Key result
HCM links to ~38% lower subendocardial arteriolar density and impaired coronary vasodilator reserve.
Why the study?
The coronary microvasculature is thought to be abnormal in hypertrophic cardiomyopathy (HCM), with subendocardial arterioles suspected of playing a key role in regulating intramyocardial blood flow and coronary vasodilator reserve.
Is the architecture of subendocardial arterioles altered and associated with impaired coronary vasodilator reserve in patients with hypertrophic cardiomyopathy and angina pectoris compared to normotensive controls?
Case-Control (n=18)
Is the architecture of subendocardial arterioles altered and associated with impaired coronary vasodilator reserve in patients with hypertrophic cardiomyopathy and angina pectoris compared to normotensive controls?
Patients with hypertrophic cardiomyopathy and angina have reduced subendocardial arteriolar density and lumen area, which directly correlates with impaired coronary vasodilator reserve and may predispose them to myocardial ischemia.
Microvascular rarefaction may underlie ischemia in HCM; extends prior observations but leaves open therapeutic relevance.
Objectives The study was designed to investigate the architecture of subendocardial arterioles of patients with hypertrophic cardiomyopathy (HCM) and angina pectoris with respect to coronary vasodilator reserve. Background There is growing evidence that the coronary microvasculature is abnormal in HCM. Arterioles, which mainly regulate intramyocardial blood flow, are especially suspect. Methods Thirteen patients with HCM (50.1+/-12.6 years old, mean value +/- SD) were studied after exclusion of any relevant coronary stenoses. Subendocardial arterioles (density [n/mm2], wall area [microm2], percent lumen area [%lumen], periarteriolar collagen area [microm2]), myocyte diameter (microm) and interstitial collagen fraction (Vv%) were evaluated by means of stereologic morphometry of transvenous biopsy samples. Coronary blood flow was measured quantitatively with the inert chromatographic argon method at basal conditions and after dipyridamole (0.5 mg/kg body weight over 4 min intravenously), and coronary vasodilator reserve was calculated as the ratio of coronary resistance at basal conditions and after pharmacologic vasodilation. Data from five normotensive subjects (45.4+/-11 years old, p = NS) served as control data. Results Arteriolar density was diminished by 38% (p = 0.004) and %lumen by 13% (p = 0.009) in patients with HCM compared with control subjects. Coronary reserve was impaired in patients with HCM (2.28+/-0.6 vs. 5.34+/-1.49, p = 0.003) because of higher coronary resistance after vasodilation (0.48+/-0.14 vs. 0.22+/-0.06 mm Hg x min x 100 g/ml, p = 0.004). Coronary vasodilator reserve correlated with arteriolar density (r = +0.47, p = 0.045) and with %lumen (r = 0.65, p = 0.003). Conclusions In HCM, the architecture of preterminal subendocardial arterioles is altered by a reduced total cross-sectional lumen area, corresponding to an impaired coronary vasodilator capacity that may predispose to myocardial ischemia.
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Schwartzkopff et al. (1998) conducted a case-control in Hypertrophic cardiomyopathy (HCM) with angina pectoris (n=18). Hypertrophic cardiomyopathy vs. Normotensive control subjects was evaluated on Coronary vasodilator reserve and subendocardial arteriolar density and % lumen area (p=0.003). Patients with HCM had 38% lower subendocardial arteriolar density (p=0.004), 13% smaller %lumen area (p=0.009), and impaired coronary vasodilator reserve (2.28 vs 5.34, p=0.003) vs controls.
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