#heart attacks

@whumperless-whump-event Day 13: "I thought you were getting better." Leverage. Nate and Sophie. 200 words Double Drabble

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“I thought you were getting better.”

The words hung in the air..

𝗕𝗮𝗰𝘁𝗲𝗿𝗶𝗮𝗹 𝗕𝗶𝗼𝗳𝗶𝗹𝗺𝘀 𝗶𝗻 𝗔𝘁𝗵𝗲𝗿𝗼𝘀𝗰𝗹𝗲𝗿𝗼𝘁𝗶𝗰 𝗣𝗹𝗮𝗾𝘂𝗲𝘀: 𝗔 𝗡𝗼𝘃𝗲𝗹 𝗠𝗲𝗰𝗵𝗮𝗻𝗶𝘀𝗺 𝗶𝗻 𝗠𝘆𝗼𝗰𝗮𝗿𝗱𝗶𝗮𝗹 𝗜𝗻𝗳𝗮𝗿𝗰𝘁𝗶𝗼𝗻 𝗣𝗮𝘁𝗵𝗼𝗴𝗲𝗻𝗲𝘀𝗶𝘀

Abstract -Atherosclerotic cardiovascular disease, the leading cause of mortality worldwide, has traditionally been attributed to dyslipidemia, hypertension, and lifestyle factors. However, emerging evidence implicates microbial infections in plaque instability and acute coronary events. This review synthesizes recent findings on viridans streptococcal biofilms within coronary plaques, highlighting their role in evading immune surveillance and precipitating inflammation-driven rupture.

Introduction -Coronary artery disease (CAD) manifests through the accumulation of lipid-rich plaques in arterial walls, culminating in myocardial infarction (MI) via plaque rupture and thrombosis. While cholesterol deposition and endothelial dysfunction are central, chronic inflammation is a key driver of plaque vulnerability. Recent investigations reveal that bacterial biofilms—structured communities encased in extracellular matrix—may colonize plaque cores, remaining latent for extended periods. These biofilms, primarily composed of oral viridans group streptococci (VGS), originate from transient bacteremia and embed deeply within atheromas, resisting antibiotics and innate immunity.

Evidence from Recent Studies

In a landmark autopsy and surgical cohort study involving 217 subjects, quantitative PCR detected VGS DNA in 42.1% of coronary plaques from sudden cardiac death victims and 42.9% of endarterectomy samples.this Immunohistochemistry confirmed VGS immunopositivity correlating with severe atherosclerosis (P<0.0001), coronary heart disease mortality (P=0.021), and MI (P=0.042)Biofilms evaded macrophage detection in plaque cores but dispersed virulent streptococci infiltrated ruptured fibrous caps, activating pattern-recognition receptors (e.g., TLR2) and adaptive immunity. Genome-wide expression analysis of endarterectomy tissues showed upregulated bacterial recognition pathways, supporting infection-induced inflammation. External triggers, such as viral infections, may disrupt biofilms, amplifying local inflammation and precipitating rupture.

Discussion -These findings challenge the lipid-centric paradigm, proposing an infectious etiology for MI. VGS biofilms' dormancy explains prior antibiotic trial failures, as matrix barriers hinder penetration. Implications include novel diagnostics via biofilm-specific imaging or serology, and preventive strategies like VGS-targeted vaccines or oral hygiene interventions to mitigate bacteremia. Future research should validate causality through animal models and longitudinal cohorts.

Conclusion -Integrating microbial factors into CAD models could revolutionize prevention, emphasizing interdisciplinary approaches to combat this infectious component of heart disease.

References

1. Karhunen PJ, et al. Viridans Streptococcal Biofilm Evades Immune Detection and Contributes to Inflammation and Rupture of Atherosclerotic Plaques. J Am Heart Assoc. 2025;14(16):e041521. doi:10.1161/JAHA.125.041521.

2. Pessi T, et al. Myocardial infarction may be an infectious disease. Tampere University Press Release. 2025. #MedTwitter #MedEd #MedX