Viral Cardiac Infections — Questions

a. Pathogenesis. After a respiratory or gastrointestinal infection the virus, typically an enterovirus such as coxsackievirus B, reaches the heart by viraemia. Injury then occurs in two phases: direct viral damage to myocytes, followed by immune-mediated injury in which cytotoxic T cells attack both infected and, through autoreactivity, uninfected myocytes. Interstitial inflammation and myocyte loss cause ventricular dilation and failure, and healing fibrosis and viral persistence may progress to dilated cardiomyopathy.

b. Acute investigation for a viral cause. Combine cardiac and virological tests. Troponin and creatine kinase MB confirm myocardial injury, the ECG shows sinus tachycardia with low-voltage complexes, and echocardiography or cardiac magnetic resonance imaging shows the dilated, inflamed ventricle. The specific viral evidence comes from endomyocardial biopsy with PCR (and in situ hybridisation) on heart tissue, since peripheral samples are unreliable; supporting serology and throat or stool viral studies may identify a circulating enterovirus. Note that a genome detected in the myocardium supports, but does not alone prove, causation.

Sinus tachycardia with low-voltage QRS complexes and T-wave changes is typical, sometimes with a pseudo-infarct pattern or arrhythmia.

Peaked T waves, a short PR, U waves and delta waves point to other conditions.

The inflammation is patchy and widely distributed, so sampling frequently misses it, giving biopsy a low and variable sensitivity.

Biopsy can detect genomes by PCR, the Dallas criteria are applied to it, and its risk is greatest, not absent, in small children.

Neonatal myocarditis is typically fulminant with high mortality, often acquired in utero and frequently due to coxsackievirus B.

It is not mild, not rarely enteroviral, not exclusively postnatal, and not treated with immunosuppression.

Both share the coxsackievirus and adenovirus receptor (CAR), which is important in cardiac development and is expressed more highly in the young and in dilated cardiomyopathy.

The other receptors listed are not the shared entry route for these agents.

Endocardial fibroelastosis, linked to intrauterine mumps, has all but disappeared since mumps vaccination, supporting a viral cause.

There is no coxsackievirus B vaccine, and the decline is not explained by neonatal care, prophylaxis or screening.

The Myocarditis Treatment Trial showed no benefit from immunosuppression in viral myocarditis, though it does help in giant-cell myocarditis.

It neither improves survival routinely, eradicates the virus, serves as first-line therapy, nor prevents dilated cardiomyopathy.

Troponin marks myocardial injury but is not specific for myocarditis or for a viral cause, so it is interpreted in clinical context.

It does not confirm a viral aetiology, exclude pericarditis, stay normal, or identify the agent.

Injury occurs in two phases: direct viral damage to myocytes, then immune-mediated injury by cytotoxic and autoreactive T cells.

The process is not ischaemic, not toxin-mediated, not purely autoantibody-driven, and microabscesses indicate bacterial rather than viral disease.

A causal role is hard to affirm because the parvovirus B19 genome persists in many hearts without disease, so detection does not prove causation.

It is not the established commonest cause, is not neonate-restricted, is not readily cultured, and does persist in the myocardium.

The enteroviruses, above all coxsackievirus B, are the classical and commonest cause of viral myocarditis.

The other viruses can involve the heart but do so far less often, and rhinovirus and rotavirus are essentially confined to the respiratory and enteric tracts.

The Dallas criteria are histopathological, grading a biopsy as active, borderline or no myocarditis by the infiltrate and myocyte damage.

They are not based on troponin, ejection fraction, blood viral load or the chest film.

Protease 2A cleaves dystrophin, the cytoskeletal protein whose inherited mutation causes familial dilated cardiomyopathy and the cardiomyopathy of Duchenne and Becker muscular dystrophy, giving a direct link to chronic disease.

The other mechanisms are not how protease 2A damages the myocardium.

Cardiac magnetic resonance imaging with gadolinium maps the site and extent of myocardial inflammation and has become a valuable non-invasive test.

The chest film and electrocardiogram are non-specific, angiography is invasive and assesses coronaries, and abdominal ultrasound is irrelevant.