Myocardial injury in diabetic patients with multivessel coronary artery disease after revascularization interventions

Carregando...
Imagem de Miniatura
Citações na Scopus
4
Tipo de produção
article
Data de publicação
2017
Título da Revista
ISSN da Revista
Título do Volume
Editora
BIOMED CENTRAL LTD
Citação
DIABETOLOGY & METABOLIC SYNDROME, v.9, article ID 92, 9p, 2017
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
Background: Diabetic patients may be more susceptible to myocardial injury after coronary interventions. Thus, the aim of this study was to assess the release of cardiac biomarkers, CK-MB and troponin, and the findings of new late gadolinium enhancement (LGE) on cardiac magnetic resonance (CMR) in patients with type 2 diabetes mellitus after elective revascularization procedures for multivessel coronary artery disease (CAD). Methods: Patients with multivessel CAD and preserved systolic ventricular function underwent either elective percutaneous coronary intervention (PCI), off-pump or on-pump bypass surgery (CABG). Troponin and CK-MB were systematically collected at baseline, 6, 12, 24, 36, 48 and 72 h after the procedures. CMR with LGE was performed before and after the interventions. Patients were stratified according to diabetes status at study entry. Biomarkers and CMR results were compared between diabetic and nondiabetics patients. Analyses of correlation were also performed among glycemic and glycated hemoglobin (A1c) levels and troponin and CK-MB peak levels. Patients were also stratified into tertiles of fasting glycemia and A1c levels and were compared in terms of periprocedural myocardial infarction (PMI) on CMR. Results: Ninety (44.5%) of the 202 patients had diabetes mellitus at study entry. After interventions, median peak troponin was 2.18 (0.47, 5.14) and 2.24 (0.69, 5.42) ng/mL (P = 0.81), and median peak CK-MB was 14.1 (6.8, 31.7) and 14.0 (4.2, 29.8) ng/mL (P = 0.43), in diabetic and nondiabetic patients, respectively. The release of troponin and CK-MB over time was statistically similar in both groups and in the three treatments, besides PCI. New LGE on CMR indicated that new myocardial fibrosis was present in 18.9 and 17.3% (P = 0.91), and myocardial edema in 15.5 and 22.9% (P = 0.39) in diabetic and nondiabetic patients, respectively. The incidence of PMI in the glycemia tertiles was 17.9% versus 19.3% versus 18.7% (P = 0.98), and in the A1c tertiles was 19.1% versus 13.3% versus 22.2% (P = 0.88). Conclusions: In this study, diabetes mellitus did not add risk of myocardial injury after revascularization interventions in patients with multivessel coronary artery disease.
Palavras-chave
Type 2 diabetes mellitus, Coronary artery disease, Percutaneous coronary intervention, Coronary artery bypass, Myocardial infarction
Referências
  1. Alegria JR, 2007, AM HEART J, V154, P743, DOI 10.1016/j.ahj.2007.06.020
  2. American Diabetes Association, 2016, DIABETES CARE S1, V39, pS1, DOI 10.2337/DC13-S011
  3. Barsotti A, 2009, CURR PHARM DESIGN, V15, P836, DOI 10.2174/138161209787582066
  4. Dagenais GR, 2011, CIRCULATION, V123, P1492, DOI 10.1161/CIRCULATIONAHA.110.978247
  5. Devereux RB, 2000, CIRCULATION, V101, P2271
  6. Di Filippo C, 2005, DIABETES, V54, P803
  7. Domanski MJ, 2011, JAMA-J AM MED ASSOC, V305, P585, DOI 10.1001/jama.2011.99
  8. Feuvray D, 1997, CARDIOVASC RES, V34, P113, DOI 10.1016/S0008-6363(97)00037-0
  9. Grodzinsky A, 2017, CIRC-CARDIOVASC QUAL, V10, DOI 10.1161/CIRCOUTCOMES.117.003553
  10. GWILT DJ, 1985, BRIT HEART J, V54, P466
  11. Hadour G, 1998, J MOL CELL CARDIOL, V30, P1869, DOI 10.1006/jmcc.1998.0751
  12. Hasdai D, 2000, J AM COLL CARDIOL, V35, P1502, DOI 10.1016/S0735-1097(00)00591-X
  13. Hueb W, 2016, ANN THORAC SURG, V101, P2202, DOI 10.1016/j.athoracsur.2015.11.034
  14. Korkmaz-Icoz S, 2015, J DIABETES RES, V2015, DOI [10.1155/2015/396414262299694502305, DOI 10.1155/2015/39641426229969]
  15. LEHTO S, 1994, J INTERN MED, V236, P291, DOI 10.1111/j.1365-2796.1994.tb00799.x
  16. Matsumoto S, 2009, CARDIOVASC DRUG THER, V23, P263, DOI 10.1007/s10557-009-6184-5
  17. Miki T, 2009, DIABETES, V58, P2863, DOI 10.2337/db09-0158
  18. Moussa ID, 2013, J AM COLL CARDIOL, V62, P1563, DOI 10.1016/j.jacc.2013.08.720
  19. Mukamal KJ, 2001, DIABETES CARE, V24, P1422, DOI 10.2337/diacare.24.8.1422
  20. Murcia AM, 2004, ARCH INTERN MED, V164, P2273, DOI 10.1001/archinte.164.20.2273
  21. Nomura S, 2009, CURR DIABETES REV, V5, P245, DOI 10.2174/157339909789804404
  22. Norhammar A, 2004, J AM COLL CARDIOL, V43, P585, DOI 10.1016/j.jacc.2003.08.050
  23. Paulson DJ, 1997, CARDIOVASC RES, V34, P104, DOI 10.1016/S0008-6363(97)00018-7
  24. Rezende Paulo Cury, 2015, Cardiovasc Diabetol, V14, P66, DOI 10.1186/s12933-015-0228-x
  25. STONE PH, 1989, J AM COLL CARDIOL, V14, P49, DOI 10.1016/0735-1097(89)90053-3
  26. Thygesen K, 2012, J AM COLL CARDIOL, V60, P1581, DOI 10.1016/j.jacc.2012.08.001
  27. Thygesen K, 2012, EUR HEART J, V33, P2252, DOI 10.1093/eurheartj/ehs154
  28. Verdoia M, 2015, DIABETES-METAB RES, V31, P85, DOI 10.1002/dmrr.2567
  29. Zhang ZG, 2011, CIRC-CARDIOVASC QUAL, V4, P172, DOI 10.1161/CIRCOUTCOMES.110.940502