Analgesia epidural torácica para el tratamiento de la angina inestable

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Abstract

La miocardiopatía isquémica en pacientes con angina inestable refractaria al tratamiento médico constituye un escenario clínico complicado. Una anatomía desfavorable o un riesgo quirúrgico excesivamente alto pueden desaconsejar la realización de una angioplastia o de una cirugía de derivación coronaria. En este artículo se pretende revisar la utilización de la analgesia/anestesia epidural torácica para el tratamiento y estabilización de este tipo de pacientes, a través de una breve descripción de la fisiopatología de la isquemia cardiaca, estudios experimentales en animales y humanos, uso en cirugía cardiaca y efectos secundarios.

Translated abstract

Ischemic cardiomyopathy in patients with unstable angina refractory to medical therapy is a difficult medical condition. Unfavorable anatomy or excessive surgical risk can advise against the performance of angioplasty or coronary bypass surgery. This study has reviewed the use of thoracal epidural analgesia/anesthesia for the management and stabilization of this type of patients, with a brief description of the physiopathology of cardiac ischemia, experimental studies in animals and human beings, use of cardiac surgery and side effects.

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Most cited references 54

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Platelet activation in unstable coronary disease.

D J Fitzgerald, L Roy, F Catella … (1986)

Pathological and clinical studies have suggested that platelets have a role in the pathogenesis of unstable angina and myocardial infarction. However, the relation of platelet activation to episodic ischemia in patients with unstable angina is unknown. We assessed the biosynthesis of thromboxane and prostacyclin as indexes of platelet activation in patients with stable and unstable coronary disease by physicochemical analysis of metabolites in plasma and urine. Prostacyclin biosynthesis was markedly elevated in patients with acute myocardial infarction and correlated with plasma creatine kinase (r = 0.795; P less than 0.001). The largest rise in thromboxane synthesis was observed in patients with unstable angina, in whom 84 percent of the episodes of chest pain were associated with phasic increases in the excretion of thromboxane and prostacyclin metabolites. However, 50 percent of such increases were not associated with chest pain, possibly reflecting silent myocardial ischemia. These data indicate that platelet activation occurs during spontaneous ischemia in patients with unstable angina. The increment in prostacyclin biosynthesis during such episodes may be a compensatory response of vascular endothelium that limits the degree or effects of platelet activation. If so, biochemically selective inhibition of the synthesis or action of thromboxane A2 would be desirable in the treatment of unstable angina. In contrast, thromboxane inhibitors or antagonists would not be expected to be effective in patients with chronic stable angina, in whom there was no increase in the formation of thromboxane A2.