РЕНТГЕНОХИРУРГИЯ В ЛЕЧЕНИИ ОСТРЫХ ИНФАРКТОВ И ИНСУЛЬТОВ. СОВРЕМЕННОЕ СОСТОЯНИЕ ВОПРОСА.ЧАСТЬ 1
Обзорная статья
Дата публикации: сентября 16, 2019
Ключевые слова
инфаркт миокарда
блок интенсивной кардиологической терапии
реперфузия миокарда
интракраниальные вмешательства
инсульт
тромболизис
блок интенсивной кардиологической терапии
реперфузия миокарда
интракраниальные вмешательства
инсульт
тромболизис
Как цитировать
[1]
Б. Реймерс, «РЕНТГЕНОХИРУРГИЯ В ЛЕЧЕНИИ ОСТРЫХ ИНФАРКТОВ И ИНСУЛЬТОВ. СОВРЕМЕННОЕ СОСТОЯНИЕ ВОПРОСА.ЧАСТЬ »1, КМКВ, вып. 3, сс. 73-81, сен. 2019.
Аннотация
После того, как Херрик описал клиническую картину острого инфаркта миокарда более 100 лет назад (1912 г.), лечения ОИМ прошло три фазы развития: фаза 1 (1912–1961 гг., постельный режим и «выжидательное» лечение); фаза 2 (1961–1974, создание и развитие отделений и блоков интенсивной кардиологической терапии); и фаза 3 (с 1975 года по настоящее время, реперфузионная тактика лечения ишемии миокарда). Сейчас мы находимся на пороге фазы 4, которая включает в себя усилия по сокращению перфузионного повреждения миокарда, а также регенеративную медицину. Лечение острого ишемического инсульта претерпело кардинальные изменения в последнее время после продемонстрированной эффективности внутриартериальной тромболитической терапии (IA) на основе данных многочисленных исследований. Отбор пациентов для внутривенной и IA-терапии основан на своевременной визуализации с помощью компьютерной томографии или магнитно-резонансной томографии, с последующей прямой ангиографией для документирования окклюзии крупного сосуда, поддающейся вмешательству. Современные методы визуализации являются основой для выявления ишемического ядра и зоны состоявшегося некроза, и эта информация вносить все больший вклад в принятие решений о тактики лечения по мере увеличения терапевтического временного окна. Внутривенный тромболизис с использованием активатора плазминогена тканевого типа остается основой терапии острого инсульта в течение первых 4.5 часов после начала инсульта. У пациентов с проксимальными окклюзиями крупных сосудов лечение следует начинать на основе IA в течение 6 часов после начала инсульта. Организация и внедрение региональных систем лечения инсульта необходимы для лечения как можно большего числа подходящих пациентов. Новые парадигмы лечения, сочетающие нейропротекцию, высокотехнологические методики и терапию, потенциально увеличивает число пациентов, которых можно лечить, несмотря на длительное время транспортировки, и смягчить последствия реперфузионного повреждения. Лечение острого инсульта вступило в золотой век, и можно ожидать многих дополнительных достижений.Литература
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3. Harrison TR, Resnik WH. Etiologic aspects of heart disease (including treatment of the different etiologic types). In Harrison TR, Beeson PB, Thorn GW, et al. (eds). Principles of internal medicine. New York: Blackiston; 1950. p. 1287–1289.
4. Julian DG. Treatment of cardiac arrest in acute myocardial ischemia and infarction. Lancet. 1961; 840–844.
5. Pantridge JF, Geddes JS. A mobile coronary care unit in the management of myocardial infarction. Lancet. 1967; 271–273.
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7. Ginks WR, Sybers PR, Maroko PR, Covell JW, Sobel BE, Ross J. Coronary artery reperfusion. II. Reduction of myocardial infarct size at one week after the coronary occlusion. J Clin Invest. 1972; 51: 2717–2723.
8. Maroko PR, Braunwald E. Modification of myocardial infarct size after coronary occlusion. Ann Intern Med. 1973; 79: 720–733. doi: 10.7326/0003-4819-79-5-720
9. Chazov EI, Matveeva LS, Mazaev AV, Sargin KE, Sadovskaia GV, Ruda MI. Intracoronary administration of fibrinolysin in acute myocardial infarction. Terapeuticheskii Arkhiv. 1976; 48: 8–19.
10. Markis JE. Malagold M. Parker JA, Silverman KJ, Barry WH, Als AV et al. Myocardial salvage after intracoronary thrombolysis with streptokinase in acute myocardial infarction: assessment of intracoronary thallium-201. N Engl J Med. 1981; 305: 777–782.
