Concerning new research is linking viral infections to inflammatory cardiomyopathy, an infiltration of inflammatory cells into the myocardium. This infiltration can compromise heart function.
Although bacteria, fungal, and protozoal infections, as well as drugs and autoimmune disease, can precipitate inflammatory cardiomyopathy, viruses are the main cause. Unfortunately, inflammatory cardiomyopathy has a poor prognosis. Not all viruses cause heart diseases, but it is important to arm yourself with knowledge of the ones that do.
Myocardial injury frequently occurs in patients with COVID-19. The inflammatory nature of the infection likely contributes to residual myocardial inflammation.
Early recognition and assessment of residual cardiac disease is important in those with COVID-19, according to an article published in Expert Review of Cardiovascular Therapy. These steps help facilitate disease-modifying treatments for subclinical damage that prevent or mitigate the pathogenesis of heart failure. Nevertheless, ECG and echocardiography usually detect only advanced stages of heart damage, when left ventricular function presents.
The authors recommended using cardiovascular magnetic resonance (CMR) for in-depth tissue characterization and identification of pathology of the myocardium, such as inflammation, edema, ischemia, and fibrosis.
“The availability of new, highly reliable, and reproducible techniques that not only detect, but also measure and quantify these processes, offers us the possibility of a shift of paradigm, from treating the late consequences of established HF, to going ahead of the disease, starting therapy at an early stage and preventing the consequences of advanced HF,” they wrote. “Additionally, CMR allows for monitoring of disease activity and response to treatment, guiding pharmacologic therapy.”
These enteroviruses are the most common causes for myocarditis and dilated cardiomyopathy, amounting to half of all infections. The good news is that myocarditis is relatively rare, affecting only 1% of the US population and presenting at an average age of 42 years, according to information presented by Stanford University.
The incubation period for coxsackie virus infection is between 2 and 10 days, with heart symptoms occurring about 2 weeks after infection. From the gut, this infection spreads to the heart and damages heart cells by allowing white blood cells into heart tissue.
These white blood cells trigger an autoimmune process that results in death of both infected and healthy heart cells. This pathologic process occurs long after the virus is cleared, resulting in myocarditis and heart failure.
Keys to preventing heart damage secondary to coxsackie virus infection include fecal-oral control via handwashing and improved sanitation. Myocarditis can be treated with analgesics to decrease inflammation.
Salt intake should be limited due to reduced heart functioning, and oxygen can be given to decrease workload. Heart transplantation is an option with heart failure.
Traditional risk factors for atherosclerosis include elevated cholesterol levels, hypertension, and smoking, but a growing amount of epidemiologic research is centered on the role of herpesvirus as a risk factor for the condition.
With an estimated worldwide prevalence of 35% to 40%, the risk could be substantial.
Chronic inflammation by herpesvirus also may promote thrombosis. HSV-1 and HSV-2 are the major subtypes of herpesvirus and spark the most concern.
“The atherogenic mechanisms of HSV may involve increasing adherence of leukocytes to endothelium, inducing lipid accumulation in vascular smooth muscle cells (VSMCs), and contributing to deposition of thrombin in atherosclerotic plaque,” according to the authors of a meta-analysis published in BioMed Research International.
In that analysis, the authors found significant elevated risks for atherosclerosis and myocardial ischemia in those patients with HSV-1 infection. HSV-2 infection was only tied to myocardial ischemia, but not other types of atherosclerosis.
Researchers recently discovered an interesting mechanism by which cytomegalovirus (CMV) could lead to cardiovascular death, according to an article in Theranostics. They found that CMV infection is intimately related to the accumulation of CD28null T-cells, which damage the endothelium and trigger cardiovascular events.
The accumulation of CD28null T-cells is a normal consequence of aging, but it remains to be elucidated whether these CD28null T-cell populations are expanded due to aging or CMV infection.
“Simply treating CMV might have real potential to achieve this,” wrote the authors. “For example, acyclovir was shown to dramatically reduce the frequencies of CMV-specific CD4 T-cells in older humans, and valacyclovir was shown to reduce CMV-specific T-cells in mice. Attempting to reduce the frequencies of CD28null CD4 T-cells with these drugs in individuals at risk could be the next decisive step forward.”
Bisma R. Association of Viruses in the Development of Cardiovascular Diseases. Current Pharmaceutical Design. 2021.
Pera A. CD28null pro-atherogenic CD4 T-cells explain the link between CMV infection and an increased risk of cardiovascular death. Theranostics. 2018.
Shchendrygina A. COVID-19 myocarditis and prospective heart failure burden. Expert Review of Cardiovascular Therapy. 2020.
Wu Y. Herpes Simplex Virus Type 1 and Type 2 Infection Increases Atherosclerosis Risk: Evidence Based on a Meta-Analysis. BioMed Research International. 2018.