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Acute severe mitral regurgitation presenting as acute coronary syndrome: a case report

Session Poster Session 2

Speaker Marta Pellegrino

Congress : Acute Cardiovascular Care 2019

  • Topic : imaging
  • Sub-topic : Echocardiography
  • Session type : Poster Session
  • FP Number : P628

Authors : M Pellegrino (Rozzano,IT), M Chiarito (Rozzano,IT), F Cannata (Rozzano,IT)

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Authors:
M Pellegrino1 , M Chiarito1 , F Cannata1 , 1Clinical Institute Humanitas IRCCS - Rozzano - Italy ,

Citation:

Case report: A 49-year-old male was admitted to the emergency department reporting two days of effort chest pain regressing with rest and some transient chest pain episodes during the night before. He suffered from hypertension and obesity, had a familial history for ischemic cardiac disease. Vital parameters, ECG and chest x-ray were normal. Physical examination revealed a systolic murmur, apparently known for years. Blood tests showed slightly elevated cardiac troponin, white cell count and C-reactive protein. He was admitted to a cardiological ward for suspected acute coronary syndrome. During the subsequent day he developed a high fever and non-productive cough, with rapid worsening. He suddenly became dyspnoeic and tachycardic, severely hypertensive, with desaturation and marked elevation of inflammatory markers. Bedside transthoracic echocardiography (TTE) showed mitral regurgitation (MR), though of difficult evaluation due to hyperkinesis of left ventricle (Fig 1, middle). Chest x-ray showed diffuse lung congestion with possible associated pneumonia (Fig 1, top). Given the high suspicion of endocarditis of the mitral valve and associated pneumonia, blood cultures were drawn and empiric antibiotic therapy was started. Non-invasive ventilation, nitrates and diuretics were started. Few hours later, further worsening lead to the decision to invasively ventilate the patient. Transoesophageal echocardiography (TEE) documented ruptured mitral chords with flail leaflet and massive MR, no regional wall motion abnormalities, excluding ischemic etiology; no visible vegetations (Fig 1, bottom). The patient underwent urgent surgical valve replacement: intra-operative findings documented complete chordal rupture of P2 without endocarditis. Post-operative course was uneventful; chest x-ray rapidly and completely normalized and blood cultures resulted negative, excluding the hypothesis of pneumonia and endocarditis. Discussion and conclusions: Acute severe MR is a surgical emergency. The most common causes include endocarditis, spontaneous chordal rupture in degenerative or myxomatous mitral valve and rupture or dysfunction of the papillary muscle due to acute myocardial ischemia. Classical presentation comprises acute pulmonary congestion, associated with reduced cardiac output, hypotension and shock, but findings may be subtle, mimicking other conditions such as sepsis or pneumonia. A high degree of clinical suspicion is required to make the diagnosis. Typical MR findings, such as holosystolic murmur, may be attenuated and TTE may be inconclusive in severely ill patients with eccentric regurgitant jets, often TEE is required. Medical and supportive therapy may be necessary to provide hemodynamic compensation: sodium nitroprusside reduces afterload; nitrates and diuretics reduce filling pressure; in hypotension and hemodynamic instability, intra-aortic balloon pump is indicated. In acute primary MR, valve surgery is the only effective treatment.

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