Posteromedial Papillary Muscle Rupture Associated with Inferoposterior Wall Myocardial Infarction

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IMAGE SECTION Posteromedial Papillary Muscle Rupture Associated with Inferoposterior Wall Myocardial Infarction NASIR SHAIKH, M.D., NAJEEB UR REHMAN, M.D., and RICHARD S. GRODMAN, M.D. Department of Medicine, Division of Cardiology, St. Vincent’s Medical Center of Richmond, Staten Island, New York, a Teaching Hospital of New York Medical College, Valhalla, New York cardiogenic shock, posteromedial papillary muscle rupture, subacute inferoposterior myocardial infarction We present the case of a patient who presented with cardiogenic shock secondary to posterome- dial papillary muscle rupture associated with subacute inferoposterior myocardial infarction. Case Report A 40-year-old man with no significant risk factors for coronary artery disease presented to the emergency department with severe dys- pnea and dizziness of 4 hours’ duration. He denied any chest pain at that time but had been seen in the emergency department 9 days earlier with atypical chest pain of 24 hours’ duration. There had been no ischemic changes on the electrocardiogram (ECG), and he was discharged home. This time, he was found to be hypotensive and in pulmonary edema with a modest mitral regurgitation (MR)murmur. His ECG showed evidence of subacute inferoposte- rior myocardial infarction. He was endotrache- ally intubated, mechanically ventilated, and treated with vasopressor drugs. Transthoracic (technically limited) and transesophageal echo- cardiograms were performed immediately and showed evidence of rupture of the left ventric- ular posteromedial papillary muscle with free flow of the chordal segment and papillary mus- Address for correspondence and reprint requests: Richard S. Grodman, M.D., Division of Cardiology, St. Vincent’s Medical Center of Richmond, 355 Bard Avenure, Staten Island, NY 10310. Fax: 718-876-2755. cle head into the left atrium (LA) (Figs. 1 and 2). MR appeared to be mild to moderate by Doppler color flow mapping of the regurgitant jet area, but the width of the vena contracta was 6-7 mm, which is consistent with more severe MR. Neither a pulmonary venous flow sample nor a proximal flow conversion zone estimate of the severity of MR was obtained. There was severe hypokinesia of posterior wall of the left ventricle (LV). The patient continued to be hypotensive and in cardiogenic shock. An intraaortic balloon pump was inserted immedi- ately at the bedside, but there was no improve- ment in hemodynamic status. Before the pa- tient could be transferred to another institu- tion where cardiothoracic surgery could be performed, he had cardiac arrest and could not be resuscitated. The family refused consent for postmortem examination. Discussion Rupture of the papillary muscle is a rare but often fatal complication of acute myocardial in- farction, usually occurring 2-7 days after the ini- tial event and accounting for 5% of all deaths from acute myocardial infarction (AMI).Isolated cases have been reported as a result of syphilis, endocarditis, and trauma. Unlike acute ventric- ular septa1 defect, papillary muscle rupture oc- curs with relatively small infarctions in approx- imately half of cases, suggesting that relatively good LV systolic function may result in a greater sheering force at the site of the rupture. Com- Vol. 16, No. 3, 1999 ECHOCARDIOGRAPHY: A Jrnl. of CV Ultrasound & Allied Tech. 269

Transcript of Posteromedial Papillary Muscle Rupture Associated with Inferoposterior Wall Myocardial Infarction

Page 1: Posteromedial Papillary Muscle Rupture Associated with Inferoposterior Wall Myocardial Infarction

IMAGE SECTION

Posteromedial Papillary Muscle Rupture Associated with Inferoposterior Wall Myocardial Infarction

NASIR SHAIKH, M.D., NAJEEB UR REHMAN, M.D., and RICHARD S. GRODMAN, M.D. Department of Medicine, Division of Cardiology, St. Vincent’s Medical Center of Richmond, Staten Island, New York, a Teaching Hospital of New York Medical College, Valhalla, New York

cardiogenic shock, posteromedial papillary muscle rupture, subacute inferoposterior myocardial infarction

We present the case of a patient who presented with cardiogenic shock secondary to posterome- dial papillary muscle rupture associated with subacute inferoposterior myocardial infarction.

