Феномен no-reflow и реперфузионное повреждение миокарда: механизмы и методы лечения
https://doi.org/10.17650/1818-8338-2021-15-1-4-K645
Аннотация
В настоящее время одним из ключевых методов лечения пациентов с инфарктом миокарда с подъемом сегмента ST является как можно более быстрое, полное и устойчивое восстановление кровотока в инфарктсвязанной артерии. Однако в ряде случаев добиться адекватной реперфузии миокарда не удается, несмотря на восстановление коронарного кровотока. Данный феномен получил название “no-reflow”, или «синдром невосстановленного коронарного кровотока». В связи с отсутствием единого подхода к диагностике no-reflow его встречаемость варьируется в широких пределах – от 2 до 44 %. Недостижение адекватной перфузии миокарда приводит к более высокой летальности – от 7,4 до 30,3 %, а также к более агрессивному ремоделированию миокарда. Длительное время одним из ведущих механизмов считалась дистальная эмболия при чрескожном коронарном вмешательстве. Однако рутинное использование защитных устройств не показало выраженного влияния на исход и прогноз, хотя и является оправданным в отдельных клинических ситуациях. Существенную роль играет непосредственно ишемическое повреждение за счет перегрузки кардиомиоцитов ионами кальция, клеточного отека, некроза и апоптоза, что значительно усугубляется при реперфузии миокарда и формирует обструкцию на уровне микроциркуляторного русла. Все больше данных накапливается об иммуноопосредованном повреждении посредством активации клеточного иммунитета, интенсивного воспаления и тромбоза in situ. Несмотря на успехи экспериментов на животных, клиническое применение отдельных групп препаратов показало неоднозначный результат. Согласно последним рекомендациям Европейского общества кардиологов и Европейской ассоциации кардиоторакальных хирургов (European Society of Cardiology / European Association for Cardio-Thoracic Surgery, ESC / EACTS) от 2018 г. в случае no-reflow рекомендовано использование ингибиторов GPIIb / IIIa-рецепторов тромбоцитов. Кроме того, согласно данным литературы перспективным кажется применение никорандила и нитропруссида натрия, а также антагонистов интерлейкина 1β. В качестве немедикаментозной терапии заслуживает внимания селективная интракоронарная гипотермия, показавшая свою эффективность и безопасность в пилотном исследовании. На сегодняшний день ясно, что феномен no-reflow является проявлением сложного каскада реакций, включающих ишемическое, реперфузионное и иммунное повреждение, а также дистальную эмболию. Учитывая его весомый вклад в частоту неблагоприятных исходов и поздних осложнений, кажется необходимым введение единого подхода к диагностике, профилактике и лечению, что требует проведения качественных клинических исследований.
Об авторах
М. Ю. ГиляровРоссия
Россия, 117049 Москва, Ленинский пр-кт, 8
Россия, 117997 Москва, ул. Островитянова, 1
И. И. Иванов
Россия
Россия, 117997 Москва, ул. Островитянова, 1
Е. В. Константинова
Россия
Екатерина Владимировна Константинова
Россия, 117049 Москва, Ленинский пр-кт, 8
Россия, 117997 Москва, ул. Островитянова, 1
Н. И. Расчётнова
Россия
Россия, 117997 Москва, ул. Островитянова, 1
Н. А. Шостак
Россия
Россия, 117997 Москва, ул. Островитянова, 1
Список литературы
1. Fletcher A.P., Alkjaersig N., Smyrniotis F.E. et al. The treatment of patients suffering from early myocardial infarction with massive and prolonged streptokinase therapy. Trans Assoc Am Physicians 1958;71:287–96.
2. Lincoff A.M., Topol E.J. Illusion of reperfusion. Does anyone achieve optimal reperfusion during acute myocardial infarction? Circulation 1993;88(3):1361–74. DOI: 10.1161/01.cir.88.3.1361.
3. Krug A., Du Mesnil de Rochemont null, Korb G. Blood supply of the myocardium after temporary coronary occlusion. Circ Res 1966;19(1):57–62. DOI: 10.1161/01.res.19.1.57.
