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PubMedDate not supplied

Effect of oral H2-receptor antagonists on left ventricular systolic function and exercise capacity in patients with chronic stable heart failure.

STUDY OBJECTIVE: To evaluate the effect of cimetidine, famotidine, ranitidine, and placebo on left ventricular systolic function, aerobic metabolic performance, and exercise capacity in patients with chronic, stable heart failure. DESIGN: Double-blind, randomized, placebo-controlled, four-way crossover study. SETTING: Outpatient, university-affiliated cardiology clinic. PATIENTS: Twelve men with stable New York Heart Association class II or III heart failure secondary to ischemic heart disease or hypertension. INTERVENTIONS: Patients received in random sequence cimetidine 400 mg twice/day, famotidine 40 mg/day, ranitidine 150 mg twice/day, and placebo. Each treatment was administered for 7 days, and the periods were separated by a 1-week washout. MEASUREMENTS AND MAIN RESULTS: Before and after each treatment, patients underwent a bicycle stress echocardiogram with aerobic metabolic assessment. Left ventricular function was evaluated by calculating ejection phase indexes from Doppler echocardiographic measurements. All 12 patients successfully completed the study. No patient reported any adverse effect attributed to study drugs. None of the treatments was associated with significant changes in any measure of left ventricular systolic function, aerobic metabolic performance, or exercise capacity, nor were placebo-subtracted differences for the agents significantly different for any of the three measures. CONCLUSION: The three H2-receptor antagonists administered for 7 days at clinical dosages have no significant effect on left ventricular systolic function, aerobic metabolic performance, or exercise capacity in men with class II or III stable heart failure.

Administration, Oral↗

PubMed1992

Effects of impaired lung function and pulmonary regurgitation on maximal exercise capacity in patients with repaired tetralogy of Fallot.

Long-term haemodynamic results and exercise capacity were studied in 34 patients with tetralogy of Fallot (24 men and 10 women) repaired 10.0 +/- 4.9 (mean +/- SD) years previously and compared to 34 healthy matched controls. All subjects were studied by resting spirometry, echocardiography and a symptom limited treadmill exercise test (modified Bruce protocol). The maximal oxygen consumption was 38.2 +/- 8.0 ml.kg-1.min-1 in patients and 48.1 +/- 8.1 ml.kg-1.min-1 in the control group (P < 0.001). Reduced maximal oxygen consumption was found in patients with low vital capacity (VC) and pulmonary regurgitation (PR). The ventilatory anaerobic threshold (VAT) was 23.8 +/- 0.6 ml.kg-1.min-1 and 29.9 +/- 0.6 ml.kg-1.min-1 in patients and controls, respectively (P < 0.001). VC was 3.4 +/- 1.21 in patients and 4.0 +/- 1.31 in controls (P < 0.02). In the patients, maximal ventilation was reduced and at submaximal exercise, the breathing frequency increased. Heart rates during exercise were similar in patients and controls. Tricuspid regurgitation (TR) was detected in 20 patients (58.8%); however, the exercise capacity was not reduced. Thus, impaired exercise capacity in tetralogy of Fallot is partly due to reduced resting lung function, pulmonary regurgitation and low ventilatory anaerobic threshold.

Adolescent↗

PubMed2000

Role of the etiology of cardiomyopathies on exercise capacity and oxygen consumption in patients with severe congestive heart failure.

