Kardioprotekcja — czy nie zapominamy o ochronie krążenia wieńcowego. Część I. Podstawy patofizjologiczne
Streszczenie
Choroby układu sercowo-naczyniowego, a wśród nich choroba wieńcowa, od lat pozostają jedną z najczęstszych przyczyn zgonów na świecie. Podczas niedokrwienia reperfuzja jest jedyną metodą pozwalającą na zachowanie żywotności mięśnia sercowego. Niestety, już w latach 70. XX wieku wiadomo było, że do uszkodzenia miokardium dochodzi nie tylko w trakcie niedokrwienia, ale również w czasie reperfuzji. Publikowane są liczne prace omawiające patomechanizm powstawania uszkodzenia związanego z niedokrwieniem i reperfuzją. Większość autorów skupia się na zmianach zachodzących w miokardium, jednakże coraz częściej nacisk kładziony jest też na mikrokrążenie wieńcowe, które nie tylko jest „sprawcą”, ale powinniśmy myśleć o nim również jako o „ofierze” uszkodzenia związanego z niedokrwieniem i reperfuzją. W tej części artykułu chcemy zaprezentować podstawy patofizjologiczne takiego rozumowania.
Słowa kluczowe: miokardiumhartowaniemikrokrążenie wieńcowe
Referencje
- Mendis S, Davis S, Norrving Bo. Organizational update: the world health organization global status report on noncommunicable diseases 2014; one more landmark step in the combat against stroke and vascular disease. Stroke. 2015; 46(5): e121–e122.
- GBD 2013 Mortality and Causes of Death Collaborators. Global, regional, and national age-sex specific all-cause and cause-specific mortality for 240 causes of death, 1990-2013: a systematic analysis for the Global Burden of Disease Study 2013. Lancet. 2015; 385(9963): 117–171.
- Ginks WR, Sybers HD, Maroko PR, et al. Coronary artery reperfusion. II. Reduction of myocardial infarct size at 1 week after the coronary occlusion. J Clin Invest. 1972; 51(10): 2717–2723.
- Maroko PR, Libby P, Ginks WR, et al. Coronary artery reperfusion. I. Early effects on local myocardial function and the extent of myocardial necrosis. J Clin Invest. 1972; 51(10): 2710–2716.
- Serruys PW, Kutryk MJB, Ong ATL. Coronary-artery stents. N Engl J Med. 2006; 354(5): 483–495.
- Krug A, Korb G. Blood supply of the myocardium after temporary coronary occlusion. Circ Res. 1966; 19(1): 57–62.
- Kloner RA, Ganote CE, Jennings RB, et al. The "no-reflow" phenomenon after temporary coronary occlusion in the dog. J Clin Invest. 1974; 54(6): 1496–1508.
- Reimer KA, Jennings RB. The "wavefront phenomenon" of myocardial ischemic cell death. II. Transmural progression of necrosis within the framework of ischemic bed size (myocardium at risk) and collateral flow. Lab Invest. 1979; 40(6): 633–644.
- Reimer KA, Lowe JE, Rasmussen MM, et al. The wavefront phenomenon of ischemic cell death. 1. Myocardial infarct size vs duration of coronary occlusion in dogs. Circulation. 1977; 56(5): 786–794.
- Zhao ZQ, Corvera J, Halkos M, et al. Inhibition of myocardial injury by ischemic postconditioning during reperfusion: comparison with ischemic preconditioning. American Journal of Physiology - Heart and Circulatory Physiology. 2003; 285(2): H579–H588.
- Yellon DM, Hausenloy DJ. Myocardial reperfusion injury. N Engl J Med. 2007; 357(11): 1121–1135.
- Heusch G, Kleinbongard P, Skyschally A, et al. The coronary circulation in cardioprotection: more than just one confounder. Cardiovasc Res. 2012; 94(2): 237–245.
- Heusch G. Molecular basis of cardioprotection: signal transduction in ischemic pre-, post-, and remote conditioning. Circ Res. 2015; 116(4): 674–699.
