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Predictors of rapid progression of carotid atherosclerosis in patients with stable coronary artery disease after myocardial revascularization

Authors: Sokolova N.Yu. 1, Bakulina A.V. 1 3, Magomedova N.M. 2, Kazanovskaya S.N. 2, Golukhova E.Z. 2

Company: 1 Tver’ «Regional clinical hospital», Peterburgskoe shosse, 105, Tver’, Region Tver’, 170036, Russian Federation;
2 Bakoulev National Scientific and Practical Center for Cardiovascular Surgery of Ministry of Health of the Russian Federation, Rublevskoe shosse, 135, Moscow, 121552, Russian Federation;
3 Tver’ State Medical University of Ministry of Health of the Russian Federation, ulitsa Sovetskaya, 4, Tver’, 170100, Russian Federation

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Type:  Ischemic heart disease


DOI: https://doi.org/10.24022/1997-3187-2017-11-3-222-234

For citation: Sokolova N.Yu., Bakulina A.V., Magomedova N.M., Kazanovskaya S.N., Golukhova E.Z. Predictors of rapid progression of carotid atherosclerosis in patients with stable coronary artery disease after myocardial revascularization. Kreativnaya Kardiologiya (Creative Cardiology). 2017; 11 (3): 222–34 (in Russ.). DOI: 10.24022/1997-3187-2017-11-3-222-234

Received / Accepted:  August 03, 2017 / August 11, 2017

Keywords: coronary artery disease stenosis of the internal carotid artery accelerated atherosclerosis systemic inflammatory response

Full text:  

 

Abstract

Objective. To identify predictors of rapid progression of carotid atherosclerosis in patients with stable coronary artery disease (SCAD) after different methods of myocardial revascularization.

Material and methods. The study included 111 patients with SCAD without hemodynamically significant lesions of the internal carotid artery (ICA) who underwent myocardial revascularization. The criteria for inclusion in this study was the indication for myocardial revascularization, the exclusion criteria – severe heart valves dysfunction, left ventricular (LV) aneurysm, acute myocardial infarction, severe systolic left ventricular dysfunction (ejection fraction less 35%), significant ICA stenosis, age more than 80 years, pre-operative acute neurological disease associated with cancer and rheumatologic diseases. Myocardial revascularization in patients with stable coronary artery disease and concomitant non-significant lesion of the brachiocephalic arteries was performed using coronary artery bypass grafting (CABG), including on-pump CABG (n=32), off-pump CABG (n=30); percutaneous coronary intervention (PCI) (n=49) with drug-eluting stents implantation. The mean age was 60.2±8.1 years; all clinical characteristics were comparable among 3 groups. The average follow-up period was 37.9±6 months.

Results. Conducted univariate logistic regression analysis revealed a correlation of accelerated progression of the brachiocephalic atherosclerosis after surgical and interventional procedures in patients with concomitant diabetes (HbA1c more 7,5% (p=0.038), elevated high-sensitivity CRP (p=0.041), smoking continuation (p=0.046), I (p=0.049) and IV types (p=0.034) atherosclerotic plaques in the ICA, elevated values of metalloproteinase-9 (MMP-9) (p=0.017) and myocardial revascularization with on-pump CABG (p=0.029).

Сonclusion. Syndrome of accelerated atherosclerosis of ICA was observed in patients with complex morphology of brachiocephalic stenosis, chronic nicotine consumption, a concomitant poorly controlled diabetes, high values of inflammation markers (hs-CRP and MMP-9) and on-pump CABG.

References

  1. Huh J., Wall M.J., Soltero E.R. Treatment of combined coronary and carotid artery disease. Curr. Opin. Cardiol. 2003; 18: 447–53.

  2. Libby P. Braunwald’s heart disease: a textbook of cardiovascular medicine. 10th ed. Boston, Mass, USA: Saunders; 2014: 873–90.