Peak oxygen consumption is of great importance for the decision of heart transplantation in congestive heart failure. Moreover, the level of exercise capacity seems to depend on the etiology of congestive heart failure. This study compared 14 heart failure patients with idiopathic dilated cardiomyopathy (group 1) to 14 heart failure patients with cardiomyopathy due to ischemic heart disease (group 2), matched for sex (13 male, one female in each group), age +/-10 years, left ventricular ejection fraction +/-5% and pulmonary artery mean pressure +/-5 mm Hg, to assess exercise capacity and oxygen consumption independently of the age, sex and the level of left ventricular dysfunction. Right ventricular function was also assessed. No difference existed in terms of right ventricular parameters. Maximal exercise parameters were significantly higher in group 1 than in group 2. Peak oxygen consumption was statistically higher in group 1 than in group 2. In the whole population, a significant correlation was found between peak oxygen consumption and right ventricular ejection fraction (r=0. 44, P<0.02) but not between peak oxygen consumption and left ventricular ejection fraction. For similar levels of left ventricular dysfunction, exercise capacity and oxygen consumption appear to be better in idiopathic dilated cardiomyopathy than in ischemic cardiomyopathy, thereby suggesting that functional tolerance of left ventricular dysfunction might depend on the etiology of severe congestive heart failure.

Cardiomyopathies↗

PubMed1996

Serial assessment of cardiopulmonary exercise capacity after cardiomyoplasty for either ischemic or idiopathic dilated cardiomyopathy.

Cardiomyoplasty is a surgical procedure aimed at assisting the left ventricle during ejection. We describe the long-term effects of cardiomyoplasty on peak exercise capacity, with serial assessments for up to 3 years after operation. Sixteen patients (12 in New York Heart Association class III and 4 in class IV) were enrolled. The mean left ventricular ejection fraction was 18 +/- 8%. Bicycle exercise tests with respiratory gas analysis were performed preoperatively and 6, 12, 18, 24, and 36 months after operation. Mean follow-up was 12 +/- 5 months (range 6 to 24). At 6 months, peak oxygen consumption and the ventilatory threshold were unchanged (from 17.8 +/- 5.8 to 15.8 +/- 5.3 ml/min/kg, and from 12.1 +/- 2.7 to 11.4 +/- 3.4 ml/min/kg, respectively). Ventilation at 50 W, viewed as an index of polypnea at submaximal exercise, was also unchanged. Serial assessment of exercise capacity thereafter showed no changes. However, ejection fraction tended to increase from 18 +/- 8% to 21 +/- 9% (p=0.08) and 14 patients reported an improvement in their functional status, resulting in a significant change in New York Heart Association functional class (3.3 +/- 0.5 to 2.2 +/- 0.4 at 6 months and 2.4 +/- 0.4 at the last visit, p <0.005) and improvement in quality-of-life scores. Thus, cardiomyoplasty does not appear to increase peak exercise capacity in the long term, despite an improvement in the left ventricular ejection fraction. Symptoms and quality of life, however, appear to improve. This may be related in part to an insufficient number of assisted systoles during exercise, persistent deconditioning, or changes in pulmonary mechanics.

Cardiomyopathy, Dilated↗

PubMed2002

Left atrial function: bridge to central and hormonal determinants of exercise capacity in patients with chronic heart failure.

UNLABELLED: The stroke volume response to exercise is a critical determinant in meeting peripheral metabolic demands in patients with chronic hear failure. The Left atrium, by its position, is important in coupling right and left ventricles, to left preload reserve and to modulate sympathetic activity. We performed this study to investigate the relationship between exercise capacity and diastolic and systolic left atrium function in patients with chronic heart failure. METHODS: We considered 128 consecutive patients with severe chronic heart failure (EF < 35%) due to ischemic or idiopathic dilated cardiomyopathy. Cardiac output, right atrial pressure, pulmonary artery pressures and mean pulmonary wedge pressure (A, X, V, Y wedge pressures) were determined during right cardiac catheterization. By Echocardiography evaluation, we measured atrial pressures and volume during early and late left atrial systolic filling and we calculated left atrial chamber stiffness by this equation P = A*eKV1. (P = left atrial pressure; A = elastic constant (mmHg*ml); e = the base of the natural logarithm; V1 = left atrial volume (ml); K = left atrial chamber stiffness constant (ml-1) = ln (V/X)/(maximal--minimal left atrial volumes)). All patients performed cardiopulmonary exercise test with modified Noughton protocol. Plasma norepinephrine and Atrial natriuretic factor levels were determined. RESULTS: Maximal and minimal left atrial volumes were inversely related to oxygen consumption (r = -.44, p < .001; r = -.61, p < .001). At rest, no differences were found in plasma norepinephrine concentrations (309 +/- 152 pg/ml vs 309 +/- 394 pg/ml; p = ns) and systemic vascular resistance (1706 +/- 435 vs 1771 +/- 524 dynes/cm sec-5; p = ns) in patients with large or normal left atrial volumes. During exercise the chronotropic response increased less in patients with large atrial volumes (56 +/- 13 vs 45 +/- 14; p = .001). The left atrial chamber stiffness constant was inversely related to peak oxygen consumption and exercise time. Patients with different chamber stiffness showed statistical difference in peak VO2 (16 +/- 4 vs 11 +/- 3 ml/kg/min; p = .0001). Left atrial ejection fraction was directly related to peak oxygen consumption (r = 0.55), but the most strongly correlation was with atrial filling fraction (r = .67). CONCLUSIONS: This study demonstrates a strong relationship between left atrial function and exercise capacity in patients with chronic heart failure.

