心脏病可能由细菌引发。
Myocardial infarction may be an infectious disease

原始链接: https://www.tuni.fi/en/news/myocardial-infarction-may-be-infectious-disease

最新研究表明,感染可能是导致心脏病发作(心肌梗塞)的关键诱因。科学家们发现细菌可以在动脉中的动脉粥样硬化斑块*内部*形成隐蔽且持久的生物膜。这些生物膜可以保护细菌免受免疫系统和抗生素的攻击。 感染或其他诱因会激活这些休眠细菌,引起炎症。这种炎症会削弱斑块,导致破裂、血栓形成,最终导致心脏病发作。 由佩卡·卡胡宁教授领导的研究发现了这些斑块中存在的口腔细菌DNA,并开发出一种抗体来证实生物膜的存在。这挑战了传统观点,即只有氧化低密度脂蛋白会引发冠状动脉疾病。 这些发现为新的诊断工具、疗法——甚至可能包括疫苗——的开发,以预防和治疗心脏病打开了大门。这项研究是多家机构合作的结果,并得到了欧盟和芬兰组织的资助。

## 心脏病发作与细菌关联 - 摘要 最新研究表明,心脏病发作可能由动脉斑块内的细菌触发。研究人员在动脉粥样硬化组织中发现了口腔细菌,并推测身体对这些细菌的免疫反应会导致炎症,最终导致斑块破裂并引发心脏病发作。这为长期以来已知的炎症(通过hs-CRP测量)与心脏病风险之间的关联提供了一种潜在机制。 除了这种细菌关联外,其他关键风险因素包括ApoB水平、Lp(a)(一种遗传因素)、HbA1c(胰岛素抵抗)和eGFR(肾功能)。所有这些都可以通过血液检查来测量。 讨论还强调了寄生虫(如恰加斯病和莱姆病)在诱发炎症和心脏问题方面的潜在作用,以及使用噬菌体穿透细菌生物膜的可能性。重要的是,研究表明细菌充当*触发器*,而不是心脏病发作的唯一原因,可能解释了像流感引发的病例。还需要进一步的流行病学验证。
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原文

According to the recently published research, 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.

Professor Pekka Karhunen, 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. Our study demonstrated the presence of genetic material – DNA – from several oral bacteria inside atherosclerotic plaques,” Karhunen explains.

The findings were 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 study was conducted by Tampere and Oulu Universities, Finnish Institute for Health and Welfare and the University of Oxford. Tissue samples were obtained from individuals who had died from sudden cardiac death, as well as from patients with atherosclerosis who were undergoing surgery to cleanse carotid and peripheral arteries.

The research is part of an extensive EU-funded cardiovascular research project involving 11 countries. Significant funding was also provided by the Finnish Foundation for Cardiovascular Research and Jane and Aatos Erkko Foundation. 

The research article Viridans Streptococcal Biofilm Evades Immune Detection and Contributes to Inflammation and Rupture of Atherosclerotic Plaques was published in the Journal of the American Heart Association on 6 August 2025. Read the article online

Professor Pekka Karhunen
Faculty of Medicine and Health Technology
Tampere University
pekka.j.karhunen [at] tuni.fi (pekka[dot]j[dot]karhunen[at]tuni[dot]fi)
Tel. +358 400 511361

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