Brief Reports
Myocardial Infarction Mimicked by Acute Cholecystitis Edward T. Ryan, MD; Peter H. Pak, MD; and Roman W. DeSanctis, MD Annals of Internal Medicine.
1992;116:218-220.
Acute cholecystitis, pancreatitis, myocarditis, and pneumonia have each been associated with transient electrocardiographic changes consistent with myocardial ischemia or infarction (1-5). Although these changes usually take the form of T-wave inversions or ST-segment depressions, rare reports of ST-segment elevations do exist (1-3). We describe a patient with persistent and marked anterior ST-segment elevations without evidence of obstruction or spasm of coronary arteries, pericarditis, or myocardial cell damage. These changes resolved rapidly after removal of an acutely inflamed gallbladder. This is the first report of such ST-segment elevations to include angiographic data. Case Report A previously healthy 46-year-old man presented to the emergency department an hour after the sudden onset of a constant, substernal, nonpleuritic chest pressure. The pain began at rest, did not radiate, and was associated with nausea, vomiting, and diaphoresis. The patient's temperature was 36.1 °C; blood pressure, 110/60 mmHg; and pulse, 50 beats per minute. Results of physical examination and hematologic tests, including tests of hepatobiliary function, were normal. Roentgenographic examination of the chest showed clear lungs and no enlargement of the heart. An electrocardiogram showed ST-segment elevations in leads V, through V3 (Figure IB) compared with electrocardiographic results at baseline (Figure 1A). The patient's chest discomfort was incompletely relieved after treatment with nitroglycerine and morphine. Streptokinase was administered intravenously over 1 hour without complications. The discomfort resolved completely 20 minutes after completion of the infusion; the electrocardiogram was unchanged. Five hours after completion of the streptokinase infusion, the patient's temperature increased to 40 °C and he experienced rigors and chills. His blood pressure was 90/60 mm Hg, and his pulse was 80 beats per minute. Inspiratory crackles were present in the lower From Massachusetts General Hospital, Boston, Massachusetts: Harvard Medical School, Boston, Massachusetts. For current author addresses, see end of text. 218
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quarter of each lung field. Cardiac and abdominal examinations were unchanged. A repeat roentgenogram showed increased pulmonary vascular markings without congestive heart failure. The electrocardiogram showed increased ST-segment elevations in leads V, through V3 (Figure 1C). An emergent cardiac catheterization was done, and coronary arteries and ventricular function were found to be normal. The cardiac index was 4.1 L/min • m2, the systemic vascular resistance to 596 dynes • sec/cm~ \ and the pulmonary capillary wedge pressure was 11 to 14 mm Hg. No source of infection was evident, and echocardiographic examination showed no pericardial fluid. Examination of blood, urine, sputum, and stool and enzymatic assays of hepatic and pancreatic function were normal. The creatine phosphokinase level and erythrocyte sedimentation rate remained low. The patient's condition stabilized, but he remained febrile. Seventy-two hours after hospitalization, electrocardiographic examination showed persistent, marked STsegment elevations without the development of Q-waves. At this time, the patient began to complain of pain in the right upper quadrant; Murphy sign was present. Ultrasonographic examination showed multiple stones in a thickened gallbladder with pericholecystic fluid but without ductal dilation. Total serum bilirubin was mildly elevated at 24 ju,mol/L (1.4 mg/dL) (normal range, 0 to 17 /i,mol/L [0 to 1.0 mg/dL]). The patient had surgery, during which an acutely inflamed gallbladder was removed without complications. An electrocardiogram done 10 hours after surgery showed complete resolution of the ST-segment elevations (Figure ID). Discussion Electrocardiographic changes consistent with acute myocardial ischemia have been associated with several inflammatory conditions. Inflammation of the hepatobiliary system, pancreas, and lung as well as viral myocarditis has been noted to produce electrocardiographic injury patterns (1-6). These changes are often transient and diffuse, and they most frequently involve T-wave inversion or ST-segment depressions (1, 4, 5). Other investigators have suggested that such changes represent spasm or constriction of coronary arteries or exacerbations of underlying coronary artery disease (1, 4). Our case has several unique features. We observed in our patient biliary-tract-associated ST-segment elevations that were not diffuse but were observed in the distribution of only a single coronary artery—the anterior descending. The observed ST-segment changes were strongly suggestive of myocardial infarction, prompting the administration of thrombolytic therapy.
