Endothelial nitric oxide synthase and cardiac remodelling: location, location, location?

This editorial refers to ‘Endothelial nitric oxide synthase of the bone marrow regulates myocardial hypertrophy, fibrosis, and angiogenesis’ by A. Kazakov et al. , pp. 397–405, this issue. Left ventricular hypertrophy (LVH) in response to an increased systolic load is a compensatory mechanism that aims to restore LV pump function to normal levels. Clinically, chronic systolic LV overload most commonly results from myocardial infarction (MI), or chronic pressure overload, including hypertension and aortic stenosis.1 Despite the apparent appropriateness of the hypertrophy process, LVH in response to these pathological processes constitutes an independent risk factor for developing angina pectoris and congestive heart failure.1 The mechanisms underlying the progressive deterioration in LV function remain incompletely understood but include myocardial blood flow abnormalities, as the coronary vascular tree fails to grow commensurate with the degree of LVH.2,3 The resulting impaired myocardial O2 delivery contributes to cardiac contractile dysfunction, apoptosis, and fibrosis.2,3 In contrast to LVH produced by MI or pressure overload, LVH produced by regular dynamic physical exercise is associated with a decreased risk for coronary artery disease and congestive heart failure. Indeed, exercise-induced LVH is associated with an increased myocardial perfusion capacity and normal to increased LV contractile function,4 …