Chronic Disease↗

PubMed1987

[Exercise capacity in ischemic heart disease evaluated by continuous wave Doppler echocardiography].

To evaluate exercise capacity in ischemic heart disease, we measured the peak aortic flow velocity by continuous wave Doppler (CWD) echo from the suprasternal notch at rest and during multiple load ergometer testing in the supine position. The study subjects consisted of 14 normal controls, 10 patients with effort angina and 21 patients with old myocardial infarction (OMI). In all the patients and in five normal subjects, thallium-201 emission CT (SPECT) was also performed immediately after exercise and four hours subsequently. Change in the peak aortic flow velocity during exercise was compared with the extent of perfusion defects and the presence or absence of redistribution images on SPECT. At rest, the peak aortic flow velocity was not different from that of the other three groups. During exercise, it increased progressively (crescendo type) as the exercise was increased in normal subjects. In patients with angina pectoris it increased at the initial stage of exercise, but was unchanged (crescendo-plateau type) or decreased (crescendo-decrescendo type) at the maximum exercise stage. Redistribution images on SPECT were seen in nine of 10 patients with angina pectoris. In patients with OMI, change in the peak aortic flow velocity was of the crescendo type in 14, crescendo-decrescendo in three and crescendo-plateau in one. In the remaining three it decreased from the beginning of exercise (decrescendo type). Redistribution images were seen in all patients with the crescendo-decrescendo, crescendo-plateau or decrescendo types. Furthermore, myocardial damage was much more extensive in the decrescendo type. We conclude that exercise continuous wave Doppler echocardiography is a useful means of evaluating exercise capacity in ischemic heart disease.

Adult↗

PubMed1988

The acute effect of an oral "inotropic" placebo on the exercise capacity of patients with chronic cardiac failure.

Uncontrolled studies have suggested that the newer oral phosphodiesterase inhibitors milrinone and enoximone acutely improve exercise performance in patients with severe chronic cardiac failure. To determine whether an oral placebo presented as an inotropic agent could acutely enhance exercise capacity, two separate groups of stable heart failure patients were studied by serial exercise testing and respiratory gas exchange analysis. Group 1 had nine patients studied four hours after a single oral dose of placebo, and group 2 had ten patients retested after one to two weeks of placebo therapy. No significant change was seen in the mean exercise time, mean peak oxygen consumption, and the mean oxygen consumption at anaerobic threshold after placebo administration in both group 1 and group 2 patients. Improvements in exercise time, peak oxygen consumption, and oxygen consumption at anaerobic threshold occurred in five patients in group 1 and seven patients in group 2. The improvements exceeded the baseline variability of 10 percent in three group 1 patients. Among group 2 patients, the increase in exercise time, peak oxygen consumption, and oxygen consumption at anaerobic threshold exceeded 10 percent in six, four, and four patients, respectively. Thus, stable chronic heart failure patients can achieve a true baseline exercise capacity. Small improvements in exercise performance seen acutely after oral inotropic drug therapy in individual heart failure patients must be interpreted with caution, as they may be due to a placebo effect.

