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Acute myocardial ischemia can induce a reversible form of systolic anterior motion (SAM) of the mitral valve in the absence of left ventricular hypertrophy, likely mediated by transient apical dysfunction and compensatory basal hyperkinesis. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

March 3, 2026Open Access

Reversible Systolic Anterior Motion in the Absence of Left Ventricular Hypertrophy Following Acute Myocardial Infarction: A Report of a Rare Case

Key Points

Systolic anterior motion of the mitral valve was found, causing moderate mitral regurgitation and a left ventricular outflow tract gradient of 30 mmHg.
Transthoracic echocardiography revealed normal left ventricle size and preserved systolic function, excluding hypertrophy.

Structured PICO

Population

54-year-old woman presenting with non-ST-elevation myocardial infarction (NSTEMI) and ischemia-induced systolic anterior motion (SAM) of the mitral valve without left ventricular hypertrophy (n=1).

Intervention

Percutaneous coronary intervention with drug-eluting stent (DES) to the mid-left anterior descending artery, combined with medical management (beta-blocker therapy, volume optimization, avoidance of inotropes).

Outcome

Resolution of systolic anterior motion (SAM), mitral regurgitation, LVOT gradient, and apical wall-motion abnormalities on follow-up transesophageal echocardiography.surrogate

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.

Abstract

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.

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