Sanneke P M de Boer1, Jin M Cheng1, Hélène Rangé2, Hector M Garcia-Garcia1, Jung Ho Heo1, K Martijn Akkerhuis1, Olivier Meilhac3, Guillaume Cosler4, Pirkko J Pussinen5, Robert-Jan van Geuns1, Patrick W Serruys1, Eric Boersma1, Isabella Kardys6. 1. Erasmus MC, Department of Cardiology, Rotterdam, The Netherlands. 2. INSERM UMRS 1148 Laboratory for Vascular Translational Science, Bichat Hospital, Paris, France; Periodontology Department, Rothschild Hospital, Paris, France; UFR of Odontology, Paris Diderot University, Paris, France. 3. INSERM UMRS 1148 Laboratory for Vascular Translational Science, Bichat Hospital, Paris, France; CHU de La Réunion, Saint-Denis, La Réunion, France. 4. INSERM UMRS 1148 Laboratory for Vascular Translational Science, Bichat Hospital, Paris, France. 5. Institute of Dentistry, University of Helsinki, Helsinki, Finland. 6. Erasmus MC, Department of Cardiology, Rotterdam, The Netherlands. Electronic address: i.kardys@erasmusmc.nl.
Abstract
OBJECTIVE: Previous studies have suggested positive associations between periodontal infection and cardiovascular disease. We aimed to investigate the associations of circulating antibodies against periodontal pathogens with 1-year cardiovascular outcome, as well as the extent of coronary atherosclerosis, plaque vulnerability and lesion remodeling on intravascular ultrasound (IVUS) imaging. METHODS: Between 2008 and 2011, radiofrequency IVUS imaging of a non-culprit coronary artery was performed in 581 patients who underwent coronary angiography. Immunoglobulin G (IgG) and A (IgA) against Porphyromonas gingivalis, Aggregatibacter actinomycetemcomitans, Tannerella forsythia and Prevotella intermedia were measured in plasma. RESULTS: None of the antibody levels were associated with coronary plaque burden, radiofreqeuncy-IVUS-derived thin-cap fibroatheroma lesion morphology or 1-year incidence of major adverse cardiac events (MACE), which included all-cause mortality, acute coronary syndrome and unplanned coronary revascularization. IgA against A. actinomycetemcomitans, T. forsythia and P. intermedia were inversely associated with extent of positive lesion remodeling (OR for highest versus lowest tertile 0.55, 95%CI 0.35-0.88, p = 0.012; 0.53, 95%CI 0.32-0.87, p = 0.012; and 0.64, 95%CI 0.40-1.02, p = 0.061, respectively). In diabetic patients specifically, IgG against P. gingivalis tended to be associated with coronary plaque burden (p = 0.080), while IgA against P. gingivalis tended to be associated with incident MACE (p = 0.060). CONCLUSION: Plasma IgG and IgA against major periodontal pathogens were not associated with the extent of coronary atherosclerosis (with the exception of a trend in diabetics) nor with coronary plaque vulnerability. IgA against periodontal pathogens were inversely associated with extent of coronary remodeling. Altogether, these results do not add evidence for a substantial role of systemic exposure to periodontal pathogens in coronary artery disease.
OBJECTIVE: Previous studies have suggested positive associations between periodontal infection and cardiovascular disease. We aimed to investigate the associations of circulating antibodies against periodontal pathogens with 1-year cardiovascular outcome, as well as the extent of coronary atherosclerosis, plaque vulnerability and lesion remodeling on intravascular ultrasound (IVUS) imaging. METHODS: Between 2008 and 2011, radiofrequency IVUS imaging of a non-culprit coronary artery was performed in 581 patients who underwent coronary angiography. Immunoglobulin G (IgG) and A (IgA) against Porphyromonas gingivalis, Aggregatibacter actinomycetemcomitans, Tannerella forsythia and Prevotella intermedia were measured in plasma. RESULTS: None of the antibody levels were associated with coronary plaque burden, radiofreqeuncy-IVUS-derived thin-cap fibroatheroma lesion morphology or 1-year incidence of major adverse cardiac events (MACE), which included all-cause mortality, acute coronary syndrome and unplanned coronary revascularization. IgA against A. actinomycetemcomitans, T. forsythia and P. intermedia were inversely associated with extent of positive lesion remodeling (OR for highest versus lowest tertile 0.55, 95%CI 0.35-0.88, p = 0.012; 0.53, 95%CI 0.32-0.87, p = 0.012; and 0.64, 95%CI 0.40-1.02, p = 0.061, respectively). In diabeticpatients specifically, IgG against P. gingivalis tended to be associated with coronary plaque burden (p = 0.080), while IgA against P. gingivalis tended to be associated with incident MACE (p = 0.060). CONCLUSION: Plasma IgG and IgA against major periodontal pathogens were not associated with the extent of coronary atherosclerosis (with the exception of a trend in diabetics) nor with coronary plaque vulnerability. IgA against periodontal pathogens were inversely associated with extent of coronary remodeling. Altogether, these results do not add evidence for a substantial role of systemic exposure to periodontal pathogens in coronary artery disease.
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