Terapevticheskii arkhiv

Терапевтический архив

0040-36602309-5342

LLC Obyedinennaya Redaktsiya

30316

Editorial article

Передовая статья

Spontaneous reperfusion of infact-related artery in patients with ST elevation myocardial infarction

Спонтанная реперфузия артерии, ответственной за развитие инфаркта, у больных инфарктом миокарда с подъемом сегмента ST

Ruda

M Ya

Руда

М Я

Kuz'min

A I

Кузьмин

А И

Merkulova

I N

Меркулова

И Н

Samko

A N

Самко

А Н

Merkulov

E V

Меркулов

Е В

Sozykin

A V

Созыкин

А В

Akasheva

D U

Акашева

Д У

Ruda

M Ya

Kuzmin

A I

Merkulova

I N

Samko

A N

Merkulov

E V

Sozykin

A V

Akasheva

D U

15052009

815

NO5 (2009)

ТОМ 81, №5 (2009)

202909042020

2009

Consilium Medicum

ООО "Консилиум Медикум"

https://creativecommons.org/licenses/by-nc-sa/4.0

https://ter-arkhiv.ru/0040-3660/article/view/30316

Aim. To characterize a clinical course of ST elevation myocardial infarction (STEMI) and spontaneous reperfusion of the coronary arteries (SR) as well as in patients after reperfusion trombolytic therapy (TLT) and/or transluminal ballon coronary angioplasty (TBCA); to compare effectiveness of different approaches to treatment of SR patients: conservative - early medication and active - TBCA on the first postmyocardial 24 hours. Material and methods. We studied 479 patients admitted to hospital not later than 6 hours since STEMI onset and either having SR (n = 49) or treated using active methods of coronary circulation restoration - prehospital thrombolysis (n = 127), thrombolysis after hospitalization (n = 127), primary TBCA (n = 60) and TBCA after initiation of TLT (n = 116). We made a more detailed analysis on the sample of 149 SR patients. Results. SR was diagnosed in 10.2% cases with STEMI and occurred much earlier than recovery of coronary circulation due to TLT and/or TBCA. Patients with SR developed Q-MI, right ventricular infarction, cardiac failure and atrioventricular block less frequently. They had the lowest peak activity of creatin phosphokinase and a higher left ventricular ejection fraction versus patients without SR (50.7 ± 6.8 and 45.4 ± 6.6%, respectively; p < 0.05). As showen by coronaroangiography, SR patients had no"no reflow" phenomenon (0% and 17%, respectively). Active policy of SR patients treatment had no significant advantages over conservative treatment. Conclusion. Early SR had more favourable course of MI, less mass of the affected myocardium and better contractile function of the left ventricle. The conservative policy of STEMI treatment in the presence of SR is more effective than the active one if a due control over the patients' condition is provided.

Материалы и методы. В исследование включили 479 больных, поступивших в клинику до 6 ч от начала ИМnST, у которых либо наблюдалась СР (49 больных), либо применялись активные методы восстановления коронарного кровотока - догоспитальный тромболизис (127 больных), тромболизис после госпитализации (127 больных), первичная ТБКА (60 больных) и ТБКА после начала ТЛТ (116 больных). Более детальный анализ был выполнен на выборке из 149 больных с СР. Результаты. СР диагностировалась у 10,2% больных с ИМпST и выявлялась существенно раньше, чем восстановление коронарного кровотока под влиянием ТЛТ и/или ТБА. У больных с СР по сравнению с больными без СР реже отмечались формирование Q-ИМ и инфаркта правого желудочка, сердечная недостаточность и атриовентрикулярная блокада. У них наблюдалась самая низкая "пиковая" активность креатинфосфокиназы и более высокая фракция выброса левого желудочка (50,7 ± 6,8 % против 45,4 ± 6,6% у больных без СР; p < 0,05). По данным коронароангиографии у больных с СР фактически отсутствовал феномен "no reflow" (0 % против 17%). Активная тактика лечения больных со СР не имела существенных преимуществ перед консервативной. Заключение. Ранняя СР сопровождается более благоприятным течением ИМ, у таких больных меньше масса пораженного миокарда и лучше сократительная функция левого желудочка. Консервативная тактика ведения больных с ИМnST и СР при условии тщательного контроля за состоянием пациентов, по-видимому, является более предпочтительной, чем активная.