  3. Ip J.H., Fuster V., Badimon L., Badimon J., Taubman M.B., Chesebro J.H. Syndromes of accelerated atherosclerosis: role of vascular injury and smooth muscle cell proliferation. J. Am. Coll. Cardiol. 1990; 15 (7): 1667–87. DOI: 10.1016/0735-1097(90)92845-s.

  4. Zouridakis E.G., Schwartzman R., Garcia-Moll X. et al. Increased plasma endothelin levels in angina patients with rapid coronary artery disease progression. Eur. Heart J. 2001; 22 (17): 1578–84.

  5. Nakachi T., Kosuge M., Hibi K. et al. C-reactive protein elevation and rapid angiographic progression of nonculprit lesion in patients with non-STsegment elevation acute coronary syndrome. Circ. J. 2008; 72 (12): 1953–9.

  6. Mazzone A., Parri M.S., Giannessi D. et al. Osteopontin plasma levels and accelerated atherosclerosis in patients with CAD undergoing PCI: a prospective clinical study. Coronary Artery Dis. 2011; 22 (3): 179–87.

  7. Kataoka Y., Wolski K., Uno K. et al. Spotty calcification as a marker of accelerated progression of coronary atherosclerosis. J. Am. Coll. Cardiol. 2012; 59 (18): 1592–7.

  8. Bockeria L.A., Kamchatnov P.R., Klyuchnikov I.V.et al. Cerebrovascular disorders in patients withcoronary artery bypass graft. Zhurnal Nevrologii iPsikhiatrii imeni S.S. Korsakova (S.S. KorsakovJournal of Neurology and Psychiatry). 2008; 3: 90–4(in Russ.).

  9. Kuntsevich G.I. Ultrasonic methods for studyingthe branches of the aortic arch. Minsk: Aversev;2006 (in Russ.).

  10. Kuntsevich G.I., Belolapotko E.A. UltrasonicDoppler diagnostics of vascular diseases. Eds.Nikitina Yu.M., Trukhanova A.I. Moscow: Vidar;1998 (in Russ.).

  11. Schiller N.B., Shah P.M., Crawford M. et al. Recommendations for quantitation of the left ventricle by towd imensional echocardiography. J. Am. Soc. Echocardiogr. 1989; 43 (2): 358–67.

  12. Charlson M.E., Pompei P., Ales K.L., McKenzie C.R. A new method of classifying prognostic comorbidity in longitudinal studies: development and validation. J. Chron. Dis. 1987; 40 (5): 373–83.

  13. Fihn S.D., Blankenship J.C., Alexander K.P., Bittl J.A., Byrne J.G. et al. 2014 ACC/AHA/AATS/PCNA/SCAI/STS Focused Update of the Guideline for the diagnosis and management of patients with stable ischemic heart disease. J. Am. Coll. Cardiol. 2014; 64 (18): 1929–49. DOI: 10.1016/j.jacc.2014.07.017.

  14. Windecker S., Kolh P., Alfonso F. 2014 ESC/EACTS. Guidelines on Myocardial Revascularization. The Task Force on Myocardial Revascularization of the European Society of Cardiology (ESC) and the European Association for Cardio-Thoracic Surgery (EACTS) Eur. Heart J. 2014; 35 (37): 2541–619. DOI: 10.1093/eurheartj/ehu278.

  15. Shah P., Bajaj S., Virk H., Bikkina M., Shamoon F. Rapid progression of coronary atherosclerosis: a review. Thrombosis. 2015; 2015: article ID 634983. DOI: 10.1155/2015/634983.

  16. Bulaeva N.I., Golukhova E.Z. Endothelial dysfun-ction and oxidative stress: a role in the developmentof cardiovascular pathology. Kreativnaya Kardiolo-giya (Creative Cardiology).2013; 1: 14–22 (in Russ.).

  17. Mather K., Anderson T.J., Verma S. Insulin action in the vasculature: physiology and pathophysiology. J. Vasc. Res. 2001; 38: 415–22.

  18. Verma S., Anderson T.J. Fundamentals of endothelial function for the clinical cardiologist. Circulation. 2002; 105: 546–9.

