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Published on: July 3, 2018
Presence of bacterial DNA in thrombotic material of patients with myocardial infarction
P Piñon-Esteban1, L Núñez2, R Moure3
1Servicio de Cardiología. Complexo Hospitalario Universitario de A Coruña (CHUAC), Sergas, Instituto de Investigación Biomédica de A Coruña (INIBIC), Universidade da Coruña(UDC), As Xubias 84, 15006, A Coruña, Spain. pablopesteban@mail.com.
Abstract:
Infectious agents have been suggested to be involved in etiopathogenesis of Acute Coronary Syndrome (ACS). However, the relationship between bacterial infection and acute myocardial infarction (AMI) has not yet been completely clarified. The objective of this study is to detect bacterial DNA in thrombotic material of patients with ACS with ST-segment elevation (STEMI) treated with Primary Percutaneous Coronary Intervention (PPCI). We studied 109 consecutive patients with STEMI, who underwent thrombus aspiration and arterial peripheral blood sampling. Testing for bacterial DNA was performed by probe-based real-time Polymerase Chain Reaction (PCR). 12 probes and primers were used for the detection of Aggregatibacter actinomycetemcomitans, Chlamydia pneumoniae, viridans group streptococci, Porphyromonas gingivalis, Fusobacterium nucleatum, Tannarella forsythia, Treponema denticola, Helycobacter pylori, Mycoplasma pneumoniae, Staphylococus aureus, Prevotella intermedia and Streptococcus mutans. Thus, DNA of four species of bacteria was detected in 10 of the 109 patients studied. The most frequent species was viridans group streptococci (6 patients, 5.5%), followed by Staphylococus aureus (2 patients, 1.8%). Moreover, a patient had DNA of Porphyromonas gingivalis (0.9%); and another patient had DNA of Prevotella intermedia (0.9%). Bacterial DNA was not detected in peripheral blood of any of our patients. In conclusion, DNA of four species of endodontic and periodontal bacteria was detected in thrombotic material of 10 STEMI patients. Bacterial DNA was not detected in the peripheral blood of patients with bacterial DNA in their thrombotic material. Bacteria could be latently present in plaques and might play a role in plaque instability and thrombus formation leading to ACS.
Insights
Bacterial DNA from four species, including viridans group streptococci and Staphylococcus aureus, was found in the thrombi of STEMI patients. This suggests bacteria may contribute to plaque instability and acute coronary syndrome.
Area of Science:
- Cardiology
- Microbiology
- Pathogenesis
Background:
- Infectious agents are implicated in Acute Coronary Syndrome (ACS) pathogenesis.
- The specific role of bacterial infection in Acute Myocardial Infarction (AMI) requires further clarification.
Purpose of the Study:
- To investigate the presence of bacterial DNA within the thrombotic material of patients experiencing ST-segment elevation myocardial infarction (STEMI).
- To determine if specific bacterial species are associated with STEMI through analysis of thrombus aspirates.
Main Methods:
- 109 consecutive STEMI patients undergoing thrombus aspiration and peripheral blood sampling were analyzed.
- Real-time Polymerase Chain Reaction (PCR) with 12 specific probes and primers was used to detect bacterial DNA.
- Targeted bacteria included Aggregatibacter actinomycetemcomitans, Chlamydia pneumoniae, viridans group streptococci, Porphyromonas gingivalis, and others.
Main Results:
- Bacterial DNA was detected in the thrombotic material of 10 out of 109 patients (9.2%).
- Viridans group streptococci were most frequent (5.5%), followed by Staphylococcus aureus (1.8%).
- DNA from Porphyromonas gingivalis and Prevotella intermedia was each found in one patient (0.9%).
- No bacterial DNA was found in the peripheral blood samples of any patient.
Conclusions:
- Four species of endodontic and periodontal bacteria were identified in STEMI patient thrombi.
- The absence of bacterial DNA in peripheral blood suggests localized presence within thrombi.
- These findings support a potential role for latent bacterial presence in atherosclerotic plaques, contributing to plaque instability and thrombus formation in ACS.
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