonspectral parameters of heart rate variability were investigated. Mean heart rate was similar in patients with syndrome X and in control subjects. Patients with syndrome X had significantly lower standard deviation of all normal RR intervals, a lower percentage of adjacent normal RR intervals > 50 ms in difference (126.4 +/- 22 vs 149 +/- 43 ms, p < 0.05; 6.3 +/- 4 vs 11.2 +/- 7%, p < 0.05; respectively), and a trend toward lower values of time-domain parameters. Lower values of total power and low frequency were also observed in patients with syndrome X (1273 +/- 693 vs 1790 +/- 989 ms2, p < 0.05; 406 +/- 176 vs 729 +/- 455 ms2, p < 0.01, respectively). An inverse correlation between heart rate and measures of heart rate variability was found in syndrome X but not in control subjects. High- and low-frequency power showed a similar circadian pattern in syndrome X patients and control subjects. Patients and control subjects were then allocated into 2 groups according to the median RR duration: syndrome X1 and control 1 with high mean heart rate, and syndrome X2 and control 2 with low mean heart rate.(ABSTRACT TRUNCATED AT 250 WORDS)

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PubMed1994

Neurohormonal mechanisms and the role of angiotensin-converting enzyme (ACE) inhibitors in heart failure.

Clinical evidence accumulated over the past decade suggests that neurohormonal mechanisms significantly influence the pathogenesis and eventual outcome of congestive heart failure (CHF). Pharmacologic modulation of this neuroendocrine activity can, consequently, be expected to improve patient prognosis. Results of several recent clinical trials--the Studies of Left Ventricular Dysfunction (SOLVD), the second Veterans Administration Cooperative Vasodilator Heart Failure Trial (VH eFT-II), and the Cooperative North Scandinavian Enalapril Survival Study (CONSENSUS)--provide substantial evidence that addition of the angiotensin-converting enzyme (ACE) inhibitor enalapril to conventional therapeutic regimens can significantly reduce mortality and improve prognosis in patients with all grades of heart failure. Moreover, data from all three trials confirm the involvement of neurohormonal systems in the development and progression of CHF and suggest that the beneficial effects of enalapril in heart failure may in part be due to the suppression of this neurohormonal activity. It is now apparent that some form of neurohormonal activation is present early in the course of the disease before the emergence of overt heart failure symptoms. On the basis of such findings, it would seem that early introduction of therapy targeted at neurohormonal influences may well become a central component of any future CHF treatment program.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1994

Predictors of exercise capacity in chronic heart failure.

Abnormalities of skeletal muscle rather than of haemodynamics may be important determinants of exercise capacity in chronic heart failure. We investigated an array of indicators of central haemodynamics and peripheral muscle function to establish which resting measurements predicted exercise performance. In 20 patients quadriceps strength, resting and peak leg blood flow and leg muscle cross sectional area were measured. In 18 patients average daytime blood pressure and pulse rate, haemodynamic variables at rest and during exercise, and autonomic activity were measured. There were correlations between peak oxygen consumption and quadriceps strength (0.65; P = 0.007), thigh muscle cross sectional area (r = 0.63; P = 0.004), and average daytime systolic blood pressure (r = 0.66; P < 0.01). There were no correlations with indices of peripheral blood flow, measures of haemodynamic function, or autonomic function. Quadriceps strength was the most important individual correlate of exercise tolerance (r = 0.73). With total muscle cross sectional area and left quadriceps strength also taken into consideration, 82% of the variation in peak oxygen consumption was explained. Of the haemodynamic variables, only average daytime systolic blood pressure predicted exercise performance. The resting variables that best predict exercise performance in chronic heart failure are measures of skeletal muscle function and bulk, and average daytime systolic blood pressure. These findings suggest that abnormalities in the periphery largely determine exercise performance in chronic heart failure, and that the ability of the heart to generate an adequate blood pressure response to daily activities is also predictive of functional status.

Autonomic Nervous System↗

PubMed1994

Time course of haemodynamic changes after maximal exercise.

