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PubMed2003

Effects of a comprehensive rehabilitation program on quality of life in patients with chronic heart failure.

This evaluation was performed to assess the effects of a new, comprehensive outpatient rehabilitation program on generic and disease-specific quality of life related to exercise tolerance in stable chronic heart failure patients. Fifty-one patients (aged 59+/-11 years; 84% men) were treated for 12 weeks. Patients underwent optimized drug treatment, exercise training, and counseling and education. At baseline and at the end of the program, functional status, exercise capacity, and quality of life were assessed using the Medical Outcomes Study 36-item Short-Form Health Survey and the Minnesota Living with Heart Failure Questionnaire. Left ventricular ejection fraction and New York Heart Association functional class, as well as measures of physical fitness and walking distance covered in 6 minutes, improved significantly (by 11%-20% and by 58% on average, respectively). Physical functioning (effect size, 0.38; p<0.0001), role functioning (effect size, 0.17; p<0.05), and mental component score (effect size, 0.47; p<0.0001) on the questionnaire improved significantly. Disease-specific quality of life improved in sum score (effect size, 0.24; p<0.0001) and physical component score (effect size, 0.35; p<0.0001). The latter was inversely correlated to improvement in peak power output (r= -0.31; p<0.05). In patients with stable chronic heart failure, significant improvements in both generic and disease-specific quality of life related to improved exercise tolerance can be achieved within 12 weeks of comprehensive rehabilitation.

Aged↗

PubMed1997

Effect of exercise rehabilitation on heart rate variability in hypertensives after myocardial infarction.

OBJECTIVE: The aim of the study was to find out whether the presence of hypertension affects heart rate variability in patients rehabilitated after myocardial infarction. DESIGN: Echocardiography, exercise testing and 24 h Holter monitoring were performed before and after 27 days of early postdischarge cardiac rehabilitation. PATIENTS: The study population consisted of 64 patients aged 34-65 years (mean+/-SD 51.6+/-6.6) discharged from hospital after a first myocardial infarction who were subdivided into two groups, group A comprising 34 patients with arterial hypertension which had lasted 4.8+/-2.1 years and group B comprising 30 normotensives. MAIN OUTCOME: We expected exercise rehabilitation to affect heart rate variability, exercise tolerance and myocardial ischemia in patients after myocardial infarction with and without arterial hypertension. RESULTS: At baseline no intergroup differences were seen in the duration of exercise, workload and heart rate variability parameters. All parameters increased significantly after cardiac rehabilitation (P < 0.01): SD of all normal RR intervals 123.4+/-30.0 versus 123.8+/-30.0 ms; SD of the averages of normal RR intervals in all 5-min segments of the entire recording 115.1+/-30.5 versus 116.3+/-28.3 ms; mean of the SD of all normal RR intervals for all 5-min segments of the entire recording 49.0+/-12.5 versus 48.3+/-11.8 ms; square root of the mean of the sum of the squares of differences between adjacent RR intervals 29.7+/-9.1 versus 28.0+/-8.5 ms; percentage of differences between adjacent RR intervals > 50 ms 7.9+/-6.0 versus 7.1+/-6.1% (group A versus group B, respectively, NS). The duration of exercise and the workload were significantly increased (the rise was higher in normotensives). No differences were seen in the frequency and severity of silent myocardial ischemia. CONCLUSIONS: Early stationary exercise rehabilitation after myocardial infarction improves heart rate variability parameters and exercise tolerance both in hypertensives and in normotensives.

Adult↗

PubMedDate not supplied

Cardiopulmonary exercise testing in Fabry disease.