  19. Davignon J., Ganz P. Role of endothelial dysfunction in atherosclerosis. Circulation. 2004; 109: 27–32.

  20. Warren O.J., Watret A.L., de Wit K.L., Alexiou C., Vincent C., Darzi A.W., Athanasiou T. The inflammatory response to cardiopulmonary bypass: part 2–anti-inflammatory therapeutic strategies. J. Cardiothorac. Vasc. Anesth. 2009; 23: 384–93.

  21. Onorati F., Rubino A.S., Nucera S., Foti D., Sica V., Santini F. et al. Off-pump coronary artery bypass surgery versus standard linear or pulsatile cardiopulmonary bypass: endothelial activation and inflammatory response. Eur. J. Cardiothorac. Surg. 2010; 37: 897–904.

  22. Shumkov K.V., Lefterov N.P., Pak N.L., Kaku-chaya T.T. et al. Aortocoronary bypass in condi-tions of artificial circulation and working heart: acomparative analysis of immediate and long-termresults and postoperative complications (cardiacrhythm disturbances, cognitive and neurologicaldisorders, rheological features and the state of thehemostatic system). Kreativnaya Kardiologiya(Creative Cardiology).2009; 1: 28–50 (in Russ.)

  23. Aird W.C. Endothelial cell heterogeneity. Crit. Care Med. 2003; 31: S221–30.

  24. Jongman R.M., Zijlstra J.G., Kok W.F., van Harten A.E et al. Off-Pump CABG surgery reduces systemic inflammation compared with on-pump surgery but does not change systemic endothelial responses: a prospective randomized study. Shock. 2014; 42 (2): 121–8.

  25. Parolari A., Camera M., Alamanni F., Naliato M., Polvani G.L., Agrifoglio M., Brambilla M., Biancardi C., Mussoni L., Biglioli P. et al. Systemic inflammation after on-pump and off-pump coronary bypass surgery: a one-month follow-up. Ann. Thorac. Surg. 2007; 84: 823–8.

  26. Karu I., Taal G., Zilmer K., Pruunsild C., Starkopf J., Zilmer M. Inflammatory/oxidative stress during the first week after different types of cardiac surgery. Scand. Cardiovasc. J. 2010; 44: 119–24.

  27. Suleiman M.S., Zacharowski K., Angelini G.D. Inflammatory response and cardioprotection during open-heart surgery: the importance of anaesthetics. Br. J. Pharmacol. 2008; 153: 21–33.

  28. Plicner D., Stoliński J., Wc5 sowicz M., Gawc5 da B., Hymczak H. et al. Preoperative values of inflammatory markers predict clinical outcomes in patients after CABG, regardless of the use of cardiopulmonary bypass. Ind. Heart J. 2016; 68: 10–5.

  29. Jankowski P., Czarnecka D., Łukaszewska A., Łysek R., Wolfshaut-Wolak R. et al. Factors related to the effectiveness of hypercholesterolemia treatment following hospitalization for coronary artery disease. Pol. Arch. Med. Wewn. 2016; 126: 388–94.

  30. Raja S.G., Berg G.A. Impact of off-pump coronary artery bypass surgery on systemic inflammation: current best available evidence. J. Card. Surg. 2007; 22: 445–55.

  31. Boehm J., Hauner K., Grammer J. et al. Tumor necrosis factor-a-863 C/A promoter polymorphism affects the inflammatory response after cardiac surgery. Eur. J. Cardiothorac. Surg. 2011; 40: 50–4.

  32. Wypasek E., Undas A., Sniezek-Maciejewska M. et al. The increased plasma creactive protein and interleukin-6 levels in patients undergoing coronary artery bypass grafting surgery are associated with the interleukin-6-174G > C gene polymorphism. Ann. Clin. Biochem. 2010; 47: 343–9.

  33. Lehmann L.E., Schroeder S., Hartmann W. et al. A single nucleotide polymorphism of macrophage migration inhibitory factor is related to inflammatory response in coronary bypass surgery using cardiopulmonary bypass. Eur. J. Cardiothorac. Surg. 2006; 30: 59–63.

