Periodontal Bacteria in Thrombi of Patients With AMI
Periodontal Bacteria in Thrombi of Patients With AMI
Backgrounds Numerous reports have demonstrated that periodontal bacteria are present in plaques from atherosclerotic arteries. Although periodontitis has recently been recognized as a risk factor for coronary artery disease, the direct relationship between periodontal bacteria and coronary artery disease has not yet been clarified. It has been suggested that these bacteria might contribute to inflammation and plaque instability. We assumed that if periodontal bacteria induce inflammation of plaque, the bacteria would be released into the bloodstream when vulnerable plaque ruptures. To determine whether periodontal bacteria are present in thrombi at the site of acute myocardial infarction, we tried to detect periodontal bacteria in thrombi of patients with acute myocardial infarction by polymerase chain reaction (PCR).
Methods We studied 81 consecutive adults with ST-segment elevation acute myocardial infarction who underwent primary percutaneous coronary intervention (PCI). All patients underwent removal of thrombus with aspiration catheters at the beginning of percutaneous coronary intervention, and a small sample of thrombus was obtained for PCR.
Results The detection rates of periodontal bacteria by PCR were 19.7% for Aggregatibacter actinomycetemcomitans, 3.4% for Porphyromonas gingivalis, and 2.3% for Treponema denticola.
Conclusions Three species of periodontal bacteria were detected in the thrombi of patients with acute myocardial infarction. This raises the possibility that such bacteria are latently present in plaque and also suggests that these bacteria might have a role in plaque inflammation and instability.
Rupture of coronary atherosclerotic plaque with consequent platelet aggregation and thrombus formation is the major cause of acute coronary syndrome. Clinical and pathologic studies have indicated that rupture, erosion, and ulceration of plaque participate in thrombus formation and that vulnerable plaque consists of a lipid core covered by a thin fibrous cap. Vulnerable plaque is also prone to local inflammation, and chronic inflammation may cause plaque instability.
Recently, many studies have shown a correlation between periodontal disease and coronary artery disease. Periodontitis has been recognized as a new risk factor for coronary artery disease alongside hypertension, diabetes, hyperlipidemia, and smoking. However, the direct relationship between local inflammation of periodontitis and distant coronary arterial inflammation has not yet been clarified. Chiu performed a histologic analysis of human carotid endoatherectomy specimens and found Porphyromonas gingivalis (PG) and Streptococcus sanguis in unstable plaques. In addition, we have detected Actinobacillus actinomycetemcomitans (AA), PG, Bacteroides forsythus, Treponema denticola (TD), and Campylobacter rectus in samples of coronary artery plaques by polymerase chain reaction (PCR). Furthermore, the presence of AA, Fusobacterium nucleatum-periodonticum-simiae group, PG, Prevotella intermedia (PI), Prevotella nigrescens, and Tannerella forsythia (TF) in atheromatous plaques from coronary arteries have been demonstrated by Gaetti-Jardim Jr et al using PCR. Because periodontal bacteria have been detected in atherosclerotic plaques, it has been suggested that such bacteria might take part in causing inflammation and plaque instability. We assumed that if periodontal bacteria induced inflammation and disruption of plaques, the bacteria would be released into the bloodstream or into the thrombus when the vulnerable plaque ruptured. To the best of our knowledge, periodontal pathogens have never been found in the thrombus. Therefore, we tried to detect periodontal bacteria in thrombus obtained from the occluded site in patients with acute myocardial infarction.
Abstract and Introduction
Abstract
Backgrounds Numerous reports have demonstrated that periodontal bacteria are present in plaques from atherosclerotic arteries. Although periodontitis has recently been recognized as a risk factor for coronary artery disease, the direct relationship between periodontal bacteria and coronary artery disease has not yet been clarified. It has been suggested that these bacteria might contribute to inflammation and plaque instability. We assumed that if periodontal bacteria induce inflammation of plaque, the bacteria would be released into the bloodstream when vulnerable plaque ruptures. To determine whether periodontal bacteria are present in thrombi at the site of acute myocardial infarction, we tried to detect periodontal bacteria in thrombi of patients with acute myocardial infarction by polymerase chain reaction (PCR).
Methods We studied 81 consecutive adults with ST-segment elevation acute myocardial infarction who underwent primary percutaneous coronary intervention (PCI). All patients underwent removal of thrombus with aspiration catheters at the beginning of percutaneous coronary intervention, and a small sample of thrombus was obtained for PCR.
Results The detection rates of periodontal bacteria by PCR were 19.7% for Aggregatibacter actinomycetemcomitans, 3.4% for Porphyromonas gingivalis, and 2.3% for Treponema denticola.
Conclusions Three species of periodontal bacteria were detected in the thrombi of patients with acute myocardial infarction. This raises the possibility that such bacteria are latently present in plaque and also suggests that these bacteria might have a role in plaque inflammation and instability.
Introduction
Rupture of coronary atherosclerotic plaque with consequent platelet aggregation and thrombus formation is the major cause of acute coronary syndrome. Clinical and pathologic studies have indicated that rupture, erosion, and ulceration of plaque participate in thrombus formation and that vulnerable plaque consists of a lipid core covered by a thin fibrous cap. Vulnerable plaque is also prone to local inflammation, and chronic inflammation may cause plaque instability.
Recently, many studies have shown a correlation between periodontal disease and coronary artery disease. Periodontitis has been recognized as a new risk factor for coronary artery disease alongside hypertension, diabetes, hyperlipidemia, and smoking. However, the direct relationship between local inflammation of periodontitis and distant coronary arterial inflammation has not yet been clarified. Chiu performed a histologic analysis of human carotid endoatherectomy specimens and found Porphyromonas gingivalis (PG) and Streptococcus sanguis in unstable plaques. In addition, we have detected Actinobacillus actinomycetemcomitans (AA), PG, Bacteroides forsythus, Treponema denticola (TD), and Campylobacter rectus in samples of coronary artery plaques by polymerase chain reaction (PCR). Furthermore, the presence of AA, Fusobacterium nucleatum-periodonticum-simiae group, PG, Prevotella intermedia (PI), Prevotella nigrescens, and Tannerella forsythia (TF) in atheromatous plaques from coronary arteries have been demonstrated by Gaetti-Jardim Jr et al using PCR. Because periodontal bacteria have been detected in atherosclerotic plaques, it has been suggested that such bacteria might take part in causing inflammation and plaque instability. We assumed that if periodontal bacteria induced inflammation and disruption of plaques, the bacteria would be released into the bloodstream or into the thrombus when the vulnerable plaque ruptured. To the best of our knowledge, periodontal pathogens have never been found in the thrombus. Therefore, we tried to detect periodontal bacteria in thrombus obtained from the occluded site in patients with acute myocardial infarction.
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