BACKGROUND: Fabry disease is a rare X-linked disorder that results from a deficiency in a lysosomal enzyme known as alpha-galactosidase A, with accumulation of globotriaosylceramide (Gl3). Early manifestations include angiokeratomas, acroparesthesias, and hypohidrosis and may progress to renal failure, cardiac dysfunction, and stroke. Patients exhibit decreased exercise tolerance and often complain of fatigue. OBJECTIVE: Our study evaluates the cardiopulmonary characteristics in a cohort of Fabry disease patients at rest and during exercise. METHODS: Thirty-nine patients with a diagnosis of Fabry disease underwent a health screening history and physical examination, an electrocardiogram, an echocardiogram, pulmonary function testing (spirometry), and a non-invasive cardiopulmonary exercise test. A control group was selected for comparison. RESULTS: Eighteen of the 39 Fabry patients (46%) exhibited a significant decrease in diastolic blood pressure (DBP) during exercise. The average decrease in DBP was 10 mm Hg. The maximum drop in DBP was 44 mm Hg. The drop in DBP was evident in 9 of the 24 female patients (38%). None of the control patients had a significant drop in DBP during exercise. CONCLUSIONS: Our finding of a significant decrease in DBP in patients with Fabry disease may explain deficits in exercise tolerance. It is notable that this abnormality is manifested in female patients, even though they are typically not as severely affected as males.

Adolescent↗

PubMed1992

Propionyl-L-carnitine: a new compound in the metabolic approach to the treatment of effort angina.

The effects of propionyl-L-carnitine on exercise tolerance of 12 patients with stable exertional angina were assessed in a double-blind, placebo-controlled, cross-over protocol using serial exercise tests. Compared to placebo, propionyl-L-carnitine significantly increased total work from 514 +/- 199 to 600 +/- 209 W (P less than 0.05) (17%) and prolonged exercise time and time to ischemic threshold from 515 +/- 115 to 565 +/- 109 sec (P less than 0.05) (10%) and from 375 +/- 102 to 427 +/- 93 sec (P less than 0.01) (14%), respectively. ST segment depression at the highest common work level was significantly reduced from 0.19 +/- 0.08 to 0.15 +/- 0.08 mV (P less than 0.05) (21%). No significant changes in heart rate, systolic blood pressure, and rate-pressure product at rest, at the highest common work level, on appearance of the ischemic threshold, or at peak exercise were observed after propionyl-L-carnitine treatment. No side effects were observed under propionyl-L-carnitine treatment. This study shows that propionyl-L-carnitine can significantly improve exercise tolerance in patients with stable angina. Our data seem to confirm that propionyl-L-carnitine most likely exerts its protective action via the metabolic pathway.

Adult↗

PubMed1981

Double-blind trial of nifedipine in angina patients with normal coronary arteries.

A double-blind trial was carried out in 33 patients with the syndrome of angina and normal coronary arteries, comparing the effects of nifedipine and placebo on the frequency and severity of anginal attacks, glyceryl trinitrate consumption and exercise tolerance. Electrocardiograms were abnormal at rest in 16 and normal in 17 patients. Five patients developed electrocardiographic changes suggestive or myocardial ischaemia on exertion. Exercise thallium 201 scintigraphy showed evidence of regional myocardial ischaemia in 4 patients. Of 30 patients who completed the trial, 16 reported fewer, less severe anginal attacks on nifedipine than on placebo; glyceryl trinitrate consumption was lower during nifedipine thn during placebo therapy. However, the reduction in angina and glyceryl trinitrate consumption in the group as a whole was not statistically significant; the results from 1 particular patient heavily influenced the statistical analysis against significant benefit from nifedipine. Exercise tolerance was similar on nifedipine and placebo. Two-thirds of the patients reported unwanted effects from nifedipine; 3 patients withdrew because of intolerable side-effects. It is concluded that nifedipine may reduce the frequency and severity of anginal attacks in some patients with angina and normal coronary arteries but the high incidence of side-effects may limit its usefulness.

Adult↗

PubMed1981

[Serial evaluation by effort test of the effects of coronary artery bypass on effort angina (author's transl)].