Case Report

A 40-year-old man with no significant risk factors for coronary artery disease presented to the emergency department with severe dys- pnea and dizziness of 4 hours’ duration. He denied any chest pain at that time but had been seen in the emergency department 9 days earlier with atypical chest pain of 24 hours’ duration. There had been no ischemic changes on the electrocardiogram (ECG), and he was discharged home. This time, he was found to be hypotensive and in pulmonary edema with a modest mitral regurgitation (MR) murmur. His ECG showed evidence of subacute inferoposte- rior myocardial infarction. He was endotrache- ally intubated, mechanically ventilated, and treated with vasopressor drugs. Transthoracic (technically limited) and transesophageal echo- cardiograms were performed immediately and showed evidence of rupture of the left ventric- ular posteromedial papillary muscle with free flow of the chordal segment and papillary mus-

Address for correspondence and reprint requests: Richard S. Grodman, M.D., Division of Cardiology, St. Vincent’s Medical Center of Richmond, 355 Bard Avenure, Staten Island, NY 10310. Fax: 718-876-2755.

cle head into the left atrium (LA) (Figs. 1 and 2). MR appeared to be mild to moderate by Doppler color flow mapping of the regurgitant jet area, but the width of the vena contracta was 6-7 mm, which is consistent with more severe MR. Neither a pulmonary venous flow sample nor a proximal flow conversion zone estimate of the severity of MR was obtained. There was severe hypokinesia of posterior wall of the left ventricle (LV). The patient continued to be hypotensive and in cardiogenic shock. An intraaortic balloon pump was inserted immedi- ately at the bedside, but there was no improve- ment in hemodynamic status. Before the pa- tient could be transferred to another institu- tion where cardiothoracic surgery could be performed, he had cardiac arrest and could not be resuscitated. The family refused consent for postmortem examination.

Discussion

Rupture of the papillary muscle is a rare but often fatal complication of acute myocardial in- farction, usually occurring 2-7 days after the ini- tial event and accounting for 5% of all deaths from acute myocardial infarction (AMI). Isolated cases have been reported as a result of syphilis, endocarditis, and trauma. Unlike acute ventric- ular septa1 defect, papillary muscle rupture oc- curs with relatively small infarctions in approx- imately half of cases, suggesting that relatively good LV systolic function may result in a greater sheering force at the site of the rupture. Com-

Vol. 16, No. 3, 1999 ECHOCARDIOGRAPHY: A Jrnl. of CV Ultrasound & Allied Tech. 269

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SHAIKH, REHMAN, AND GRODMAN

plete transection of the LV papillary muscle is usually incompatible with life because of the sud- den massive MR, which is usually characterized by the dramatic onset of cardiogenic shock and a new systolic murmur. The murmur may not be impressive because of the early equalization of the LV and LA pressures and a large regurgitant orifice producing insufficient turbulence. As the blood pressure falls, the murmur may become softer and even disappear. Thus, the diagnosis depends on a high index of suspicion.1 Similarly, the severity of acute severe MR may be underes- timated by standard Doppler color flow mapping techniques2 due to the brevity of the regurgitant signal and perhaps other factors present in a severely hypotensive patient whose LA and LV systolic pressures have equalized. In this situa- tion, the width of the vena contracta may be of more value because the regurgitant orifice is ex- pected to be large. Echocardiography, especially transesophageal echocardiography, helps to di- agnose and differentiate papillary muscle rup- ture from other less severe forms of MR and other mechanical complications of AMI. The sev- ered papillary muscle head seen moving freely in the heart or the flail mitral leaflet with systolic prolapse into the left atrium, usually in the pres-

Figure 1. Transesophageal echocardiogram, mul- tiplane (138 degrees) esophageal view, showing both ends of the transected posteromedial papillary mus- cle head (*) within the left ventricle at end-diastole. AR = aortic root; L A = left atrium; LV = left ventri- cle; MV = mitral valve; RV = right ventricle.

Figure 2. Transesophageal echocardiogram, hori- zontal (0 degrees) four-chamber esophageal view, showing the chordal end of the transected posterome- dial papillary muscle head (*) fully protruding into the left atrium (LA) at end-systole. AR = aortic root.

ence of preserved LV systolic function, suggests papillary muscle r ~ p t u r e . ~ Medical therapy, in- cluding vasodilators (if blood pressure allows) and intra-aortic balloon counterpulsation for he- modynamically unstable patient, should be insti- tuted early. Patients requiring pharmacological and mechanical support, as was the case with our patient, should undergo immediate cardiac surgery (consisting of mitral valve repairhe- placement with or without coronary artery by- pass graft. surgery), which may be life saving.

References

Samman B, Korr KS, Katz AS, et al: Pitfalls in the diagnosis and management of papillary muscle rupture: A study of four cases and re- view of the literature. Clin Cardiol 1995;18:

Smyllie JH, Sutherland GR, Geuskens R, et al: Doppler color flow mapping in the diagnosis of ventricular septa1 rupture and acute mitral re- gurgitation after myocardial infarction. J Am Coll Cardiol 1990;15:1449-1455. Moursi MH, Bhatnagar SK, Vilacosta I, et al: Transesophageal echocardiographic assessment of papillary muscle rupture. Circulation 1996;

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