Aged↗

PubMed1998

Exercise capacity in heart transplant recipients: relation to impaired endothelium-dependent vasodilation of the peripheral microcirculation.

OBJECTIVES: The aim of this study was to examine the responses to endothelium-dependent and -independent vasodilators on the peripheral microcirculation in heart transplant recipients in relation to exercise capacity compared with that in healthy controls. BACKGROUND: Impaired endothelium-dependent vasodilation of the microcirculation may play an important role in the limitation of exercise capacity after heart transplantation. METHODS: Microvascular perfusion responses to four graded levels of iontophoretically applied 1% acetylcholine (endothelium-dependent vasodilator) and 1% sodium nitroprusside (SNP) (endothelium-independent) in the forearm skin of 42 transplant recipients and 16 age-matched controls were determined by laser Doppler perfusion measurements. Maximal exercise capacity was assessed by peak oxygen uptake (peak VO2) during progressive, symptom-limited, upright bicycle exercise. RESULTS: With similar baseline perfusion levels in transplant recipients and controls (4.2 +/- 0.4 vs 4.6 +/- 0.6 arbitrary units [AU]), the increases in perfusion to acetylcholine, but not to SNP, were significantly attenuated in the transplant recipients: 7.0 +/- 1.0 vs 11.0 +/- 2.0, 12.7 +/- 1.5 vs 21.0 +/- 2.8, 21.0 +/- 1.9 vs 32.7 +/- 2.4, and 28.0 +/- 1.6 vs 39.2 +/- 2.4 AU, respectively (all p < 0.01). Peak VO2 was significantly lower in the transplant recipients (22.4 +/- 1.0 vs 38.0 +/- 2.9 ml/kg/min; p < 0.01). Furthermore, acetylcholine responses of the transplant recipients correlated closely to their peak VO2, irrespective of level of application (r = 0.63; p < 0.001, all four acetylcholine responses taken together), whereas no such correlation was found for SNP responses. In the control group, no relation was observed in acetylcholine/SNP responses to peak VO2. CONCLUSIONS: Exercise limitation in transplant recipients appears strongly associated with attenuated endothelium-dependent vasodilation of the peripheral microcirculation.

Acetylcholine↗

PubMed1989

Effects of DBcAMP on exercise capacity in patients with and without chronic heart failure.

The acute effects of vasodilation on exercise capacity in cardiac patients with (group 1) and without (group 2) congestive heart failure were studied using dibutyryl cyclic AMP (DBcAMP). Exercise was performed on an upright bicycle ergometer using a graded protocol. DBcAMP increased cardiac output and decreased pulmonary capillary wedge pressure and systemic vascular resistance both at rest and during maximal exercise in these two groups. However, before and after DBcAMP neither exercise duration (371 +/- 52 seconds vs. 388 +/- 44, NS, in group 1, 645 +/- 148 vs. 635 +/- 143 seconds, NS, in group 2, respectively) nor maximal oxygen consumption (12.8 +/- 2.3 ml/kg/min vs. 13.1 +/- 1.6, NS, in group 1, 20.3 +/- 1.4 vs. 20.1 +/- 1.5, NS, in group 2, respectively) was improved. In both groups the arteriovenous oxygen differences were lower at rest and during exercise performed while on DBcAMP than in the control state. In group 2 patients excess vasoconstriction mediated by abnormally increased neurohormonal activities or edema were absent. Failure of the vasodilator to increase exercise capacity is probably due to nonspecific vasodilation and maldistribution of increased cardiac output, and not to tight vasoconstriction or narrowed arteriolar lumen.

Adolescent↗

PubMed1998

Oral branched-chain amino acids do not improve exercise capacity in McArdle disease.