The haemodynamic changes during 4 h following maximal upright bicycle exercise were evaluated in six normals in a randomized controlled crossover design. Total peripheral resistance was reduced to 2 h (-6.7 mmHg min l-1, P < 0.05); exercising and non-exercising vascular beds were vasodilated for 2 h (-24.1 and -23.8 mmHg min ml-1 100 ml-1 tissue, respectively, P < 0.05), associated with reductions in systolic (-5.8 mmHg, P < 0.05) and diastolic pressure (-8.3 mmHg, P < 0.05). Rise in cardiac index for 1 h (+0.51 min-1 m-2, P < 0.05) was accounted for by an elevated heart rate (+14.4 beats min-1, P < 0.01) as stroke volume was unchanged. Body temperature was elevated until 40 min (+0.20 degrees C, P < 0.05). The return of all haemodynamic variables to control by 3 h suggests a 3 h limit for a hypotensive effect of exercise. Rise in body temperature is not the only factor responsible for the hypotension.

Adult↗

PubMed1994

Training partially reverses skeletal muscle metabolic abnormalities during exercise in heart failure.

Using 31P-magnetic resonance spectroscopy during and after exercise, we studied whether forearm metabolic responses to exercise were improved by 1 mo of training in 10 males with heart failure. In the control (untrained) arm, there were no changes in any of the measured variables. In the trained arm, maximal voluntary contraction increased 6% (P = 0.05). During incremental exercise, duration increased 19% (P < 0.05) and submaximal responses improved for pH (6.78 +/- 0.13 pretraining vs. 6.85 +/- 0.17 posttraining; P < 0.01) and PCr/(PCr+Pi) (where PCr is phosphocreatine; 0.48 +/- 0.09 pretraining vs. 0.52 +/- 0.07 posttraining; P < 0.01). The PCr resynthesis rate increased by 48% (P < 0.01), and estimated effective maximal rate of mitochondrial ATP synthesis increased by 37% (P < 0.05). Endurance exercise duration increased by 67% (P < 0.01), and submaximal levels of PCr/(PCr+Pi) (P < 0.05) and pH (P = 0.07) improved. The PCr resynthesis rate (P < 0.01) and the effective maximal rate of mitochondrial ATP synthesis (P < 0.05) also improved. These findings document that impaired oxidative capacity of skeletal muscle can be improved by local muscle training in heart failure, which is compatible with the hypothesis that a part of the abnormality present in heart failure may be due to inactivity.

Adenosine Triphosphate↗

PubMed1993

Physical training improves skeletal muscle metabolism in patients with chronic heart failure.

OBJECTIVES: This study investigated the effects of physical training on skeletal muscle metabolism in patients with chronic heart failure. BACKGROUND: Skeletal muscle metabolic abnormalities in patients with chronic heart failure have been associated with exercise intolerance. Muscle deconditioning is a possible mechanism for the intrinsic skeletal muscle metabolic changes seen in chronic heart failure. METHODS: We used phosphorus-31 nuclear magnetic resonance spectroscopy to study muscle metabolism during exercise in 12 patients with stable ischemic chronic heart failure undergoing 8 weeks of home-based bicycle exercise training in a randomized crossover controlled trial. Changes in muscle pH and concentrations of phosphocreatine and adenosine diphosphate (ADP) were measured in phosphorus-31 spectra of calf muscle obtained at rest, throughout incremental work load plantar flexion until exhaustion and during recovery from exercise. Results were compared with those in 15 age-matched control subjects who performed a single study only. RESULTS: Before training, phosphocreatine depletion, muscle acidification and the increase in ADP during the 1st 4 min of plantar flexion exercise were all increased (p < 0.04) compared with values in control subjects. Training produced an increase (p < 0.002) in incremental plantar flexion exercise tolerance. After training, phosphocreatine depletion and the increase in ADP during exercise were reduced significantly (p < 0.003) at all matched submaximal work loads and at peak exercise, although there was no significant change in the response of muscle pH to exercise. After training, changes in ADP were not significantly different from those in control subjects, although phosphocreatine depletion was still greater (p < 0.05) in trained patients than in control subjects. The phosphocreatine recovery half-time was significantly (p < 0.05) shorter after training, although there was no significant change in the half-time of adenosine diphosphate recovery. In untrained subjects, the initial rate of phosphocreatine resynthesis after exercise (a measure of the rate of oxidative adenosine triphosphate [ATP] synthesis) and the inferred maximal rate of mitochondrial ATP synthesis were reduced compared with rates in control subjects (p < 0.003) and both were significantly increased (p < 0.05) by training, so that they were not significantly different from values in control subjects. CONCLUSIONS: The reduction in phosphocreatine depletion and in the increase in ADP during exercise, and the enhanced rate of phosphocreatine resynthesis in recovery (which is independent of muscle mass) indicate that a substantial correction of the impaired oxidative capacity of skeletal muscle in chronic heart failure can be achieved by exercise training.

