Myocardial ischemia/reperfusion-injury, a clinical view on a complex pathophysiological process. Int J Cardiol

Laboratory of Cell Biology & Histology , University of Antwerp, Antwerpen, Flemish, Belgium
International Journal of Cardiology (Impact Factor: 4.04). 05/2005; 100(2):179-90. DOI: 10.1016/j.ijcard.2004.04.013
Source: PubMed


Myocardial infarction is the major cause of death in the world. Over the last two decades, coronary reperfusion therapy has become established for the management of acute myocardial infarction (AMI). However, restoration of blood flow to previously ischemic myocardium results in the so-called ischemia/reperfusion (IR)-injury. The different clinical manifestations of this injury include myocardial necrosis, arrhythmia, myocardial stunning and endothelial- and microvascular dysfunction including the no-reflow phenomenon. The pathogenesis of ischemia/reperfusion injury consists of many mechanisms. Recently, there's increasing evidence for an important role in IR-injury on hypercontracture induced by high levels of cytosolic calcium or by low concentrations of ATP. In the last years, many studies on experimental models were investigated, but the clinical trials confirming these effects remain spare. Recently, the beneficial effect of Na(+)/H(+)-exchange inhibitor cariporide and of the oxygen-derived free radical (ODFR) scavenger vitamin E on coronary bypass surgery-induced IR-injury were demonstrated. Also recently, the beneficial effect of allopurinol on the recovery of left ventricular function after rescue balloon-dilatation was demonstrated. The beneficial effect of magnesium and trimetazidine on IR-injury remains controversial. The beneficial effect of adenosine remains to be further confirmed. There's also increasing interest in agentia combining the property of upregulating NO-synthase (e.g. L-arginine) and restoring the balance between NO and free radicals (e.g. tetrahydrobiopterin). One of such agents could be folic acid. In this review article the authors give an overview of the recent insights concerning pathogenesis and therapeutic possibilities to prevent IR-induced injury.

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    • "Se ha demostrado que la reperfusión miocárdica también se asocia a un daño reflejado en la disminución de la contractilidad, menor umbral arritmogénico, la muerte de miocitos dañados pero viables y la disfunción microvascular. La causa de este daño por reperfusión parece estar relacionada con sobrecarga celular de calcio, radicales libres de oxígeno y actuación de los neutrófilos [25][26]. Así la reperfusión coronaria produce un beneficio al aportar flujo sanguíneo de nuevo al miocardio pero también un daño en el territorio isquémico, aunque el balance es favorable, con más tejido salvado que dañado, sobre todo cuanto más precozmente se restaura el flujo arterial coronario. "
    Dataset: TESIS-JMVR

    Full-text · Dataset · Apr 2015
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    • "Current treatments for myocardial I–R injury targeting inflammation Myocardial I–R injury, MI and resultant heart failure remains a major cause of death and disability in Western societies, despite clinical advances such as thrombolysis and percutaneous revascularization interventions to facilitate reperfusion. In the next decade, this morbidity will expand to all corners of the globe (Moens et al., 2005; Murphy & Steenbergen, 2008; Peart & Headrick, 2009; Thygesen et al., 2012). The most recent recommendations from the American Heart Association for patients presenting with MI include fibrinolysis within the subsequent 30 min and primary percutaneous coronary intervention (PCI) by 90 min after patient presentation (Masoudi et al., 2008; Anderson et al., 2011). "
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    ABSTRACT: Myocardial infarction (MI) and its resultant heart failure remains a major cause of death in the world. The current treatments for patients with MI are revascularization with thrombolytic agents or interventional procedures. These treatments have focused on restoring blood flow to the ischemic tissue to prevent tissue necrosis and preserve organ function. The restoration of blood flow after a period of ischemia, however, may elicit further myocardial damage, called reperfusion injury. Pharmacological interventions, such as antioxidant and Ca(2+) channel blockers, have shown premises in experimental settings; however, clinical studies have shown limited success. Thus, there is a need for the development of novel therapies to treat reperfusion injury. The therapeutic potential of glucocorticoid-regulated anti-inflammatory mediator annexin-A1 (ANX-A1) has recently been recognized in a range of systemic inflammatory disorders. ANX-A1 binds to and activates the family of formyl peptide receptors (G protein-coupled receptor family) to inhibit neutrophil activation, migration and infiltration. Until recently, studies on the cardioprotective actions of ANX-A1 and its peptide mimetics (Ac2-26, CGEN-855A) have largely focused on its anti-inflammatory effects as a mechanism of preserving myocardial viability following I-R injury. Our laboratory provided the first evidence of the direct protective action of ANX-A1 on myocardium, independent of inflammatory cells in vitro. We now review the potential for ANX-A1 based therapeutics to be seen as a "triple shield" therapy against myocardial I-R injury, limiting neutrophil infiltration and preserving both cardiomyocyte viability and contractile function. This novel therapy may thus represent a valuable clinical approach to improve outcome after MI. Copyright © 2014. Published by Elsevier Inc.
    Full-text · Article · Nov 2014 · Pharmacology [?] Therapeutics
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    • "Corresponding author: Dick H.J. Thijssen (e-mail: to activate endothelial NO synthase (eNOS) (Loke et al. 2010), improve anti-oxidative capacity (Neyestani et al. 2010), and (or) decrease oxidative stress (Luczaj and Skrzydlewska 2005; Steffen et al. 2008). Myocardial infarction leads to injury because of the period of prolonged ischaemia, but significant injury is also caused by (surgical ) reperfusion of the ischemic area (Moens et al. 2005). This damage is known as ischaemia–reperfusion (IR) injury. "
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    ABSTRACT: Tea consumption is associated with reduced cardiovascular risk. Previous studies found that tea flavonoids work through direct effects on the vasculature, leading to dose-dependent improvements in endothelial function. Cardioprotective effects of regular tea consumption may relate to the prevention of endothelial ischaemia-reperfusion (IR) injury. Therefore, we examined the effect of black tea consumption on endothelial function and the ability of tea to prevent IR injury. In a randomized, crossover study, 20 healthy subjects underwent 7 days of tea consumption (3 cups per day) or abstinence from tea. We examined brachial artery (BA) endothelial function via flow-mediated dilation (FMD), using high resolution echo-Doppler, before and 90 min after tea or hot water consumption. Subsequently, we followed a 20-min ischaemia and 20-min reperfusion protocol of the BA after which we measured FMD to examine the potential of tea consumption to protect against IR injury. Tea consumption resulted in an immediate increase in FMD% (pre-consumption: 5.8 ± 2.5; post-consumption: 7.2 ± 3.2; p < 0.01), whilst no such change occurred after ingestion of hot water. The IR protocol resulted in a significant decrease in FMD (p < 0.005), which was also present after tea consumption (p < 0.001). This decline was accompanied by an increase in the post-IR baseline diameter. In conclusion, these data indicate that tea ingestion improves BA FMD. However, the impact of the IR protocol on FMD was not influenced by tea consumption. Therefore, the cardioprotective association of tea ingestion relates to a direct effect of tea on the endothelium in humans in vivo.
    Full-text · Article · Feb 2014 · Applied Physiology Nutrition and Metabolism
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