To determine whether oral branched-chain amino acids (BCAAs) improve exercise capacity, six fasting patients with McArdle's disease were given a solution of BCAA (77 mg/kg) or a control noncaloric beverage 30 minutes before exercise. The BCAA meal tripled plasma BCAA levels, increased BCAA catabolism as indicated by greater exercise increases in plasma glutamine and alanine, but lowered mean peak free fatty acid levels and reduced exercise capacity in five of six patients. Lower work capacity may be attributed to a net reduction in muscle fuel availability after BCAA administration.

Administration, Oral↗

PubMed2005

Supported and unsupported arm exercise capacity following lung volume reduction surgery: a pilot study.

STUDY OBJECTIVES: Lung volume reduction surgery (LVRS) has been shown to improve lung function, leg exercise capacity and quality of life in subjects with severe COPD. This is the first study to examine the effect of LVRS on supported and unsupported arm exercise capacity. DESIGN: Eight subjects with COPD (% pred FEV1 +/- SD = 31.1 +/- 9.8%) completed testing. At baseline (T1), after eight weeks pulmonary rehabilitation (T2) and four months after LVRS (T3), each subject had tests of lung function, and performed three symptom-limited exercise tests to peak work capacity: supported arm exercise (SAE), unsupported arm exercise (UAE) and leg exercise (LE). MEASUREMENTS: The FEV1 (% pred) increased from 27.8 +/- 7.4 (mean +/- SD) at T2 to 36.3 +/- 7.1 at T3 (P < 0.05). Peak oxygen consumption (VO2) remained similar from T1 to T2 for SAE, UAE and LE (all P = 1.0) but increased from T2 to T3 (P < 0.05) (SAE: T2 = 0.59 +/- 0.2 L/min, T3 = 0.72 +/- 0.1 L/min; UAE: T2 = 0.45 +/- 0.1 L/min, T3 = 0.54 +/- 0.1 L/min; LE: T2 = 0.68 +/- 0.2 L/min, T3 = 0.81 +/- 0.2 L/min). The ratio of end-expiratory lung volume to total lung capacity was reduced at peak SAE and LE from T2 to T3 (P < 0.01) (SAE: T2 = 81 +/- 4.0%, T3 = 76 +/- 2.7%; LE: T2 = 81 +/- 5.1%, T3 = 75 +/- 3.6%). CONCLUSION: There was a significant increase in SAE and UAE capacity following LVRS. Dynamic hyperinflation was reduced during SAE following LVRS.

Aged↗

PubMed1998

Effects of spironolactone on exercise capacity and neurohormonal factors in patients with heart failure treated with loop diuretics and angiotensin-converting enzyme inhibitor.

1. Treatment with spironolactone is reported to be useful when combined with loop diuretics and an angiotensin-converting enzyme (ACE) inhibitor in severe congestive heart failure (CHF). However, the effects of the addition of spironolactone on exercise capacity and neurohormonal variables have not been demonstrated. This study determined the effects of additive spironolactone on exercise capacity and neurohormonal factors in patients with mild CHF. 2. Oxygen uptake (VO2), plasma norepinephrine (NE), renin activity (PRA), angiotensin II (AII), aldosterone (ALD), and atrial natriuretic peptide (ANP) were measured at rest and after peak exercise in nine patients with CHF (six idiopathic and three ischemic cardiomyopathy; New York Heart Association (NYHA) classes II and III) who were already taking furosemide (mean 29 +/- 5 mg/day) and enalapril (mean 4.7 +/- 0.8 mg/day). Studies were repeated after 16 weeks of treatment with additive single daily dose of 25 mg of spironolactone. In four of nine patients, the exercise test was repeated after a 4-weeks washout of spironolactone. 3. Treatment with spironolactone caused natriuresis, decreased cardiothoracic ratio in chest X-ray (before vs. after treatment: 53.7 +/- 1.2 vs. 50.7 +/- 1.4%, P < 0.01), and improved NYHA functional class. Peak VO2 (17.1 +/- 1.6 vs. 17.5 +/- 2.2 ml/min/kg, NS) and heart rate and blood pressure responses to exercise were not altered. Resting NE (215 +/- 41 vs. 492 +/- 85 pg/ml, P < 0.01) and resting PRA (8.2 +/- 2.3 vs. 16.2 +/- 4.1 ng/ml/hr, P < 0.01) as well as peak NE (1618 +/- 313 vs. 2712 +/- 374 pg/ml, P < 0.01) and peak PRA (12.8 +/- 3.2 vs. 28.1 +/- 11.8 ng/ml/hr, P = 0.17) were augmented after additive spironolactone. ALD and AII were insignificantly increased, and ANP was insignificantly decreased at peak exercise after spironolactone treatment. Spironolactone washout was associated with a trend of the neurohormones to return toward pretreatment values. 4. In conclusion, chronic additive treatment with spironolactone was associated with neurohormonal activation both at rest and during exercise without changing the exercise capacity of patients with mild CHF who were already on loop diuretics and ACE inhibitor therapy.

