Abstract
In their recently published article, Sharma et al. [1] have shown that patients with end-stage renal disease have high prevalence (12%) of dobutamine-induced significant left ventricular outflow tract obstruction (LVOTO). None of the patients have been detected to have LVOTO at rest. Of patients with angina, 26% have been reported to have dynamic LVOTO compared to only 1% in those without angina. They have suggested that the development of dynamic LVOTO may be the potential cause of angina in patients with end-stage renal disease. Hypertrophic obstructive cardiomyopathy is the most frequent cause of dynamic LVOTO. Significant hypertrophy of basal septum and a frequently accompanied systolic anterior motion of the mitral valve are the reported explanations for this dynamic obstruction [2]. Other rare conditions as excessive sympathetic stimulation, hyperdynamic state, dehydration, and vasodilation have been reported to be associated with dynamic LVOTO [3–7]. Previously, Auer et al. [3] have reported a patient without left ventricular hypertrophy who developed severe dynamic LVOTO during catecholamine stimulation for shock that complicated severe pancreatitis. They have suggested that hypovolemia together with a hyperdynamic state resulting from catecholamine administration may result in the development of dynamic LVOTO even if baseline cardiac evaluation is unremarkable. Similarly, Mingo et al. [4] have reported two patients with normal left ventricular structure who developed significant LVOTO in the context of
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