To evaluate the duration of favourable effects of coronary artery bypass (CAB) on exercise-induced angina (A), 58 patients: 13 with single 21 with double and 24 with triple vessel disease, were studied. All patients underwent CAB for stable angina on effort. Patients underwent exercise testing (ET) before surgery at one, two and three years. Heart rate peak (HR), HR x systolic blood pressure peak (DP), work load (W), exercise-induced ST segment depression (ST) and incidence of A were evaluated; the results of ET before surgery were compared with those found after CAB. Our findings show that HR, DP, W and ST were significantly improved by surgery for at least 3 years. The lowest incidence of A was found at one year ET (20.6%), while it increased at two years (27,5%) and three years ET (37.9%). Most patients with A had angiographic evidence of left ventricular abnormal wall motion and ec-graphic signs of previous myocardial infarction. Our data indicate that serial exercise testing can objectively monitor the results of CAB. Most patients show an improved exercise tolerance for up to 3 years after CAB. Some patients, with more extensive CAD, showed a progressive deterioration of the clinical pattern and a decrease of the exercise tolerance.

Angina Pectoris↗

PubMed1995

[Indicators of bicycle ergometry after heart transplantation].

Exercise tolerance in postcardiac transplantation patients versus healthy controls was studied at different intervals after the surgery using bicycle ergometry. Being low after the transplantation, exercise tolerance in the patients increased throughout the rehabilitation period but still did not reach the values characteristic for healthy subjects. Initial heart rate in the above patients was higher, while chronotropic and inotropic reserves of the transplanted heart appeared lower than in the controls. The data obtained help objectively assess the condition of the patients with transplanted heart.

Adolescent↗

PubMed1985

Effects of cold stimulation on coronary haemodynamics during exercise in patients with coronary artery disease.

To assess if cold-induced vasoconstriction may persist during exercise and contribute to the development of myocardial ischaemia, we studied 11 patients with exertional angina and angiographically proven coronary artery disease, in all cases involving the proximal portion of the left anterior descending artery. Great cardiac vein flow (GCVF) was measured by the thermodilution technique and the coronary resistance of the abnormally perfused anterior region (ARCR) was calculated as the quotient of mean arterial pressure and GCVF. All patients performed a supine bicycle exercise test (ET1) until angina occurred. After recovery, they underwent a cold pressor test (CPT) and then performed a second exercise test (ET2) while cold stimulation was continued. During ET1, ARCR decreased (from 1.53 +/- 0.43 to 1.04 +/- 0.35 mmHg ml-1 min-1, P less than 0.001) as a result of the metabolic vasodilation, while it rose, although non significantly, during CPT despite the increase in double product (P less than 0.001), reflecting the augmented myocardial oxygen consumption. However, such abnormal response to CPT did not persist during ET2, because ARCR decreased to a value non significantly different from that achieved at peak ET1. In five patients, who showed a reduced exercise tolerance during ET2, ARCR dropped by 22% during ET2 compared with 34% decrease during ET1. However, such a difference was unlikely to account for the reduction in exercise tolerance, because the double product at peak ET2 was never lower than the corresponding value at peak ET1. Our data show that the inappropriate vasoconstriction induced by CPT in an abnormally perfused myocardial region does not persist during exercise, when metabolic vasodilation occurs.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed2001

Progression from hypertrophic to dilated cardiomyopathy in mice that express a mutant myosin transgene.

A mouse model of hypertrophic cardiomyopathy (HCM) was created by expression of a cardiac alpha-myosin transgene including the R(403)Q mutation and a deletion of a segment of the actin-binding domain. HCM mice show early histopathology and hypertrophy, with progressive hypertrophy in females and ventricular dilation in older males. To test the hypothesis that dilated cardiomyopathy (DCM) is part of the pathological spectrum of HCM, we studied chamber morphology, exercise tolerance, hemodynamics, isolated heart function, adrenergic sensitivity, and embryonic gene expression in 8- to 11-mo-old male transgenic animals. Significantly impaired exercise tolerance and both systolic and diastolic dysfunction were seen in vivo. Contraction and relaxation parameters of isolated hearts were also decreased, and lusitropic responsiveness to the beta-adrenergic agonist isoproterenol was modestly reduced. Myocardial levels of the G protein-coupled beta-adrenergic receptor kinase 1 (beta-ARK1) were increased by more than twofold over controls, and total beta-ARK1 activity was also significantly elevated. Induction of fetal gene expression was also observed in transgenic hearts. We conclude that transgenic male animals have undergone cardiac decompensation resulting in a DCM phenotype. This supports the idea that HCM and DCM may be part of a pathological continuum rather than independent diseases.

