دورية أكاديمية

[Predictors of acute coronary syndrome in patients with ischaemic heart disease].

التفاصيل البيبلوغرافية
العنوان: [Predictors of acute coronary syndrome in patients with ischaemic heart disease].
عنوان ترانسليتريتد: Prediktory ostrogo koronarnogo sindroma u patsientov s ishemicheskoĭ bolezn'iu serdtsa.
المؤلفون: Kochergin NA; Laboratory of Roentgenoendovascular and Reconstructive Surgery of the Heart and Vessels, Research Institute for Complex Problems of Cardiovascular Diseases, Kemerovo, Russia., Kochergina AM; Laboratory of Roentgenoendovascular and Reconstructive Surgery of the Heart and Vessels, Research Institute for Complex Problems of Cardiovascular Diseases, Kemerovo, Russia., Ganiukov VI; Laboratory of Roentgenoendovascular and Reconstructive Surgery of the Heart and Vessels, Research Institute for Complex Problems of Cardiovascular Diseases, Kemerovo, Russia.
المصدر: Angiologiia i sosudistaia khirurgiia = Angiology and vascular surgery [Angiol Sosud Khir] 2020; Vol. 26 (3), pp. 179-184.
نوع المنشور: Journal Article
اللغة: Russian
بيانات الدورية: Publisher: Izd-vo Info-Media Country of Publication: Russia (Federation) NLM ID: 9604504 Publication Model: Print Cited Medium: Print ISSN: 1027-6661 (Print) Linking ISSN: 10276661 NLM ISO Abbreviation: Angiol Sosud Khir Subsets: MEDLINE
أسماء مطبوعة: Original Publication: [Moskva] : Izd-vo Info-Media, c1995-
مواضيع طبية MeSH: Acute Coronary Syndrome*/complications , Acute Coronary Syndrome*/diagnosis , Coronary Artery Disease* , Plaque, Atherosclerotic*/complications , Plaque, Atherosclerotic*/diagnosis, Humans
مستخلص: Acute coronary syndrome has for a long time been giving no way of decreasing mortality related to ischaemic heart disease. The primary cause of acute coronary syndrome in the majority of cases is rupture of an unstable atherosclerotic plaque in the coronary artery followed by thrombosis thereof. The main missions of modern cardiology include: assessment of the risk of acute coronary syndrome, identification of predictors of adverse events, and working-out of measures aimed at prevention and optimal management of patients with ischaemic heart disease. This article deals with clinical and morphological factors associated with destabilization of coronary plaques, their rupture, and the development of an acute coronary event.
References: Kochergin NA, Kochergina AM, Khorlampenko AA, et al. Nestabil'nye ateroskleroticheskie blyashki koronarnykh arterii pri stabil'noi ishemicheskoi bolezni serdtsa: 12-mesyachnoe nablyudenie. Kardiologiya. 2020; 60: 2: 1–6. (In Russ.). doi: 10.18087/cardio.2020.2.n467.
Laimoud M, Faris F, Elghawaby H. Coronary atherosclerotic plaque vulnerability rather than stenosis predisposes to non-ST elevation acute coronary syndromes. Cardiol. Res. Pract. 2019; 2019: 2642740. doi: 10.1155/2019/2642740.
Roth GA, Johnson C, Abajobir A, et al. Global, regional, and national burden of cardiovascular diseases for 10 causes, 1990 to 2015. J. Am. Coll. Cardiol. 2017; 70: 1: 1–25. doi: 10.1016/j.jacc.2017.04.052.
Theodorou K, Boon RA. Endothelial cell metabolism in atherosclerosis. Front. Cell Dev. Biol. 2018; 6: 82. doi: 10.3389/fcell.2018.00082.
Muller JE, Tofler GH, Stone PH. Circadian variation and triggers of onset of acute cardiovascular disease. Circulation. 1989; 79: 4: 733–743. doi: 10.1161/01.cir.79.4.733.
Yonetsu T, Jang IK. Advances in intravascular imaging: new insights into the vulnerable plaque from imaging studies. Korean Circ. J. 2018; 48: 1: 1–15. doi: 10.4070/kcj.2017.0182.
Costopoulos C, Huang Y, Brown AJ, et al. Plaque rupture in coronary atherosclerosis is associated with increased plaque structural stress. JACC Cardiovasc. Imaging. 2017; 10: 12: 1472–1483. doi: 10.1016/j.jcmg.2017.04.017.
