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1、Journal of Electrocardiology Vol. 32 No. 1 1999 ECG Changes After Rabbit Coronavirus Infection Lorraine K. Alexander, DRPH,* Bruce W. Keene, DVM, t Boyd L. Yount, BS,* Joachim Dieter Geratz, MD,: J. David Small, DVM, MPH,* and Ralph S. Baric, PhD* Abstract: This study examines the electrocardiograph
2、ic (ECG) changes fol- lowing rabbit coronavirus (RbCV) infection. We have shown that infection with RbCV results in the development of myocarditis and congestive heart failure and that some survivors of RbCV infection go on to develop dilated cardiomyopathy in the chronic phase. Serial ECGs were rec
3、orded on 31 RbCV-infected rabbits. Measurements of heart rate; P-R interval; QRS dura- tion; QTc interval; and P-, QRS-, and T-wave voltages were taken. The recordings were also examined for disturbances of conduction, rhythm, and repolarization. The acute and subacute phases were characterized by s
4、inus tachycardia with depressed R- and T-wave voltages as well as disturbances of conduction, rhythm, and repolarization. In most animals in the chronic phase, the sinus rate returned to near-baseline values with resolution of the QRS voltage changes. The ECG changes observed during RbCV infection a
5、re similar to the spectrum of interval/segment abnormalities, rhythm disturbances, conduction defects, and myocardial pathology seen in human myocarditis, heart failure, and dilated cardiomyopathy. Because animals often died sud- denly in the absence of severe clinical signs of congestive heart fail
6、ure during the acute phase, RbCV infection may increase ventricular vulnerability, resulting in sudden cardiac death. RbCV infection may provide a rare oppor- tunity to study sudden cardiac death in an animal model in which the ventricle is capable of supporting veutricular fibrillation, and invasiv
7、e techniques monitoring cardiac function can be performed. Key words: coronavirus, myocarditis, heart failure, ECG. From the * Department of Epidemiology, School of Public Health, $ Department of Pathology, School of Medicine, The University of North Carolina at Chapel Hill, Chapel Hill NC; and the
8、I College of Veterinary Medicine, North Carolina State University, Raleigh, NC. Supported by grants from the American Heart Association, 90112, the National Institutes of Health, AI23946, and a fellowship from the American Heart Association, North Carolina Affiliate, NC-93-FW-01, to LICA. This work
9、was performed during an Established Investigator Award from the American Heart Association, 890193, to RSB. Reprint requests: Ralph S. Baric, PhD, Department of Epidemiology, School of Public Health, The University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-7400. Copyright 1999 by Churc
10、hill Livingstone 0022-0736l 99l 3201-0004510.00/0 21 22 Journal of Electrocardiology Vol. 32 No. 1 January 1999 Viral infection of the heart can lead to myocardi- tis, dilated cardiomyopathy, progressive heart fail- ure, and sudden cardiac death (1,2). Myocarditis is thought to develop in approximat
11、ely 2 to 5% of patients following acute viral infection (3,4). The diagnosis of viral myocarditis is problematic due to the lack of definitive clinical signs and the paucity of sensitive diagnostic tests (1). Diagnosis can be fur- ther complicated by the variable time course of progression of viral
12、myocarditis, with clinically un- apparent viral infection (even early in childhood), potentially resulting in dilated cardiomyopathy weeks, months, or even years later (5). Rapidly accumulating evidence based on nucleic acid hy- bridization and other molecular techniques sup- ports the hypothesis th
13、at cardiotropic viruses play an important role in the pathogenesis of myocardi- tis and dilated cardiomyopathy (6-10). Difficulties inherent in diagnosing and studying the pathogen- esis of viral myocarditis have prevented an accurate assessment of the prevalence of virus-induced heart disease in th
14、e human population. Animal models of viral myocarditis offer a valu- able opportunity to study the complex interactions between virus and host with respect to both viral infection and the pathogenesis of virus-induced myocarditis and dilated cardiomyopathy. An appro- priate animal model could provid
15、e useful clinical diagnostic markers for the disease and serve as a model for potential therapeutic intervention once the natural history of the infection is known. A good model should induce a reproducible spectrum of disease clinically similar to that observed in humans. Recently, our laboratory h
16、as described a model of viral myocarditis, congestive heart failure (CHF), and dilated cardiomyopathy in rabbits in- fected with rabbit coronavirus (RbCV). The RbCV model of myocarditis and dilated cardiomyopathy has been divided into acute, subacute, and chronic phases based on duration of survival after infection, clinical signs, and pathologic findings (11-I3). Sur- vivors of RbCV infection (chronic phase) have been further categorized into those exhibiting slight myocyte hypertro