Adrenergic beta-Agonists↗

PubMed1989

Comparison of the effects of captopril and enoximone in patients with severe heart failure: a placebo controlled double-blind study.

The effects of enoximone, a new cyclic adenosine monophosphate phosphodiesterase inhibitor, were compared with those of captopril in a double-blind study in a group of 10 patients with severe heart failure. Four weeks treatment with enoximone improved symptom-limited exercise tolerance from a mean value of 11.33 to 13.36 minutes (P less than 0.05) and 4 weeks of captopril treatment from 11.01 to 13.92 minutes (P less than 0.05). Four of the patients had a greater exercise tolerance taking enoximone, the remaining 6 while taking captopril. Both drugs reduced perceived exertion during submaximal exercise. Minute ventilation measured at rest and during submaximal exercise was also reduced by both drugs. Resting and post exercise calf blood flow was increased to a similar extent with captopril (P less than 0.03) and enoximone (P less than 0.005). There was no difference in calf blood flow and calf vascular resistance between the drugs suggesting that the peripheral haemodynamic effects of enoximone are due to peripheral vasodilatation. Enoximone is a useful drug for the treatment of patients with severe heart failure.

Adult↗

PubMed1993

Treatment of hypertension with felodipine in patients with concomitant diseases.

Coexisting medical conditions often complicate the selection of antihypertensive drugs. Felodipine, a new vascular-selective calcium antagonist with demonstrated antihypertensive efficacy, has not been found to alter lipid profiles in hypertensive patients. Studies in additional patient populations have yielded insights into the effects of the drug on other diseases that may coexist with hypertension. In individuals with stable angina pectoris or congestive heart failure, acute administration of felodipine reduces systemic vascular resistance and increases cardiac output and total coronary blood flow; myocardial contractility is not depressed at doses that produce a clinically significant reduction in vascular resistance. In patients with coronary stenoses, the drug increases vessel diameter in the vicinity of obstructive lesions. Single-dose and long-term studies in patients with exertional angina have found that felodipine reduces anginal frequency and improves exercise tolerance. In patients with congestive heart failure, chronic dosing with felodipine produces a persistent reduction in vascular resistance and an increase in cardiac output, both at rest and during exercise. Symptomatic improvement and increased exercise tolerance have been noted in some studies. In patients with Raynaud's phenomenon, felodipine has been associated with a dose-dependent improvement in symptomatology. Among individuals with exercise-induced bronchospasm, the drug has no effect on resting bronchial tone and may exert some positive effects during exercise. In hypertensive patients with Type II diabetes, felodipine has not been found to raise glucose levels significantly. The data obtained thus far suggest that felodipine is safe for use in hypertensive patients with a variety of concomitant diseases.

Disease↗

PubMed1982

Normal exercise capacity in patients with severe left ventricular dysfunction: compensatory mechanisms.

About one-third of patients who have severe left ventricular dysfunction can achieve normal levels of exercise. To elucidate the mechanisms that permit this to occur, we studied six patients with severe left ventricular dysfunction (average left ventricular ejection fraction 17 +/- 2.5% [mean +/- SEM]) who achieved nearly normal levels of exercise tolerance (greater than 11 minutes of treadmill exercise, Sheffield protocol). All patients had normal pulmonary function at rest and during exercise. Hemodynamics were measured at rest and during supine and upright exercise. The major mechanisms of the preserved exercise capacity in these patients were chronotropic competence, ability to tolerate elevated wedge pressures (33 +/- 3 mm Hg) without dyspnea, ventricular dilation, and increased levels of plasma norepinephrine at rest and during exercise. Also, whereas peripheral vascular resistance was unchanged during supine exercise, it decreased by 50% during similar levels of upright exercise. As a consequence, increases in cardiac output from rest to exercise were greater during upright than supine exercise (100% vs 50%, respectively) (p less than 0.05), and pulmonary wedge pressures were lower during upright than supine exercise (21 +/- 5 mm Hg vs 33 +/- 3 mm Hg). Thus, multiple mechanisms permit some patients with severe left ventricular dysfunction to achieve normal levels of exercise. These studies emphasize that left ventricular function must be assessed by direct means rather than inferring function of the left ventricle from the results of an exercise tolerance test.

