The collaborative research investigated the role of bacteria in coronary artery disease. The study used advanced molecular and imaging techniques on tissue samples collected from individuals who had died from sudden cardiac death and patients undergoing surgery for atherosclerosis.
The researchers found that atherosclerotic plaques in the arteries, long believed to be the primary culprits behind myocardial infarctions, can contain dormant bacterial biofilms. These gelatinous structures, composed of bacteria embedded in a self-produced matrix, are capable of surviving undetected in the body for years, shielded from both immune responses and antibiotics.
According to the study, an external trigger such as a viral infection may disturb the dormant biofilm, leading to bacterial proliferation and an immune system response. This inflammation can rupture the fibrous cap of a cholesterol-rich plaque, causing a thrombus (blood clot) that ultimately leads to a heart attack.
To validate their findings, the researchers developed a targeted antibody, which revealed biofilm structures in arterial tissues. In cases of myocardial infarction, bacteria released from the biofilm were detected and shown to have provoked inflammatory responses.
“Bacterial involvement in coronary artery disease has long been suspected, but direct and convincing evidence has been lacking,” said Professor Karhunen, lead author of the study. “Our study demonstrated the presence of genetic material – DNA – from several oral bacteria inside atherosclerotic plaques.”
Reference: Pekka J. Karhunen, Tanja Pessi, Sohvi Hörkkö, Vesa Karhunen, Sirkka Goebeler, Anne‐Mari Louhelainen, Mika Martiskainen, Teppo Haapaniemi, Johanna Lappeteläinen, Tommi Ijäs, Leo‐Pekka Lyytikäinen, Emma Raitoharju, Thanos Sioris, Sari Tuomisto, Heini Huhtala, Chunguang Wang, Claudia Monaco, Niku Oksala, Terho Lehtimäki, Reijo Laaksonen. Viridans Streptococcal Biofilm Evades Immune Detection and Contributes to Inflammation and Rupture of Atherosclerotic Plaques. Journal of the American Heart Association, 2025; 14 (16) DOI: 10.1161/JAHA.125.041521
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