Periodontal Disease, Inflammation and Atherosclerosis Progression in Patients with Acute Coronary Syndromes – the ATHERODENT Study

Theodora Benedek 1 , 2 , Ioana Rodean 1 , Mihaela Ratiu 1 , 2 , Nora Rat 1 , 2 , Lia Yero Eremie 3 , Carmen Biriș 3 , Luminița Lazăr 3 , Mariana Păcurar 3 , and Imre Benedek 1 , 2
  • 1 Clinic of Cardiology, University of Medicine and Pharmacy, Tîrgu Mureș, Romania
  • 2 Center of Advanced Research in Multimodality Cardiac Imaging, Cardio Med Medical Center, , Tîrgu Mureș, Romania
  • 3 Faculty of Dental Medicine, University of Medicine and Pharmacy, Tîrgu Mureș, Romania

Abstract

Recent studies have shown that systemic inflammation caused by periodontal disease (PD) can determine important changes in the coronary arteries, favoring atherosclerosis progression and the development of acute coronary syndromes (ACS). The aim of the ATHERODENT study (Protocol Record Number CM0117-ATD) is to assess the interrelation between PD, inflammation, and the progression of coronary atherosclerosis in patients with ACS.

Material and methods: This case-control observational study will enroll 100 patients (group 1 – ACS and associated PD, and group 2 – ACS and no PD), in whom the following data will be collected: (1) demographic and clinical data; (2) cardiovascular risk factors; (3) full characterization of PD markers; (4) systemic inflammatory biomarkers; (5) imaging biomarkers derived from transthoracic echocardiography, computed tomography, coronary angiography, optical coherence tomography, and intravascular ultrasound; and (6) assessment of the presence of specific oral bacteria in samples of coronary plaques collected by coronary atherectomy, which will be performed during percutaneous revascularization interventions, when indicated in selected cases, in the atherectomy sub-study. The follow-up will be performed at 1, 3, 6, 12, 15, 18, and 24 months. The primary endpoint of the study will be represented by the rate of major adverse cardiovascular events (MACE) in PD vs. non-PD patients and in correlation with: (1) the level of systemic inflammation triggered by PD and/or by ACS at baseline; (2) the vulnerability degree of atheromatous plaques in the coronary tree (culprit and non-culprit lesions); and (3) the presence and burden of oral bacteria in atheromatous plaques. Secondary endpoints will be represented by: (1) the rate of progression of vulnerability degree of non-culprit coronary plaques; (2) the rate of progression of atheromatous burden and calcium scoring of the coronary tree; and (3) the rate of occurrence of left ventricular remodeling and post-infarction heart failure. The ATHERODENT study has been registered in clinicaltrials.gov (ClinicalTrials.gov Identifier: NCT03395041).

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  • 12. Sethi NJ, Safi S, Korang SK, et al. Antibiotics for secondary prevention of coronary heart disease. Cochrane Database of Systematic Reviews. 2017;7:CD003610. doi: 10.1002/14651858. CD003610.pub3.

  • 13. World Health Organization. Cardiovascular Diseases fact sheet (updated May 2017). Available at: http://www.who.int/mediacentre/factsheets/fs317/en/

  • 14. Hamilton JA, Hasturk H, Kantarci A, Serhan CN, Van Dyke T. Atherosclerosis, Periodontal Disease, and Treatment with Resolvins. Curr Atheroscler Rep. 2017;19:57. doi: 10.1007/s11883-017-0696-4.

  • 15. Theodora Benedek. The Link between Periodontal Disease, Inflammation and Atherosclerosis – an Interdisciplinary Approach. Journal of Interdisciplinary Medicine. 2017;2(S1):11-16. doi: 1.0.1515/jim-2017-0016.

  • 16. Lawson JS. Multiple Infectious Agents and the Origins of Atherosclerotic Coronary Artery Disease. Front Cardiovasc Med. 2016;3:30. doi:10.3389/fcvm.2016.00030.

  • 17. B Kalra DK, Heo R, Valenti V, Nakazato R, Min JK. Role of Computed Tomography for Diagnosis and Risk Stratification of Patients with Suspected or Known Coronary Artery Disease. Arterioscler Thromb Vasc Biol. 2014;34:1144-1154. doi: 10.1161/ATVBAHA.113.302074.

  • 18. Fatkhullina AR, Peshkova IO, Koltsova EK. The Role of Cytokines in the Development of Atherosclerosis. Biochemistry (Mosc). 2016;81:1358-1370. doi: 10.1134/S0006297916110134.

  • 19. Hansen GM, Egeberg A, Holmstrup P, Hansen PR. Relation of Periodontitis to Risk of Cardiovascular and All-Cause Mortality (From a Danish Nationwide Cohort Study). Am J Cardiol. 2016;118:489-493. doi: 10.1016/j.amjcard.2016.05.036.

  • 20. Nazir MA. Prevalence of periodontal disease, its association with systemic diseases and prevention. Int J Health Sci (Qassim). 2017;11:72-80.

  • 21. Gualtero DF, Lafaurie GI, Fontanilla MR. Two-dimensional (2D) and three-dimensional (3D) models for studying atherosclerosis pathogenesis induced by periodontopathogenic microorganisms. Mol Oral Microbiol. 2017. doi: 10.1111/omi.12201.

  • 22. Martu S, Nicolaiciuc O, Solomon S, et al. The Evaluation of the C Reactive Protein Levels in the Context of the Periodontal Pathogens Presence in Cardiovascular Risk Patients. Revista de Chimie. 2017;68:605-607.

  • 23. Fonseca FAH, de Oliveira Izar MC. High-Sensitivity C-Reactive Protein and Cardiovascular Disease Across Countries and Ethnicities”. Clinics (Sao Paulo). 2016;71:235-242. doi: 10.6061/clinics/2016(04)11.

  • 24. Assadpour Piranfar M. The Correlation between High-Sensitivity C-Reactive Protein (hsCRP) Serum Levels and Severity of Coronary Atherosclerosis. Int Cardiovasc Res J. 2014;8:6-8.

  • 25. van Soesta G, Marcub L, Boumac BE, Regardet E. Intravascular imaging for characterization of coronary atherosclerosis. Current Opinion in Biomedical Engineering. 2017;3:1-12. doi. org/10.1016/j.cobme.2017.07.001.

  • 26. Libby P, Theroux P. Pathophysiology of Coronary Artery Disease. Circulation. 2005;111:3481-3488. doi: 10.1161/CIRCULATIONAHA.105.537878.

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