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.