Brown AJ, Teng Z, Evans PC, et al. Role of biomechanical forces in the natural history of coronary atherosclerosis. Nat. Rev. Cardiol. 2016; 13: 4: 210–220. doi: 10.1038/nrcardio.2015.203.
Stefanadis C, Antoniou CK, Tsiachris D, Pietri P. Coronary atherosclerotic vulnerable plaque: current perspectives. J. Am. Heart Assoc. 2017; 6: 3: 5543. doi: 10.1161/JAHA.117.005543.
Wu MY, Li CJ, Hou MF, Chu PY. New insights into the role of inflammation in the pathogenesis of atherosclerosis. Int. J. Mol. Sci. 2017; 18: 10: 2034. doi: 10.3390/ijms18102034.
Ji Y, Fish PM, Strawn TL, et al. C-reactive protein induces expression of tissue factor and plasminogen activator inhibitor-1 and promotes fibrin accumulation in vein grafts. J. Thromb. Haemost. 2014; 12: 10: 1667–1677. doi: 10.1111/jth.12680.
Stancel N, Chen C, Ke L, et al. Interplay between CRP, atherogenic LDL, and LOX-1 and its potential role in the pathogenesis of atherosclerosis. Clin. Chem. 2016; 62: 2: 320–327. doi: 10.1373/clinchem.2015.243923.
Peilkert A, Kaier K, Merz J, et al. Residual inflammatory risk in coronary heart disease: incidence of elevated high-sensitive CRP in a real-world cohort. Clin. Res. Cardiol. 2020; 109: 3: 315–323. doi: 10.1007/s00392-019-01511-0.
Lahdentausta L, Leskela J, Winkelmann A, et al. Serum MMP-9 diagnostics, prognostics, and activation in acute coronary syndrome and its recurrence. J. Cardiovasc. Transl. Res. 2018; 11: 3: 210–220. doi: 10.1007/s12265-018-9789-x.
Tong DC, Whitbourn R, Maclsaac A, et al. High-sensitivity C-reactive protein is a predictor of coronary microvascular dysfunction in patients with ischemic heart disease. Front. Cardiovasc. Med. 2018; 4: 81. doi: 10.3389/fcvm.2017.00081.
Liu HH, Cao YX, Sun D, et al. High-sensitive C-reactive protein and hypertension: combined effects on coronary severity and cardiovascular outcomes. Hypertens. Res. 2019; 42: 11: 1783–1793. doi: 10.1038/s41440-019-0293-8.
Cheng JM, Oemrawsingh RM, Garcia-Garcia HM, et al. Relation of C-reactive protein to coronary plaque characteristics on grayscale, radiofrequency intravascular ultrasound, and cardiovascular outcome in patients with acute coronary syndrome or stable angina pectoris (from the ATHEROREMO-IVUS Study). Am. J. Cardiol. 2014; 114: 10: 1497–1503. doi: 10.1016/j.amjcard.2014.08.013.
Tay C, Liu YH, Hosseini H, et al. T. B-cell-specific depletion of tumour necrosis factor alpha inhibits atherosclerosis development and plaque vulnerability to rupture by reducing cell death and inflammation. Cardiovasc. Res. 2016; 111: 4: 385–397. doi: 10.1093/cvr/cvw186.
Cherneva ZV, Denchev SV, Gospodinova MV, et al. Inflammatory cytokines at admission-independent prognostic markers in patients with acute coronary syndrome and hyperglycaemia. Acute Cardiac. Care. 2012; 14: 1: 13–19. doi: 10.3109/17482941.2011.655292.
Battes LC, Cheng JM, Oemrawsingh RM, et al. Circulating cytokines in relation to the extent and composition of coronary atherosclerosis: results from the ATHEROREMO-IVUS study. Atherosclerosis. 2014; 236: 1: 18–24. doi: 10.1016/j.atherosclerosis.2014.06.010.
Ait-Oufella H, Taleb S, Mallat Z, Tedgui A. Recent advances on the role of cytokines in atherosclerosis. Arterioscler. Thromb. Vasc. Biol. 2011; 31: 5: 969–979. doi: 10.1161/ATVBAHA.110.207415.
