Non-compaction cardiomyopathy with acute mitral regurgitation due to chordae tendineae rupture and mechanical valve replacement – a case report

Abstract

Left ventricular non-compaction cardiomyopathy (LVNC) is an infrequent cardiac disorder characterized by prominent trabeculations, deep intertrabecular recesses, and thinning of the compacted myocardial layer, predisposing to heart failure, arrhythmias, and thromboembolic complications. The relationship between myocardial inflammation and chordae tendineae rupture is clinically relevant, as prior inflammatory processes may compromise valvular structures, leading to acute mitral regurgitation and ventricular overload. We present the case of a 45-year-old male with a history of severe mitral regurgitation and heart failure with preserved ejection fraction, who presented with progressive dyspnea, oppressive chest pain, diaphoresis, and lower extremity edema. Clinical assessment revealed arterial hypertension, tachycardia, hypoxemia, a loud systolic mitral murmur, jugular venous distension, and peripheral edema. Complementary studies demonstrated LVNC, severe prolapse of the posterior mitral leaflet with chordae tendineae rupture, acute mitral regurgitation, and pulmonary hypertension. Thoracic computed tomography revealed chronic lesions compatible with a previous viral infection, although specific SARS-CoV-2 testing results were unavailable. The patient underwent mitral valve replacement with a mechanical prosthesis, with postoperative complications including acute pulmonary edema, pleural effusion, renal insufficiency, and left ventricular dysfunction, which resolved favorably during hospitalization. This case highlights the importance of early recognition of LVNC and its valvular complications, as well as a comprehensive approach and timely surgical intervention to optimize clinical outcomes in complex cardiovascular scenarios.