11. Gruppo Italiano per lo Studio della Streptochinasi nell’Infarto Miocardico (GISSI). Effectiveness of intravenous thrombolytic treatment in acute myocardial infarction. Lancet. 1986; 397–402.
12. Dalen JE, Gore JM. Braunwald E, Borer J, Goldberg RJ, Passaman ER et al. Six and twelve- month follow-up of the Phase I Thrombolysis in Myocardial Infarction (TIMI) Trial. Am J Cardiol. 1988; 62: 179–185.
13. TIMI Study Group. The Thrombolysis in Myocardial Infarction (TIMI) Trial. N Engl J Med. 1985; 312: 932–936.
14. ISIS-2 Collaborative Group. Randomized trial of intrave- nous streptokinase, oral aspirin, both, or neither among 17187 cases of suspected acute myocardial infarction: ISIS- 2. Lancet. 1988; 349–360.
15. Sabatine MS, Cannon CP, Gibson CM, López-Sendón JL, Montalescot G, Theroux P et al. Addition of clopidogrel to aspirin and fibrinolytic therapy for myocardial infarction with ST-segment elevation. N Engl J Med. 2005; 352: 1179–1189.
16. Keeley EC, Boura JA, Grines CL. Primary angioplasty versus intravenous thrombolytic therapy for acute myocardial infarction: a quantitative review of 23 randomized trials. Lancet. 2003; 361: 13–20.
17. Zhu MM, Feit A, Chadow H, Alam M, Kwan T, Clark LT. Primary stent implan- tation compared with primary balloon angioplasty for acute myocardial infarction. A meta-analysis of randomized clini- cal trials. Am J Cardiol. 2001; 88: 297–301.
18. Brodie BR. Aspiration thrombectomy with primary PCI for STEMI: review of the data and current guidelines. J Invasive Cardiol. 2011; 22(10 Suppl B): 2B–5B.
19. Jennings RB, Sommers HM, Smyth GA, Flack H, Linn H. Myocardial necrosis induced by temporary occlusion of a coronary artery in the dog. Arch Pathol. 1960; 70: 68–78.
20. Krug A, Du Mesnil de Rochemont R, Korb G. Blood supply of the myocardium after temporary coronary occlusion. Circ Res. 1966; 19: 57–62.
21. Kloner RA, Ganote CE, Jennings RB. The «no-reflow» phenomenon after temporary coronary occlusion in the dog. J Clin Invest. 1974; 54: 1496–1508.
22. Ndrepepa G, Tiroch K, Fusaro M, Keta D, Seyfarth M, Byrne RA et al. 5-year prognostic value of no-reflow phenomenon after percutaneous coronary intervention in patients with acute myocardial infarction. J Am Coll Cardiol. 2010; 55: 2383–2389. doi: 10.1016/j.jacc.2009.12.054.
23. Braunwald E, Kloner RA. Myocardial reperfusion: a double-edged sword? J Clin Invest. 1985; 76: 1713–19. doi: 10.1172/JCI112160
24. Yellon DM, Hausenloy DJ. Myocardial reperfusion injury. N Engl J Med. 2007; 357: 1121–1135.
25. Schwartz Longacre L, Kloner RA, Arai AE, Baines CP, Bolli R, Braunwald E et al. New horizons in cardioprotection: recommendations from the 2010 National Heart, Lung and Blood Institute Workshop. Circulation. 2011; 124: 1172–1179.
26. Murry CE, Jennings RB, Reimer KA. Preconditioning with ischemia: a relay of lethal cell injury in ischemic myocardium. Circulation. 1986; 74: 1124–1136.
27. Hausenloy DJ, Yellon DM. Remote ischemic preconditioning underlying mechanisms and clinical application. Cardiovasc Res. 2008; 79: 377–386. doi: 10.1093/cvr/cvn114.
28. Zhao ZQ, Corvera JS, Halkos ME, Kerendi F, Wang NP, Guyton RA et al. Inhibition of myocardial injury by ischemic postconditioning during reperfusion: Comparison with ischemic preconditioning. Am J Physiol Heart Circ Physiol. 2003; 285: H579–H588.
29. Kerendi F, Kin H, Halkos ME, Jiang R, Zatta AJ, Zhao ZQ et al. Remote postconditioning: brief renal ischemia and reperfusion applied before coronary artery reperfusion reduces myocardial infarct size via endogenous activation of adenosine receptors. Basic Res Cardiol. 2005; 100: 404–412.
