Epicardial Coronary Vessels and Coronary Microcirculation in Pressure Overload Hypertrophy: A Complex Interaction

Pressure overload left ventricular (LV) hypertrophy (LVH) is associated with abnormalities in coronary perfusion distinct from those due to atheromatous disease.1 Such abnormalities would explain greater vulnerability to ischemia and hypoxia in hypertrophied myocardium. Coronary vasculature changes of hypertensive heart involve both epicardial vessels and microvessels. Increase of total coronary blood flow and epicardial luminal diameter would be expected in relation with the magnitude of LVH, which reduces wall stress and normalizes myocardial energy demand per gram of myocardium. On the contrary, Kozakova et al2 show that at rest, hypertensive LVH is not associated with increased epicardial vessel size. When normalized for LV mass (LVM) magnitude, left main coronary artery (LMA), measured by transesophageal echocardiography, gradually decreases from normotensive controls through hypertensive patients without LVH to those with LVH. Normalized LMA appears even lower in athletes with physiologic LVH than in controls. These findings are important but cannot explain the entire physiopathology of the coronary circulation in LVH. Under resting condition, coronary flow autoregulation is a resultant of two opposite determinants: coronary perfusion pressure, reflecting arterial pressure, and coronary impedance, due to combined interaction of vascular, myocardial, and hemodynamic forces. All these components are altered in hypertensive LVH and exert their maximal effect at the level of coronary microvessels, in particular on subendocardial myocardial layers, more vulnerable to LVM increase and to myocardial fibrosis. At present, transthoracic Doppler echocardiography allows the analysis of the impact of these factors on coronary microcirculation under maximal hyperemic stimulation (adenosine or dipyridamole), by calculating coronary flow reserve (CFR), that is, the ratio between hyperemic and resting flow velocity at any given pressure. In the absence of epicardial coronary stenosis, CFR of the distal left anterior descending artery reflects the functional state of coronary microcirculation and the coronary perfusion in physiologic and pathologic LVH. Athletes with LVH have a greater LMA size, which corresponds to increased CFR and the possibility of dilating maximally the coronary microvascular bed when the myocardial oxygen demand is the highest. Also Kozakova et al2 found a positive association between the degree of CFR and epicardial vessel size in their athletes. An opposite situation occurs in hypertensive LVH, where the maximal coronary microvascular diastolic dilation is negatively affected, not only by increased afterload, but also by compressive forces developing in parallel with LVM increase. Under these circumstances, the degree of CFR reduction progresses with the excess of LVM beyond the values compensatory for individual hemodynamic load,3 even before the evidence of LVH (Fig. 1). This state corresponds to LV concentric geometry4 and reflects the development of myocardial fibrosis. Such deep modifications of the myocardial interstitium explain how the relation of CFR impairment is even greater with LV diastolic dysfunction—direct expression of fibrosis—than with LVM increase.5 In the hypertensive heart, the inadequate response of the epicardial vessel size to LVH is accompanied by microvascular dysfunction, whose degree is related to myocardial structural changes. The interaction between changes of coronary macrocirculation and microcirculation progresses through accelerated atherosclerosis to onset of myocardial ischemia in arterial hypertension.1