Welsh P, Murray HM, Ford I, et al. Circulating interleukin-10 and risk of cardiovascular events: a prospective study in the elderly at risk. Arterioscler. Thromb. Vasc. Biol. 2011; 31: 10: 2338–2344. doi: 10.1161/ATVBAHA.111.231795.
Oemrawsingh RM, Lenderink T, Akkerhuis KM, et al. Multimarker risk model containing troponin-T, interleukin 10, myeloperoxidase and placental growth factor predicts long-term cardiovascular risk after non-ST-segment elevation acute coronary syndrome. Heart. 2011; 97: 13: 1061–1066. doi: 10.1136/hrt.2010.197392.
Kato M, Dote K, Naganuma T, et al. Clinical predictors of culprit plaque rupture assessed on intravascular ultrasound in acute coronary syndrome. Circ. J. 2010; 74: 9: 1936–1942.
Lloyd-Jones DM, Morris PB, Ballantyne CM, et al. 2016 ACC expert consensus decision pathway on the role of non-statin therapies for LDL-cholesterol lowering in the management of atherosclerotic cardiovascular disease risk: a report of the American College of Cardiology Task Force on Clinical Expert Consensus Documents. J. Am. Coll. Cardiol. 2016; 68: 1: 92–125. doi: 10.1016/j.jacc.2016.03.519.
Grundy SM, Stone NJ, Bailey AL, et al. 2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the management of blood cholesterol: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. J. Am. Coll. Cardiol. 2019; 73: 24: 3168–3209. doi: 10.1016/j.jacc.2018.11.002.
Hafiane A, Kellett S, Genest J. Treatment options for low high-density lipoproteins. Curr. Opin. Endocrinol. Diabetes Obes. 2014; 21: 2: 134–139. doi: 10.1097/MED.0000000000000049.
Androulakis E, Zacharia E, Papageorgiou N, et al. High-density lipoprotein and low-density lipoprotein therapeutic approaches in acute coronary syndromes. Curr. Cardiol. Rev. 2017; 13: 3: 168–182. doi: 10.2174/1573403X13666170209145622.
Rosenson RS, Brewer HB, Ansell BJ, et al. Dysfunctional HDL and atherosclerotic cardiovascular disease. Nat. Rev. Cardiol. 2016; 13: 1: 48–60. doi: 10.1038/nrcardio.2015.124.
Tang X, Yang Y, Luo S, et al. The effect of statin therapy on plaque regression following acute coronary syndrome: a meta-analysis of prospective trials. Coron. Artery Dis. 2016; 27: 8: 636–649.
Ye H, Wang S, Hu Y, et al. Therapeutic effects of different atorvastatin doses on vulnerable plaques in coronary arteries assessed by intracoronary optical coherence tomography. Medicine (Baltimore). 2018; 97: 31: 11718. doi: 10.1097/MD.0000000000011718.
Tsujita K, Sugiyama S, Sumida H, et al. PRECISE–IVUS Investigators. Impact of dual lipid-lowering strategy with ezetimibe and atorvastatin on coronary plaque regression in patients with percutaneous coronary intervention: the multicenter randomized controlled PRECISE-IVUS Trial. J. Am. Coll. Cardiol. 2015; 66: 5: 495–507. doi: 10.1016/j.jacc.2015.05.065.
Cheng JM, Oemrawsingh RM, Garcia-Garcia HM, et al. PCSK9 in relation to coronary plaque inflammation: results of the ATHEROREMO-IVUS study. Atherosclerosis. 2016; 248: 117–122. doi: 10.1016/j.atherosclerosis.2016.03.010.
Tang WH, Hazen SL. Atherosclerosis in 2016: advances in new therapeutic targets for atherosclerosis. Nat. Rev. Cardiol. 2017; 14: 2: 71–72. doi: 10.1038/nrcardio.2016.216.
Huang Y, Cai X, Mai W, et al. Association between prediabetes and risk of cardiovascular disease and all cause mortality: systematic review and meta-analysis. BMJ. 2016; 355: 5953. doi: 10.1136/bmj.i5953.
Su G, Mi S, Tao H, et al. Association of glycemic variability and the presence and severity of coronary artery disease in patients with type 2 diabetes. Cardiovasc. Diabetol. 2011; 10: 19. doi: 10.1186/1475-2840-10-19.