ST elevation myocardial infarctionspontaneous reperfusion of the coronary arterythrombolytic therapytransluminal ballon coronary angioplasty

инфаркт миокарда с подъемом сегмента STспонтанная реперфузия коронарной артериитромболитическая терапиятранслюминальная баллонная коронарная ангиопластика

Uriel N., Moravsky G., Blatt A. et al. Acute myocardial infarction with spontaneous reperfusion: clinical characteristics and optimal timing for revascularization. IMAJ 2007; 9: 243-246.

Rimar D., Crystal E., Battler A. et al. Improved prognosis of patients presenting with clinical markers of spontaneous reperfusion during acute myocardial infarction. Heart 2002; 88: 352-356.

Lee C. W., Hong M. K., Lee J. H. et al. Determinants and prognostic significance of spontaneous coronary recanalization in acute myocardial infarction. Am. J. Cardiol. 2001; 87: 951-954.

Ishihara M., Inoue I., Kawagoe T. et al. Impact of spontaneous anterograde flow of the infarct artery on left ventricular function in patients with a first anterior wall acute myocardial infarction. Am. J. Cardiol. 2002; 90: 5-9.

Stone G. W., Cox D., Garcia E. et al. Normal flow (TIMI-3) before mechanical reperfusion therapy is an independent determinant of survival in acute myocardial infarction: analysis from the primary angioplasty in myocardial infarction trials. Circulation 2001; 104: 636-641.

Christian T. F., Milavetz J. J., Miller T. D. et al. Prevalence of spontaneous reperfusion and associated myocardial salvage in patients with acute myocardial infarction. Am. Heart J. 1998; 135: 421-427.

Steg P. G., Himbert D., Benamer H. et al. Conservative management of patients with acute myocardial infarction and spontaneous acute patency of the infarct-related artery. Am. Heart J. 1997; 134 (2, pt 1): 248-252.

Christian T. F., Bjarne L. N., Jens F. L. et al. Potential significance of spontaneous and interventional ST-changes in patients transferred for primary pecutaneous coronary intervention: observations from the ST-MONitoring in Acute Myocardial Infarction study (The MONAMI study). Eur. Heart J. 2006; 27 (3): 267-275.

Taher T., Fu Y., Wagner G. S. et al. Aborted myocardial infarction in patients with ST-segment elevation: insights from the Assessment of the Safety and Efficacy of a New Thrombolytic Regimen-3 Trial. Electrocardiographic substudy. J. Am. Coll. Cardiol. 2004; 44: 38-43.

10.

Hackworthy R. A., Vogel M. B., Harris P. J. Effect of spontaneous reperfusion on myocardial infarct size. Clin. Cardiol. 1987; 10: 168-174.

11.

Grines C. L., Browne K. F., Marco J. et al. for the Primary Angioplasty in Myocardial infarction Study Group. A comparison of immediate angioplasty with thrombolytic therapy for acute myocardial infarction. N. Engl. J. Med. 1993; 328: 673.

12.

Weaver W. D., Simes R. J., Betriu A. et al. Comparison of primary coronary angioplasty and intravenous thrombolytic therapy for acute myocardial infarction. A quantitative review. J. A. M. A. 1997; 278: 2093.

13.

Nunn C. M., O'Neill W. W., Rothbaum D. et al. for the Primary Angioplasty in Myocardial Infarction I Study Group. Long-term outcome after primary angioplasty: Report from the Primary Angioplasty in Myocardial Infarction (PAMI-1) trial. J. Am. Coll. Cardiol. 1999; 33: 640.

14.

Haider A. W., Andreotti F., Hackett D. R. et al. Early spontaneous intermittent myocardial reperfusion during acute myocardial infarction is associated with augmented thrombogenic activity and less myocardial damage. J. Am. Coll. Cardiol. 1995; 26: 662-667.

15.

Topol E. J., Califf R. M., George B. S. et al. A randomized trial of immediate versus delayed elective angioplasty after intravenous tissue plasminogen activator in acute myocardial infarction. N. Engl. J. Med. 1987; 317: 581-588.

16.

Simoons M. L., Arnold A., Betriu A. et al. Thrombolysis with tissue plasminogen activator in acute myocardial infarction: no additional benefit from immediate percutaneous transluminal coronary angioplasty. Lancet 1988; 1: 197-202.

17.

18.

