Changes In Exercise Tolerance Research Articles

Usefulness of changes in exercise tolerance induced by nitroglycerin in identifying patients with syndrome X

Two exercise tests, one under basal conditions and one after sublingual nitroglycerin (NTG), were performed in 39 patients with stable angina pectoris—16 with critical coronary stenoses and 23 with normal coronary arteries (syndrome X). Under basal conditions, times at ischemic threshold, at peak exercise, and at complete ECG recovery were similar in the two groups. Peak ST depression was significantly higher in patients with coronary artery disease (CAD). In a similar proportion of patients, ST-segment depression developed earlier or at a low heart rate. Patterns of heart rate, blood pressure, and rate-pressure product during exercise and recovery were also similar. After NTG an increase in the ischemic threshold was observed in a significantly higher proportion of patients with CAD (93.8% vs 39.1%). Furthermore, a subgroup of patients with syndrome X showed a worsening of exercise performance. This suggests that NTG does not directly affect small coronary vessels. Our results confirm that no relevant differences exist in exercise responses between patients with CAD and those with syndrome X uncer basal conditions. NTG-induced changes in this response could be useful in indentifying patients with normal coronary arteries. Moreover, this test could be used as a guide to therapeutic approaches.

Nitrates versus angiotensin-converting enzyme inhibitors for congestive heart failure

The efficacy of nitrates versus that of angiotensin-converting enzyme (ACE) inhibitors in heart failure may be evaluated based on 3 treatment aims: hemodynamic improvement, symptom relief, and survival benefit. Nitrates used in conjunction with hydralazine produce a relatively large increase in stroke volume and a prominent reduction of left ventricular filling pressure, whereas ACE inhibitors produce a comparatively modest increase in stroke volume with a prominent reduction in filling pressure. The effect of these drugs on arterial compliance has been evaluated using a modified Windkessel model of the circulation to define their mechanism of action. Nitrates appear to affect the large arteries and arterial bed as well as the venous circulation. Intermediate-term response to therapy is often evaluated by changes in exercise tolerance. A review of multicenter trials reveals that, although both ACE inhibitors and hydralazine/nitrate have favorable hemodynamic actions, the effect of hydralazine/nitrate on exercise capacity appears to be slightly better. ACE inhibitors and nitrates both may reduce dysfunctional myocardial remodeling, as evaluated in a canine model of chronic left ventricular dysfunction. The increase in the ejection fraction by these drugs and the decrease of plasma norepinephrine levels by ACE inhibitors may contribute to improved long-term survival. It appears, therefore, that the long-term benefits of nitrates and ACE inhibitors in heart failure probably relate to their ability both to affect cardiac remodeling and to relax vascular smooth muscle.

The acute response of left ventricular filling dynamics to intravenous verapamil predicts the changes in exercise tolerance after oral verapamil therapy in patients with hypertrophic cardiomyopathy.

We studied the correlation between changes in left ventricular filling dynamics induced by acute intravenous administration of verapamil and the changes in exercise tolerance induced by oral administration of the agent in 30 patients with hypertrophic cardiomyopathy. Diastolic cardiac function was measured by means of a nuclear stethoscope before and 10 min after intravenous administration of verapamil, 0.15 mg.kg-1 over 2 min. Treadmill exercise tests using a modified Bruce protocol were performed before the initiation of oral verapamil treatment and after 4 weeks of oral therapy at a dose of 320-360 mg.day-1 (mean +/- SD 332 +/- 17 mg.day-1). Peak filling rate (PFR) increased in 21 patients, 18 of whom (86%) also had an increase in exercise duration, PFR showed no increase in nine patients, eight of whom (89%) had no change in exercise duration (sensitivity 95%, specificity 73%, predictive value of the positive result 86%, predictive value of the negative result 89%). Acute changes in time from the beginning of rapid filling to PFR (t-PFR) and in left ventricular end-diastolic volume (EDV) were less useful in predicting improvement in exercise tolerance. In 19 patients the changes in PFR and EDV paralleled. Twelve of the 13 patients (92%) with an increase in both parameters also had an increase in exercise duration, whereas all six in whom these parameters were reduced showed no increase in exercise duration (sensitivity 100%, specificity 86%, predictive value of positive results 92%, and predictive value of negative results 100%).(ABSTRACT TRUNCATED AT 250 WORDS)