4. Kloner R.A., Ganote C.E., Jennings R.B. The “no-reflow” phenomenon after temporary coronary occlusion in the dog. J Clin Invest 1974;54(6):1496–508. DOI: 10.1172/JCI107898.
5. Ames A., Wright R.L., Kowada M. et al. Cerebral ischemia. II. The no-reflow phenomenon. Am J Pathol 1968;52(2):437–53.
6. Eeckhout E., Kern M.J. The coronary no- reflow phenomenon: a review of mechanisms and therapies. Eur Heart J 2001;22(9):729–39. DOI: 10.1053/euhj.2000.2172.
7. Hearse D.J., Bolli R. Reperfusion induced injury: manifestations, mechanisms, and clinical relevance. Cardiovasc Res 1992;26(2):101–8. DOI: 10.1093/cvr/26.2.101.
8. Kloner R.A. Does reperfusion injury exist in humans? J Am Coll Cardiol 1993;21(2):537–45. DOI: 10.1016/0735-1097(93)90700-b.
9. Kloner R.A., Przyklenk K., Whittaker P. Deleterious effects of oxygen radicals in ischemia/reperfusion. Resolved and unresolved issues. Circulation 1989;80(5):1115–27. DOI: 10.1161/01.cir.80.5.1115.
10. Gregorini L., Marco J., Kozàkovà M. et al. Alpha-adrenergic blockade improves recovery of myocardial perfusion and function after coronary stenting in patients with acute myocardial infarction. Circulation 1999;99(4):482–90. DOI: 10.1161/01.cir.99.4.482.
11. Lefroy D.C., Wharton J., Crake T. et al. Regional changes in angiotensin II receptor density after experimental myocardial infarction. J Mol Cell Cardiol 1996;28(2):429–40. DOI: 10.1006/jmcc.1996.0039.
12. Lyons D., Webster J., Benjamin N. Angiotensin II. Adrenergic sympathetic constrictor action in humans. Circulation 1995;91(5):1457–60. DOI: 10.1161/01.cir.91.5.1457.
13. Murohara T., Buerke M., Lefer A.M. Polymorphonuclear leukocyte-induced vasocontraction and endothelial dysfunction. Role of selectins. Arterioscler Thromb J Vasc Biol 1994;14(9):1509–19. DOI: 10.1161/01.atv.14.9.1509.
14. Seydoux C., Goy J.J., Davies G. Platelet and neutrophil imaging techniques in the investigation of the response to thrombolytic therapy and the no-reflow phenomenon. Am Heart J 1993;125(4):1142–7. DOI: 10.1016/0002-8703(93)90127-u.
15. Piana R.N., Paik G.Y., Moscucci M. et al. Incidence and treatment of “no-reflow” after percutaneous coronary intervention. Circulation 1994;89(6):2514–8. DOI: 10.1161/01.cir.89.6.2514.
16. Jaffe R., Charron T., Puley G. et al. Microvascular obstruction and the noreflow phenomenon after percutaneous coronary intervention. Circulation 2008;117(24):3152–6. DOI: 10.1161/CIRCULATIONAHA.107.742312.
17. Gupta S., Gupta M.M. No reflow phenomenon in percutaneous coronary interventions in ST-segment elevation myocardial infarction. Indian Heart J 2016;68(4):539–51. DOI: 10.1016/j.ihj.2016.04.006.
18. Wang L., Cheng Z., Gu Y. et al. Shortterm effects of verapamil and diltiazem in the treatment of no reflow phenomenon: A meta-analysis of randomized controlled trials. BioMed Res Int 2015;2015:382086. DOI: 10.1155/2015/382086.
19. Abu Arab T., Rafik R., El Etriby A. Efficacy and safety of local intracoronary drug delivery in treatment of no-reflow phenomenon: A pilot study. J Intervent Cardiol 2016;29(5):496–504. DOI: 10.1111/joic.12318.