The TIMI Research Group. Immediate versus delayed catheterization and angioplasty following thrombolytic therapy for acute myocardial infarction: TIMI-IIA results. J. A. M. A. 1988; 260: 2849-2858.

19.

Российские рекомендации. Диагностика и лечение больных острым инфарктом миокарда с подъемом сегмента ST электрокардиограммы. Кардиоваск. тер. и профилакт. 2007; 6, прил.: 26.

20.

Смирнов А. А., Хакимов А. Г., Дорогун Б. Н. Электрокардиографические признаки коронарной реперфузии у больных инфарктом миокарда. Кардиология 1988; 5: 14-19.

21.

Oldroyd K. G. Identifying failure to achieve complete (TIMI 3) reperfusion following thrombolytic treatment: how to do it, when to do it, and why it's worth doing. Heart 2000; 84: 113-115.

22.

Vaturi M., Birnbaum Y. The use of the electrocardiogram to identify epicardial coronary and tissue reperfusion in acute myocardial infarction. J. Thromb. Thrombolys. 2000; 10: 137-147.

23.

De Wood M. A., Spores J., Notske R. et al. Prevalence of total coronary occlusion during the early hours of transmural myocardial infarction. N. Engl. J. Med. 1980; 303: 897-902.

24.

Rentrop K. P. Thrombi in acute coronary syndromes: revisited and revised. Circulation 2000; 101: 1619-1626.

25.

Betriu A., Castaner A., Sanz G. A. et al. Angiographic findings 1 month after myocardial infarction: a prospective study of 259 survivors. Circulation 1982; 65: 1099-1105.

26.

Rentrop K. P., Feit F., Sherman W. et al. Late thrombolytic therapy preserves left ventricular function in patients with collateralized total coronary occlusion: primary end point findings of the Second Mount Sinai-New York University Reperfusion Trial. J. Am. Coll. Cardiol. 1989: 14: 58-64.

27.

Blanke H., von Hardenberg D., Cohen M. et al. Patterns of creatine kinase release during acute myocardial infarction after nonsurgical reperfusion: comparison with conventional treatment and correlation with infarct size. J. Am. Coll. Cardiol. 1984; 3: 675-680.

28.

Zijlstra F., Ernst N., de Boer M. J. et al. Influence of prehospital administration of aspirin and heparin on initial patency of the infarct-related artery in patients with acute ST elevation myocardial infarction. J. Am. Coll. Cardiol. 2002; 39: 1733-1737.

29.

Matetzky S., Freimark D., Chouraqui P. et al. The distinction between coronary and myocardial reperfusion after thrombolytic therapy by clinical markers of reperfusion. J. Am. Coll. Cardiol. 1998; 32: 1326-1330.

30.

Huey B. L., Gheorghiade M., Crampton R. S. et al. Acute non-Q wave myocardial infarction associated with early ST segment elevation: evidence for spontaneous coronary reperfusion and implications for thrombolytic trials. J. Am. Coll. Cardiol. 1987; 9: 18-25.

31.

Hata K., Whittaker P., Kloner R. A. et al. Brief antecedent ischemia attenuates platelet-mediated thrombosis in damaged and stenotic canine coronary arteries: role of adenosine. Circulation 1998; 97: 692-702.

32.

Przyklenk K., Whittaker P. Brief antecedent ischemia enhances recombinant tissue plazminogen activator-induced coronary thrombolysis by adenosine-mediated mechanism. Circulation 2000; 102: 88-95.

33.

Anzai T., Yoshikawa T., Asakura Y. et al. Preinfarction angina as a major predictor of left ventricular function and long-term prognosis after a first Q wave myocardial infarction. J. Am. Coll. Cardiol. 1995; 26: 19-27.

34.

Lincoff A. M., Topol E. J. Illusion of reperfussion: does anyone achieve optimal repercussion during acute myocardial infarction. Circulation 1993; 88: 1361-1374.

35.

De Luca G., Ernst N., Zijlstra F. et al. Preprocedural TIMI flow and mortality in patients with acute myocardial infarction treated by primary angioplasty. J. Am. Coll. Cardiol. 2004; 43: 1363.

36.

Каган-Пономарев М. Я., Добровольский А. Б., Староверов И. И. и др. Коагулологические особенности у больных инфарктом миокарда при раннем спонтанном и медикаментозном восстановлении коронарного кровотока. Кардиология 1994; 11: 4-10.