Improvement in exercise capacity after correction of anemia in patients with end-stage renal failure

Changes in exercise tolerance occurring after correction of anemia with recombinant human erythropoietin in a group of patients with end-stage renal failure were evaluated. Ten patients, aged 29 ± 11 years, on chronic hemodialysis treatment, with no associated diseases, were evaluated by cardiopulmonary bicycle exercise testing and M-mode, 2-dimensional and pulsed doppler echocardiography before and after anemia correction. After 1 and 3 months of therapy, hemoglobin plasma levels increased from 5.9 ± 1.2 to 7.7 ± 1.3 and 9.9 ± 1.4 g/dl, with a concomitant increase in peak oxygen consumption (VO 2) from 21.4 ± 4.3 to 24.4 ± 4.3 and 26.6 ± 4.6 ml/kg/min and of VO 2 at the ventilatory threshold from 15.0 ± 3.7 to 17.3 ± 3.7 and 16.8 ± 3.4 ml/kg/min. After 3 months of therapy, systolic blood pressure significantly decreased both at peak exercise (159 ± 35 to 134 ± 22 mm Hg) and ventilatory threshold (140 ± 27 to 123 ± 19 mm Hg), whereas cardiac index at rest decreased from 3.3 ± 0.7 to 2.8 ± 0.5 liters/min/m 2 and heart rate from 77 ± 12 to 70 ± 10 beats/min. However, no significant relation was found between hemoglobin plasma levels and peak VO 2, whereas a significant relation was found between hemoglobin concentration and cardiac index at rest.

Changes in exercise tolerance and resting haemodynamics during long-term treatment of heart failure with xamoterol

The long-term efficacy of xamoterol in improving effort capacity and haemodynamics was investigated in a study lasting 1 year in heart failure patients. Following a 3 month, double-blind period of treatment with xamoterol, patients continued therapy for a further 9 months. Exercise duration rose by 27% at 3 months and this improvement was maintained at 12 months. Similarly, the statistically significant increase in cardiac index and reduction in pulmonary wedge pressure and exercise heart rate persisted for 12 months.

Effect of vasodilator and inotropic drugs on clinical symptoms and long-term survival in chronic congestive heart failure

The major therapeutic goals in the treatment of congestive heart failure are the relief of symptoms and the prolongation of life, but it remains unclear whether there is a relation between changes in exercise tolerance and alterations in the risk of death. Although all vasodilator and inotropic agents produce short-term haemodynamic benefits, these acute effects do not predict the long-term clinical responses to these drugs. Converting-enzyme inhibitors appear to improve symptoms and survival. A combination of hydralazine and isosorbide dinitrate produces variable effects on exercise tolerance but appears to prolong life. Catecholamines and phosphodiesterase inhibitors may reduce dyspnea and fatigue but adversely affect mortality. Calcium channel blocking drugs may exert deleterious effects on both symptoms and prognosis. alpha-Adrenergic blocking drugs produce no beneficial or adverse effects on clinical status or mortality. Hence, there is no consistent relation between the symptomatic and prognostic effects of drug therapy in patients with chronic heart failure. This variability makes it impossible to predict the effects of any drug on exercise tolerance or survival based on an evaluation of the agent's short-term haemodynamic effects.

Exercise tolerance changes following renal transplantation.

Maximal exercise capacity was measured in 20 nondiabetic patients with end-stage renal disease before and soon after successful renal transplantation. Maximal oxygen consumption increased significantly in all patients posttransplant. Increases in maximal heart rate and heart rates at 70% of maximal levels were also observed. The changes in maximal oxygen consumption were not significantly correlated with changes in hematocrit. The removal of uremia may result in improved functioning of one or more of the systems involved in oxygen transport and utilization that determine exercise capacity.

