This review highlights the multifactorial mechanisms contributing to impaired coronary vasodilator reserve in hypertensive heart disease.
Highlights the multifactorial nature of microvascular dysfunction in hypertensive heart disease; leaves open the.
Time for primary review 35 days. Essential hypertension is a main risk factor for left ventricular hypertrophy (LVH), ischemic heart disease and hypertensive cardiomyopathy [1]. In addition to the increased prevalence of atherosclerotic stenoses in epicardial arteries, hypertensive subjects with no relevant coronary artery disease or LVH have impaired coronary vasodilator reserve [2, 3]that has been reported to correlate with scintigraphic evidence of myocardial ischemia [4]. Impaired coronary reserve could be an important factor for inadequate delivery of oxygen and substrate to myocytes, precipitating myocardial ischemia and contributing to deterioration of myocardial function [2–4]. The potential mechanisms of impaired coronary reserve include abnormal processes of contraction and relaxation of a structurally remodeled myocardium, increased extravascular compressive forces, rheologic factors, metabolic factors as well as functional and structural alterations of the intramyocardial coronary arteries and arterioles (Fig. 1). The purpose of the present review is to discuss the pathophysiological mechanisms that may be involved in reduced vasodilator capacity in human hypertensive heart disease and to report about therapeutic interventions. Fig. 1 Potential factors to influence coronary reserve in hypertensive heart disease. In the coronary venous blood, oxygen content is about 5 ml/100 ml, which corresponds to about 25–30% saturation and a p O2 of 18–25 mm Hg. Thus, given significant oxygen extraction, any relevant additional oxygenation can only be made available by a proportional increase in coronary blood flow. The normal heart can increase its blood flow by a factor of 4 to 5 [2–5]. Coronary autoregulation enables the heart to keep coronary flow unchanged over a wide range of perfusion pressures (from ∼50 to 120 mm Hg) (review [5, 6]). This is reflected by a pressure–flow relationship with a central portion running parallel to the pressure axis that is followed by a steep increase in flow …
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B. Schwartzkopff (1998) studied this question.
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