Protection against myocardial ischemia-reperfusion injury in clinical practice.
Even when reperfusion therapy is applied as early as possible, survival and quality of life are compromised in a considerable number of patients with ST-segment elevation acute myocardial infarction. Some cell death following transient coronary occlusion occurs during reperfusion, due to poor handling of calcium in the sarcoplasmic reticulum-mitochondria system, calpain activation, oxidative stress, and mitochondrial failure, all promoted by rapid normalization of intracellular pH. Various clinical trials have shown that infarct size can be limited by nonpharmacological strategies--such as ischemic postconditioning and remote ischemic conditioning--or by drugs--such as cyclosporine, insulin, glucagon-like peptide-1 agonists, beta-blockers, or stimulation of cyclic guanosine monophosphate synthesis. However, some clinical studies have yielded negative results, largely due to a lack of consistent preclinical data or a poor design, especially delayed administration. Large-scale clinical trials are therefore necessary, particularly those with primary clinical variables and combined therapies that consider age, sex, and comorbidities, to convert protection against reperfusion injury into a standard treatment for patients with ST-segment elevation acute myocardial infarction.
Hospital Universitario e Institut de Recerca Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Electronic address: dgdorado@vhebron.net.
David
D
Garcia-Dorado
Hospital Universitario e Institut de Recerca Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain.
Antonio
A
Rodríguez-Sinovas
Hospital Universitario e Institut de Recerca Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain.
Marisol
M
Ruiz-Meana
Hospital Universitario e Institut de Recerca Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain.
Javier
J
Inserte
D002986:Clinical Trials as Topic; D006801:Humans; D009203:Myocardial Infarction / Q000150:complications* / Q000628:therapy*; D015425:Myocardial Reperfusion / Q000009:adverse effects*; D015428:Myocardial Reperfusion Injury / Q000188:drug therapy / Q000517:prevention & control*
Condicionamiento isquémico remoto; Daño por reperfusión; Infarto de miocardio; Myocardial infarction; Proteicinasa G; Protein kinase G; Remote ischemic conditioning; Reperfusion injury