acute mitral regurgitation MR following STEMI

This patient has acute severe mitral regurgitation (MR) secondary to acute papillary muscle rupture, a complication of her recent ST-elevation myocardial infarction. Because she is in cardiogenic shock, the insertion of an intraaortic balloon pump (IABP) as a bridge to surgical mitral valve replacement (definitive treatment) is the best next step to optimize her hemodynamics preoperatively (choice A is correct).

The clinical presentation of acute pulmonary edema with hypoxemic respiratory failure and cardiogenic shock 2 to 7 days after completion of an ST-elevation myocardial infarction is highly suggestive of severe acute MR from acute papillary muscle rupture. Additional clinical findings supportive of this diagnosis include her jugular venous distension with V wave, a systolic murmur, and signs of cardiogenic shock (cool extremities). Transthoracic echocardiography performed at a time of her acute decompensation demonstrated new severe MR (4+ MR) with a severe posterior MR jet. She underwent right-sided heart catheterization; pulmonary capillary wedge pressure of 34 mm Hg with V wave decreased to 22 mm Hg after IABP placement, and she ultimately underwent a surgical mitral valve replacement.

Mechanical complications after acute myocardial infarctions (AMIs) are infrequent, yet they are associated with high mortality rates and require urgent surgical interventions, often using temporary mechanical circulatory support as a bridge to definitive treatment. Therefore, it is important for critical care doctors to recognize acute mechanical complications of AMI and initiate management strategies to stabilize the patient as a bridge to the definitive surgical intervention. Acute mechanical complications of AMI include papillary muscle rupture with acute MR, ventricular septal defect, and rupture of the ventricular free wall.

Acute papillary muscle rupture causing acute MR has an associated mortality rate of 10% to 40% and typically manifests with acute hemodynamic decompensation and acute pulmonary edema within 2 to 5 days of an inferior or lateral wall myocardial infarct. Management is aimed at improving the patient’s hemodynamics by reducing left ventricular afterload, thus preferentially directing blood flow across the aortic valve, which reduces MR, increases cardiac output, and decreases pulmonary venous congestion. Infusion of vasodilators, such as nitroglycerin, nicardipine, or sodium nitroprusside, to reduce afterload are often limited by systemic hypotension. In patients who are hemodynamically unstable, the 2020 American College of Cardiology/American Heart Association guidelines recommend the insertion of an IABP to reduce left ventricular afterload and augment cardiac output through balloon counterpulsation. 

Venovenous extracorporeal membrane oxygenation (ECMO) is used to support respiratory gas exchange, and although she has hypoxemic respiratory failure, it is in the setting of pulmonary edema from acute, severe MR, and she is in cardiogenic shock. Venovenous ECMO does not provide circulatory support and is therefore not indicated in the management of severe, acute MR with hemodynamic instability (choice D is incorrect). Peripheral venoarterial ECMO does provide circulatory support; however, the retrograde flow from the femoral arterial cannula towards the aortic valve will increase afterload and may exacerbate pulmonary edema from her severe acute MR. Thus, venoarterial ECMO in isolation would also not be the optimal management strategy in this patient.

Mitral valve transcatheter edge-to-edge repair to clip anterior and posterior leaflets of the mitral valve is indicated in patients with chronic primary MR with severe symptoms who have a high surgical risk and in chronic secondary (functional) MR (choice B is incorrect).

Percutaneous coronary intervention would be indicated if her acute decompensation was due to acute thrombosis of her right circumflex artery stent. Her ECG has elevations in II, III, and aVF; however, her ECG was unchanged from prior ECGs, and although her troponin and creatine phosphokinase levels were elevated, they were trending down (choice C is incorrect).123

Footnotes

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  2. Damluji AA, van Diepen S, Katz JN, et al; American Heart Association Council on Clinical Cardiology; Council on Arteriosclerosis, Thrombosis and Vascular Biology; Council on Cardiovascular Surgery and Anesthesia; and Council on Cardiovascular and Stroke Nursing. Mechanical complications of acute myocardial infarction: a scientific statement from the American Heart Association. Circulation. 2021;144(2):e16-e35. PubMed ↩

  3. Otto CM, Nishimura RA, Bonow RO, et al. 2020 ACC/AHA guideline for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2021;143(5):e72-e227. PubMed ↩