Key result
Patients with nonobstructive hypertrophic cardiomyopathy had significantly blunted endothelium-independent vasodilation compared to normotensive controls (13% vs. 23%, P<0.01).
Why the study?
Does nonobstructive hypertrophic cardiomyopathy impair endothelium dependent and independent vasodilation compared to healthy normotensive subjects and hypertensive patients?
Observational
Does nonobstructive hypertrophic cardiomyopathy impair endothelium dependent and independent vasodilation compared to healthy normotensive subjects and hypertensive patients?
Absolute Event Rate: 13% vs 23%
p-value: p=<0.01
Patients with nonobstructive hypertrophic cardiomyopathy exhibit impaired endothelium-independent vasodilation in systemic conduit arteries, suggesting vascular wall remodeling or smooth muscle cell dysfunction.
Impaired endothelium-independent vasodilation in nonobstructive HCM may indicate smooth muscle dysfunction; hypothesis-generating and should not yet change practice.
BACKGROUND: In patients with hypertrophic cardiomyopathy (HCM) an impaired microvascular function is reported not only in the hypertrophied septum but also in the nonhypertrophied left ventricular free wall as well as in forearm resistance vessels, thus suggesting a generalized alteration in vascular function. However, information on conduit artery involvement is still sparse and controversial. The aim of this study was to evaluate whether functional abnormalities are detectable in the arteries of HCM patients. METHODS: In a group of newly diagnosed, previously untreated, patients with nonobstructive HCM, conduit artery endothelium dependent and independent vasodilation (EDV and NEDV, respectively) were assessed with high resolution ultrasound by measuring respectively flow-mediated vasodilation and response to sublingual nitroglycerine of the brachial artery. Normotensive subjects free of cardiovascular disease and risk factors and untreated hypertensive patients with left ventricular hypertrophy were studied as control groups. RESULTS: Compared to normotensives, HCM patients showed significantly blunted NEDV (13 ± 6% vs. 23 ± 7%, P < 0.01), whereas EDV was not significantly different between the two groups (11 ± 4 for HCM vs. 13 ± 4% for normotensives, P = 0.25). In the hypertensive group, both NEDV and EDV were significantly decreased compared to normotensives (P = 0.01 and P < 0.01, respectively). CONCLUSIONS: Patients with HCM show a reduced vasodilator response of systemic conduit arteries to nitroglycerine, suggesting a remodeling of vascular wall or smooth muscle cell dysfunction.
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Bartolomucci et al. (2011) conducted an observational in Nonobstructive Hypertrophic Cardiomyopathy. Nonobstructive Hypertrophic Cardiomyopathy vs. Normotensive subjects and untreated hypertensive patients was evaluated on Conduit artery endothelium independent vasodilation (NEDV) (p=<0.01). Patients with nonobstructive hypertrophic cardiomyopathy had significantly blunted endothelium-independent vasodilation compared to normotensive controls (13% vs. 23%, P<0.01).
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