Thick Hearts Can't Keep Up: Exercise Limitations in Patients With Hypertrophic Cardiomyopathy

Abstract

Patients with hypertrophic cardiomyopathy (HCM) may experience intolerance to submaximal and maximal exercise. While ejection fraction is generally preserved, reduced left ventricular end diastolic volume may limit stroke volume reserve and potentially attenuate maximal oxygen uptake (V̇O2max). Whether the relationship between supply (cardiac output, Q̇c) and demand (oxygen uptake, V̇O2) remains intact in these patients is unclear.PURPOSETo quantify the cardiac output response to a given metabolic demand during submaximal and maximal exercise in patients with HCM.METHODSEight patients with HCM (45.8±8.8 years, 75% female, left ventricular outflow tract pressure gradient 13±12mmHg) completed two bouts of submaximal steady‐state treadmill exercise (SS1 ~45% and SS2 ~60% V̇O2max), followed by an incremental treadmill test to exhaustion. V̇O2 (Douglas bag technique), Q̇c, (acetylene rebreathing), stroke volume (Q̇c/heart rate) and arterio‐venous difference (av‐O2 diff, Fick principle) were measured during rest, SS1, SS2 and maximal exercise. Stroke volume reserve was calculated as the percent increase in stroke volume from rest to maximal exercise. The relationship between Q̇c and V̇O2 (Q̇c/V̇O2 slope) was quantified using data collected at rest, submaximal and maximal exercise. Healthy sedentary adults (n=8) and subjects with left ventricular hypertrophy from hypertension (LVH, n=8) were included for age and sex‐matched comparison.RESULTSPatients with HCM had lower relative V̇O2max than healthy subjects and patients with LVH (HCM: 21.1±4.8mL/kg/min, healthy: 27.5±3.4 mL/kg/min, LVH 24.4±7.5 mL/kg/ min). The Q̇c response to a given metabolic demand was impaired in patients with HCM when compared to healthy controls and patients with LVH (HCM: 4.6, control: 5.4, LVH: 5.5; Figure 1). The blunted Q̇c/V̇O2 slope was primarily due to a smaller stroke volume reserve (HCM 28.8±27.0%, healthy 52.2±19.6%, LVH 48.6±25.0%), but also a significantly lower maximal heart rate compared to healthy controls (154±24 vs. 178±10 beats per minute, respectively; P<0.05), though 75% of HCM patients were on beta‐blockade and/or calcium channel‐blockade therapy. Remarkably, five HCM patients were able to compensate for a blunted Q̇c/V̇O2 slope (4.2±0.4) and still achieve >80% of predicted V̇O2max by significantly augmenting av‐O2 diff from rest to maximal exercise (Δav‐O2 diff 10.6±1.6 vs. 6.2±1.5 in HCM patients who did not achieve 80% of predicted V̇O2 max, P<0.05).CONCLUSIONAlthough ejection fraction is preserved, patients with HCM may be unable to sufficiently match Q̇c to metabolic demands. However, some patients appear to compensate by significantly augmenting peripheral oxygen extraction and achieve at least 80% of predicted V̇O2max.Support or Funding InformationSupported by The Center for Regenerative Science and Medicine, UTSW Medical Center, Biotronik Inc., and the Research Endowment from The American College of Sports Medicine Foundation.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.