Sudden Deterioration Following Acute Myocardial Infarction

April 16, 2008
Ronald N. Rubin, MD

Two days before a 72-year-old woman is admitted to the cardiac care unit (CCU), she had substernal discomfort she described as "heartburn," accompanied by episodes of nausea and vomiting. She attributed her symptoms to GI upset.

Two days before a 72-year-old woman is admitted to the cardiac care unit (CCU), she had substernal discomfort she described as "heartburn," accompanied by episodes of nausea and vomiting. She attributed her symptoms to GI upset. The GI symptoms abated but significant fatigue and malaise continued, prompting a neighbor to take her to the hospital.

On admission, temperature is 38°C (100.4°F); heart rate, 110 beats per minute and regular; blood pressure, 110/70 mm Hg; and oxygen saturation, 92% on room air. Neck veins are not distended. No S3 gallop or murmurs are audible. Soft rales are heard in both lung bases. The remainder of the physical findings are unremarkable.

White blood cell count is 11,000/µL with a slight left shift. Cardiac troponin levels are normal, but the creatinine kinase level is 1400 U/L, with a cardiac creatine kinase-myocardial band fraction of 15%. The ECG shows sinus tachycardia with 3-mm ST-segment elevation and deep symmetrical T-wave inversion in leads II, III, and aVF. Acute myocardial infarction (AMI) is diagnosed. Additional leads V3R and V4R are normal.

Catheterization reveals a 100% occlusion in the proximal third of the right coronary artery; this is successfully treated with thrombolysis, dilation, and stent placement. In the remainder of the coronary artery anatomy, there is minimal narrowing that does not require intervention. The left ventricular ejection fraction is 55%.

The patient does well in the CCU for 38 hours, and her cardiac and pulmonary findings return to normal. On the afternoon of the fourth day, acute dyspnea develops. She has no new chest pain, and neither the ECG nor her cardiac enzyme levels show any evidence of new ischemia. However, cardiac examination reveals regular tachycardia (120 beats per minute), a loud S3 gallop, and a new holosystolic murmur along the left sternal border that radiates anteriorly and to the left. Rales to the scapulae are audible bilaterally, and a chest radiograph obtained emergently reveals pulmonary edema.

Which of the following best explains the patient's recent clinical findings?A. Acute endocarditis with aortic valve perforation resulting from Staphylococcus aureus endocarditis.
B. Cardiac tamponade secondary to free ventricular wall rupture.
C. Cardiogenic shock as a consequence of right ventricular infarction.
D. Ischemic papillary muscle rupture with mitral regurgitation.

(Answer on next page.)


This patient sustained a classic inferior transmural AMI 4 days before her acute deterioration. Appropriate interventions, including stenting, were performed. However, because her presentation was delayed, MI with necrosis had already occurred. Dramatic new deterioration occurred during her fourth day with the development of new and severe congestive heart failure (CHF), evident on physical examination and chest radiograph, and the appearance of a new cardiac murmur. These findings are all consistent with myocardial rupture-specifically, rupture of the posterior papillary muscle-resulting in the development of acute mitral regurgitation and acute mechanical heart failure (choice D).

Pathophysiology of myocardial rupture after AMI. The histological events that ensue after AMI explain the timing of post-MI ventricular rupture. Neutrophils appear in the infarct zone on day 1; maximal myocyte necrosis occurs from day 2 to day 5. Removal of necrotic cells begins on day 5 and reaches a maximum rate by day 14. Finally, granulation tissue accrues, and a firm scar is present by 4 weeks.1

This histological pattern correlates perfectly with clinical studies that indicate that the incidence of myocardial rupture is greatest 2 to 7 days after AMI.1,2 Rupture may be more common and may occur earlier-even on day 1-in patients who undergo thrombolysis.2Types of post-MI myocardial rupture. The most common sites of rupture are the ventricular septum (1% to 4% of affected patients) and the free wall (also 1% to 4%). Papillary muscle rupture occurs in about 1%.2 Free wall rupture (choice B) is frequently fatal. It prompts acute pericardial tamponade physiology with hypotension, pulsus paradoxus, and the ECG finding of electromechanical dissociation-cardiac electrical activity in the absence of a pulse in a moribund patient.

Ventricular septum rupture can elicit new, severe CHF. However, septal rupture almost always causes a harsh holosystolic murmur along the left sternal border and in at least half of patients induces a palpable thrill.3 Once cardiac output has severely declined, the murmur and thrill may markedly diminish and be difficult to detect.

Papillary muscle rupture can involve the inferior or the anterior papillary muscle. Rupture of the inferior papillary muscle is more common and is associated with inferior or right coronary artery infarction; rupture of the anterior papillary muscle is associated with anterior myocardial infarction or infarction of marginal or obtuse branches of the left coronary artery. Rupture results in acute disruption of the papillary muscle apparatus, which gives rise to acute mitral regurgitation.2,4 A new holosystolic murmur at the base is audible with radiation either anteriorly (if the inferior papillary muscle is destroyed) or posteriorly (if the anterior muscle is involved). Unlike the auscultatory sounds caused by septal rupture, the associated murmur is soft and thrills are rare.2,4Other causes of acute deterioration after AMI. Right ventricular infarction (choice C) is another acute cause of CHF after AMI. In this scenario, the infarcted right ventricle cannot effectively fill the left heart and cardiac output diminishes. The ECG pattern associated with right ventricle infarction is very different from that seen in this patient: it includes ST-segment elevation in V1 through V4 and is confirmed by ST-segment elevation in V3R and V4R in suspect cases. These findings are not present on this patient's tracing. Also, a new murmur is typically not present in right ventricular infarction.

Aortic valve perforation (choice A) is a dreaded complication of infective endocarditis, especially to be feared when the latter is caused by aggressive organisms, such as S aureus. This patient has no obvious risk factors for endocarditis. Her fever was low-grade and brief, related to her AMI. Moreover, she had a systolic murmur rather than the diastolic murmur that would be expected with aortic regurgitation.

Outcome of this case. A bedside echocardiogram confirmed new, severe mitral valve regurgitation as the result of a ruptured inferior papillary muscle. Left ventricular ejection fraction was 40% with roughly half of cardiac output via the mitral regurgitation. After a second catheterization to better delineate the anatomy and physiology, an aortic balloon pump was placed. The patient underwent urgent mitral valve replacement. She was discharged on day 24.




Fishbein MC, Maclean D, Maroko PR. The histopathologic evolution of myocardial infarction. Chest. 1978;73:843-849.


Johnson PA, Jaffer FA, Neilan TG, et al. Case records of the Massachusetts General Hospital. Case 34-2006. A 72-year-old woman with nausea followed by hypotension and respiratory failure. N Engl J Med. 2006;355:2022-2031.


Birnbaum Y, Fishbein MC, Blanche C, Siegel RJ. Ventricular septal rupture after acute myocardial infarction. N Engl J Med. 2002;347:1426-1432.


Carabello BA, Crawford FA Jr. Valvular heart disease. N Engl J Med. 1997;337:32-41.

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