20. Assali A.R., Sdringola S., Ghani M. et al. Intracoronary adenosine administered during percutaneous intervention in acute myocardial infarction and reduction in the incidence of “no reflow” phenomenon. Catheter Cardiovasc Interv Off J Soc Card Angiogr Interv 2000;51(1):27–31. DOI: 10.1002/1522-726x(200009)51:1<27::aid-ccd7>3.0.co;2-0.
21. Niccoli G., Rigattieri S., De Vita M.R. et al. Open-label, randomized, placebocontrolled evaluation of intracoronary adenosine or nitroprusside after thrombus aspiration during primary percutaneous coronary intervention for the prevention of microvascular obstruction in acute myocardial infarction: the REOPEN-AMI study (intracoronary nitroprusside versus adenosine in acute myocardial infarction). JACC Cardiovasc Interv 2013;6(6):580–9. DOI: 10.1016/j.jcin.2013.02.009.
22. Prati F., Romagnoli E., Limbruno U. et al. Randomized evaluation of intralesion versus intracoronary abciximab and aspiration thrombectomy in patients with ST-elevation myocardial infarction: The COCTAIL II trial. Am Heart J 2015;170(6):1116–23. DOI: 10.1016/j.ahj.2015.08.020.
23. Sakakura K., Funayama H., Taniguchi Y. et al. The incidence of slow flow after rotational atherectomy of calcified coronary arteries: A randomized study of low speed versus high speed. Catheter Cardiovasc Interv Off J Soc Card Angiogr Interv 2017;89(5):832–40. DOI: 10.1002/ccd.26698.
24. Hahn J.Y., Song Y.B., Kim E.K. et al. Ischemic postconditioning during primary percutaneous coronary intervention: the effects of postconditioning on myocardial reperfusion in patients with ST-segment elevation myocardial infarction (POST) randomized trial. Circulation 2013;128(17):1889–96. DOI: 10.1161/CIRCULATIONAHA. 113.001690.
25. Harrison R.W., Aggarwal A., Ou F.S. et al. Incidence and outcomes of no-reflow phenomenon during percutaneous coronary intervention among patients with acute myocardial infarction. Am J Cardiol 2013;111(2):178–84. DOI: 10.1016/j.amjcard.2012.09.015.
26. Choo E.H., Kim P.J., Chang K. et al. The impact of no-reflow phenomena after primary percutaneous coronary intervention: a time-dependent analysis of mortality. Coron Artery Dis 2014;25(5):392–8. DOI: 10.1097/MCA.0000000000000108.
27. Resnic F.S., Wainstein M., Lee M.K.Y. et al. No-reflow is an independent predictor of death and myocardial infarction after percutaneous coronary intervention. Am Heart J 2003;145(1):42–6. DOI: 10.1067/mhj.2003.36.
28. Galiuto L., Garramone B., Scarà A. et al. The extent of microvascular damage during myocardial contrast echocardiography is superior to other known indexes of post-infarct reperfusion in predicting left ventricular remodeling: results of the multicenter AMICI study. J Am Coll Cardiol 2008;51(5):552–9. DOI: 10.1016/j.jacc.2007.09.051.
29. Reffelmann T., Hale S.L., Dow J.S. et al. No-reflow phenomenon persists longterm after ischemia/reperfusion in the rat and predicts infarct expansion. Circulation 2003;108(23):2911–7. DOI: 10.1161/01.CIR.0000101917.80668.E1.
30. Webb J., Cox D.A. et al. Distal microcirculatory protection during percutaneous coronary intervention in acute ST-segment elevation myocardial infarction: a randomized controlled trial. JAMA 2005;293(9):1063–72. DOI: 10.1001/jama.293.9.1063.
31. Matsuo A., Inoue N., Suzuki K. et al. Limitations of using a GuardWire temporary occlusion and aspiration system in patients with acute myocardial infarction: multicenter investigation of coronary artery protection with a distal occlusion device in acute myocardial infarction (MICADO). J Invasive Cardiol 2007;19(3):132–8. PMID: 17341781.