30. Botker HE, Kharbanda R, Schmidt MR, Bøttcher M, Kaltoft AK, Terkelsen CJ et al. Remote ischemic conditioning before hospital admission, as a complement to angioplasty, and effect on myocardial salvage in patients with acute myocardial infarction: a randomized trial. Lancet. 2010; 375: 727–734.
31. Griffiths EJ, Halestrap AP. Protection by Cyclosporin A of ischemia/reperfusion-induced damage in isolated rat hearts. J Mol Cell Cardiol. 1993; 25: 1461–1469.
32. Piot C, Croisille P, Staat P, Thibault H, Rioufol G, Mewton N et al. Effect of cyclosporine on reperfusion injury in acute myocardial infarction. N Engl J Med. 2008; 359: 473–481. doi: 10.1056/NEJMoa071142.
33. Miura T, Miki T. Limitation of myocardial infarct size in the clinical setting: status and challenges in translating animal experiments into clinical therapy. Basic Res Cardiol. 2008; 1031: 501–512. doi: 10.1007/s00395-008-0743-y.
34. Braunwald E. Clinical efforts to reduce myocardial infarct size – the next step. J Cardiovasc Pharmacol Ther. 2011; 16: 349–353. doi: 10.1177/1074248411407637.
2. Levine SA. Coronary thrombosis: its various clinical features. Baltimore: Williams & Wilkins; 1929.
3. Harrison TR, Resnik WH. Etiologic aspects of heart disease (including treatment of the different etiologic types). In Harrison TR, Beeson PB, Thorn GW, et al. (eds). Principles of internal medicine. New York: Blackiston; 1950. p. 1287–1289.
4. Julian DG. Treatment of cardiac arrest in acute myocardial ischemia and infarction. Lancet. 1961; 840–844.
5. Pantridge JF, Geddes JS. A mobile coronary care unit in the management of myocardial infarction. Lancet. 1967; 271–273.
6. Maroko PR, Kjekshus JK, Sobel BE, Watanabe T, Covell JW, Ross JR et al. Factors influencing infarct size following experimental coronary artery occlusion. Circulation. 1971; 43: 67–82.
7. Ginks WR, Sybers PR, Maroko PR, Covell JW, Sobel BE, Ross J. Coronary artery reperfusion. II. Reduction of myocardial infarct size at one week after the coronary occlusion. J Clin Invest. 1972; 51: 2717–2723.
8. Maroko PR, Braunwald E. Modification of myocardial infarct size after coronary occlusion. Ann Intern Med. 1973; 79: 720–733. doi: 10.7326/0003-4819-79-5-720
9. Chazov EI, Matveeva LS, Mazaev AV, Sargin KE, Sadovskaia GV, Ruda MI. Intracoronary administration of fibrinolysin in acute myocardial infarction. Terapeuticheskii Arkhiv. 1976; 48: 8–19.
10. Markis JE. Malagold M. Parker JA, Silverman KJ, Barry WH, Als AV et al. Myocardial salvage after intracoronary thrombolysis with streptokinase in acute myocardial infarction: assessment of intracoronary thallium-201. N Engl J Med. 1981; 305: 777–782.
11. Gruppo Italiano per lo Studio della Streptochinasi nell’Infarto Miocardico (GISSI). Effectiveness of intravenous thrombolytic treatment in acute myocardial infarction. Lancet. 1986; 397–402.
12. Dalen JE, Gore JM. Braunwald E, Borer J, Goldberg RJ, Passaman ER et al. Six and twelve- month follow-up of the Phase I Thrombolysis in Myocardial Infarction (TIMI) Trial. Am J Cardiol. 1988; 62: 179–185.
13. TIMI Study Group. The Thrombolysis in Myocardial Infarction (TIMI) Trial. N Engl J Med. 1985; 312: 932–936.
14. ISIS-2 Collaborative Group. Randomized trial of intrave- nous streptokinase, oral aspirin, both, or neither among 17187 cases of suspected acute myocardial infarction: ISIS- 2. Lancet. 1988; 349–360.
15. Sabatine MS, Cannon CP, Gibson CM, López-Sendón JL, Montalescot G, Theroux P et al. Addition of clopidogrel to aspirin and fibrinolytic therapy for myocardial infarction with ST-segment elevation. N Engl J Med. 2005; 352: 1179–1189.
