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ACUTE HYPOXIC RESPIRATORY FAILURE SECONDARY TO ACUTE PAPILLARY MUSCLE RUPTURE
1039 JACC April 5, 2016 Volume 67, Issue 13
FIT Clinical Decision Making ACUTE HYPOXIC RESPIRATORY FAILURE SECONDARY TO ACUTE PAPILLARY MUSCLE RUPTURE Oral Contributions Room S503 Sunday, April 03, 2016, 8:30 a.m.-8:50 a.m. Session Title: FIT Forum: Stump the Professor Abstract Category: Heart Failure and Cardiomyopathies Presentation Number: 906-08 Authors: Jeremy S. Pollock, Tala Al-Talib, Christopher DeFilippi, University of Maryland Medical Center, Baltimore, MD, USA
Background: Papillary muscle rupture is an emergent complication after acute myocardial infarction that typically occurs two to seven days after the event. Diagnosis is usually made by transthoracic echocardiography (TTE), but sometimes requires transecophageal echocardiography (TEE).
Case: An 88 year old male presented with two weeks of progressively worsening shortness of breath and chest pain. His medical history included rheumatoid arthritis, hypertension and hyperlipidemia. Troponin was found to be elevated, and he was brought for urgent left heart catheterization which found left main and triple-vessel disease. An intra-aortic balloon pump was placed and he was referred for coronary artery bypass grafting. His oxygenation continued to worsen, and a stat TTEwas ordered. Physical examination at the time of the TTE showed signs of left-sided heart failure: sp02 of 88% on non-rebreather mask, blood pressure of 85/60, elevated jugular venous pulse, a soft 2/6 holosystolic murmur best heard at the base, an S3, bilateral pulmonary crackles to the mid-thorax, and peripheral edema. Decision Making: Stat TTE performed by the on-call fellow revealed a preserved ejection fraction (60%) with anterior wall hypokinesis, normal RV function, mild mitral regurgitation, and no pericardial effusion. Given the profound hypoxia in setting a recent NSTEMI, we had a high clinical suspicion for acute mitral regurgitation as the etiology for his oxygenation issues. We proceeded to a TEE which revealed a rupture of the anterolateral papillary muscle and a flail anterior leaflet with associated severe, eccentric mitral regurgitation. The patient was taken for emergent mitral valve repair and three-vessel cabg. He tolerated the procedure well, and was able to be discharged to a rehabilitation center seven days later.
Conclusions: This case demonstrates the importance of not only maintaining a high clinical suspicion for acute mitral regurgitation in a patient that is post acute coronary syndrome who presents with profound hypoxia, but also continuing investigation with a TEE despite lack of MR or a flail leaflet on TTE.
FIT Clinical Decision Making ACUTE HYPOXIC RESPIRATORY FAILURE SECONDARY TO ACUTE PAPILLARY MUSCLE RUPTURE Oral Contributions Room S503 Sunday, April 03, 2016, 8:30 a.m.-8:50 a.m. Session Title: FIT Forum: Stump the Professor Abstract Category: Heart Failure and Cardiomyopathies Presentation Number: 906-08 Authors: Jeremy S. Pollock, Tala Al-Talib, Christopher DeFilippi, University of Maryland Medical Center, Baltimore, MD, USA
Background: Papillary muscle rupture is an emergent complication after acute myocardial infarction that typically occurs two to seven days after the event. Diagnosis is usually made by transthoracic echocardiography (TTE), but sometimes requires transecophageal echocardiography (TEE).
Case: An 88 year old male presented with two weeks of progressively worsening shortness of breath and chest pain. His medical history included rheumatoid arthritis, hypertension and hyperlipidemia. Troponin was found to be elevated, and he was brought for urgent left heart catheterization which found left main and triple-vessel disease. An intra-aortic balloon pump was placed and he was referred for coronary artery bypass grafting. His oxygenation continued to worsen, and a stat TTEwas ordered. Physical examination at the time of the TTE showed signs of left-sided heart failure: sp02 of 88% on non-rebreather mask, blood pressure of 85/60, elevated jugular venous pulse, a soft 2/6 holosystolic murmur best heard at the base, an S3, bilateral pulmonary crackles to the mid-thorax, and peripheral edema. Decision Making: Stat TTE performed by the on-call fellow revealed a preserved ejection fraction (60%) with anterior wall hypokinesis, normal RV function, mild mitral regurgitation, and no pericardial effusion. Given the profound hypoxia in setting a recent NSTEMI, we had a high clinical suspicion for acute mitral regurgitation as the etiology for his oxygenation issues. We proceeded to a TEE which revealed a rupture of the anterolateral papillary muscle and a flail anterior leaflet with associated severe, eccentric mitral regurgitation. The patient was taken for emergent mitral valve repair and three-vessel cabg. He tolerated the procedure well, and was able to be discharged to a rehabilitation center seven days later.
Conclusions: This case demonstrates the importance of not only maintaining a high clinical suspicion for acute mitral regurgitation in a patient that is post acute coronary syndrome who presents with profound hypoxia, but also continuing investigation with a TEE despite lack of MR or a flail leaflet on TTE.