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Papillary Muscle Rupture Complicating Acute Myocardial Infarction

Papillary Muscle Rupture Complicating Acute Myocardial Infarction

Niranjan Seshadri MD, Sasan Ghaffari MD, William J. Stewart MD
Department of Cardiology, Heart and Vascular Institute, Cleveland Clinic 

Introduction
Papillary muscle rupture (PMR) is an infrequent but potentially devastating complication of acute myocardial infarction (AMI). It is important to recognize this complication early because surgical repair is possible and life saving in most cases. We present a case illustrating this mechanical complication of AMI.

Case report
A 74-year old female presented to the emergency room with chest pain of 12 hours’ duration. Past medical history was remarkable for asthma, idiopathic pulmonary fibrosis (on chronic maintenance steroids for the past 3 years), hypertension and diabetes mellitus. In addition she had undergone a left heart catheterization (LHC) 10 years earlier which was reported to be normal.

The patient was admitted to the coronary care unit (CCU) with a diagnosis of non-ST segment elevation myocardial infarction (peak CKMB 223, troponin T 1.18) and became chest pain free on aspirin, intravenous (IV) heparin, beta-blockers, IV nitrates and eptifibatide. About 12 hours after admission to the CCU she reexperienced severe chest pain and rapidly became hypotensive and went into cardiogenic shock. A transthoracic echo showed rupture of the anterolateral papillary muscle with severe 4+ mitral regurgitation (MR) (Figures 1-4). A prompt surgical consultation was obtained and an intraaortic balloon pump (IABP) was inserted. An emergent LHC showed severe 3 vessel atherosclerotic coronary artery disease (Figures 5-6). The patient underwent a mitral valve replacement (#27 Carpentier-Edwards valve) and coronary artery bypass grafting. She was discharged in good condition on the 10th postoperative day.

Figure 1

Figure 2

Figure 3

Figure 4

Figure 5

Figure 6

FIGURE LEGENDS

Figure 1: Transthoracic apical 4 chamber view (LA= left atrium, LV= left ventricle, RA= right atrium, RV= right ventricle) showing a portion of the ruptured anterolateral papillary muscle attached to the anterior mitral leaflet.

Figure 2: Transthoracic apical 4 chamber view (LA= left atrium, LV= left ventricle) with a close-up of the mitral valve apparatus in systole showing the ruptured anterolateral papillary muscle attached to the anterior mitral leaflet (arrow).

Figure 3: Transthoracic apical 4 chamber view (LA= left atrium, LV= left ventricle) with a close-up of the mitral valve apparatus in diastole showing the ruptured anterolateral papillary muscle attached to the anterior mitral leaflet (arrow).

Figure 4: Transthoracic apical 4 chamber view (LA= left atrium, LV= left ventricle, RA= right atrium, RV= right ventricle) with color flow imaging showing severe 4+ mitral regurgitation.

Figure 5: Coronary angiography demonstrating the left anterior descending (A) and left circumflex coronary (B) arteries in the left anterior oblique projection with severe narrowings in the proximal portions of both arteries (arrows).

Figure 6: Coronary angiography demonstrating severe narrowing of the proximal portion of the right coronary artery in the left anterior oblique projection (arrow).

Discussion

Following AMI, MR is relatively common and often has variable clinical severity. The presence of post-infarct MR, irrespective of the hemodynamic burden, is associated with a worse prognosis 1. MR due to PMR entails <5% of ischemic MR and is a potentially catastrophic complication, usually occurring 2-7 days post AMI 2. The incidence of this complication is 1% of all AMIs and accounts for 5% of the mortality following AMI 3 4. PMR is more common with inferior AMI and the use of thrombolytics has decreased its incidence, however, it tends to occur earlier 3. The posteromedial papillary muscle is more frequently involved due to its single blood supply via the posterior descending coronary artery. The anterolateral papillary muscle has dual blood supply from both the left anterior descending (LAD) and left circumflex (LCX) coronary arteries. In our patient, both the LAD and LCX coronary arteries were severely stenosed resulting in compromised blood flow to the anterolateral papillary muscle (Figures 5-6). A high index of suspicion is the key to early diagnosis and prompt management in a hemodynamically compromised patient with AMI. A new pansystolic murmur may be audible on physical examination. However, the murmur may be soft or inaudible in severe cases due to rapid equalization of left atrial and left ventricular pressures. Advances in echocardiography have made it the key diagnostic modality. Transthoracic views are usually adequate, but a transesophageal echo may be required in a few cases. Treatment includes aggressive medical therapy with vasodilators and IABP as a bridge to immediate surgical treatment. In one series, perioperative mortality was 27%, and both short- and long-term post-operative mortality was influenced by the presence of left ventricular dysfunction 5.

In conclusion, papillary muscle rupture following acute myocardial infarction is a rare but serious complication warranting immediate recognition and aggressive medical therapy as a bridge to urgent surgical intervention.

Comments from Dr. Eric Topol:

This is a prototypic case of an elderly female with acute MI complicated by PMR. The key was rapid diagnosis with full hemodynamic support and urgent triage to surgery. Fortunately she did well and her course reflects a better than expected outcome. In the era or reperfusion therapy, PMR is less likely to occur---but in patients who have unsuccessful reperfusion, or present too late to receive this therapy, we need to be on the lookout.

References:

  1. Maisel AS, Gilpin EA, Klein L, Le Winter M, Henning H, Collins D. The murmur of papillary muscle dysfunction in acute myocardial infarction: clinical features and prognostic implications. American Heart Journal 1986; 112:705-11.
  2. Lehmann KG, Francis CK, Dodge HT. Mitral regurgitation in early myocardial infarction. Incidence, clinical detection, and prognostic implications. TIMI Study Group [published erratum appears in Ann Intern Med 1992 Aug 15;117(4):349] [see comments]. Annals of Internal Medicine 1992; 117:10-7.
  3. Reeder GS. Identification and treatment of complications of myocardial infarction. Mayo Clinic Proceedings 1995; 70:880-4.
  4. Manning WJ, Waksmonski CA, Boyle NG. Papillary muscle rupture complicating inferior myocardial infarction: identification with transesophageal echocardiography. American Heart Journal 1995; 129:191-3.
  5. Kishon Y, Oh JK, Schaff HV, Mullany CJ, Tajik AJ, Gersh BJ. Mitral valve operation in postinfarction rupture of a papillary muscle: immediate results and long-term follow-up of 22 patients [see comments]. Mayo Clinic Proceedings 1992; 67:1023-30.

Address for correspondence:
William J. Stewart MD
Cleveland Clinic/ Desk F15
9500 Euclid Avenue
Cleveland, Ohio 44195
Phone: (216) 444 5923