Adenosine Diphosphate↗

PubMed1993

Persistent peripheral vasodilation and sympathetic activity in hypotension after maximal exercise.

Hemodynamics (by aortic Doppler), autonomic factors (power spectrum analysis of heart rate and blood pressure variabilities and baroreceptor sensitivity), and plasma renin activity during the hypotension after maximal exercise were studied in 10 normal subjects on two separate days: a nonexercise (control) day (30 min of upright rest followed by 60 min of supine rest) and an exercise day (maximal upright bicycle exercise followed by 60 min supine) in random order. After exercise, diastolic pressure was reduced for the entire hour, cardiac output increased (+33.8%, P < 0.05), stroke volume was unchanged, and systemic vascular resistance fell (-28.6%, P < 0.01). Indexes of vagal activity were reduced for 60 min, whereas the sympathetic indexes were elevated. Baroreflex sensitivity was also reduced for the first 10 min after exercise. Renin activity increased threefold after exercise. The postexercise hypotension results from a persisting peripheral vasodilation despite an increase in renin activity: the persistent sympathetic activity and reduced vagal tone are probably reflex responses to this vasodilatation.

Adult↗

PubMed1993

Angina and coronary artery disease in patients with aortic valve disease.

The significance of angina pectoris in patients with aortic valve disease (AVD) and the need for coronary arteriography before valve replacement are controversial. The history of chest pain and coronary arteriographic findings were reviewed in 333 patients > or = forty years old, with AVD: 142 with aortic stenosis, 87 with mixed AVD and 104 with aortic regurgitation. The prevalence of coronary artery disease (CAD) was similar among different types of AVD. Angina pectoris was more frequent in patients with aortic stenosis (56%) and mixed AVD (53%) than in patients with aortic regurgitation (24%) (p < 0.0001). Similar results were found in patients with and without CAD. Twenty-six of 95 (27%) patients with CAD had no chest pain at all. The absence of any chest pain in CAD patients was more frequent in those > or = sixty years old than in those < sixty (p < 0.05). Thus, since a significant number of patients had CAD in the absence of any chest pain, the authors recommend coronary arteriography for all patients > or = forty years of age before aortic valve replacement.

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PubMed1992

Comparison of different methods for assessing sympathovagal balance in chronic congestive heart failure secondary to coronary artery disease.

Twenty-five patients (aged 62 +/- 2 years) with stable, moderate to severe ischemic congestive heart failure (CHF) (New York Heart Association class II/III: 15/10; ejection fraction 21.6 +/- 2%; and peak oxygen uptake 13.6 +/- 0.7 ml/kg/min) were studied to evaluate the ability of different methods to characterize autonomic tone in chronic CHF. Sympathovagal balance was assessed by: (1) heart rate variability in the time domain, assessed by the SD of RR intervals; (2) heart rate variability in the frequency domain, assessed by low- (0.03 to 0.14 Hz) and high- (0.18 to 0.40 Hz) frequency components of heart rate variability by autoregressive power spectral analysis; (3) 24-hour, daytime and nighttime heart rate; (4) submaximal heart rate during upright bicycle exercise, with respiratory gas analysis to obtain peak oxygen uptake; and (5) radiolabeled norepinephrine spillover. These methods did not correlate, with the exception of day and nighttime heart rate (r = 0.74; p < 0.001) and the expected inverse correlation between low and high frequency (r = -0.92; p < 0.001). No method correlated significantly with peak oxygen uptake, exercise tolerance or ejection fraction. After 8 weeks of physical training at home, all methods showed improvement in autonomic balance: increases in SD of RR intervals (+21%; p < 0.02) and high frequency (+41%; p < 0.007), and decreases in low frequency (-19%; p < 0.002), low-/high-frequency ratio (-48%; p < 0.03), norepinephrine spillover (-28.9%; p < 0.03), 24-hour heart rate (-2.7%; p < 0.005) and submaximal heart rate (-10.8%; p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Autonomic Nervous System Diseases↗

PubMed1992

Impairment of endothelium dependent responses in a rat model of chronic heart failure: effects of an exercise training protocol.

