Study Links Myocardial Infarction to Bacterial Infection

A recent study by researchers from Tampere University presents evidence that myocardial infarction may originate from bacterial infection, challenging long‑standing interpretations of coronary artery disease. The work suggests that infections could not only contribute to the development of myocardial infarction but also raise the possibility of diagnostics and vaccines aimed at prevention.

The study focused on coronary artery disease and the role of atherosclerotic plaques, which contain cholesterol deposits in arterial walls. The researchers discovered that such plaques can harbor biofilms—structured communities of bacteria encased in a gelatinous layer. These biofilms may develop silently over years or decades, with bacteria remaining in a dormant state protected from both immune surveillance and antibiotic exposure. Because the immune system and drug treatments cannot readily penetrate the biofilm structure, the bacteria persist in a sheltered environment.

A viral infection or other external trigger can reactivate the dormant bacteria. Once active, the microbes multiply, initiating an inflammatory immune response. This process increases the risk of the fibrous cap covering an atherosclerotic plaque rupturing. When rupture occurs, a thrombus may form, which can block blood flow and lead directly to myocardial infarction.

Pekka Karhunen, first author of the study published in JAHA, noted that prior understanding attributed the origins of coronary artery disease primarily to oxidized low‑density lipoprotein (LDL), recognized by the body as a harmful structure. As he explains, “Bacterial involvement in coronary artery disease has long been suspected, but direct and convincing evidence has been lacking. Our study demonstrated the presence of genetic material—DNA—from several oral bacteria inside atherosclerotic plaques." 

The research further validated these findings with an antibody designed against the identified bacterial strains. Unexpectedly, this antibody revealed distinct biofilm architectures in arterial tissue samples. In patients experiencing myocardial infarction, bacteria were observed leaving the biofilm, followed by immune activation and inflammation sufficient to rupture plaque deposits rich in cholesterol. 

By framing myocardial infarction as potentially infectious in origin, the study highlights new directions for therapeutic research. It establishes the possibility of infection‑based interventions ranging from biomarker‑driven diagnostics to vaccine strategies aimed at disease prevention.