Game-Changer in Myocarditis: Identifying the True Culprit
Traditionally, the belief held that viral infections trigger inflammation, resulting in acute myocarditis, potentially leading to fatal heart arrhythmias in young, healthy adults. However, a recent study has revealed a groundbreaking finding: the virus directly harms heart cells before inflammation occurs, questioning established beliefs.
Viral infections lead to the primary cause of acute inflammation in the heart muscle, termed myocarditis, which contributes to up to 42% of sudden cardiac deaths among young adults. Viruses such as the common cold (adenovirus), hepatitis B and C, and parvovirus are linked to myocarditis.
Virus-Induced Myocardial Damage
The conventional explanation for myocarditis attributes its cause to inflammation, which occurs due to the body’s immune response to a virus, potentially leading to life-threatening rapid or irregular heart rhythms known as arrhythmias. However, a recent study led by researchers at the Fralin Biomedical Research Institute at Virginia Tech challenges this conventional wisdom, suggesting that the virus itself inflicts damage on the heart muscle prior to the onset of inflammation.
James Smyth, the corresponding author of the study, commented, “From a clinical standpoint, our understanding of viral infection in the heart has primarily centered on inflammation, which disrupts the heart’s rhythm or rate. However, we have identified an acute phase when the virus initially infects the heart, occurring before the body’s immune response triggers inflammation. Thus, even before inflammation occurs, the heart becomes susceptible to arrhythmias.”
Exploring Biomarkers for Elevated Risk of Arrhythmia Following Viral Infection
The subsequent phase involves identifying biomarkers indicative of an elevated risk of arrhythmia in individuals post-viral infection.
Smyth stated, “Individuals with acute infections may exhibit normal MRI and echocardiography results, but upon scrutinizing at the molecular level, we observed the potential for significant risks.” He continued, “Regarding diagnostics, we can collaborate with our colleagues to explore methods for detecting a blood biomarker associated with this more severe issue. While individuals often recover from cardiac infections, can we pinpoint what sets apart those at higher risk of experiencing arrhythmia? This might be achievable through a straightforward blood test administered in a clinical setting.”
Read the original article on: New Atlas
