Do infections cause heart attacks? Lessons from COVID
During the COVID-19 pandemic, there was an elevation of myocardial infarctions and strokes in infected patients, which raised the question as to why this happens. Many cardiologists involved in studies during the pandemic and in following long-COVID patients said we might just be noticing what happens in may types of infections, but we just have not been paying attention. This includes the ability of infections to promote inflammation in atherosclerotic plaques.
To find out more, Cardiovascular Business spoke with Peter Libby, MD, a cardiovascular medicine specialist, Brigham and Women’s Hospital, and Mallinckrodt Professor of Medicine, Harvard Medical School. Libby also was heavily involved in COVID-19 research during and after the pandemic to help answer questions about how SARS-CoV2 damages the endothelium on blood vessels. This has been implicated as the primary cause of thrombosis in COVID patients, and the possible cause of many post-COVID sequelae symptoms.
However, he said there is more to the story and COVID is not necessarily special in the way it may cause heart attacks. He said many types of infections are known to amplify what was previously dominant inflammation in coronary plaques. He suggested the research focus on COVID just made this process much more visible and is changing how some researchers think about the association of infections and their relation to cardiovascular disease.
"I think remote infections, be it influenza, SARS-CoV2 or sepsis from bacterial infector of pneumonia, can cause an echo at the prepared soil of atherosclerotic plaques. Most people my age will have plaques lying in wait and will remain inactive, but if I get a urinary tract infection with urosepsis or a viral infection, I would have a release of cytokines in response to that remote infection that could then impinge on that prepared soil," Libby explained.
He said the cytokines can activate the inflammatory cells in coronary plaques that otherwise would be in a resting phase. This has been tested in animal studies where remote infections created increased inflammatory response in atherosclerotic plaques that were very remote from the source of the infection.
"We also have pretty robust literature showing that, for example with influenza, you harvest some coronary events in the wake of an acute viral infection, Libby said.
The pandemic spurred a massive amount of research on the association of COVID infection with just about every biological process, resulting in more research focused on a specific viral pathogen than any other in just four years. Many researchers have said this focus on COVID has opened their eyes to how these biological processes and impacts may be all around us with other types of infection that went somewhat unnoticed because the numbers of impacted patients has been relatively low and dispersed across the national healthcare system.
Libby's research on COVID clotting mechanisms
Libby presented on mechanism for COVID's proclivity for vascular beds at the 2022 American Heart Association (AHA) meeting. Libby also has been a major researcher in the role of inflammation in vascular diseases, and early on saw COVID-19 as a vascular disease as much as it is a respiratory virus. He explained one of main mechanisms that caused clotting inside blood vessels throughout the body in COVID patients.
"What we learned early on is that when we activate these pathogen-associated molecular patterns (PAMPs), we trigger a coordinated series of changes in the endothelial surface," he said of the research presented at AHA last fall. "There are only a few surfaces, synthetic or natural, that can maintain blood in a liquid state in prolonged contact. When we expose the endothelial lawyer of blood vessels to these PAMPs, we flip from the hemostatic, anticoagulant, pro fibrinlytic, anti-inflammatory, vasodilatory set of functions of a normal endothelium to just the opposite," Libby explained.
Find our more on Libby's research in the VIDEO: Why does COVID-19 damage vascular beds?