Hypertensive left ventricular hypertrophy is associated with abnormal myocardial fatty acid metabolism and myocardial efficiency

Abstract

Hypertension-induced left ventricular hypertrophy (LVH) is associated with an increased risk of cardiovascular morbidity and death by mechanisms not well characterized. Myocardial fatty acid (FA) metabolism and left ventricular (LV) mass were evaluated in 13 patients with hypertensive LVH with normal LV ejection fraction and 42 normal control subjects (primary cohort). Contractile performance was also evaluated in 5 hypertensive LVH patients and 5 matched normal control subjects (magnetic resonance [MR] substudy). Myocardial FA utilization (MFAU) and myocardial FA oxidation (MFAO) were assessed by positron emission tomography by use of 1-carbon-11 palmitate. Myocardial contractile function (strain and stress) was determined by cardiac MR imaging with tissue tagging and calibrated arterial pressure traces; myocardial external minute work and efficiency were derived. In the primary cohort decreased MFAO was predictive of increased LV mass (model r(2) = 0.61, P = .03). In the MR substudy decreased MFAO (corrected for myocardial oxygen consumption [MVO(2)]) in the hypertensive LVH group compared with the normal group (MFAU/MVO(2), 26 +/- 5 vs 37 +/- 8; MFAO/MVO(2), 24 +/- 6 vs 35 +/- 7; both P = .03) was paralleled by decreased myocardial external minute work (0.13 +/- 0.03 J x g(-1) x min(-1) vs 0.17 +/- 0.04 J x g(-1) x min(-1), P = .07) and decreased myocardial efficiency (5.2% +/- 1.4% vs 7.1% +/- 1.0%, P = .03). Abnormalities in myocardial FA metabolism are apparent in hypertensive LVH, and these abnormalities may be responsible, at least in part, for a reduction in myocardial efficiency.