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Myocardial Infarction After Dog Bite glance suggest transmural ischemia and an acute inferolateral myocardial infarction, it is uncharacteristic to find ST elevation in lead I and an upsloping ST segment in V2 and V3, rather than reciprocal ST depression given this degree of ST elevation in inferolateral leads; (2) echocardiography showed diffuse left ventricular hypokinesia and not the typical regional akinesia expected with an inferolateral infarction; and (3) in the absence of embolic endocarditis or severe sustained hypotension, there is no plausible pathogenic link (and the authors suggest none) between bacteremia/disseminated intravascular coagulation and the acute occlusion of an epicardial coronary artery leading to myocardial infarction, and the latter is rarely, if ever, described as a complication of the former. The far more likely diagnosis is toxic-infectious myocarditis, which can notoriously mimic acute myocardial infarction.2 Acute myocarditis would better account for the atypical ECG features and the diffuse left ventricular hypokinesia in the context of a severe systemic clinical presentation. Downloaded from http://circ.ahajournals.org/ by guest on June 16, 2017 To the Editor: We do not agree with the diagnosis of myocardial infarction in the case of a 36-year-old man 2 days after a dog bite1. For several reasons, we believe that the patient had myopericarditis rather than myocardial infarction. First, the patient had symptoms, signs, and laboratory findings consistent with sepsis, and blood cultures yielded Capnocytophaga canimorsus. Myocardial infarction occurs occasionally in patients with bacteremia, and it usually results from sepsisassociated hypotension or from endocarditis with septic embolism to the coronary arteries. However, viral and bacterial infections are more commonly the cause of pericarditis and myocarditis.2,3 ECG patterns of acute myopericarditis are known to resemble those seen with acute myocardial infarction.4 The presented ECG demonstrated ST elevations in both anterior and inferior leads in a manner consistent with the pattern found in acute myopericarditis.4,5 Second, the absence of regional wall motion abnormalities and the documentation of diffuse hypokinesia with left ventricular systolic dysfunction are typically seen in myopericarditis. Abnormal regional wall motion is nearly universally present in acute myocardial infarction. Presentation with chest discomfort and laboratory examinations with elevated levels of creatine kinase and raised troponin-I concentrations are consistent with myopericarditis as well as with myocardial infarction. Third, coronary angiography demonstrating normal vessels without signs of atherosclerosis is also consistent with the diagnosis of myopericarditis. This finding makes acute myocardial infarction less likely but does not definitely rule out previous coronary artery occlusion. In summary, we think that the diagnosis of acute myopericarditis is more likely than acute myocardial infarction in the reported case.1 Peter Bogaty, MD Quebec Heart Institute/Laval Hospital 25 Chemin Ste-Foy Ste-Foy, Quebec, Canada G1V 4G5 [email protected] 1. Scharf C, Widmer U. Myocardial infarction after dog bite. Circulation. 2000;102:713–714. 2. Narula J, Khaw BA, Dec GW Jr, et al. Brief report: recognition of acute myocarditis masquerading as acute myocardial infarction. N Engl J Med. 1993;328:100 –104. Myocardial Infarction After Dog Bite To the Editor: I read with interest the report by Scharf et al1 of a 36-year-old man with an acute myocardial infarction presenting 2 days after a dog bite that was associated with leucocytosis and elevated C-reactive protein (CRP). Although I agree with the authors that infection and bacteremia may precipitate an acute myocardial infarction,2 I disagree with their statement that “it usually results from hypotension or from endocarditis with septic emboli to the coronary arteries.” None of my patients with pharyngitis and consequent acute myocardial infarction had hypotension or evidence of endocarditis, and those catheterized had normal or minor coronary artery disease.2 Inflammation, both local and systemic, plays a role in plaque vulnerability. Inflammation at the systemic level leads to elevated CRP and amyloid A levels and to activation of monocytes and adhesion molecules,3,4 all of which have been associated with acute coronary syndromes. Thus, the inflammatory response to the dog bite and the elevated CRP and leucocytosis, among other factors, led to endothelial dysfunction and changes in circulating clotting factors such as fibrinogen, which led to an increased clotting tendency and thrombotic coronary occlusion.5 Because no intravascular ultrasound was done, a minor atheroma instability or small plaque rupture associated with the inflammatory response cannot be excluded. Johann Auer, MD Robert Berent, MD Bernd Eber, MD Department of Cardiology and Intensive Care General Hospital Wels Wels, Austria 1. Scharf C, Widmer U. Myocardial infarction after dog bite. Circulation. 2000;102:713–714. 2. Lorell BH, Braunwald E. Pericardial disease. In: Braunwald E, ed. Heart Disease. 4th ed. Philadelphia: Saunders; 1992:1465–1472. 3. Zayas R, Anguita M, Torres F, et al. Incidence of specific etiology and role of methods for specific etiologic diagnosis of primary acute pericarditis. Am J Cardiol. 1995;75:378 –382. 4. Goldberger AL, Goldberger E. Miscellaneous ECG patterns: pericarditis and pericardial effusion; myocarditis. In: Goldberger AL, Goldberger E, eds. Clinical Electrocardiography. 5th ed. St Louis: Mosby Year Book; 1994:131–133. 