Adult↗

PubMed1998

Abnormal transoesophageal Doppler coronary flow reserve in patients with dilated cardiomyopathy: relationship to exercise capacity.

1. In patients with dilated cardiomyopathy, abnormal myocardial blood flow may contribute to poor myocardial function. 2. The aim of this study was to investigate the possible contribution of abnormal myocardial blood flow to the limitation of exercise capacity in patients with dilated cardiomyopathy. 3. Coronary flow reserve was assessed in 16 patients with dilated cardiomyopathy and 9 matched normal control individuals. All participants had angiographically normal coronary arteries. At rest and after dipyridamole infusion (0.56 mg/kg intravenously), peak systolic and diastolic coronary flow velocities were measured in the proximal left anterior descending coronary artery using transoesophageal pulsed Doppler echocardiography, guided by colour flow imaging. Coronary flow reserve was calculated as the ratio of hyperaemic to basal diastolic and systolic peak coronary flow reserve. 4. Baseline diastolic and systolic coronary flow velocities were significantly higher in patients (50 +/- 6 and 30 +/- 4 cm/s respectively) compared with control individuals (37 +/- 3 and 20 +/- 1 cm/s respectively) (mean +/- S.E.M.) (P < 0.05). Diastolic and systolic peak coronary flow reserve were significantly lower in patients (1.60 +/- 0.14 and 1.40 +/- 0.09 respectively) compared with control individuals (2.89 +/- 0.15 and 2.17 +/- 0.17 respectively) (P < 0.001). Although peak VO2 and exercise time were significantly lower in patients compared with control individuals, coronary flow reserve did not correlate to exercise capacity in patients with dilated cardiomyopathy. 5. These results confirm the abnormalities of coronary flow reserve previously observed in patients with dilated cardiomyopathy, but suggest that such abnormalities do not contribute to the limitation of exercise capacity in these patients.

Blood Flow Velocity↗

PubMed2003

Quality of life and exercise capacity in patients with prolonged PQ interval and dual chamber pacemakers: a randomized comparison of permanent ventricular stimulation vs intrinsic AV conduction.