Aged↗

PubMedDate not supplied

[Diagnosis of coronary artery restenosis after radiologic endovascular dilatation].

Altogether 40 patients with stable angina of effort were investigated in a long-term period after roentgenovascular dilatation of one or two coronary arteries. Control coronarography was performed in 22 patients with lowered exercise tolerance. A reliable feature in the development of hemodynamically significant restenosis and/or "new" coronary stenosis in 11 patients was a combination of average and low exercise tolerance with its negative dynamics. For patients with I functional class, a sign of restenosis and/or "new" stenosis was the appearance of the ischemic shift of the CT-segment on ECG during bicycle testing. An efficient selection of patients resulted in increased sensitivity and specificity of noninvasive tests.

Adult↗

PubMed1991

[Long-acting nitrate-induced changes in microcirculation and tissue oxygen balance in patients with coronary heart disease].

A total of 56 patients with Functional Class II angina pectoris and 25 healthy subjects were examined. Long-acting nitrates were ascertained to result in profound venular dilatation, slight arteriolar dilatation, moderately decreased erythrocyte aggregation and improvement of tissue oxygen supply. The most marked increase in exercise tolerance and reduction in the frequency of anginal attacks were noted in patients with normal and narrowed venules. There were no significant changes in microcirculation and exercise tolerance in patients with baseline dilated venules. It is concluded that the microvasculature may be one of the criteria for applying long-acting nitrates in patients with coronary heart disease on an individual basis.

Adult↗

PubMed2006

Effect of low altitude at the Dead Sea on exercise capacity and cardiopulmonary response to exercise in cystic fibrosis patients with moderate to severe lung disease.

Oxygen supplementation may improve exercise tolerance and the physiological response to exercise in cystic fibrosis (CF) patients. Elevated barometric pressure at low altitude is a simple means of increasing the quantity of inspired oxygen. Our objectives were to examine the effect of natural oxygen enrichment (at the Dead Sea, 396 m below sea level) on exercise capacity, and the physiological responses to maximal and submaximal exercise in CF patients. Patients were tested twice: at sea level (barometric pressure, 754 +/- 6 mmHg, mean +/- SD), and at the Dead Sea (barometric pressure, 791 +/- 3 mmHg), in a randomized crossover design. We studied 14 CF patients (6 females, 8 males), aged 15-45 years, with moderate to severe lung disease (mean forced expired volume in 1 sec = 50.0 +/- 11.2% predicted). Tests at each site included resting spirometry, anthropometry, a graded submaximal exercise test, a maximal exercise test on a treadmill, and a 6-min walk test. Tests were performed in identical order at both sites. Tests at the Dead Sea were performed 72 hr after arrival. No differences between sites were observed in lung function at rest. Peak oxygen consumption was significantly improved at the Dead Sea compared with sea level (1.68 +/- 0.73 vs. 1.57 +/- 0.74 l/min, respectively, P = 0.05), along with an improvement in the ventilatory equivalent for oxygen (41.2 +/- 6.3 vs. 46.1 +/- 7.1, respectively, P < 0.05). During submaximal exercise, blood oxygen saturation improved at the Dead Sea compared with sea level at all exercise intensities (P < 0.05). In conclusion, these results suggest that even a brief stay at the Dead Sea area may have physiological benefits for CF patients with moderate to severe lung disease.

Adolescent↗

PubMed2006

Evaluation of a specific activity questionnaire to predict mortality in men referred for exercise testing.

