United States: In a recent study by the National Institutes of Health, the SARS-CoV-2, which is the pathogen responsible for COVID-19, seems to have the capability to inflict heart damage even when there is no direct tissue infiltration. The findings of the study published in the Journal Circulation, chiefly concerning the hearts of SARS-CoV-2-related acute respiratory distress syndrome (ARDS) patients, also known as a major lung illness, pointed out that the physical status of the patients was in great danger. However, the same findings have such widespread intimation for the cardiac field and the same reach as for other organs and various viral strains outside SARS-CoV-2.
Thorough scientific investigations as to the risks of heart complications like heart attacks and strokes during and after the period of the disease have been reported in medical journals. Previous imaging studies have made it evident that around 50 percent of COVID-19 patients would develop myocardial inflammation or damage during the disease. However, the pivotal question remains unanswered: Is the damage a direct result of the virus attacking the heart cells, or is it a consequence of the chronic inflammation provoked by the entire immune system’s host reaction?
“The quest for an answer to this quandary is of paramount importance, as it unravels a fresh comprehension of the nexus between severe pulmonary afflictions and the inflammatory cascades predisposing individuals to cardiovascular adversities,” remarked Michelle Olive, Ph.D., serving as the associate director of the Basic and Early Translational Research Program at the National Heart, Lung, and Blood Institute (NHLBI), an arm of the NIH,” according to a news release by Health and Human Services National Institutes of Health of the US.
“Furthermore, the research intimates that quelling the inflammatory response through therapeutic interventions could potentially mitigate these deleterious outcomes,” the expert added.
To unravel their discoveries, the researchers directed their focus towards cardiac macrophages, immune entities pivotal in maintaining tissue integrity but susceptible to inflammatory transformations following injuries such as cardiac arrests or heart failures. Delving into heart tissue specimens obtained from 21 deceased patients succumbing to SARS-CoV-2-related ARDS and contrasting them with samples from 33 individuals meeting their demise due to non-COVID-19 causes, the researchers embarked on a comparative analysis. Additionally, they subjected mice to SARS-CoV-2 infection to delineate the repercussions on macrophages post-infection.
In both human and murine subjects, the researchers observed an escalation in the total count of cardiac macrophages subsequent to SARS-CoV-2 infection, coupled with a transition towards an inflammatory phenotype.
“When cardiac macrophages deviate from their normative functions, encompassing the maintenance of cardiac metabolism and the clearance of pathogenic entities, the ramifications extend beyond cardiac debilitation to systemic repercussions,” elucidated Matthias Nahrendorf, MD, Ph.D., holding the position of a professor of Radiology at Harvard Medical School and serving as the senior author of the study, the news release added.
Subsequently, the researchers devised an experiment in mice to discern whether the observed response stemmed from direct cardiac invasion by SARS-CoV-2 or if the severity of pulmonary inflammation precipitated a heightened inflammatory state in cardiac macrophages. This experiment simulated pulmonary inflammation cues sans the presence of the actual virus. The outcome was revelatory: even in the virus’s absence, the mice exhibited immune responses potent enough to elicit the same phenotypic transition in cardiac macrophages observed in both deceased COVID-19 patients and SARS-CoV-2-infected mice.
“This study underscores the capacity of the immune system to orchestrate remote organ damage subsequent to COVID-19 infection, instigating systemic inflammation in addition to the direct pulmonary insult inflicted by the virus,” articulated Nahrendorf. “Moreover, our findings harbor broader implications, insinuating that any grave infection can reverberate through the entirety of the organism.”
Furthermore, the research cohort discovered that neutralizing antibodies effectively intercepted the inflammatory cascade in murine subjects, thereby preserving cardiac function. While the translation of this intervention to human subjects awaits empirical validation, Nahrendorf opined that such a therapeutic approach holds promise as a prophylactic measure for individuals with pre-existing conditions or those predisposed to severe outcomes associated with SARS-CoV-2-induced ARDS.