Acute Ischemic Mitral Regurgitation
I am a huge fan of using the New England Journal of Medicine’s weekly Massachusetts General Hospital (MGH) cases as a way to keep up with medicine in general and cardiology in particular. These are interesting cases discussed by excellent clinicians. Case #23 from 2019 presented a 52-year-old man who appeared in the emergency room of the proverbial “outside hospital” with a fever of 37.7C, shortness of breath, a right upper lobe infiltrate and a prominent murmur at the right upper sternal border. His ECG showed a heart rate of 120 bpm with anterior ST segment depressions. He was treated with antibiotics and IV fluids but worsened and was sent to MGH. He was ultimately diagnosed with MINOCA (MI with nonobstructive coronary arteries) and partial rupture of the posterior medial papillary muscle (PMPM). Here are the key take home messages, some from the case discussants and some from me.
The patient had a right upper lobe infiltrate that was diagnosed as infection, but PMPM dysfunction can produce an eccentric regurgitant jet directed toward the right upper pulmonary vein. Heart failure (HF) with only a right upper lobe infiltrate is clearly unusual, but many times we see patients diagnosed with infection by CHX who have HF. We need to remember that HF can generate low-grade fevers and produce pulmonary infiltrates that look more like pneumonia than pulmonary edema. I use a couple of rules: Any patient who calls with a self-diagnosed “cold”, but who has a history of cardiac disease and a cough but no coryza has HF until proven otherwise. I make patients have a runny nose before I give them the right to diagnose their cold. Any patient treated in the ED for pneumonia who gets worse or does not get better rapidly with antibiotics and fluids has HF until proven otherwise. Also, anyone seen in the ED for pneumonia who bounces back despite antibiotics needs a HF evaluation.
The papillary muscles are the most vulnerable area of the heart for ischemic rupture because they are little peninsulas of tissue as far away as possible from the epicardial blood supply. They also have the highest oxygen consumption of any cardiac structure because they are contracting while holding onto those parachute-like leaflets.
The PMPM is more vulnerable to ischemic rupture than the anterior lateral papillary muscle because the PMPM has one source of blood supply, the posterior descending coronary artery. Partial disruption of the PMPM should always be considered in any patient with an inferior or posterior wall myocardial infarction who is not doing well.
The murmur of acute mitral regurgitation is not holosystolic so does not sound like MR. It is not holosystolic because the left atrium has not yet dilated so fills rapidly and then regurgitant flow and the murmur stop. That leads to a short, early systolic murmur that often sounds like aortic stenosis. Furthering the confusion is that it is often heard at the right upper sternal border because of the blood flow being directed into that right upper pulmonary vein and because the left atrium sits behind the aorta. The amount of regurgitation also produces severe hypoxia because the non-dilated left atrium increases pressure so rapidly that pulmonary vascular flow is greatly reduced. The rapid increase in pressure also creates the classic peaked V wave of acute MR. I tell the fellows that if a V wave looks uncomfortable to sit on, DON’T. Get a cardiac surgeon to fix the mitral valve.
So that is it. Take home messages:
1. Keep up with cardiology by reviewing the NEJM MGH cardiology cases.
2. Keep heart failure in the differential diagnosis of any pulmonary infiltrate.
3. Think of papillary muscle disruption when a patient with an inferior or posterior wall MI is not doing well.
