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Sudden Deterioration Following Acute Myocardial Infarction

Sudden Deterioration Following Acute Myocardial Infarction

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.)


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