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Figure 1. Serial electrocardiograms. Panel A. Baseline, obtained 5 years before hospitalization. Panel B. At presentation to the emergency department with substernal chest pressure. Panel C. Patient had no pain five hours after streptokinase infusion. Panel D. After removal of the inflamed gallbladder.
Despite severe electrocardiographic abnormalities, no evidence of myocardial cell damage, coronary hypoperfusion, coronary artery spasm, myocarditis, or pericarditis was evident. Similarly, no evidence of ventricular failure was noted during ventriculography, echocardiography, or pulmonary capillary wedge measurements. The patient's ST-segment elevations were unrelated to exogenous vasopressors, and the low systemic vascular resistance precluded endogenous hypercatecholemic vasospasm or ischemia. The mechanism of such electrocardiographic elevations is unknown. It is unlikely that a coronary clot was partially lysed by the thrombolysis, because all distal lumens were clear on angiographic examination and because enzymatic assays showed no myocardial cell damage, despite persistent ST-segment elevations. Other investigators have postulated the existence of a biliary-cardiac reflex (4, 5, 7-9). In addition, bacterial infections of the lungs and acute pancreatitis have also been noted to result in similar manifestations (1, 2). Electrocardiographic elevations have been observed only in patients with hemodynamic compromise result-
ing from their inflammatory disease (1, 2, 10). Our patient also had a decreased systemic vascular resistance and increased cardiac index consistent with sepsis. It is possible that sepsis and other severe inflammatory states may alter myocardial repolarization in an as yet unknown way. Acknowledgments: The authors thank Gerard J. Nau, MD, PhD; Kathleen M. McKibbin. MD; Rachel J. Givelber, MD; Adriane P. Concus, MD; and Debra A. Bakal, MD for their contributions. Requests for Reprints: Edward T. Ryan, MD, Division of Infectious Diseases, Gray 5, Massachusetts General Hospital, Fruit Street, Boston, MA 02114. Current Author Addresses: Dr. Ryan: Division of Infectious Diseases, Gray 5, Massachusetts General Hospital, Fruit Street, Boston, MA 02114. Dr. Pak: Department of Internal Medicine, Massachusetts General Hospital, Fruit Street, Boston, MA 02114. Dr. DeSanctis: 15 Parkman Street, Suite 467, Boston, MA 02114.
References 1. Terradellas JB, Bellot JF, Saris AB, Gil CL, Torrallardona AT, Garriga JR. Acute and transient ST segment elevation during bacterial shock in seven patients without apparent heart disease. Chest. 1982;81:444-8.
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2. Fulton MC, Marriott HJ. Acute pancreatitis simulating myocardial infarction in the electrocardiogram. Ann Intern Med. 1963;59:730-2. 3. Waldman HM, Palacios IF, Hutter AM, Dec GW. Biopsy proven myocarditis mimicking acute myocardial infarction. Circulation. 1988;78(Supl II):457. 4. Krasna MJ, Flancbaum L. Electrocardiographic changes in cardiac patients with acute gallbladder disease. Am Surg. 1986;52:541-3. 5. Dickerman JL. Electrocardiographic changes in acute cholecystitis. J Am Osteopath Assoc. 1989;89:630-5. 6. Ferguson DW, Farwell AP, Bradley WA, Rollings RC. Coronary artery vasospasm complicating acute myocarditis. West J Med. 1988;148:664-9. 7. Hodge GB, Messer AL, Hill H. Effect of distension of the biliary tract on the electrocardiogram. Arch Surg. 1947;55:710-22. 8. Hampton AG, Beckwith JR, Wood JE. The relationship between heart disease and gallbladder disease. Ann Intern Med. 1957,50: 1135-45. 9. Hodge GB, Messer AL. The electrocardiogram in biliary tract disease and during experimental biliary distension: clinical observations on 26 patients. Surg Gynecol Obstet. 1948;86:617-26. 10. Weil MH, Shubin H, Biddle M. Shock caused by gram negative microorganisms: analysis of 169 cases. Ann Intern Med. 1964;60: 384-400. © 1992 American College of Physicians
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