Squeezing tubes: a case of remodeling and regulation: coronary reserve in hypertensive heart disease.

1. Introduction pressure–flow relationship with a central portion running parallel to the pressure axis that is followed by a steep Essential hypertension is a main risk factor for left increase in flow at higher perfusion pressures (Fig. 2). If, ventricular hypertrophy (LVH), ischemic heart disease and however, coronary vessels are maximally dilated then such hypertensive cardiomyopathy [1]. In addition to the in-autoregulation is lost and a steep, almost linear pressure– creased prevalence of atherosclerotic stenoses in epicardial flow relationship results for a wide range of perfusion arteries, hypertensive subjects with no relevant coronary pressure. On the side of low inflow pressures (,40 mm artery disease or LVH have impaired coronary vasodilator Hg), pressure–flow curves in the maximally dilated state reserve [2,3] that has been reported to correlate with may become curvilinear due to discharge of vascular scintigraphic evidence of myocardial ischemia [4]. capacitance [6], and here the intercept with the pressure Impaired coronary reserve could be an important factor axis defines 'back pressure', reflecting the combined for inadequate delivery of oxygen and substrate to effects of extravascular myocardial compression and in-myocytes, precipitating myocardial ischemia and contribut-traventricular pressure [5,6]. Coronary autoregulation is ing to deterioration of myocardial function [2–4]. The affected by metabolic, myogenic, vascular, adrenergic and potential mechanisms of impaired coronary reserve include neural factors as well as tissue pressure [2,6–9]. Regional abnormal processes of contraction and relaxation of a differences in pressure and flow exist within the myocar-structurally remodeled myocardium, increased extravascu-dium, where pressure is higher in the subendocardium than lar compressive forces, rheologic factors, metabolic factors in the subepicardium, which is associated with an in-as well as functional and structural alterations of the creased metabolic demand and a greater coronary blood intramyocardial coronary arteries and arterioles (Fig. 1). flow (endo / epi ratio 1.1–1.4); but during vasodilatation The purpose of the present review is to discuss the (metabolic / tachycardial / pharmacological) the endo / epi pathophysiological mechanisms that may be involved in ratio may be dramatically inverted with a relative under-reduced vasodilator capacity in human hypertensive heart perfusion of the subendocardium [10]. disease and to report about therapeutic interventions. The coronary flow reserve is defined as the maximal coronary flow [5] above its resting level at a given perfusion pressure when coronary vasculature is maximally 2. Physiological conditions of coronary circulation dilated. Small differences in perfusion pressure can produce big differences in coronary flow reserve, thus In …