OBJECTIVE: The aim was to document the response of aortic rings from a rat model of heart failure to endothelium dependent and endothelium independent vasodilating agents. The effects of an exercise training schedule upon these responses was studied. METHODS: Heart failure was produced in one group of female Wistar rats by coronary artery occlusion, and sham operations were performed in a matched group. The rats were allowed to recover for six weeks, following which half the rats with heart failure were started on a treadmill exercise schedule for a further six weeks. After this time the rats were killed, and rings of aorta were studied in an organ bath to measure the response to both endothelium dependent and endothelium independent vasoactive agents. RESULTS: The presence of heart failure was confirmed in both the non-trained (NT, n = 5) and trained rats (TR, n = 5), but not in the sham operated animals (SH, n = 6). The constrictor response to prostaglandin F2 alpha was similar in aortic rings from all the animals. The relaxation response to the endothelium dependent vasodilator acetylcholine (10(-7) and 10(-6) M) was impaired in the rats with heart failure compared to the sham operated animals (10% v 33% with 10(-7) M acetylcholine, p < 0.005). The dilator response in the trained rats was not significantly greater than in the non-trained rats (TR 35% v NT 24% with 10(-6) M acetylcholine). There was no difference in the response to sodium nitroprusside (10(-7) and 10(-6) M) between the three groups. CONCLUSIONS: Chronic heart failure impairs the response of aortic rings to the endothelium dependent vasodilator acetylcholine in a rat model of heart failure. The response to sodium nitroprusside, an endothelium independent relaxing agent, is not impaired by heart failure. These findings may help to explain the raised systemic vascular resistance and the failure of vasodilatation in skeletal muscle vasculature which limits exercise capacity in subjects with heart failure.

Acetylcholine↗

PubMed1992

Ascending aortic Doppler velocity and the prediction of exercise capacity in post-infarction left ventricular dysfunction.

A system to improve analysis of the aortic pulsed Doppler velocity signal has been developed and used to study cardiac performance during a 4 min, 25 W incremental stage supine bicycle exercise to exhaustion. Twenty-two male subjects with stable chronic ischaemic heart disease were studied (15 with NYHA class II/III heart failure, and seven age-matched class I subjects). None had evidence of reversible ischaemia. Peak velocity (PV) from the intensity weighted mean velocity profile, early acceleration (eA) and stroke distance (SD) were all significantly lower at rest in class II/III compared to class I. For the change from rest to 50 W, PV did not alter, eAC increased significantly (P less than 0.05) and to a similar extent in both groups (18.6% class II/III vs 16.4% class I) and SD was reduced from 7.8 to 5.9 in class II/III (P less than 0.01) but did not change in class I (12.4 vs 11.8, ns). There was also a greater increase in heart rate (HR) in class II/III subjects (P less than 0.05). The duration of exercise was correlated with resting PV (r = 0.48, P less than 0.025) but was correlated best with the change in blood momentum (PV x Stroke volume x HR) between rest and peak exercise (r = 0.80, P less than 0.001). Thus Doppler velocimetry can give quantitative information on the response to exercise which discriminates between grades of ventricular dysfunction and is predictive of exercise capacity.

Adult↗

PubMed1992

Effects of mild physical activity, atenolol and the combination on ambulatory blood pressure in hypertensive subjects.

OBJECTIVE: To evaluate whether beta-blocker treatment could enhance the effect of a mild physical training programme upon blood pressure. DESIGN AND METHODS: In 12 hypertensive subjects (mean age: 40.3 years) a prospective randomized Latin square-design trial was performed with three treatments: physical training and placebo tablets; atenolol 50 mg once a day and inactivity; and physical training and atenolol 50 mg once a day. RESULTS: Training significantly increased maximal ventilatory oxygen consumption (VO2MAX), and there was a decrease in ambulatory diastolic blood pressure (DBP) which did not reach statistical significance. Atenolol alone significantly reduced ambulatory systolic blood pressure (SBP) and DBP. Atenolol alone did not reduce VO2MAX. The combination of training and atenolol resulted in an increase in VO2MAX compared with atenolol alone, but no additional significant fall in blood pressure. CONCLUSIONS: Atenolol did not enhance the effect of physical training upon blood pressure and had little if any effect upon the training-induced increase in exercise tolerance.

Adult↗

PubMed1992

Ventilation in chronic heart failure: effects of physical training.