32. Gick M., Jander N., Bestehorn H.P. et al. Randomized evaluation of the effects of filter-based distal protection on myocardial perfusion and infarct size after primary percutaneous catheter intervention in myocardial infarction with and without ST-segment elevation. Circulation 2005;112(10):1462–9. DOI: 10.1161/CIRCULATIONAHA. 105.545178.
33. Cura F.A., Escudero A.G., Berrocal D. et al. Protection of distal embolization in high-risk patients with acute ST-segment elevation myocardial infarction (PREMIAR). Am J Cardiol 2007;99(3):357–63. DOI: 10.1016/j.amjcard.2006.08.038.
34. Levine G.N., Bates E.R., Blankenship J.C. et al. 2011 ACCF/AHA/SCAI guideline for percutaneous coronary intervention. Circulation 2011;124(23):574–651. DOI: 10.1161/CIR.0b013e31823ba622.
35. Levine G.N., Bates E.R., Blankenship J.C. et al. 2015 ACC/AHA/SCAI focused update on primary percutaneous coronary intervention for patients with ST-elevation myocardial infarction: An Update of the 2011 ACCF/AHA/SCAI guideline for percutaneous coronary intervention and the 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction. Circulation 2016;133(11):1135–47. DOI: 10.1161/CIR.0000000000000336.
36. Bers D.M. Cardiac excitation – contraction coupling. Nature 2002;415(6868):198–205. DOI: 10.1038/415198a.
37. Eisner D.A., Choi H.S., Díaz M.E. et al. Integrative analysis of calcium cycling in cardiac muscle. Circ Res 2000;87(12):1087–94. DOI: 10.1161/01.res.87.12.1087.
38. Jennings R.B., Shen A.C. Calcium in experimental myocardial ischemia. Recent Adv Stud Cardiac Struct Metab 1972;1:639–55.
39. Murphy E., Steenbergen C. Mechanisms underlying acute protection from cardiac ischemia-reperfusion injury. Physiol Rev 2008;88(2):581–609. DOI: 10.1152/physrev.00024.2007.
40. Barrabés J.A., Garcia-Dorado D., Ruiz- Meana M. et al. Myocardial segment shrinkage during coronary reperfusion in situ. Relation to hypercontracture and myocardial necrosis. Pflugers Arch 1996;431(4):519–26. DOI: 10.1007/BF02191898.
41. Ruiz-Meana M., Inserte J., Fernandez- Sanz C. et al. The role of mitochondrial permeability transition in reperfusioninduced cardiomyocyte death depends on the duration of ischemia. Basic Res Cardiol 2011;106(6):1259–68. DOI: 10.1007/s00395-011-0225-5.
42. Gaschler M.M., Stockwell B.R. Lipid peroxidation in cell death. Biochem Biophys Res Commun 2017;482(3):419–25. DOI: 10.1016/j.bbrc.2016.10.086.
43. Amier R.P., Tijssen R.Y.G., Teunissen P.F.A. et al. Predictors of intramyocardial hemorrhage after reperfused ST‐segment elevation myocardial infarction. J Am Heart Assoc 6(8):e005651. DOI: 10.1161/JAHA.117.005651.
44. Kloner R.A., Rude R.E., Carlson N. et al. Ultrastructural evidence of microvascular damage and myocardial cell injury after coronary artery occlusion: which comes first? Circulation 1980;62(5):945–52. DOI: 10.1161/01.cir.62.5.945.
45. Lasukova T.V., Zykova M.V., Belousov M.V. et al. The role of NO synthase in the cardioprotective effect of substances of humic origin on the model of ischemia and reperfusion of isolated rat heart. Bull Exp Biol Med 2019;166(5):598–601. DOI: 10.1007/s10517-019-04399-y.
46. Drexler S.K., Foxwell B.M. The role of toll-like receptors in chronic inflammation. Int J Biochem Cell Biol 2010;42(4):506–18. DOI: 10.1016/j.biocel.2009.10.009.
47. Vallejo J.G. Role of toll-like receptors in cardiovascular diseases. Clin Sci Lond Engl 2011;121(1):1–10. DOI: 10.1042/CS20100539.
