Common infections may trigger some heart attacks, researchers say

New research by teams in Finland and the United Kingdom suggests that common infections may act as triggers for heart attacks by activating bacteria that reside within cholesterol-rich arterial plaques.

The investigators reported finding genetic material from oral bacteria inside atherosclerotic plaques and identified biofilm-like bacterial structures in arterial tissue. They say that when a person develops an unrelated infection — such as a respiratory illness or a urinary tract infection (UTI) — the resulting systemic inflammatory response can cause plaque instability, increase platelet stickiness and, in some cases, lead to a clot that blocks blood flow to the heart.

The study was led by Professor Pekka Karhunen of Tampere University, working in collaboration with researchers at the University of Oxford. The team analysed arterial tissue from people who had died suddenly of cardiac causes and from patients undergoing procedures to remove plaque buildup. They reported detecting DNA from several oral bacteria inside the plaques and said they developed an antibody that marks biofilm structures in arterial tissue.

"Bacterial involvement in coronary artery disease has long been suspected, but direct and convincing evidence has been lacking," Karhunen said. "Our study demonstrated the presence of genetic material — DNA — from several oral bacteria inside atherosclerotic plaques." The authors say the findings point to a mechanism in which bacteria protected within biofilms persist in the artery wall and are reactivated by systemic infection.

According to the researchers, cholesterol-rich material inside plaques may provide a niche that shields bacteria from the immune system and from antibiotics. When an infection elsewhere in the body provokes an inflammatory response, the biofilm may be disturbed and bacteria can proliferate or release substances that promote inflammation. That inflammation, in turn, can weaken plaque caps and raise the tendency for blood to clot.

The research team said the work does not negate established cardiovascular risk factors such as high cholesterol, smoking, poor diet and hypertension, but that the findings could inform the development of new diagnostic approaches and preventive strategies, including vaccines against common pathogens that may trigger events.

The new analysis echoes earlier observational research linking infections with acute coronary events. A 2018 study in the Journal of the American Heart Association followed more than 1,300 people who had experienced a heart attack or other coronary event and found that roughly 37% had suffered an infection in the preceding three months, with UTIs and pneumonia among the most frequently reported. "The infection appears to be the trigger for changing the finely tuned balance in the blood and making us more prone to blood clot formation," said Dr. Kamakshi Lakshminarayan, the lead author of that study.

Cardiovascular disease remains the leading cause of death worldwide, accounting for an estimated 17.9 million deaths annually. In the United Kingdom, recurrent UTIs affect an estimated 1.7 million people, most of them women, and contribute substantially to outpatient visits and hospital bed days, the authors noted. Public health experts have also raised concerns about rising premature cardiovascular deaths in recent years and an apparent increase in heart attacks among younger adults in some datasets.

The investigators acknowledged limitations in the current work. Detection of bacterial DNA and biofilm markers in plaques establishes the presence of microbial material but does not by itself prove a direct causal sequence from infection to plaque rupture in every case. The authors called for further research to replicate the findings, to characterise the organisms and molecular signals involved, and to determine whether preventing or treating specific infections can reduce the risk of acute coronary events.

Antibiotic resistance and the variable effectiveness of treatments for common infections were cited by the researchers as complicating factors. They said additional study is needed to assess whether targeted prevention measures — including better vaccines, improved infection control and new diagnostics to detect bacterial activity in plaques — could reduce the number of heart attacks attributable to infection-related mechanisms.

Clinicians not involved in the study emphasized that established preventive measures for heart disease remain critical. Controlling blood pressure and cholesterol, quitting smoking, managing diabetes and maintaining a healthy diet and activity level continue to be the primary strategies to lower heart attack risk, they said, while acknowledging that a better understanding of the interplay between infection and atherosclerosis could add new tools to prevention and treatment efforts.