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A left ventricular outflow tract pressure gradient (LVOT PG) ≥50 mmHg at rest in hypertrophic cardiomyopathy (HCM) is a predictor of heart failure and cardiovascular death [1, 2]. The clinical indication for myectomy and alcohol septal ablation is also LVOT PG ≥50 mmHg at rest or with physiological exercise [ 3 ].
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These data suggest that in the absence of increased wall stress and concomitant microtubule densification, pressure-overload LV hypertrophy invokes favorable compensatory modification (s) of the contractile apparatus, or of its regulation, in the hypertrophied cardiocyte.
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