Angina microvascular y síndrome X / Microvascular angina and syndrome X

RESUMEN

El término síndrome X se emplea habitualmente para definir a un grupo de pacientes que presentan dolor torácico característico, depresión del segmento ST durante el esfuerzo y arterias coronarias angiográficamente normales. Los mecanismos fisiopatológicos propuestos para explicar la naturaleza de este síndrome son heterogéneos y, en ocasiones, controvertidos. Muchos datos apuntan a un posible origen isquémico de los síntomas, como la depresión del segmento ST durante los episodios de dolor precordial, los defectos transitorios de perfusión miocárdica, la producción transmiocárdica de lactato y otras evidencias objetivas, recientemente descritas. Sin embargo, la isquemia miocárdica sólo se ha podido demostrar en aproximadamente un 20-25% de los pacientes. En el presente artículo se expone la evidencia existente sobre el papel potencial que la isquemia miocárdica puede ejercer en la patogenia del síndrome X (AU)

ABSTRACT

Cardiac syndrome X defines patients with typical chest pain, transient ischemic ST segment changes during effort and normal coronary angiograms. An ischemic origin has been postulated for syndrome X since its description over 30 years ago. This has been based on the fact that patients with cardiac syndrome X have abnormal perfusions cans, a drop in both pH and oxygen saturation of the coronary sinus blood during chest pain and transmyocardiallactate production during stress testing. