ORIGINAL PAPERS, CLINICAL CARDIOLOGY

L eft ventricular hypertrophy (LVH) is a cardiac adaptationresponse to arterial hypertension in an attempt to over-come the enhanced peripheral vascular resistance. LVH has been proven to be a major independent risk factor for cardio-vascular morbidity and mortality [1–6]. The exact mecha-nism leading to the increased occurrence of cardiac events in patients with LVH is not fully understood; it is probably mul-tifactorial, including an increased oxygen consumption, a de-creased coronary blood flow reserve, and susceptibility to malignant atrial and ventricular arrhythmias [7–12]. Cardiac hypertrophy comprises cardiomyocyte hypertrophy, intersti-tial fibrosis, and consequent structural alterations in the coro-nary microcirculation with a decreased coronary flow reserve, which results in impairment of the diastolic and systolic function of the left ventricle despite the normal anatomy of the epicardial coronary arteries [13]. Doppler-echocardio