788-3 Effect of Body Composition on Exercise Performance in Patients with Heart Failure

Changes in fat and skeletal muscle Volume may contribute to the exercise intolerance reported by patients with heart failure. To test this hypothesis, we measured hemodynamic and ventilatory responses to exercise in 65 patients with chronic heart failure. Body composition was determined by dual-energy x-ray absorptiometry. Peak exercise VO2 averaged 13.2±2.9ml/min/kg, peak exercise cardiac index 4.5±1.1 L/min/m2, lean body weight 55±12kg, lean leg weight 17.2±3.8kg and total fat 27±11kg. Thirty-eight (58%) of the patients were obese, as defined by a percentage fat >30%. Twenty-four patients (37%) exhibited lean body wt/height <300gm/cm, consistent with muscle atrophy. Peak exercise VO2 correlated closely with total leg muscle:There was no relationship between VO2/gm leg muscle and the lean body wt/height index, suggesting that muscle atrophy does not affect muscle performance/unit of muscle. VO2/kg muscle was higher in obese vs non-obese patients (72+14 vs 59+13 mllmin/kg (p<0.01) whereas peak VO2/kg body weight was similar (13.0+3.3 vs 13.2+2.6 mllmin/kg). since body weight inCludes fat. These findings suggest that skeletal muscle volume influences exercise capacity in patients with heart failure. Exercise capacity in obese patients is underestimated by normalizing for body weight

Dissociation between peak exercise oxygen consumption and hemodynamic dysfunction in potential heart transplant candidates

AbstractObjectives. The purpose of this study was to determine how often peak exercise oxygen consumption (Vo2) misclassifies the severity of cardiac dysfunction in potential heart transplant candidates.Background. Cardiopulmonary exercise testing is being used to help select heart transplant candidates on the basis of the assumption that a low peak exercise Vo2indicates severe hemodynamic dysfunction and a poor prognosis. However, noncardiac factors, such as muscle deconditioning, can also influence exercise capacity. Therefore, peak exercise Vo2may overestimate the severity of cardiac dysfunction in some patients.Methods. Hemodynamic and respiratory responses to maximal treadmill exercise were measured in 64 sequential patientsundergoing evaluation for heart transplantation, all of whom had an ejection fraction <35% and reduced peak exercise Vo2levels (mean [±SD] 13.3 ± 2.7 ml/min per kg).Results. Twenty-eight (44%) of 64 patients exhibited a reduced cardiac output response to exercise and pulmonary wedge pressure >20 mm Hg at peak exercise, consistent with severe hemodynamic dysfunction. Twenty-three patients (36%) exhibited a normal cardiac output response to exercise but a wedge pressure >20 mm Hg at peak exercise, suggesting moderate hemodynamic dysfunction. Thirteen patients (20%) exhibited a normal cardiac output and wedge pressure <20 mm Hg at peak exercise, suggesting mild hemodynamic dysfunction. Despite these markedly different hemodynamic responses, all three groups exhibited similar peak exercise Vo2levels (mild dysfunction 14.2 ± 3.5 ml/min per kg, moderate dysfunction 13.9 ± 2.7 ml/min per kg, severe dysfunction 12.4 ± 2.1 ml/min per kg). A peak exercise Vo2level <14 ml/min per kg, considered to reflect severe hemodynamic dysfunction, was observed in 18 of the patients with a normal cardiac output response to exercise, whereas 7 patients with severe hemodynamic dysfunction had a peak Vo2level >14 ml/min per kg.Conclusions. More than 50% of potential heart transplant candidates with a reduced peak exercise Vo2level exhibit only mild or moderate hemodynamic dysfunction during exercise. Hemodynamic responses to exercise should be directly measured in potential transplant candidates to confirm severe circulatory dysfunction

Skeletal muscle mass and exercise performance in stable ambulatory patients with heart failure

Lang, Chim C., Don B. Chomsky, Glenn Rayos, T. K. Yeoh, and John R. Wilson. Skeletal muscle mass and exercise performance in stable ambulatory patients with heart failure. J. Appl. Physiol. 82(1): 257–261, 1997.—The purpose of this study was to determine whether skeletal muscle atrophy limits the maximal exercise capacity of stable ambulatory patients with heart failure. Body composition and maximal exercise capacity were measured in 100 stable ambulatory patients with heart failure. Body composition was assessed by using dual-energy X-ray absorption. Peak exercise oxygen consumption (V˙o 2 peak) and the anaerobic threshold were measured by using a Naughton treadmill protocol and a Medical Graphics CardioO2 System.V˙o 2 peak averaged 13.4 ± 3.3 ml ⋅ min−1 ⋅ kg−1or 43 ± 12% of normal. Lean body mass averaged 52.9 ± 10.5 kg and leg lean mass 16.5 ± 3.6 kg. Leg lean mass correlated linearly with V˙o 2 peak( r= 0.68, P &lt; 0.01), suggesting that exercise performance is influenced by skeletal muscle mass. However, lean body mass was comparable to levels noted in 1,584 normal control subjects, suggesting no decrease in muscle mass. Leg muscle mass was comparable to levels noted in 34 normal control subjects, further supporting this conclusion. These findings suggest that exercise intolerance in stable ambulatory patients with heart failure is not due to skeletal muscle atrophy. </jats:p