- Skyschally A, Schulz R, Heusch G. Pathophysiology of myocardial infarction: protection by ischemic pre- and postconditioning. Herz. 2008; 33(2): 88–100.
- Ibáñez B, Heusch G, Ovize M, et al. Evolving therapies for myocardial ischemia/reperfusion injury. J Am Coll Cardiol. 2015; 65(14): 1454–1471.
- Braunwald E, Kloner RA. The stunned myocardium: prolonged, postischemic ventricular dysfunction. Circulation. 1982; 66(6): 1146–1149.
- Heusch G, Schulz R, Rahimtoola SH. Myocardial hibernation: a delicate balance. Am J Physiol Heart Circ Physiol. 2005; 288(3): H984–H999.
- Schaper W, Görge G, Winkler B, et al. The collateral circulation of the heart. Prog Cardiovasc Dis. 1988; 31(1): 57–77.
- Pich S, Klein HH, Lindert S, et al. Cell death in ischemic, reperfused porcine hearts: a histochemical and functional study. Basic Res Cardiol. 1988; 83(5): 550–559.
- Yang XM, Liu Y, Liu Y, et al. Attenuation of infarction in cynomolgus monkeys: preconditioning and postconditioning. Basic Res Cardiol. 2010; 105(1): 119–128.
- Heusch G, Baumgart D, Camici P, et al. alpha-adrenergic coronary vasoconstriction and myocardial ischemia in humans. Circulation. 2000; 101(6): 689–694.
- Cinca J, Carreno A, Mont L, et al. Neurally Mediated Negative Inotropic Effect Impairs Myocardial Function During Cholinergic Coronary Vasoconstriction in Pigs. Circulation. 1996; 94(5): 1101–1108.
- Ludmer PL, Selwyn AP, Shook TL, et al. Paradoxical vasoconstriction induced by acetylcholine in atherosclerotic coronary arteries. N Engl J Med. 1986; 315(17): 1046–1051.
- Kleinbongard P, Heusch G. Extracellular signalling molecules in the ischaemic/reperfused heart - druggable and translatable for cardioprotection? Br J Pharmacol. 2015; 172(8): 2010–2025.
- Murry CE, Jennings RB, Reimer KA. Preconditioning with ischemia: a delay of lethal cell injury in ischemic myocardium. Circulation. 1986; 74(5): 1124–1136.
- Heusch G. Treatment of Myocardial Ischemia/Reperfusion Injury by Ischemic and Pharmacological Postconditioning. Comprehensive Physiology. 2015: 1123–1145.
- Noll T, Muhs A, Besselmann M, et al. Initiation of hyperpermeability in energy-depleted coronary endothelial monolayers. Am J Physiol. 1995; 268(4 Pt 2): H1462–H1470.
- Bruegger D, Rehm M, Jacob M, et al. Exogenous nitric oxide requires an endothelial glycocalyx to prevent postischemic coronary vascular leak in guinea pig hearts. Crit Care. 2008; 12(3): R73.
- Fernández-Jiménez R, García-Prieto J, Sánchez-González J, et al. Pathophysiology Underlying the Bimodal Edema Phenomenon After Myocardial Ischemia/Reperfusion. J Am Coll Cardiol. 2015; 66(7): 816–828.
- Manciet LH, Poole DC, McDonagh PF, et al. Microvascular compression during myocardial ischemia: mechanistic basis for no-reflow phenomenon. Am J Physiol. 1994; 266(4 Pt 2): H1541–H1550.
- Mewton N, Rapacchi S, Augeul L, et al. Determination of the myocardial area at risk with pre- versus post-reperfusion imaging techniques in the pig model. Basic Res Cardiol. 2011; 106(6): 1247–1257.
- Canty JM, Klocke FJ. Reduced regional myocardial perfusion in the presence of pharmacologic vasodilator reserve. Circulation. 1985; 71(2): 370–377.
- Ehring T, Krajcar M, Baumgart D, et al. Cholinergic and alpha-adrenergic coronary vasomotion [corrected] with increasing ischemia-reperfusion injury. Am J Physiol. 1995; 268(2 Pt 2): H886–H894.
