Myocarditis in Poliomyelitis

Laake, Helge

doi:10.1111/j.0954-6820.1951.tb10168.x

Cited by 18 publications

(1 citation statement)

References 13 publications

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“…Infection causes poliomyelitis disease, a paralytic disease but 99% of the disease has since been eradicated following the introduction of the polio vaccine [80]. Myocardial involvement after poliovirus infection is very rare, reported in studies in the 1950s with almost no case reports on myocarditis in poliomyelitis in recent years, possible due to successful efforts in eradication of poliomyelitis [81][82][83].…”

Section: Poliovirusmentioning

confidence: 99%

Viral Cardiomyopathy: A Review of Clinical Status and Meta-Analysis of Diagnosis and Clinical Management

Albakri¹

2019

2516-7138

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From an aetiological standpoint, viral cardiomyopathy represents an uncommon subtype of non-inflammatory dilated cardiomyopathy. The most common aetiologic agents are enteroviruses, adenoviruses and erythroviruses. Pathogenesis depends on the causative virus. Enteroviruses and adenoviruses infect and injure the cardiomyocyte through cytopathic effect and immune-mediated damage leading to cardiac remodelling, myocarditis and ultimately cardiomyopathy. Erythroviruses infect and injure the vascular endothelial cells resulting in macrovascular dysfunction. Typical clinical presentation is heart failure, arrhythmias and chest pains. Clinical diagnosis requires the presence of electrocardiographic abnormalities, markers of myocardial necrosis or evidence of functional/structural ventricular abnormalities accompanied by at least one physical sign or clinical symptom. However, endomyocardial biopsy remains the reference standard but increased risks of complications and the need for highly experienced operators limits its widespread use. The available clinical management strategies are standard heart failure medication for the management of cardiac dysfunction and antiarrhythmic drugs for those with ventricular arrhythmias. Patients with refractory symptoms greater than six months despite optimal medical therapy and with biopsy-proven virus negative myocardium may benefit from supplementary immunosuppressive therapy. However, largescale and long-term prospective randomized clinical trials are warranted to determine long-term benefits of immunosuppression.

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