Why the study?
Dynamic LVOTO after ACS is typically attributed to apical infarction with compensatory basal hyperkinesia, but alternative mechanisms in the absence of apical akinesia remain poorly understood.
Highlights that dynamic LVOTO in ACS can occur without apical akinesia, potentially driven by a sigmoid septum and ischemia-induced afterload reduction.
Severe dynamic LVOTO can occur post-ACS without apical akinesia; leaves open alternative mechanisms for prospective study.
The mechanism for dynamic left ventricular outflow tract obstruction (LVOTO) after acute coronary syndromes (ACS) is thought to be apical infarction with compensatory hyperkinesia of the residual normally perfused basal segments of the myocardium. However, herein, we report a patient with ACS and dynamic LVOTO (peak gradient of 250 mm Hg at rest) that could not be secondary to apical akinesia. We propose a potential alternative mechanism leading to dynamic LVOTO in ACS, namely, the interplay between sigmoid septum, basal hyperkinesis, and outflow tract narrowing induced by afterload reduction due to acute myocardial ischemia itself.
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Fujiwara et al. (2021) studied this question.
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