Lack of relationship between the short-term hemodynamic effects of captopril and subsequent clinical responses.

The role of hemodynamic monitoring during the initiation of vasodilator therapy for heart failure remains to be defined, despite the tremendous potential socioeconomic and clinical ramifications. We therefore performed resting and exercise hemodynamic studies before and during the initial 48 hr of captopril therapy in 14 stable patients with New York Heart Association Class II or III chronic congestive heart failure. Their clinical response to therapy was determined by evaluating changes in clinical status and the measured changes in exercise tolerance, heart size, and ejection fraction after 3 months. Significant improvement in each of these indexes was found for the group as a whole, but the baseline hemodynamics and the hemodynamic responses to captopril differed little between the patients showing marked improvement and those exhibiting little or no change. Correlations between the hemodynamic measurements and the changes in clinical class, exercise tolerance, heart size, and ejection fraction were generally poor. Even when they achieved significance, these correlations were too loose to allow prediction of the clinical efficacy of captopril in individual subjects. These findings indicate that the routine use of invasive hemodynamic monitoring during the initiation of captopril is unnecessary and potentially misleading, although such measurements remain valuable for diagnosis, the management of patients with complex conditions, and for investigation. The response to captopril may be best evaluated by serial measurements of exercise tolerance and heart size in addition to clinical assessment.

Oral sustained-release nitroglycerin in chronic stable angina: A multicenter, double-blind, randomized crossover trial

Forty-six patients with stable angina pectoris were randomized to receive either oral sustained-release nitroglycerin (SRNG, 6.5 mg) or placebo (P) 3 times a day for a 2-week double-blind trial. They were investigated for the frequency of anginal episodes, for sublingual nitroglycerin consumption and for exercise tolerance. There was a slight but significant decrease in the number of anginal episodes (6.4 ±1.5 episodes/week with P, 4.9 ± 1.7 with SRNG, p < 0.005) and sublingual nitroglycerin consumption (3.9 ± 1 tablets/week with P, 2.7 ± 1 with SRNG, p < 0.005). The patients performed 3 upright multistage (increments of 30 W every 3 minutes) exercise tests on a bicycle ergometer before the start of the study and 1 hour after the intake of SRNG or P, at the end of each double-blind phase. Exercise capacity, expressed as exercise duration, increased from 8.9 ± 3.8 minutes with P to 10.2 ± 3.8 minutes with SRNG (14.6 %; p < 0.001). At symptom-limited exercise, ST depression was significantly reduced (p < 0.05) during the SRNG phase. Thirty-four patients (74 %) reached a higher peak heart rate (139 beats/min with P, 145 beats/min with SRNG; p < 0.001) and 35 patients (76 %) a higher ratepressure product (+ 6 %; p < 0.001). These changes in exercise tolerance are relatively modest and at least 11 patients would have benefited from larger doses of nitrates. Although the individual variability of dose response to nitrates is wide, it is concluded that oral SRNG (6.5 mg 3 times daily) is an effective prophylactic therapy in stable angina pectoris and that exercise capacity, measured 1 hour after administration, is improved.

Acute and long-term effects of vasodilator therapy on resting and exercise hemodynamics and exercise tolerance.

The acute hemodynamic response to vasodilators in patients with chronic heart failure has been well characterized, but less is known about the long-term hemodynamic effects of vasodilator therapy. We measured hemodynamic variables at rest and during upright exercise in 11 patients during the initiation of therapy with oral hydralazine and sublingual isosorbide dinitrate and, in eight of these, after 3 months of continuous treatment. Marked initial increases in resting cardiac output and stroke volume and reductions in wedge pressure were sustained during chronic therapy. Similarly, the early improvement in exercise hemodynamic measurements persisted in most subjects. Exercise tolerance, quantified as the maximum duration of treadmill exercise, increased modestly (7.7 +/- 2.6 to 8.9 +/- 3.3 minutes, 0.05 less than p less than 0.10) after several days on vasodilators and further (10.2 +/- 3.7 minutes, p less than 0.01) during long-term treatment. The acute hemodynamic effects of vasodilator therapy at rest or during exercise did not correlate well with the changes in exercise tolerance. Our findings suggest that the combination of hydralazine and isosorbide dinitrate improves cardiac performance at rest and during exercise in patients with chronic heart failure and that this improvement persists during chronic therapy. In most patients, this hemodynamic improvement is accompanied by greater exercise tolerance.