- Heusch G. The Coronary Circulation as a Target of Cardioprotection. Circulation Research. 2016; 118(10): 1643–1658.
- Kleinbongard P, Baars T, Möhlenkamp S, et al. Aspirate from human stented native coronary arteries vs. saphenous vein grafts: more endothelin but less particulate debris. Am J Physiol Heart Circ Physiol. 2013; 305(8): H1222–H1229.
- Mills I, Fallon JT, Wrenn D, et al. Adaptive responses of coronary circulation and myocardium to chronic reduction in perfusion pressure and flow. Am J Physiol. 1994; 266(2 Pt 2): H447–H457.
- Sorop O, Merkus D, de Beer VJ, et al. Functional and structural adaptations of coronary microvessels distal to a chronic coronary artery stenosis. Circ Res. 2008; 102(7): 795–803.
- Heusch G, Kleinbongard P, Böse D, et al. Coronary microembolization: from bedside to bench and back to bedside. Circulation. 2009; 120(18): 1822–1836.
- Dörge H, Neumann T, Behrends M, et al. Perfusion-contraction mismatch with coronary microvascular obstruction: role of inflammation. Am J Physiol Heart Circ Physiol. 2000; 279(6): H2587–H2592.
- Beręsewicz A. Endogenne mechanizmy kardioprotekcyjne - co to takiego i jak to działa. Kardiol Pol. 2011; 69 (supl III): 59–66.
- Barrabés JA, Garcia-Dorado D, Mirabet M, et al. Antagonism of selectin function attenuates microvascular platelet deposition and platelet-mediated myocardial injury after transient ischemia. J Am Coll Cardiol. 2005; 45(2): 293–299.
- Barrabés JA, Inserte J, Agulló L, et al. Microvascular thrombosis: an exciting but elusive therapeutic target in reperfused acute myocardial infarction. Cardiovasc Hematol Disord Drug Targets. 2010; 10(4): 273–283.
- Barrabés JA, Mirabet M, Agulló L, et al. Platelet deposition in remote cardiac regions after coronary occlusion. Eur J Clin Invest. 2007; 37(12): 939–946.
- Chukwuemeka AO, Brown KA, Venn GE, et al. Changes in P-selectin expression on cardiac microvessels in blood-perfused rat hearts subjected to ischemia-reperfusion. Ann Thorac Surg. 2005; 79(1): 204–211.
- Kupatt C, Wichels R, Horstkotte J, et al. Molecular mechanisms of platelet-mediated leukocyte recruitment during myocardial reperfusion. J Leukoc Biol. 2002; 72(3): 455–461.
- Kogaki S, Sawa Y, Sano T, et al. Selectin on activated platelets enhances neutrophil endothelial adherence in myocardial reperfusion injury. Cardiovasc Res. 1999; 43(4): 968–973.
- Sheridan FM, Dauber IM, McMurtry IF, et al. Role of leukocytes in coronary vascular endothelial injury due to ischemia and reperfusion. Circ Res. 1991; 69(6): 1566–1574.
- Driesen RB, Zalewski J, Vanden Driessche N, et al. Histological correlate of a cardiac magnetic resonance imaged microvascular obstruction in a porcine model of ischemia-reperfusion. Cardiovasc Pathol. 2012; 21(3): 129–131.
- Niccoli G, Scalone G, Lerman A, et al. Coronary microvascular obstruction in acute myocardial infarction. Eur Heart J. 2015; 37(13): 1024–1033.
- Prasad A, Gersh BJ, Mehran R, et al. Effect of Ischemia Duration and Door-to-Balloon Time on Myocardial Perfusion in ST-Segment Elevation Myocardial Infarction: An Analysis From HORIZONS-AMI Trial (Harmonizing Outcomes with Revascularization and Stents in Acute Myocardial Infarction). JACC Cardiovasc Interv. 2015; 8(15): 1966–1974.
- Betgem RP, de Waard GA, Nijveldt R, et al. Intramyocardial haemorrhage after acute myocardial infarction. Nat Rev Cardiol. 2015; 12(3): 156–167.