AIMS: The aim of this study was to assess quality of life (QoL) and exercise capacity during permanent ventricular stimulation (PVS) compared with intrinsic atrioventricular conduction (IAVC) in patients with dual chamber pacemakers (PMs) and an intrinsic PQ interval >210 ms. Dual chamber PMs in patients with atrioventricular (AV) block are usually programmed to PVS in VDD or DDD mode, although IAVC is preserved, but prolonged. This results in PVS, although long periods of IAVC may occur. METHODS AND RESULTS: Fourteen consecutive patients (age 76 +/- 6 years; intermittent high degree AV block in six patients, binodal disease in eight patients) were enroled in a prospective, randomized, single blind, crossover study of IAVC vs PVC. To permit IAVC, programmed AV delays were prolonged. At the end of each phase, QoL scores were assessed using a questionnaire and echocardiography and cardiopulmonary stress tests were performed. During the study period with IAVC, 95 +/- 10% of the beats were conducted intrinsically. QoL scores (28.3 +/- 11 vs 29.3 +/- 13; P = 0.68), peak exercise capacity (5.4 +/- 2.4 vs 5.2 +/- 2.9 METs; P = 0.35) and peak oxygen uptake (19.8 +/- 4.5 vs 18.8 +/- 5.2 ml/kg/min; P = 0.16) were comparable during IAVC and PVS, respectively. Similar echocardiographic values were found for left ventricular (LV) ejection fraction (50 +/- 9% vs 51 +/- 10%; P = 0.67) and velocity time integral at the left ventricular outflow tract (24 +/- 5 vs 22 +/- 6 cm; P = 0.20), respectively. CONCLUSIONS: We conclude that in patients with dual chamber PMs and intermittent high degree AV block neither PVS nor IAVC is superior with respect to QoL or exercise capacity. Therefore, pulse generators may be programmed to IAVC to extend their longevity.

Aged↗

PubMed1997

Effects of cardiac rehabilitation and exercise programs on exercise capacity, coronary risk factors, behavior, and quality of life in patients with coronary artery disease.

Previous studies have indicated the benefits of cardiac rehabilitation programs after major coronary artery disease (CAD) events. We studied 591 consecutive patients from two academic institutions before and after completion of a cardiac rehabilitation and exercise training program to determine the effects of this therapy on exercise capacity, indices of obesity, plasma lipid values, behavioral characteristics, and quality of life parameters. After cardiac rehabilitation, statistically significant improvements occurred in exercise capacity (+33%), percent body fat (-6%), body mass index (-1%), HDL-C (+5%), triglycerides (-9%), LDL-C/HDL-C (-6%), anxiety score (-39%), depression score (-35%), somatization score (-37%), and in all parameters of quality of life studied (total +14%). These data further support the ability of cardiac rehabilitation and exercise training programs to improve exercise capacity, plasma lipid values, obesity indices, behavioral characteristics, and quality of life parameters in a large cohort of patients who have had major CAD events.

Aged↗

PubMed2001

Comorbidities and exercise capacity in older patients with intermittent claudication.

Patients with peripheral arterial disease (PAD) and intermittent claudication often have coronary artery disease (CAD) and other comorbid medical problems. There is a paucity of information on the impact of coexistent medical conditions on exercise capacity and functional status in patients with PAD. This study examined the impact of CAD, diabetes, cigarette smoking, prior peripheral surgical revascularization and other medical conditions on claudication pain times and peak oxygen capacity (VO2) during maximal effort treadmill testing in 119 male outpatient volunteers (ankle-brachial index (ABI) of 0.65 +/- 0.2, mean +/- SEM) with a history of Fontaine Stage II PAD. Smoking status was significantly related to ambulatory function. Current smokers had a lower peak VO2 expressed in l/min than either former or never smokers (ANCOVA adjusted for age, p = 0.003). However, after adjustment for body weight, there was only a trend for a difference in peak VO2 between current (13.2 +/- 0.5 ml/kg per min), former (14.2 +/- 0.4 ml/kg per min) and never (15.4 +/- 1.0 ml/kg per min) smokers (ANCOVA, p = 0.10). Current smokers had a shorter time to onset of claudication pain (p = 0.023) and shorter maximal claudication pain times (p = 0.029) than former or never smokers (p = 0.023). The ABI 1 min after cessation of exercise was also lower in smokers compared to former and never smokers (p = 0.018). There were no significant differences in functional performance measures or time to recovery from maximal claudication pain when patients were categorized on the presence or absence of CAD, diabetes, peripheral revascularization, arthritis, hypertension or dyslipidemia. Therefore, smoking adversely affected exercise capacity in these PAD patients, whereas the presence of CAD, diabetes and other medical problems had a relatively minor impact on exercise capacity. In conclusion, the relatively minor impact of comorbid medical conditions on walking ability in patients with PAD reflects the overwhelming limitation in ambulatory function due to the claudication pain.