Longitudinal study (32 years) of exercise tolerance, breathing response, blood pressure, and blood lipids in young men.

Changes in exercise tolerance, blood lipids, and blood pressure from youth to middle age was studied in 106 subjects followed 32 years. In addition, the responses to cold pressor and CO2 stress were studied as correlates of future lipids and blood pressure. Treadmill exercise test, cold pressor test, response to breathing a mixture of 6% CO2, and 21% O2, for 5 minutes, blood pressure, and lipid measurements were performed in 1947 when subjects were 20 +/- 2 years old. Exercise, blood pressure and lipid tests were repeated in 1979. Tracking of blood pressure and pulse response to exercise over the period was demonstrated. Baseline exercise response correlated with future blood pressure, cholesterol, triglycerides, and high density lipoproteins. Change in exercise pulse rate over the period correlated with change in cholesterol. Cold pressor systolic blood pressure response correlated with future systolic blood pressure and triglycerides. Pulse and blood pressure response to CO2 breathing correlated with cholesterol, triglyceride and high density lipoprotein 32 years later. These correlations were independent of baseline values of the variables and body mass index. Individuals who were judged "fit" (exercise pulse rise less than median) at both baseline and follow-up had the best cardiovascular risk profile (blood pressure and lipids). Blood pressure and pulse response to exercise tracked between ages 20 and 50. Exercise, cold pressor, and CO2 responses in youth correlated with blood lipid levels in middle age.

The influence of combined treatment with propranolol and acetylsalicylic acid on platelet aggregation in coronary heart disease.