  34. Nobuyoshi M., Tanaka M., Nosaka H. et al. Progression of coronary atherosclerosis: is coronary spasm related to progression? J. Am. Coll. Cardiol. 1991; 18 (4): 904–10.

  35. West M.J., Nestel P.J., Kirby A.C. et al. The value of N-terminal fragment of brain natriuretic peptide and tissue inhibitor of metalloproteinase-1 levels as predictors of cardiovascular outcome in the 179 LIPID study. Eur. Heart J. 2008; 29: 923–31.

  36. Eldrup N., Gronholdt M.L., Sillesen H., Nordestgaard B.G. Elevated matrix metalloproteinase-9 associated with stroke or cardiovascular death in patients with carotid stenosis. Circulation. 2006; 114: 1847–54.

  37. Ross R. Atherosclerosis – an inflammatory disease. N. Engl. J. Med. 1999; 340: 115–26.

  38. Hansson G.K. Inflammation, atherosclerosis, and coronary artery disease. N. Engl. J. Med. 2005; 352: 1685–95.

  39. Libby P., Ridker P.M., Hansson GK. Inflammation in atherosclerosis: from pathophysiology to practice. J. Am. Coll. Cardiol. 2009; 54: 2129–38.

  40. Ridker P.M., Cushman M., Stampfer M.J., Tracy R.P., Hennekens C.H. Inflammation, aspirin, and the risk of cardiovascular disease in apparently healthy men. N. Engl. J. Med. 1997; 336: 973–9.

  41. Ridker P.M., Hennekens C.H., Buring J.E., Rifai N. C-reactive protein and other markers of inflammation in the prediction of cardiovascular disease in women. N. Engl. J. Med. 2000; 342: 836–43.

  42. Del Rincón I., Polak J.F., O'Leary D.H., Battafarano D.F. et. al. Systemic inflammation and cardiovascular risk factors predict rapid progression of atherosclerosis in rheumatoid arthritis. Ann. Rheum. Dis. 2015; 74 (6): 1118–23. DOI: 10.1136/annrheumdis-2013-205058.

  43. Ridker P.M., Everett B.M., Thuren T., MacFadyen J.G., Chang W.H., Ballantyne C. et al. Antiinflammatory therapy with canakinumab for atherosclerotic disease. N. Engl. J. Med. 2017; 377: 1119–31. DOI: 10.1056/NEJMoa1707914.

  44. Kaski J. C. Rapid coronary artery disease progression and angiographic stenosis morphology. Italian Heart J. 2000; 1 (1): 21–5.

  45. Kaski J.C., Chen L., Crook R., Cox I., Tousoulis D., Chester M.R. Coronary stenosis progression differs in patients with stable angina pectoris with and without a previous history of unstable angina. Eur. Heart J. 1996; 17 (10): 1488–94.

  46. Kaski J.C., Chen L., Chester M. Rapid angiographic progression of ‘target’ and ‘nontarget’ stenoses in patients awaiting coronary angioplasty. J. Am. Coll. Cardiol. 1995; 26 (2): 416–21.

  47. Kaski J.C., Chester M.R., Chen L., Katritsis D. Rapid angiographic progression of coronary artery disease in patients with angina pectoris. Circulation. 1995; 92 (8): 2058–65.

About Authors

  • Sokolova Natal'ya Yur'evna, Cand. Med. Sc., Cardiologist, orcid.org/0000-0002-5720-304X;
  • Bakulina Aleksandra Vladimirovna, Cardiovascular Surgeon;
  • Magomedova Nargiz Magomedovna, Junior Researcher;
  • Kazanovskaya Svetlana Nikolaevna, Junior Researcher;
  • Golukhova Elena Zelikovna, Dr Med. Sc., Professor, Academician of Russian Academy of Sciences, Head of Department, orcid.org/0000-0002-6252-0322

Chief Editor

Leo A. Bockeria, MD, PhD, DSc, Professor, Academician of Russian Academy of Sciences, President of Bakoulev National Medical Research Center for Cardiovascular Surgery


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