Aged↗

PubMed1998

Skeletal muscle myosin heavy chains in heart failure: correlation between magnitude of the isozyme shift, exercise capacity, and gas exchange measurements.

BACKGROUND: Patients with congestive heart failure (CHF) have a reduced exercise capacity because of the early appearance of fatigue and dyspnea. Qualitative changes in the skeletal muscle composition and metabolism can be responsible for the origin of symptoms METHODS: We correlated the myosin heavy chain (MHC) composition of the gastrocnemius in 20 patients with different degrees of CHF to NYHA class, diuretic consumption, echocardiographic parameters, and expiratory gases measured during cardiopulmonary exercise testing. MHC composition was determined electrophoretically in skeletal muscle needle microbiopsies and the percent distribution was calculated by densitometry. Maximal cardiopulmonary exercise testing was performed on a treadmill with a modified Naughton protocol. A capnograph was used. RESULTS: There was no correlation between ejection fraction, left ventricular end systolic diameter, left ventricular end diastolic diameter, and MHC composition. We found a significant positive correlation between the percentage of MHC 1 (slow aerobic isoform) and NYHA class (r2 = 0.62, p < 0.0001), peak VO2 (r2 = 0.5, p < 0.0004), ventilatory threshold (VT) (r2 = 0.33, p = 0.008) and O2 pulse (peak VO2/HR) (r2 = 0.40, p = 0.003). There was a negative correlation between both MHC2a (fast oxidative) and MHC2b (fast glycolytic) with peak VO2 (r2 = 0.38, p = 0.004 and r2 = 0.37, p = 0.004, respectively), VT (r2 = 0.2, p = 0.046 and r2 = 0.34, p = 0.007, respectively), and O2 pulse (peak VO2/HR) (r2 = 0.39, p = 0.003 and r2 = 0.23, p = 0.03). NYHA class was also correlated positively with MHC2a and MHC2b (r2 = 0.46, p = 0.001 and r2 = 0.41, p < 0.006, respectively) and negatively with the same clinical and functional parameters. CONCLUSIONS: The correlation between the magnitude of the MHC shift from the slow aerobic to the fast glycolytic and fast oxidative with both functional and objective measurements of exercise capacity (peak VO2, VT, O2 pulse) seem to suggest that changes in skeletal muscle composition may play a determining role in exercise tolerance in patients with CHF.

Aged↗

PubMed1993

A non-invasive evaluation of flosequinan on haemodynamics and exercise capacity in chronic congestive heart failure.

The efficacy of flosequinan 100 mg once daily was evaluated in 15 patients with severe congestive heart failure (New York Heart Association [NYHA] class II-IV) who had not responded adequately to digoxin and diuretics. Efficacy assessments using non-invasive techniques included exercise capacity, haemodynamics and left ventricular function. Determinations were made after 3 and 21 days' treatment, and compared with baseline. Flosequinan significantly increased exercise capacity by 27% after 3 days (+79 seconds, p = 0.015) and by 43% after 21 days (+123 seconds, p = 0.0007) and was accompanied by an increase in heart rate (+7.2 beats/min, p = 0.03; +9.1 beats/min, p = 0.03, respectively). Cardiac index and cardiac output were also significantly increased but only after 21 days' treatment (+0.3 l/min/m2, +16% and +0.5 l/min, +14%, respectively; both p = 0.008). Flosequinan was well tolerated, with headache being the most frequently reported adverse event and only 1 patient being withdrawn. One patient died but this was not unexpected in a group of patients with severe heart failure. Using non-invasive techniques this study demonstrated that in patients with severe chronic congestive heart failure, flosequinan increased exercise capacity and cardiac output, the latter being achieved mainly by an increase in heart rate.

Aged↗