48. Shimamoto A., Chong A.J., Yada M. et al. Inhibition of Toll-like receptor 4 with eritoran attenuates myocardial ischemia/ reperfusion injury. Circulation 2006; 114(1):1270–74. DOI: 10.1161/CIRCULATIONAHA.105.000901.
49. Arslan F., Smeets M.B., O’Neill L.A.J. et al. Myocardial ischemia/reperfusion injury is mediated by leukocytic toll-like receptor-2 and reduced by systemic administration of a novel anti-toll-like receptor-2 antibody. Circulation 2010;121(1):80–90. DOI: 10.1161/CIRCULATIONAHA.109.880187.
50. Shishido T., Nozaki N., Yamaguchi S. et al. Toll-like receptor-2 modulates ventricular remodeling after myocardial infarction. Circulation 2003;108(23): 2905–10. DOI: 10.1161/01.CIR.0000101921.93016.1C.
51. He Y., Hara H., Núñez G. Mechanism and Regulation of NLRP3 inflammasome activation. Trends Biochem Sci 2016;41(12):1012–21. DOI: 10.1016/j.tibs.2016.09.002.
52. Mangan M.S.J., Olhava E.J., Roush W.R. et al. Targeting the NLRP3 inflammasome in inflammatory diseases. Nat Rev Drug Discov 2018;17(8):588–606. DOI: 10.1038/nrd.2018.97.
53. Liu Y., Lian K., Zhang L. et al. TXNIP mediates NLRP3 inflammasome activation in cardiac microvascular endothelial cells as a novel mechanism in myocardial ischemia/reperfusion injury. Basic Res Cardiol 2014;109(5):415. DOI: 10.1007/s00395-014-0415-z.
54. Van Hout G.P.J., Bosch L., Ellenbroek G.H.J.M. et al. The selective NLRP3-inflammasome inhibitor MCC950 reduces infarct size and preserves cardiac function in a pig model of myocardial infarction. Eur Heart J 2017;38(11):828–36. DOI: 10.1093/eurheartj/ehw247.
55. Marchetti C., Chojnacki J., Toldo S. et al. A novel pharmacologic inhibitor of the NLRP3 inflammasome limits myocardial injury after ischemiareperfusion in the mouse. J Cardiovasc Pharmacol 2014;63(4):316–22. DOI: 10.1097/FJC.0000000000000053.
56. Gupta N., Sahu A., Prabhakar A. et al. Activation of NLRP3 inflammasome complex potentiates venous thrombosis in response to hypoxia. Proc Natl Acad Sci USA 2017;114(18):4763–8. DOI: 10.1073/pnas.1620458114.
57. Val-Blasco A., Piedras M.J.G.M., Ruiz- Hurtado G. et al. Role of NOD1 in Heart Failure Progression via Regulation of Ca2+ Handling. J Am Coll Cardiol 2017;69(4):423–33. DOI: 10.1016/j.jacc.2016.10.073.
58. Prieto P., Vallejo-Cremades M.T., Benito G. et al. NOD1 receptor is upregulated in diabetic human and murine myocardium. Clin Sci Lond Engl 2014;127(12):665–77. DOI: 10.1042/CS20140180.
59. Mendez J.M., Kolora L.D., Lemon J.S. et al. Activation of the Endoplasmic Reticulum Stress Response Impacts the NOD1 Signaling Pathway. Infect Immun 2019;87(8):00826–18. DOI: 10.1128/IAI.00826-18.
60. Molinaro R., Mukherjee T., Flick R. et al. Trace levels of peptidoglycan in serum underlie the NOD-dependent cytokine response to endoplasmic reticulum stress. J Biol Chem 2019;294(22):9007–15. DOI: 10.1074/jbc.RA119.007997.
61. Yang H., Li N., Song L.N. et al. Activation of NOD1 by DAP contributes to myocardial ischemia/reperfusion injury via multiple signaling pathways. Apoptosis Int J Program Cell Death 2015;20(4):512–22. DOI: 10.1007/s10495-015-1089-1.
