Catecholamine Response to Exercise in Patients with Non‐Obstructive Hypertrophic Cardiomyopathy

Key Points Summary

Intense physical activity, a potent stimulus for sympathetic nervous system activation, is thought to increase the risk of malignant ventricular arrhythmias among patients with hypertrophic cardiomyopathy (HCM). As a result, the majority of patients with HCM deliberately reduce their habitual physical activity after diagnosis and this lifestyle change puts them at risk for sequelae of a sedentary lifestyle; weight gain, hypertension, hyperlipidemia, insulin resistance, coronary artery disease and increased morbidity and mortality. We show that plasma catecholamine levels remain stably low at exercise intensities below the ventilatory threshold, a parameter that can be defined during cardiopulmonary exercise testing, but rise rapidly at higher intensities of exercise. These findings suggest that cardiopulmonary exercise testing may be a useful tool to provide an individualized moderate‐intensity exercise prescription for patients with HCM.

Abstract

Intense physical activity, a potent stimulus for sympathetic nervous system activation, is thought to increase the risk of malignant ventricular arrhythmias among patients with hypertrophic cardiomyopathy (HCM). However, the impact of exercise intensity on plasma catecholamine levels among HCM patients has not been rigorously defined. We conducted a prospective observational case‐control study of men with non‐obstructive HCM and age‐matched controls. Laboratory‐based cardiopulmonary exercise testing coupled with serial phlebotomy was used to define the relationship between exercise intensity and plasma catecholamine levels. Compared to controls (C, n = 5), HCM participants (H, n = 9) demonstrated higher left ventricular mass index (115 ± 20 vs. 90 ± 16 g/m², p = 0.03) and maximal left ventricular wall thickness (16 ± 1 vs. 8 ± 1 mm, p<0.001) but similar body mass index, resting heart rate, peak oxygen consumption (H = 40 ± 13 vs. C = 42 ± 7 ml/kg/min, p = 0.81) and heart rate at the ventilatory threshold (H = 78 ± 6 vs. C = 78 ± 4 % peak heart rate, p = 0.92). During incremental effort exercise in both groups, concentrations of epinephrine and norepinephrine were unchanged through low‐ and moderate‐exercise intensity until reaching a catecholamine threshold (H = 82 ± 4 vs. C = 85 ± 3 % peak heart rate, p = 0.86) after which levels of both molecules rose rapidly. In patients with mild non‐obstructive HCM, plasma catecholamine levels remain stably low at exercise intensities below the ventilatory threshold but rise rapidly at higher intensities of exercise. Routine cardiopulmonary exercise testing may be a useful tool to provide an individualized moderate‐intensity exercise prescription for patients with HCM.

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