An Unusual Presentation of Acute Severe Mitral Regurgitation

Mitral regurgitation (MR) results from retrograde blood flow from the left ventricle to the left atrium. Common etiologies of acute severe MR include papillary muscle rupture from myocardial infarction, leaflet perforation in infective endocarditis, chordal rupture (pop) in myxomatous valve disease, acute rheumatic fever with carditis, or functional MR due to cardiomyopathies, myocarditis or Takotsubo cardiomyopathy. Here, we present an unusual case of acute severe MR due to ruptured chordae tendineae likely secondary to degenerative valve disease. A 59-year-old male with a past medical history of hypertension and renal calculi was evaluated in the outpatient office for a urologic procedure. He was sent to the emergency room with left-sided chest pain, 6/10 in intensity, burning in nature, and non-radiating with no aggravating and relieving factors. He had nausea and vomiting for the past three days. He reported similar chest pain at rest and on exertion multiple times over the past year. He also had a chronic cough with no recent changes. His examination was unremarkable. Chest X-ray showed interstitial lung markings. Electrocardiography revealed an old right bundle branch block, but no ST/T-wave changes. He was admitted and treated for atypical pneumonia with ceftriaxone and azithromycin. The following morning, he complained of persistent chest pain 9/10 in intensity which improved with nitroglycerin. His examination revealed a new onset holosystolic murmur heard over the precordium. A two-dimensional echocardiogram showed a preserved ejection fraction of 55-60%, severe MR with eccentric jet, concerning for partially flail leaflet of the mitral valve. He was transferred to the university hospital for mitral valve replacement. Patients with acute rupture of chordae tendineae usually progress to severe mitral valve regurgitation. These patients usually present with pulmonary edema, signs of heart failure, and cardiogenic shock. Papillary muscle dysfunction, as well as partial or complete rupture of the mitral chordae can be detected as a new-onset holosystolic murmur and can be a crucial sign for early recognition. In our case, the patient developed a new holosystolic murmur on day two of admission which was recognized early, and prompt surgical intervention was performed.