This case demonstrates that ischemia-induced systolic anterior motion of the mitral valve can occur without left ventricular hypertrophy and is fully reversible with appropriate revascularization and medical therapy.
Systolic anterior motion (SAM) of the mitral valve is classically associated with hypertrophic cardiomyopathy (HCM); however, it may rarely occur in the absence of left ventricular hypertrophy (LVH), particularly in the setting of acute myocardial ischemia. This phenomenon remains poorly understood and poses diagnostic and therapeutic challenges. We report the case of a 54-year-old woman presenting with non-ST-elevation myocardial infarction (NSTEMI). Transthoracic echocardiography showed a non-dilated left ventricle (LV end-diastolic diameter 45 mm), preserved systolic function (left ventricular ejection fraction (LVEF) 63%; end-diastolic volume 115 mL, end-systolic volume 42 mL), apical akinesia, and compensatory basal hyperkinesis. There was no LV hypertrophy (interventricular septum 8 mm; lateral wall 7 mm). SAM of the mitral valve was present, resulting in moderate mitral regurgitation and a dynamic left ventricular outflow tract (LVOT) gradient of 30 mmHg. The right ventricle was normal in size and function. Cardiac magnetic resonance imaging demonstrated apical myocardial edema on T2-weighted sequences and a punctiform transmural late gadolinium enhancement in the inferomedial segment on phase-sensitive inversion recovery (PSIR) sequences, with no evidence of cardiomyopathy or structural substrate that could explain LVOT obstruction. Coronary angiography revealed a significant mid-left anterior descending artery lesion, successfully treated with drug-eluting stent implantation. Medical management included beta-blocker therapy and careful volume optimization, with avoidance of inotropes. Follow-up transesophageal echocardiography at three weeks confirmed complete resolution of SAM, mitral regurgitation, LVOT gradient, and apical wall-motion abnormalities. This case illustrates a rare, ischemia-induced and reversible form of SAM without LVH. LVH was excluded based on echocardiographic wall thickness measurements below established thresholds (interventricular septum 8 mm and lateral wall 7 mm), well under the diagnostic cutoff for LVH (>11 mm), likely mediated by transient apical dysfunction and basal hyperkinesis, altering ventricular geometry and flow dynamics.
Chaddad et al. (2026) studied this question.