BACKGROUND: A self-administered symptom questionnaire developed at our institution (Veterans Specific Activity Questionnaire [VSAQ]) is routinely used to estimate a patient's exercise capacity to individualize the exercise test in accordance with current guidelines. This study was performed to evaluate the association of the VSAQ with all-cause mortality. METHODS: The VSAQ was administered to 1185 consecutive male patients (mean age 58 +/- 12 years) referred for exercise testing for clinical reasons. The VSAQ is designed to determine which specific daily activities are associated with cardiovascular symptoms (fatigue, chest pain, or shortness of breath) to provide an estimate of exercise tolerance (in metabolic equivalents [METs]) before exercise testing. Patients were classified into 1 of 3 groups according to VSAQ score: <5 METs, 5 to 8 METs, and >8 METs. The association between exercise capacity estimated by the VSAQ, other clinical and exercise test variables, and all-cause mortality was assessed by Cox proportional hazards. The mean follow-up period was 4.5 +/- 2.9 years. RESULTS: There were a total of 132 deaths during the follow-up period, resulting in an average annual mortality of 2.7%. In a multivariate analysis including clinical risk factors and exercise test variables, age-adjusted predictors of mortality, in rank order, were the VSAQ score in METs, history of chronic heart failure, history of smoking, and diabetes (for VSAQ: hazard ratio [HR] 0.90, 95% CI 0.83-0.98; for chronic heart failure: HR 2.67; 95% CI 1.51-4.72; for smoking: HR 1.74, 95% CI 1.18-2.57; and for diabetes: HR 1.84, 95% CI 1.15-2.95). Expressed in tertiles, age-adjusted relative risks for the VSAQ were 1.0, 0.54, and 0.22 (P for trend <.001). Each 1-MET increase in the VSAQ conferred a 10% survival benefit. CONCLUSIONS: A simple self-administered symptom questionnaire strongly and independently predicted all-cause mortality. The VSAQ is a useful adjunct to clinical and exercise test data for stratifying risk in patients undergoing exercise testing for clinical reasons.

Aged↗

PubMed1986

Antianginal effects of clonidine.

The effects of clonidine, a central alpha-adrenoceptor agonist, were studied in 12 patients with chronic stable effort angina pectoris in an 18-week randomized, double-blind, two-period (6 weeks each) crossover study with a 3-week inter-period washout phase. Clonidine (200 micrograms as a single dose) produced a decrease in rate-pressure product at rest and during exercise and an increase in exercise tolerance, at 1 and 2 h after administration. Chronic administration of clonidine produced a decrease in rate-pressure product at rest and during exercise and an increase in exercise tolerance after 3 weeks (200 micrograms twice a day) and 6 weeks (400 micrograms twice a day) of treatment.

Angina Pectoris↗

PubMed2005

Cardiovascular adaptations to exercise training after uncomplicated acute myocardial infarction.

OBJECTIVE: This study examined the cardiovascular adaptations of an exercise training program and evaluated the role of peripheral vasodilator capacity in contributing to these adaptations after myocardial infarction. DESIGN: A total of 44 consecutive patients with uncomplicated myocardial infarction underwent 3 wks of exercise training. Controls (n = 12) with comparable myocardial infarction were selected from our database and were restricted to a program with minimal activity. All patients performed cardiopulmonary exercise testing with hemodynamic measurements. Forearm and calf reactive hyperemic flow were measured by venous occlusive plethysmography as indices of peripheral vasodilator capacity. RESULTS: Despite no change in arteriovenous oxygen difference at peak exercise after training, training resulted in significant increases in oxygen consumption, cardiac output, and stroke volume and a significant decrease in systemic vascular resistance at peak exercise (overall, P < 0.05). Calf reactive hyperemic flow increased significantly after training (P < 0.001), but forearm reactive hyperemic flow did not. Furthermore, increase in calf reactive hyperemic flow after training had a positive correlation with increases in peak cardiac output, stroke volume, and oxygen consumption after training and an inverse correlation with peak systemic vascular resistance. CONCLUSIONS: Exercise training improved exercise tolerance by improving hemodynamic responses to exercise after myocardial infarction. This improved exercise performance was linked to a training-induced increase in calf vasodilator capacity.

Adaptation, Physiological↗