Increased cardiac output during exercise is the result of greater stroke volume and an increase in heart rate. It is therefore assumed that a limitation to heart rate rise (HRR) in response to activity, chronotropic incompetence (CI), could contribute to the exercise intolerance that is characteristic of chronic heart failure (CHF). However, HRR is closely related to workload and subjects with impaired exercise capacity have a lower peak heart rate (PHR) and a lower HRR. Hence, whether a limited increase in heart rate (HR) during exercise in patients with CHF is aetiological in their exercise limitation or merely a bystander remains unproven. The aim of this study was to examine the effects of correcting CI in patients with CHF on peak and submaximal exercise capacity.Methods
We enrolled 50 subjects with CHF due to left ventricular systolic dysfunction (LVSD), (left ventricular ejection fraction <45%, and symptoms of breathlessness or fatigue), on optimal medical therapy with cardiac pacing devices, into a randomised double blind cross-over study of rate adaptive versus fixed rate pacing. At baseline, each participant underwent a full echocardiographic assessment, and performed a peak, symptom-limited treadmill-based familiarisation cardiopulmonary exercise test with breath-by-breath metabolic gas analysis. After at least one week, subjects were invited back for two further exercise tests (at least one week apart) immediately prior to which, the pacemaker was either programmed to rate-adaptive or fixed rate pacing, with the maximum paced HR determined using the age-predicted peak HR equation (220-age).Results
Rate-adaptive pacing led to higher mean (SE) peak HR (128 (21) vs 107 (28) bpm; p < 0.0001, Figure 1) but no difference in mean peak oxygen consumption (16.6(4.7) v 15.9(4.5) ml/kg/min, p = 0.24), anaerobic threshold (11.7 (2.7) vs 11.3 (2.6) ml/kg/min; p = 0.24), exercise time (470 (239) v 451 (222)s; p = 0.33, Figure 2), stage-by-stage HR or perceived exertion levels.Conclusions
Exercise intolerance due to breathlessness and fatigue is a cardinal feature of CHF and remains a problem for many patients despite optimal medical and device therapy. Agents that lower HR and induce CI are proven to improve outcomes for patients with CHF due to LVSD yet traditional models of heart failure suggest that a lower cardiac output, potentially the consequence of CI, reduces blood supply to exercising muscles thereby limiting work. By demonstrating that higher HR throughout exercise is not associated with greater exercise capacity in CHF patients, we propose that CI does not play a major role in exercise intolerance in CHF.