British Journal of Clinical PharmacologyVolume 7, Issue 3 p. 287-291 Free Access The influence of combined treatment with propranolol and acetylsalicylic acid on platelet aggregation in coronary heart disease. I Keber, I KeberSearch for more papers by this authorM Jerse, M JerseSearch for more papers by this authorD Keber, D KeberSearch for more papers by this authorM Stegnar, M StegnarSearch for more papers by this author I Keber, I KeberSearch for more papers by this authorM Jerse, M JerseSearch for more papers by this authorD Keber, D KeberSearch for more papers by this authorM Stegnar, M StegnarSearch for more papers by this author First published: March 1979 https://doi.org/10.1111/j.1365-2125.1979.tb00934.xCitations: 16AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat References Abdulla, Y.H. (1969). Beta-adrenergic receptors in human platelets. J. Atheroscler. Res., 9, 171– 179. Born, G.V.R. (1962). Aggregation of blood platelets by adenosine diphosphate and its reversal. Nature, 194, 927– 929. Breddin, K. & Banke, J. (1965). Thrombozyten-agglutination und Gefäskrankheiten. Blut, 9, 144– 164. Deykin, D. (1974). Emerging concepts of platelet function. N. Engl. J. Med., 290, 144– 151. Frishman, W.H., Weksler, B.B., Christodoulou, J.P., Smithen, C. & Killip, T. (1974). Reversal of abnormal platelet aggregability and change in exercise tolerance in patients with angina pectoris following oral propranolol. Circulation, 50, 887– 896. Green, K.G. (1977). Reduction in mortality after myocardial infarction with long-term β-adrenoreceptor blockade. Multicentre international study, supplementary report Br. med. J., 2, 419– 421. Goldenfarb, P.B., Cathey, M.H. & Cooper, G.R. (1970). The determination of ADP-induced platelet aggregation in normal men. Atherosclerosis, 12, 335– 340. Haerem, J.W. (1971). Sudden coronary death: the occurrence of platelet aggregates in the epicardial arteries of man. Atherosclerosis, 14, 417– 432. Haft, J.I. (1976). Platelets, coronary artery disease and stress. In Thrombosis, Platelets, Anticoagulation and Acetylsalicytic Acid, Curr. Cardiovasc. Res., 2, ed. E. Donoso & J.I. Haft pp. 97– 109.Stuttgart: Georg Thieme. Haft, J.I. & Fani, K. (1973). Intravascular platelet aggregation in the heart induced by stress. Circulation, 47, 353– 358. Haft, J.I., Fani, K., Alcorta, C. & Toot, M. (1973). Effect of propranolol on stress induced intravascular platelet aggregation in the heart. Circulation, 48, Suppl. IV, 57. Haft, J.I., Kranz, P.D., Albert, F.J. & Fani, K. (1972). Intravascular platelet aggregation in the heart induced by norepinephrine. Microscopic studies. Circulation, 46, 698– 708. 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Mayo Clin., 8, 365– 370. O'Brien, J.R., Heywood, J.B. & Heady, J.A. (1966). The quantitation of platelet aggregation induced by four compounds: a study in relation to myocardial infarction. Thromb. Diath. Haemorrh., 16, 752– 767. Sacchetti, G., Bellani, D., Montanari, C. & Gibelli, A. (1973). Effects in vitro of some cardiovascular drugs and other agents on human platelet aggregation. Thromb. Diath. Haemorrh., 28, 190– 195. Smith, J.B. & Willis, A.L. (1971). Aspirin selectively inhibits prostaglandin production in human platelets. Nature New Biol., 231, 235– 237. Snedecor, G.W. & Cochran, W.G. (1972). Statistical methods. Ames: Iowa State University Press. Steele, P.P., Weily, H.S., Davies, H. & Genton, E. (1973). Platelet function studies in coronary artery disease. Circulation, 48, 1194– 1200. Thomas, D.P. (1967). Effect of catecholamines on platelet aggregation caused by thrombin. Nature, 215, 298– 299. Vedin, A., Wilhelmsson, C. & Werkö, L. (1975). Chronic alprenolol treatment of patients with acute myocardial infarction after discharge from hospital. Effects on mortality and morbidity. Acta Med. Scand., Suppl. 575, 7– 40. Weksler, B.B., Gillick, M. & Pink, J. (1977). Effect of propranolol on platelet function. Blood, 49, 185– 196. Yamazaki, H., Takahashi, T. & Sano, T. (1975). Hyperaggregability of platelets in thromboembolic disorders. Thromb. Diath. Haemorrh., 34, 94– 105. Citing Literature Volume7, Issue3March 1979Pages 287-291 ReferencesRelatedInformation

Effects of denial on mood and performance in cardiovascular rehabilitation

The influence of defensive denial was studied on the mood and physical performance of 45 patients with coronary artery disease seen in a cardiovascular rehabilitation program following hospitalization for myocardial infarction, severe angina or vein graft bypass surgery. Patients were defined as deniers and nondeniers on the Hackett-Cassem Denial Scale. Mood was assessed by the Profile of Mood States (POMS), a self-rated 65 item inventory, before and after a six week program of aerobic conditioning, group therapy and education on coronary artery disease. Patients were classed as Type A or Type B personalities by their physical therapists. Physical performance was measured as the change in exercise tolerance on the stationary bicycle and treadmill stress test over the six week period. Nondenying patients reported more initial mood disturbance on all subscales of the POMS compared to deniers. Although both groups showed mood improvement following the rehabilitation program, only nondeniers achieved statistically significant changes in Total Mood Disturbance. All patients increased their exercise tolerance with no significant difference between groups. Changes in mood were statistically independent of improvements in exercise tolerance. Type B patients had significantly higher denial scores than Type A. Nondeniers were predominantly Type A. The adaptive value of defensive denial in the convalescence and rehabilitation of the coronary patient is discussed.