Normalization of acquired QT prolongation in humans by intravenous potassium

Background QT interval prolongation and dispersion have been implicated in serious arrhythmias in congestive heart failure (CHF) and the congenital and drug-induced long-QT syndromes (LQTS). In a subset of the congenital LQTS, infusion of potassium can correct QT abnormalities, consistent with in vitro increases in outward currents such as I Kr or I K1 when extracellular potassium concentration ([K + ] o ) is increased. Furthermore, increasing [K + ] o decreases the potency of I Kr -blocking drugs in vitro. The purpose of this study was to test the hypothesis that increasing [K + ] o corrects QT abnormalities in CHF and in subjects treated with quinidine. Methods and Results KCl (maximum, 40 mEq) was infused into (1) 12 healthy subjects treated with quinidine sulfate (5 doses of 300 mg/5 h) or placebo and (2) 8 CHF patients and age-matched normal control subjects. Mean [K + ] increased from 4 to 4.2 mEq/L to 4.7 to 5.2 mEq/L. Potassium infusion significantly reversed QTU c prolongation, especially in the precordial leads (quinidine, 590±79 to 479±35 [±SD] ms 1/2 , P &lt;.001; CHF, 521±110 to 431±47 ms 1/2 , P &lt;.05). There was no effect in either control group. Similarly, potassium decreased QTU c dispersion (quinidine, 210±62 to 130±75 ms 1/2 , P &lt;.01; CHF, 132±68 to 84±35 ms 1/2 , P =.07) and was without effect in the control subjects. QT morphological abnormalities, including U waves and bifid T waves, were reversed by potassium. Conclusions Potentially arrhythmogenic QT abnormalities during quinidine treatment and in CHF can be nearly normalized by modest elevation of serum potassium. </jats:p

Health-status outcomes with invasive or conservative care in coronary disease

BACKGROUND In the ISCHEMIA trial, an invasive strategy with angiographic assessment and revascularization did not reduce clinical events among patients with stable ischemic heart disease and moderate or severe ischemia. A secondary objective of the trial was to assess angina-related health status among these patients. METHODS We assessed angina-related symptoms, function, and quality of life with the Seattle Angina Questionnaire (SAQ) at randomization, at months 1.5, 3, and 6, and every 6 months thereafter in participants who had been randomly assigned to an invasive treatment strategy (2295 participants) or a conservative strategy (2322). Mixed-effects cumulative probability models within a Bayesian framework were used to estimate differences between the treatment groups. The primary outcome of this health-status analysis was the SAQ summary score (scores range from 0 to 100, with higher scores indicating better health status). All analyses were performed in the overall population and according to baseline angina frequency. RESULTS At baseline, 35% of patients reported having no angina in the previous month. SAQ summary scores increased in both treatment groups, with increases at 3, 12, and 36 months that were 4.1 points (95% credible interval, 3.2 to 5.0), 4.2 points (95% credible interval, 3.3 to 5.1), and 2.9 points (95% credible interval, 2.2 to 3.7) higher with the invasive strategy than with the conservative strategy. Differences were larger among participants who had more frequent angina at baseline (8.5 vs. 0.1 points at 3 months and 5.3 vs. 1.2 points at 36 months among participants with daily or weekly angina as compared with no angina). CONCLUSIONS In the overall trial population with moderate or severe ischemia, which included 35% of participants without angina at baseline, patients randomly assigned to the invasive strategy had greater improvement in angina-related health status than those assigned to the conservative strategy. The modest mean differences favoring the invasive strategy in the overall group reflected minimal differences among asymptomatic patients and larger differences among patients who had had angina at baseline

Initial invasive or conservative strategy for stable coronary disease

BACKGROUND Among patients with stable coronary disease and moderate or severe ischemia, whether clinical outcomes are better in those who receive an invasive intervention plus medical therapy than in those who receive medical therapy alone is uncertain. METHODS We randomly assigned 5179 patients with moderate or severe ischemia to an initial invasive strategy (angiography and revascularization when feasible) and medical therapy or to an initial conservative strategy of medical therapy alone and angiography if medical therapy failed. The primary outcome was a composite of death from cardiovascular causes, myocardial infarction, or hospitalization for unstable angina, heart failure, or resuscitated cardiac arrest. A key secondary outcome was death from cardiovascular causes or myocardial infarction. RESULTS Over a median of 3.2 years, 318 primary outcome events occurred in the invasive-strategy group and 352 occurred in the conservative-strategy group. At 6 months, the cumulative event rate was 5.3% in the invasive-strategy group and 3.4% in the conservative-strategy group (difference, 1.9 percentage points; 95% confidence interval [CI], 0.8 to 3.0); at 5 years, the cumulative event rate was 16.4% and 18.2%, respectively (difference, 121.8 percentage points; 95% CI, 124.7 to 1.0). Results were similar with respect to the key secondary outcome. The incidence of the primary outcome was sensitive to the definition of myocardial infarction; a secondary analysis yielded more procedural myocardial infarctions of uncertain clinical importance. There were 145 deaths in the invasive-strategy group and 144 deaths in the conservative-strategy group (hazard ratio, 1.05; 95% CI, 0.83 to 1.32). CONCLUSIONS Among patients with stable coronary disease and moderate or severe ischemia, we did not find evidence that an initial invasive strategy, as compared with an initial conservative strategy, reduced the risk of ischemic cardiovascular events or death from any cause over a median of 3.2 years. The trial findings were sensitive to the definition of myocardial infarction that was used