Prognostic value of reduced heart rate reserve during exercise stress-echocardiography in hypertrophic cardiomyopathy

Abstract

Abstract Background Heart rate reserve (HRR) during exercise evaluates chronotropic incompetence and is a prognostically important marker of cardiac autonomic dysfunction, additive to regional wall motion abnormalities (RWMA) in patients with coronary artery disease. Objectives To assess determinants and prognostic value of HRR in patients with hypertrophic cardiomyopathy (HCM). Methods From 1998 to 2019, we enrolled 774 HCM patients (age = 48.8±15.9 years, 410 men) with exercise stress echocardiography (ESE) in 10 certified centres of the international stress echo network. During ESE we assessed: left ventricular outflow tract obstruction (LVOTO, significant when >50 mmHg); RWMA; HRR (peak/ rest heart rate), 344 in beta-blockers therapy (44.4%). Patients were followed for a median 49 months (IQ range, 25–78 months). The study end-point was all-cause mortality. Results During ESE, we observed stress-induced RWMA in 42 (5.4%) and LVOTO in 248 (33%); HRR was 1.92.±0.41. There were no difference in patients with normal and abnormal HRR with and without beta-blockers therapy (147, 41.1% vs 211, 58.9%, p=0.079). During follow-up, 43 deaths occurred. Beta blockers therapy in univariate analysis did not have prognostic role (HR 1.105, 95% CI 0.602–2.028, p=0.768). The lowest HRR quartile (≤1.62) had a 10-fold higher 6-year death rate (10.9%) than the highest quartile (>2.16, 1.04%): see figure. At multivariable analysis, lowest HRR quartile (HR 2.074, 95% CI 1.082–6.773, p=0.034), age (HR 1.045, 95% CI 1.014–1.077, p=0.004), maximal wall thickness (HR 1.137, 95% CI 1.054–1.226, p=0.001), stress-induced RWMA s(HR 4.289, 95% CI 1.733–10.615, p=0.002) and ≥ moderate mitral regurgitation at rest (HR 3.127, 95% CI 1.507–6.488, p=0.002) predicted death. Conclusions A blunted HRR during ESE predicts adverse outcome independent of inducible RWMA in HCM patients. Autonomic dysfunction deserves consideration as a potential therapeutic target in this disease. Figure 1 Funding Acknowledgement Type of funding source: None