The effects of oral propranolol and metoprolol on lung function and exercise performance in chronic airways obstruction

Fifteen men with chronic airways obstruction received a test dose of propranol 20 mg orally. Six developed increased breathlessness. Nine who tolerated the test dose received metoprolol (100 mg) and propranolol (80 mg) on different days in a randomized double-blind fashion. Changes in resting and excercise hear rate, spirometry and exercise tolerance were measured 1 and 6 hours later. The drugs had similar effects on heart rate. Propranol, but not metoprolol, caused significant reduction in forced expiratory volume in one second (FEV 1) and peak expiratory flow rate. Neither drug produced significant changes in forced vital capacity (FVC) or exercise performance in the group as a whole, although the range of changes was wide. Despite considerable reduction in FEV 1 and FVC in some individuals, most reported no increase in symptoms. Changes in exercise tolerance at 1 hour correlated significantly with changes in FVC but not with those in FEV 1. It is proposed that changes in FEV 1, though of pharmacological interest, may be less relevant clinically than changes in FVC.

Clinical Course Related to Preoperative and Postoperative Pulmonary Function in Patients with Bronchogenic Carcinoma

Unrotated factor analysis comparing patients who did well after operation with those who did not tolerate surgery due to respiratory causes revealed the FEV1 to be the most helpful in separating these two groups. Several other function tests also separated these two groups. Decrease in FEV1 after lung resection was inversely related to the degree of airway obstruction. The more normal patients had greater decrease in FEV1 and were more likely to experience decrease in exercise tolerance as compared to the more obstructed patients. The frequency of patients with worsening dyspnea after pneumonectomy and lobectomy was similar. Changes in exercise tolerance after resection were not related to morphologic emphysema nor bronchitis in the remaining lung as judged from examination of the resected specimen. Patients with postoperative atelectasis had higher lung volumes and compliance as compared to those without atelectasis. Chest roentgenograms of 12 pneumonectomy patients 3 and 30 months after operation showed “hyperinflation” in six. Lung volume measurements, however, showed no change. Unrotated factor analysis comparing patients who did well after operation with those who did not tolerate surgery due to respiratory causes revealed the FEV1 to be the most helpful in separating these two groups. Several other function tests also separated these two groups. Decrease in FEV1 after lung resection was inversely related to the degree of airway obstruction. The more normal patients had greater decrease in FEV1 and were more likely to experience decrease in exercise tolerance as compared to the more obstructed patients. The frequency of patients with worsening dyspnea after pneumonectomy and lobectomy was similar. Changes in exercise tolerance after resection were not related to morphologic emphysema nor bronchitis in the remaining lung as judged from examination of the resected specimen. Patients with postoperative atelectasis had higher lung volumes and compliance as compared to those without atelectasis. Chest roentgenograms of 12 pneumonectomy patients 3 and 30 months after operation showed “hyperinflation” in six. Lung volume measurements, however, showed no change.

Effects of propranolol on exercise tolerance in angina pectoris

The effect of beta adrenergic blockade with propranolol in angina pectoris was investigated by means of a standardized exercise tolerance test. The parenteral dose needed to produce satisfactory blockade, as judged by bradycardia, was about one-tenth of that required in the case of pronethalol. No side effects were noted after intravenous injection. In a preliminary study of 20 patients, the exercise tolerance of the 7 patients who were limited by angina pectoris was generally increased after propranolol was injected. Five patients limited by angina in the control test had no angina at a similar work level after the drug. Seven patients were limited by fatigue and showed no change in exercise tolerance. To distinguish the response to propranolol from a nonspecific placebo effect, 14 patients, limited by angina in an initial test, after an inert injection and after propranolol, were studied. Five patients with severe angina showed some improvement in exercise tolerance. Nine patients with moderate angina showed a significant increase in exercise tolerance beyond that found after the placebo. These studies suggest that propranolol improves the exercise tolerance of some patients with angina pectoris. However, any improvement in myocardial oxygenation after beta blockade is probably produced at the expense of an impairment in myocardial contractility and a fall in peripheral blood flow. Propranolol should therefore be avoided in patients with evidence of left ventricular failure.