New Delhi, Aug 28 Myocardial infarction, commonly known as heart attacks, may also be triggered by infectious diseases, finds a study, which showed that dormant bacteria can cause the deadly condition.
The pioneering study by researchers from Finland and the UK demonstrated that the discovery challenges the conventional understanding of the pathogenesis of heart attacks and opens new avenues for treatment, diagnostics, and even vaccine development.
Professor Pekka Karhunen, from Tampere University in Finland, who led the study, notes that until now, it was assumed that events leading to coronary artery disease were only initiated by oxidised low-density lipoprotein (LDL), which the body recognises as a foreign structure.
"Bacterial involvement in coronary artery disease has long been suspected, but direct and convincing evidence has been lacking," Karhunen added.
The study, published in the Journal of the American Heart Association, revealed that an infection may trigger myocardial infarction.
Using a range of advanced methodologies, the research found that, in coronary artery disease, atherosclerotic plaques containing cholesterol may harbour a gelatinous, asymptomatic biofilm formed by bacteria over years or even decades.
Dormant bacteria within the biofilm remain shielded from both the patient's immune system and antibiotics because they cannot penetrate the biofilm matrix.
A viral infection or another external trigger may activate the biofilm, leading to the proliferation of bacteria and an inflammatory response.
The inflammation can cause a rupture in the fibrous cap of the plaque, resulting in thrombus formation and ultimately myocardial infarction.
"Our study demonstrated the presence of genetic material -- DNA -- from several oral bacteria inside atherosclerotic plaques," the researcher said.
The findings were also validated by developing an antibody targeted at the discovered bacteria, which unexpectedly revealed biofilm structures in arterial tissue.
Bacteria released from the biofilm were observed in cases of myocardial infarction.
The body's immune system had responded to these bacteria, triggering inflammation, which ruptured the cholesterol-laden plaque.
The observations pave the way for the development of novel diagnostic and therapeutic strategies for myocardial infarction. Furthermore, they advance the possibility of preventing coronary artery disease and myocardial infarction by vaccination, the team said.
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