5. Eber B, Auer J, Berent R. Perikarditis. In: Eber B, ed. EKG: Einfach, Kurz, Genau. 2nd ed. Graz, Austria: Leykam; 1998:51. Myocardial Infarction After Dog Bite Edward G. Abinader, MD, FRCPI Bnai-Zion Medical Center Medical Faculty, Technion Golomb Street 47 Haifa, Israel To the Editor: Scharf and Widmer describe a case of dog bite resulting in sepsis, implicating the Gram-negative bacteria Capnocytophaga canimorsus, with accompanying chest discomfort, ST-segment elevation, and a cardiac enzyme rise.1 They conclude that myocardial infarction occurred as a complication of bacteremia “in the absence of both hypotension and endocarditis.” They did not consider another possibility that should have entered into the differential diagnosis given the following elements of the clinical presentation: (1) although the presenting ECG might at first 1. Scharf C, Widmer U. Myocardial infarction after dog bite. Circulation. 2000;102:713–714. 2. Abinader EG, Sharif D, Omary M. Inferior wall myocardial infarction preceded by acute exudative pharyngitis in young males. Isr J Med Sci. 1993;29:764 –769. 1 2 Correspondence 3. Liuzzo G, Biasucci LM, Gallimore JR, et al. The prognostic value of C-reactive protein and serum amyloid A protein in severe unstable angina. N Engl J Med. 1994;331:417– 424. 4. Mazzone A, De Servi S, Ricevuti G, et al. Increased expression of neutrophil and monocyte adhesion molecules in unstable coronary artery disease. Circulation. 1993;88:358 –363. 5. Meier CR, Jick SS, Derby LE, et al. Acute respiratory-tract infections and risk of first-time acute myocardial infarction. Lancet. 1998;351: 1467–1471. Response Downloaded from http://circ.ahajournals.org/ by guest on June 16, 2017 Differentiation between myocarditis and infarction cannot be made easily, and the gold standard for a positive diagnosis of myopericarditis would be a myocardial biopsy, which was not available in our patient. We still favor the diagnosis of myocardial infarction for the following reasons. The picture of the patient’s nose, together with laboratory results of disseminated intravascular coagulation, are signs of microvascular thrombosis with cutaneous and systemic manifestations. The hemorrhagic skin lesions developed at the same time as the myocardial necrosis (ie, a few hours before admission). Therefore we assume that infectious-triggered disseminated intravascular coagulation caused microvascular thrombosis and myocardial infarction initially in the inferolateral region, with subsequent spread over more than one area supplied by the main 3 coronary arteries. The occlusion of multiple small coronary vessels explains the global hypokinesia and the normal coronary angiogram. Most importantly, several other cases illustrate acute myocardial infarction after dog bite. In one case, typical chest pain and ST elevation appeared 1 day before fever and systemic infection.1 In another patient, acute coronary thrombosis was documented angiographically 3 weeks after dog bite. The patient had no signs of infection and was discharged after 10 days but had to be readmitted when blood cultures yielded Capnocytophaga canimorsus.2 In conclusion, Capnocytophaga canimorsus sepsis can rarely present as a distinct clinical pattern with disseminated intravascular coagulation and widespread capillary thrombosis, similar to Waterhouse-Friderichsen syndrome or thrombotic thrombocytopenic purpura,3 which can lead to extensive gangrene4 and a mortality ⬎30%.5 Clinical diagnosis before time-consuming microbiological isolation is mandatory to insure early antibiotic treatment. The old Roman mosaic in the “House of the Tragic Poet” in the ruins of Pompeii with the engraved Latin comment cave canem (beware of dog) and our images should be kept in mind when taking care of patients with signs of acute myocardial infarction after animal bites. Christoph Scharf, MD Urs Widmer, MD Department of Medicine University Hospital CH-8091 Zurich Switzerland 1. Ehrbar HU, Gubler J, Harbarth S, et al. Capnocytophaga canimorsus sepsis complicated by myocardial infarction in two patients with normal coronary arteries. Clin Infect Dis. 1996;23:335–336. 2. Newton NL, Sharma B. Acute myocardial infarction associated with DF-2 bacteremia after a dog bite. Am J Med Sci. 1986;291:352–354. 3. Scarlett JD, Williamson HG, Dadson PJ, et al. A syndrome resembling thrombotic thrombocytopenic purpura associated with Capnocytophaga canimorsus septicemia. Am J Med. 1991;90:127–128. 4. Kullberg BJ, Westendorp RG, van Meinders AE. Purpura fulminans and symmetrical peripheral gangrene caused by Capnocytophaga canimorsus (formerly DF-2) septicemia: a complication of dog bite. Medicine (Baltimore). 1991;70:287–292. 5. Pers C, Gahrn HB, Frederiksen W. Capnocytophaga canimorsus septicemia in Denmark, 1982–1995: review of 39 cases. Clin Infect Dis. 1996;23:71–75. Myocardial Infarction After Dog Bite Johann Auer, Robert Berent and Bernd Eber Circulation. 2001;103:e95 doi: 10.1161/01.CIR.103.18.e95 Downloaded from http://circ.ahajournals.org/ by guest on June 16, 2017 Circulation is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231 Copyright © 2001 American Heart Association, Inc. All rights reserved. Print ISSN: 0009-7322. Online ISSN: 1524-4539 The online version of this article, along with updated information and services, is located on the World Wide Web at: http://circ.ahajournals.org/content/103/18/e95.1 Permissions: Requests for permissions to reproduce figures, tables, or portions of articles originally published in Circulation can be obtained via RightsLink, a service of the Copyright Clearance Center, not the Editorial Office. 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