OBJECTIVE: To assess the effects of exercise training on ventilatory function in chronic heart failure. DESIGN: Observer blinded random allocation crossover training and detraining trial. SETTING: Assessment in hospital based clinical laboratory; training home based. PATIENTS: 22 patients with chronic heart failure (New York Heart Association (NYHA) class II or III) recruited from a tertiary referral centre. All finished the study. INTERVENTION: Bicycle ergometer exercise for 20 minutes a day, five days a week for eight weeks at 70%-80% of maximum heart rate. MAIN OUTCOME MEASURES: Exercise capacity on graded incremental exercise test, minute ventilation, oxygen consumption and carbon dioxide output. RESULTS: Peak work load increased from 96 W to 112 W and peak oxygen consumption from 14.1 ml/kg/min to 15.4 ml/kg/min (p < 0.01). At submaximal workloads carbon dioxide excretion (VCO2) and minute ventilation (Vi) decreased significantly (p < 0.05) though oxygen consumption was unchanged. The relation between Vi and carbon dioxide excretion changed: the slope of the Vi to VCO2 plot decreased from 38.6 to 35.3, indicating an improvement in overall ventilary efficiency. The instantaneous carbon dioxide ventilatory equivalent (Vi/VCO2) decreased at submaximal workloads, and reached a lower minimum value after training, indicating that optimum ventilatory performance improved. The exercise capacity of patients was related to the optimum ventilatory performance. It is suggested that this may in part be mediated through changes in skeletal muscles. CONCLUSION: Exercise training reduces the ventilatory abnormalities in chronic heart failure; thus some of these changes may be due to physical deconditioning.

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PubMed1992

Controlled trial of physical training in chronic heart failure. Exercise performance, hemodynamics, ventilation, and autonomic function.

BACKGROUND: Many secondary abnormalities in chronic heart failure (CHF) may reflect physical deconditioning. There has been no prospective, controlled study of the effects of physical training on hemodynamics and autonomic function in CHF. METHODS AND RESULTS: In a controlled crossover trial of 8 weeks of exercise training, 17 men with stable moderate to severe CHF (age, 61.8 +/- 1.5 years; left ventricular ejection fraction, 19.6 +/- 2.3%), increased exercise tolerance (13.9 +/- 1.0 to 16.5 +/- 1.0 minutes, p less than 0.001), and peak oxygen uptake (13.2 +/- 0.9 to 15.6 +/- 1.0 ml/kg/min, p less than 0.01) significantly compared with controls. Training increased cardiac output at submaximal (5.9-6.7 l/min, p less than 0.05) and peak exercise (6.3-7.1 l/min, p less than 0.05), with a significant reduction in systemic vascular resistance. Training reduced minute ventilation and the slope relating minute ventilation to carbon dioxide production (-10.5%, p less than 0.05). Sympathovagal balance was altered by physical training when assessed by three methods: 1) RR variability (+19.2%, p less than 0.05); 2) autoregressive power spectral analysis of the resting ECG divided into low-frequency (-21.2%, p less than 0.01) and high-frequency (+51.3%, p less than 0.05) components; and 3) whole-body radiolabeled norepinephrine spillover (-16%, p less than 0.05). These measurements all showed a significant shift away from sympathetic toward enhanced vagal activity after training. CONCLUSIONS: Carefully selected patients with moderate to severe CHF can achieve significant, worthwhile improvements with exercise training. Physical deconditioning may be partly responsible for some of the associated abnormalities and exercise limitation of CHF, including abnormalities in autonomic balance.

Autonomic Nervous System↗

PubMed1991

Angiotensin-converting enzyme inhibition and physical training in heart failure.

A total of 12 patients (mean age +/- SEM 63 +/- 2.6 years) with moderate to severe heart failure (ejection fraction = 23 +/- 3.2%) were included in a placebo-controlled crossover trial. Patients were randomly allocated to 4 periods of 6 weeks each: placebo, placebo and physical training, lisinopril 10 mg daily, and lisinopril and physical training. The exercise time increased from 13.6 +/- 0.9 min with placebo to 15 +/- 1 min with training alone, and to 16.1 +/- 0.7 min with lisinopril and training. With lisinopril alone there was a non-significant increase in exercise time, to 14.5 +/- 0.6 min. Improvements in exercise time were accompanied by a similar increase in peak oxygen consumption. Overall, the most significant improvements in symptoms and indices of cardiorespiratory fitness were achieved with a combination of lisinopril and training. Thus physical training is not only a useful adjunct to the existing medical therapy for heart failure, but it may also provide symptomatic benefits in its own right.

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