62. Linden J. Adenosine in tissue protection and tissue regeneration. Mol Pharmacol 2005;67(5):1385–7. DOI: 10.1124/mol.105.011783.
63. Fredholm B.B. Adenosine, an endogenous distress signal, modulates tissue damage and repair. Cell Death Differ 2007;14(7):1315–23. DOI: 10.1038/sj.cdd.4402132.
64. Mahaffey K.W., Puma J.A., Barbagelata N.A. et al. Adenosine as an adjunct to thrombolytic therapy for acute myocardial infarction: results of a multicenter, randomized, placebocontrolled trial: the Acute Myocardial Infarction STudy of ADenosine (AMISTAD) trial. J Am Coll Cardiol 1999;34(6):1711–20. DOI: 10.1016/s0735-1097(99)00418-0.
65. Ross A.M., Gibbons R.J., Stone G.W. et al. AMISTAD-II Investigators. A randomized, double-blinded, placebocontrolled multicenter trial of adenosine as an adjunct to reperfusion in the treatment of acute myocardial infarction (AMISTAD-II). J Am Coll Cardiol 2005;45(11):1775–80. DOI: 10.1016/j.jacc.2005.02.061.
66. Aung Naing K., Li L., Su Q. et al. Adenosine and verapamil for no-reflow during primary percutaneous coronary intervention in people with acute myocardial infarction. Cochrane Database Syst Rev 2013;6:CD009503. DOI: 10.1002/14651858.CD009503.pub2.
67. Su Q., Li L., Naing K.A. et al. Safety and effectiveness of nitroprusside in preventing no-reflow during percutaneous coronary intervention: a systematic review. Cell Biochem Biophys 2014;68(1):201–6. DOI: 10.1007/s12013-013-9690-9.
68. Zhao S., Qi G., Tian W. et al. Effect of intracoronary nitroprusside in preventing no reflow phenomenon during primary percutaneous coronary intervention: a meta-analysis. J Intervent Cardiol 2014;27(4):356–64. DOI: 10.1111/joic.12133.
69. Simonovic N., Jakovljevic V., Jeremic J. et al. Comparative effects of calcium and potassium channel modulators on ischemia/reperfusion injury in the isolated rat heart. Mol Cell Biochem 2019;450(1–2):175–85. DOI: 10.1007/s11010-018-3384-y.
70. Li J., Xu X., Zhou X. et al. Cardiovascular events associated with nicorandil administration prior to primary percutaneous coronary intervention in patients with acute ST-segment elevated myocardial infarction: a systematic review and meta-analysis. Expert Opin Drug Saf 2019;18(6):537–47. DOI: 10.1080/14740338.2019.1617848.
71. Zhao N., Xu J., Singh B. et al. Nitrates for the prevention of cardiac morbidity and mortality in patients undergoing noncardiac surgery. Cochrane Database Syst Rev 2016;(8):CD010726. DOI: 10.1002/14651858.CD010726.pub2.
72. Kunichika H., Ben-Yehuda O., Lafitte S. et al. Effects of glycoprotein IIb/IIIa inhibition on microvascular flow after coronary reperfusion. A quantitative myocardial contrast echocardiography study. J Am Coll Cardiol 2004;43(2):276–83. DOI: 10.1016/j.jacc.2003.08.040.
73. Kastrati A., Mehilli J., Schühlen H. et al. A clinical trial of abciximab in elective percutaneous coronary intervention after pretreatment with clopidogrel. N Engl J Med 2004;350(3):232–8. DOI: 10.1056/NEJMoa031859.
74. Valgimigli M., Percoco G., Barbieri D. et al. The additive value of tirofiban administered with the high-dose bolus in the prevention of ischemic complications during high-risk coronary angioplasty: the ADVANCE Trial. J Am Coll Cardiol 2004;44(1):14–9. DOI: 10.1016/j.jacc.2004.03.042.
