Adult Heart Disease Due to the Coxsackie Virus B Infection

Gs, Sainani; Krompotic, E; Slodki, Sheldon J.

doi:10.1097/00005792-196803000-00003

Cited by 170 publications

(40 citation statements)

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“…It might be emphasized that Q waves showonly a transient appearance in myocarditis. Likewise, Sainani et al (1) and Smith (2) found that 2 of 2 patients and 2 of 3 patients having Q waves were transient, respectively. Because of early disappearance of Q waves, frequent ECG recordings might be essential.…”

Section: Discussionmentioning

confidence: 90%

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Serial Electrocardiographic Findings in Acute Myocarditis.

1994

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The purpose of the present study was to clarify the characteristic findings of electrocardiogram (ECG) in ll patients with acute myocarditis. ST elevation without reciprocal ST depression was one of the conspicuous findings in the acute stage. Total QRSamplitudes at the acute stage were significantly decreased as compared to those before illness and during the convalescent stage. Abnormal Q waves were present in 7 patients and disappeared in a short period. The number of leads showing Q waves was inversely correlated to left ventricular (LV) ejection fraction (r=-0.87, p<0.01). Conduction disturbances were present in 7 patients. Second degree and advanced AV block was transient while bundle branch block remained over months. Corticosteroid treatment was effective for patients whohad edematous myocardial thickening and AVconduction disturbances. As the serial ECGfindings in acute myocarditis are so characteristic, and this help to differentiate it from acute myocardial infarction (AMI). (Internal Medicine 33: 659-666, 1994)

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Section: Discussionmentioning

confidence: 90%

“…It is nowbelieved that most cases of acute myocarditis are induced by viral infection (1)(2)(3). Electrocardiographic findings of these cases often mimic AMI (4)(5)(6)(7).…”

Section: Introductionmentioning

confidence: 99%

Serial Electrocardiographic Findings in Acute Myocarditis.

1994

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“…Yet, cases of persistent symptoms and cardiac manifestations with or without eventual recovery have been well documented (2,3). Although chronic myocarditis and myocardial fibrosis have been postulated as sequelae of acute viral myocarditis, the evidence in man remains circumstantial (4).…”

Section: Introductionmentioning

confidence: 99%

Heart muscle performance after experimental viral myocarditis.

Adesanya¹,

Goldberg²,

Phear³

et al. 1976

J. Clin. Invest.

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A B S T R A C T As part of an inquiry into possible antecedents of idiopathic cardiomyopathy, acute experimental coxsackie virus myocarditis was studied for late structural and functional sequelae. Myocarditis was induced in 12-and 22-day-old hamsters by inoculation with coxsackie virus B3. Early viremia occurred, followed by virus replication in heart muscle.Maximum peak developed tension (Tpd) of isometrically contracting isolated heart muscle was depressed 17 and 43% in the animals inoculated at 12 days, and studied 18 and 90 days later, respectively, as compared to their uninoculated controls. In both infected groups, less muscle stretch was required to reach the length at which Tpd was produced. Animals studied 180 days after inoculation did not differ from controls.The muscles from animals inoculated at 22 days of age and studied 18 days later showed a 15% depression of Tpd compared to their controls. Glycerinated muscles from this infected group developed 50% less tension than their controls. The muscles of hamsters inoculated with virus at 22 days and studied 90 and 180 days later showed no change in Tpd.The data suggest that contractility and compliance of heart muscle are decreased 18 days after inoculation, but recover by 90 days if the animals are inoculated at age 22 days. However, if the animals are inoculated at a younger age (12 days), depression of myocardial performance persists for at least an additional 90 days.It is concluded that the inflammatory stage of experimental acute coxsackie virus B3 myocarditis in the

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“…In most cases, these infections are associated with transient electrocardiographic changes, and patients recover uneventfully, although a small percentage succumb to acute cardiovascular collapse 17 ( Figure). By 1968, a condition referred to as postcarditic cardiomyopathy was established as a cause of DCM, 18 thereby answering Corvisart's question affirmatively. It now seems that many patients with DCM may have experienced an unrecognized acute viral myocarditis several years earlier (Figure).…”

Section: Dilated Cardiomyopathymentioning

confidence: 97%