16. Keeley EC, Boura JA, Grines CL. Primary angioplasty versus intravenous thrombolytic therapy for acute myocardial infarction: a quantitative review of 23 randomized trials. Lancet. 2003; 361: 13–20.
17. Zhu MM, Feit A, Chadow H, Alam M, Kwan T, Clark LT. Primary stent implan- tation compared with primary balloon angioplasty for acute myocardial infarction. A meta-analysis of randomized clini- cal trials. Am J Cardiol. 2001; 88: 297–301.
18. Brodie BR. Aspiration thrombectomy with primary PCI for STEMI: review of the data and current guidelines. J Invasive Cardiol. 2011; 22(10 Suppl B): 2B–5B.
19. Jennings RB, Sommers HM, Smyth GA, Flack H, Linn H. Myocardial necrosis induced by temporary occlusion of a coronary artery in the dog. Arch Pathol. 1960; 70: 68–78.
20. Krug A, Du Mesnil de Rochemont R, Korb G. Blood supply of the myocardium after temporary coronary occlusion. Circ Res. 1966; 19: 57–62.
21. Kloner RA, Ganote CE, Jennings RB. The «no-reflow» phenomenon after temporary coronary occlusion in the dog. J Clin Invest. 1974; 54: 1496–1508.
22. Ndrepepa G, Tiroch K, Fusaro M, Keta D, Seyfarth M, Byrne RA et al. 5-year prognostic value of no-reflow phenomenon after percutaneous coronary intervention in patients with acute myocardial infarction. J Am Coll Cardiol. 2010; 55: 2383–2389. doi: 10.1016/j.jacc.2009.12.054.
23. Braunwald E, Kloner RA. Myocardial reperfusion: a double-edged sword? J Clin Invest. 1985; 76: 1713–19. doi: 10.1172/JCI112160
24. Yellon DM, Hausenloy DJ. Myocardial reperfusion injury. N Engl J Med. 2007; 357: 1121–1135.
25. Schwartz Longacre L, Kloner RA, Arai AE, Baines CP, Bolli R, Braunwald E et al. New horizons in cardioprotection: recommendations from the 2010 National Heart, Lung and Blood Institute Workshop. Circulation. 2011; 124: 1172–1179.
26. Murry CE, Jennings RB, Reimer KA. Preconditioning with ischemia: a relay of lethal cell injury in ischemic myocardium. Circulation. 1986; 74: 1124–1136.
27. Hausenloy DJ, Yellon DM. Remote ischemic preconditioning underlying mechanisms and clinical application. Cardiovasc Res. 2008; 79: 377–386. doi: 10.1093/cvr/cvn114.
28. Zhao ZQ, Corvera JS, Halkos ME, Kerendi F, Wang NP, Guyton RA et al. Inhibition of myocardial injury by ischemic postconditioning during reperfusion: Comparison with ischemic preconditioning. Am J Physiol Heart Circ Physiol. 2003; 285: H579–H588.
29. Kerendi F, Kin H, Halkos ME, Jiang R, Zatta AJ, Zhao ZQ et al. Remote postconditioning: brief renal ischemia and reperfusion applied before coronary artery reperfusion reduces myocardial infarct size via endogenous activation of adenosine receptors. Basic Res Cardiol. 2005; 100: 404–412.
30. Botker HE, Kharbanda R, Schmidt MR, Bøttcher M, Kaltoft AK, Terkelsen CJ et al. Remote ischemic conditioning before hospital admission, as a complement to angioplasty, and effect on myocardial salvage in patients with acute myocardial infarction: a randomized trial. Lancet. 2010; 375: 727–734.
31. Griffiths EJ, Halestrap AP. Protection by Cyclosporin A of ischemia/reperfusion-induced damage in isolated rat hearts. J Mol Cell Cardiol. 1993; 25: 1461–1469.
32. Piot C, Croisille P, Staat P, Thibault H, Rioufol G, Mewton N et al. Effect of cyclosporine on reperfusion injury in acute myocardial infarction. N Engl J Med. 2008; 359: 473–481. doi: 10.1056/NEJMoa071142.
33. Miura T, Miki T. Limitation of myocardial infarct size in the clinical setting: status and challenges in translating animal experiments into clinical therapy. Basic Res Cardiol. 2008; 1031: 501–512. doi: 10.1007/s00395-008-0743-y.
34. Braunwald E. Clinical efforts to reduce myocardial infarct size – the next step. J Cardiovasc Pharmacol Ther. 2011; 16: 349–353. doi: 10.1177/1074248411407637.