75. Winchester D.E., Wen X., Brearley W.D. et al. Efficacy and safety of glycoprotein IIb/IIIa inhibitors during elective coronary revascularization: A meta-analysis of randomized trials performed in the era of stents and thienopyridines. J Am Coll Cardiol 2011;57(10):1190–9. DOI: 10.1016/j.jacc.2010.10.030.
76. Abbate A., Trankle C.R., Buckley L.F. et al. Interleukin-1 Blockade Inhibits the Acute Inflammatory Response in Patients With ST-Segment-Elevation Myocardial Infarction. J Am Heart Assoc 2020;9(5):014941. DOI: 10.1161/JAHA.119.014941.
77. Ridker P.M., Everett B.M., Thuren T. et al. Antiinflammatory therapy with canakinumab for atherosclerotic disease. N Engl J Med 2017;377(12):1119–31. DOI: 10.1056/NEJMoa1707914.
78. Zhou S.S., Tian F., Chen Y.D. et al. Combination therapy reduces the incidence of no-reflow after primary per- cutaneous coronary intervention in patients with ST-segment elevation acute myocardial infarction. J Geriatr Cardiol JGC 2015;12(2):135–42. DOI: 10.11909/j.issn.1671-5411.2015.02.003.
79. Herring M.J., Dai W., Hale S.L. et al. Rapid induction of hypothermia by the thermosuit system profoundly reduces infarct size and anatomic zone of no reflow following ischemiareperfusion in rabbit and rat hearts. J Cardiovasc Pharmacol Ther 2015;20(2):193–202. DOI: 10.1177/1074248414535664.
80. Dai W., Hale S., Kloner R.A. Delayed therapeutic hypothermia protects against the myocardial no-reflow phenomenon independently of myocardial infarct size in a rat ischemia/reperfusion model. Int J Cardiol 2017;236:400–4. DOI: 10.1016/j.ijcard.2017.01.079.
81. Erlinge D., Götberg M., Lang I. et al. Rapid endovascular catheter core cooling combined with cold saline as an adjunct to percutaneous coronary intervention for the treatment of acute myocardial infarction. The CHILL-MI trial: a randomized controlled study of the use of central venous catheter core cooling combined with cold saline as an adjunct to percutaneous coronary intervention for the treatment of acute myocardial infarction. J Am Coll Cardiol 2014;63(18):1857–65. DOI: 10.1016/j.jacc.2013.12.027.
82. Dixon S.R., Whitbourn R.J., Dae M.W. et al. Induction of mild systemic hypothermia with endovascular cooling during primary percutaneous coronary intervention for acute myocardial infarction. J Am Coll Cardiol 2002;40(11):1928–34. DOI: 10.1016/s0735-1097(02)02567-6.
83. Wang Y.S., Zhang J., Li Y.F. et al. A pilot clinical study of adjunctive therapy with selective intracoronary hypothermia in patients with ST-segment elevation myocardial infarction. Catheter Cardiovasc Interv Off J Soc Card Angiogr Interv 2018;92(7):433–40. DOI: 10.1002/ccd.27864.
84. Nichol G., Strickland W., Shavelle D. et al. Prospective, multicenter, randomized, controlled pilot trial of peritoneal hypothermia in patients with ST-segment elevation myocardial infarction. Circ Cardiovasc Interv 2015;8(3):001965. DOI: 10.1161/CIRCINTERVENTIONS.114.001965.
Рецензия
Для цитирования:
Гиляров М.Ю., Иванов И.И., Константинова Е.В., Расчётнова Н.И., Шостак Н.А. Феномен no-reflow и реперфузионное повреждение миокарда: механизмы и методы лечения. Клиницист. 2021;15(1-4):10-19. https://doi.org/10.17650/1818-8338-2021-15-1-4-K645
For citation:
Gilyarov M.Yu., Ivanov I.I., Konstantinova E.V., Raschetnova N.I., Shostak N.A. No-reflow phenomenon and reperfusion injury. Mechanisms and treatment. The Clinician. 2021;15(1-4):10-19. (In Russ.) https://doi.org/10.17650/1818-8338-2021-15-1-4-K645