Case report:
This report was waived from institutional review board approval as it does not constitute human subjects research, consent was not obtained as this case contains no personal health identifiers. A 59-year-old male with no medical history developed sudden onset of dyspnea shortly after strenuous physical activity loading a truck with a couch. He presented to a local community hospital but during his transport he was drowsy and required bag valve mask ventilation. On arrival to the emergency department his telemetry showed atrial fibrillation with rapid ventricular response and no ST-segment changes. The patient underwent endotracheal intubation due to respiratory distress secondary to pulmonary edema. Bedside echocardiogram was performed, showing severe mitral valve regurgitation suspect of anterior chordae leaflet rupture. An intraortic balloon pump was placed for support in addition to intravenous vasopressors (epinephrine and vasopressin). He was transferred to a tertiary center for urgent valve repair.
Arrival laboratory workup demonstrated a serum creatinine of 2.3mg/dl, hemoglobin 10.8g/L, platelets 242x 10^3/cmm, white blood cell count 1710^3/cmm, and a peak troponin-I of 0.490ng/mL. He was started on broad spectrum antibiotics for suspected aspiration pneumonia on chest x-ray. A transthoracic echocardiogram showed anterior mitral valve leaflet flail suspecting ruptured chordae, normal biventricular function, and no regional wall motions abnormalities. A cardiac catheterization was performed, demonstrating 40-50% ostial left main disease with mild-moderate disease in the rest of the coronary arteries providing TIMI III flow. A transesophageal echocardiography added supportive evidence of a ruptured chord leading to A1 flail and severe mitral regurgitation (Figure1A and 1C). The regurgitant jet was posteriorly directed and exhibited a Coanda effect (Figure 1B). The EROA by PISA was 0.79cm\S\2, VC was 0.80cm and regurgitant volume was 73mL. EROA by 3D was 1.10cm\S\2. There was evidence of reverse systolic flow in the pulmonary veins with severe mitral regurgitation. Left ventricular ejection fraction was described as normal. The patient underwent mitral valve replacement with a bioprosthetic valve and bypass grafting of two coronary vessels. There was no macroscopic evidence of acute ischemia or myocardial infarction, the coronary vessels showed mild eccentric atheromatosis. The excision of the mitral valve revealed the anterolateral PMR attached to the apparatus (Figure 1D). Pathology demonstrated a valve tissue with fibrosis and myxoid degeneration. The hospital course was complicated with self-limited gastrointestinal bleed, new onset atrial fibrillation, and a small thromboembolic cerebrovascular accident. The patient ultimately recovered and was discharged home with a NYHA I functional class and a transthoracic echocardiogram showing normal biventricular function and a bioprostethic mitral valve with normal gradients and no perivalvular leaks.