Exercise capacity in chronic heart failure is related to the aetiology of heart disease

Abstract

Objective-To assess whether the underlying aetiology of chronic heart failure is a predictor of exercise performance. Setting-Tertiary referral centre for cardiology. Patients and outcome measuresRetrospective study of maximum exercise testing with metabolic gas exchange measurements in 212 patients with chronic heart failure who had undergone coronary angiography. Echocardiography and radionucleide ventriculography were used to determine indices of left ventricular function, and coronary arteriography was used to determine whether the cause of chronic heart failure was ischaemic heart disease (n = 122) or dilated cardiomyopathy (n = 90). Results-The cardiomyopathy group was younger (mean (SD) age 58.45 (11.66) years v 61.49 (7.42); p = 0.02) but there was no diVerence between the groups in ejection fraction or fractional shortening. Peak oxygen consumption (Ṽ O 2 ) was higher in the dilated group, while the slope relating carbon dioxide production and ventilation (Ṽ E/Ṽ CO 2 slope) was the same in both groups. Both groups achieved similar respiratory exchange ratios at peak exercise, suggesting that there was near maximum exertion. There was a relation between peak Ṽ O 2 and age (peak Ṽ O 2 = 33.9 − 0.267*age; r = 0.36; p < 0.001). After correcting for age, the peak achieved Ṽ O 2 was still greater in the cardiomyopathy group than in the ischaemic group (p < 0.002). Conclusions-Exercise performance for a given level of cardiac dysfunction appears to vary with the aetiology of heart failure. Thus the two diagnostic categories should be considered separately in relation to abnormalities of exercise physiology. The diVerence may in part account for the worse prognosis in ischaemic patients.

Limitation of exercise tolerance in chronic heart failure: distinct effects of left Bundle-Branch block and coronary artery disease

“…Rather, we found that both absolute and percentage predicted values of peak VO 2 were strikingly reduced in patients with LBBB compared with those without, and to a lesser extent by CAD (19), even when exercise tolerance was not limited by acute ischemia. Patients with neither LBBB nor CAD thus had the highest absolute and percentage predicted values of peak VO 2 , whereas those with LBBB had the lowest values of all, irrespective of whether CAD was present or not.…”

Ischemic etiology of heart failure identifies patients with more severely impaired exercise capacity

“…In a retrospective analysis Clark et al [10] showed that patients with heart failure due to non-ischemic heart disease have a higher peak VO2 than patients with coronary artery disease; this did not appear to be related to any difference in ventilatory response to exercise, as measured by the VE/VCO2 slope. However, in this study the role of etiology was not assessed independently of the degree of left ventricular dysfunction.…”

“…However, for the same level of left ventricular dysfunction, different degrees of exercise impairment are found [7][8][9]. Few previous reports have proposed that the etiology of heart failure might influence functional capacity, regardless of left ventricular function, through being related to different levels of peripheral vascular disease, skeletal muscle myopathy and cardiac adaptation to excessive wall stress [10,11]. Therefore, the aim of the present study was to examine the effect of heart failure etiology on peak VO2 and on the ventilatory response to exercise in a large cohort of unselected patients with CHF.…”

The Role of NT-ProBNP in Explaining the Variance in Anaerobic Threshold and VE/VCO2 Slope

“…It is interesting that the etiology of HF (ischemic/dilated cardiomyopathy) is an independent predictor of peak VO 2 and VE/VCO 2 slope but not of AT, although all of these exercise variables differ significantly when comparing patients with ischemic or dilated cardiomyopathy. 5 Clark et al 19 have reported these differences in peak VO 2 . The worsened CPX variables (lower peak VO 2 , lower AT, and higher VE/VCO 2 slope) found in the ischemic HF patients compared with the ones in the nonischemic group may be attributed to changes in the cardiac muscle and function occurring because of ischemia in this group.…”