Relationship between exertional symptoms and functional capacity in patients with heart failure

AbstractOBJECTIVESThe present study was undertaken to investigate the relationship over time between exertional symptoms in heart failure and functional capacity.BACKGROUNDMost clinicians rely on exertional symptoms rather than on exercise testing to assess functional capacity in heart failure. However, it remains uncertain whether the subjective symptoms reported by patients provide a reliable index of functional capacity.METHODSFifty patients with heart failure underwent serial cardiopulmonary exercise testing and evaluation of exertional fatigue and dyspnea over a period of one to four years. Exercise testing was performed using the Naughton treadmill protocol and a MedGraphics metabolic cart. Fatigue and dyspnea were each scored from 0 to 3 (p = none, 1 = mild, 2 = moderate, 3 = severe). A composite symptom score was determined by adding together the fatigue and dyspnea scores.RESULTSPatients underwent a total of 185 tests at an average interval of 4.3 months (average tests/patient = 3.7). Composite symptom scores noted at the time of exercise testing correlated significantly with peak exercise minute oxygen consumption (VO2) (r = 0.47, p < 0.01). In addition, the change in symptoms scores and change in peak VO2noted between the baseline and final exercise test correlated significantly (r = 0.50, p < 0.01). However, patients reported few or no symptoms (symptom score ≤2) 45% of the time when peak VO2was <14 ml/min/kg, consistent with a severe functional disability, and 72% of the time when peak VO2was 14 to 18 ml/min/kg, consistent with moderate functional disability.CONCLUSIONSExertional symptoms reported by patients with heart failure generally correlate with maximal exercise capacity. However, exertional symptoms frequently underestimate the severity of functional disability. Cardiopulmonary exercise testing rather than symptoms should be used to assess functional capacity in heart failure

Selection of patients for heart transplantationin the current era of heart failure therapy

AbstractObjectivesWe sought to assess the relationship between survival, peak exercise oxygen consumption (Vo2), and heart failure survival score (HFSS) in the current era of heart failure (HF) therapy.BackgroundBased on predicted survival, HF patients with peak Vo2<14 ml/min/kg or medium- to high-risk HFSS are currently considered eligible for heart transplantation. However, these criteria were developed before the widespread use of beta-blockers, spironolactone, and defibrillators—interventions known to improve the survival of HF patients.MethodsPeak Vo2and HFSS were assessed in 320 patients followed from 1994 to 1997 (past era) and in 187 patients followed from 1999 to 2001 (current era). Outcomes were compared between these two groups of patients and those who underwent heart transplantation from 1993 to 2000.ResultsSurvival in the past era was 78% at one year and 67% at two years, as compared with 88% and 79%, respectively, in the current era (both p < 0.01). One-year event-free survival (without urgent transplantation or left ventricular assist device) was improved in the current era, regardless of initial peak Vo2: 64% vs. 48% for peak Vo2<10 ml/min/kg (p = 0.09), 81% vs. 70% for 10 to 14 ml/min/kg (p = 0.05), and 93% vs. 82% for >14 ml/min/kg (p = 0.04). Of the patients with peak Vo2of 10 to 14 ml/min/kg, 55% had low-risk HFSS and exhibited 88% one-year event-free survival. One-year survival after transplantation was 88%, which is similar to the 85% rate reported by the United Network for Organ Sharing for 1999 to 2000.ConclusionsSurvival for HF patients in the current era has improved significantly, necessitating re-evaluation of the listing criteria for heart transplantation

Prostaglandin production contributes to exercise-induced vasodilation in heart failure

Lang, Chim C., Don B. Chomsky, Javed Butler, Shiv Kapoor, and John R. Wilson. Prostaglandin production contributes to exercise-induced vasodilation in heart failure. J. Appl. Physiol. 83(6): 1933–1940, 1997.—Endothelial release of prostaglandins may contribute to exercise-induced skeletal muscle arteriolar vasodilation in patients with heart failure. To test this hypothesis, we examined the effect of indomethacin on leg circulation and metabolism in eight chronic heart failure patients, aged 55 ± 4 yr. Central hemodynamics and leg blood flow, determined by thermodilution, and leg metabolic parameters were measured during maximum treadmill exercise before and 2 h after oral administration of indomethacin (75 mg). Leg release of 6-ketoprostaglandin F1α was also measured. During control exercise, leg blood flow increased from 0.34 ± 0.03 to 1.99 ± 0.19 l/min ( P &lt; 0.001), leg O2 consumption from 13.6 ± 1.8 to 164.5 ± 16.2 ml/min ( P &lt; 0.001), and leg prostanoid release from 54.1 ± 8.5 to 267.4 ± 35.8 pg/min ( P &lt; 0.001). Indomethacin suppressed release of prostaglandin F1α( P &lt; 0.001) throughout exercise and decreased leg blood flow during exercise ( P &lt; 0.05). This was associated with a corresponding decrease in leg O2 consumption ( P &lt; 0.05) and a higher level of femoral venous lactate at peak exercise ( P &lt; 0.01). These data suggest that release of vasodilatory prostaglandins contributes to skeletal muscle arteriolar vasodilation in patients with heart failure. </jats:p

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