Desouza CV, Bolli GB, Fonseca V. Hypoglycemia, diabetes, and cardiovascular events. Diabetes Care. 2010; 33: 6: 1389–1394. doi: 10.2337/dc09-2082.
Kuroda M, Shinke T, Sakaguchi K, et al. Effect of daily glucose fluctuation on coronary plaque vulnerability in patients pre-treated with lipid-lowering therapy: a prospective observational study. JACC Cardiovasc. Interv. 2015; 8: 6: 800–811. doi: 10.1016/j.jcin.2014.11.025.
Kochergin NA, Kochergina AM. Vnutrisosudistyi ul'trazvuk kak metod vyyavleniya nestabil'nykh ateroskleroticheskikh blyashek koronarnykh arterii (obzor literatury). Meditsinskaya vizualizatsiya. 2017; 4: 21: 82–87. (In Russ.). doi: 10.24835/1607-0763-2017-4-82-87.
Zimetti F, Freitas WM, Campos AM, et al. Cholesterol efflux capacity does not associate with coronary calcium, plaque vulnerability, and telomere length in healthy octogenarians. J. Lipid Res. 2018; 59: 4: 714–721. doi: 10.1194/jlr.P079525.
Finn AV, Nakano M, Narula J, et al. Concept of vulnerable/unstable plaque. Arterioscler. Thromb. Vasc. Biol. 2010; 30: 7: 1282–1292. doi: 10.1161/ATVBAHA.108.179739.
Stone GW, Maehara A, Lansky A. J., et al. A prospective natural-history study of coronary atherosclerosis. N. Engl. J. Med. 2011; 364: 3: 226–235. doi: 10.1056/NEJMoa1002358.
Calvert PA, Obaid DR, O'Sullivan M, et al. Association between IVUS findings and adverse outcomes in patients with coronary artery disease: the VIVA (VH-IVUS in Vulnerable Atherosclerosis) Study. JACC Cardiovasc. Imag. 2011; 4: 8: 894–901. doi: 10.1016/j.jcmg.2011.05.005.
Cheng JM, Garcia-Garcia HM, de Boer SP, et al. In vivo detection of high-risk coronary plaques by radiofrequency intravascular ultrasound and cardiovascular outcome: results of the ATHEROREMO-IVUS study. Eur. Heart. J. 2014; 35: 10: 639–647. doi: 10.1093/eurheartj/eht484.
Bom MJ, van der Heijden DJ, Kedhi E, et al. Early detection and treatment of the vulnerable coronary plaque: can we prevent acute coronary syndromes? Circ. Cardiovasc. Imaging. 2017; 10: 5: 5973. doi: 10.1161/CIRCIMAGING.116.005973.
Kochergin NA, Ganyukov VI. Randomizirovannoe issledovanie preventivnoi revaskulyarizatsii nestabil'nykh blyashek koronarnykh arterii u bol'nykh khronicheskoi ishemicheskoi bolezn'yu serdtsa. Kompleksnye problemy serdechno-sosudistykh zabolevanii. 2019; 8: (4S): 104–110. (In Russ.). doi: 10.17802/2306-1278-2019-8-4S-104-110.
فهرسة مساهمة: Keywords: acute coronary syndrome; intravascular ultrasound; ischaemic heart disease; myocardial infarction; thin-cap fibroatheroma; unstable plaque
Local Abstract: [Publisher, Russian] Острый коронарный синдром длительное время не позволяет снизить смертность от ишемической болезни сердца. Главной причиной острого коронарного синдрома в большинстве случаев является разрыв нестабильной атеросклеротической бляшки в коронарной артерии с последующим ее тромбозом. Основные задачи современной кардиологии – оценка риска острого коронарного синдрома, выявление предикторов неблагоприятных событий и разработка мер профилактики и оптимального лечения пациентов с ишемической болезнью сердца. В статье представлены клинические и морфологические факторы, ассоциированные с дестабилизацией коронарных бляшек, их разрывом и развитием острого коронарного события.
تواريخ الأحداث: Date Created: 20201016 Date Completed: 20201019 Latest Revision: 20201019
رمز التحديث: 20221213
DOI: 10.33529/ANGI02020302
PMID: 33063766
قاعدة البيانات: MEDLINE
الوصف
تدمد:1027-6661
DOI:10.33529/ANGI02020302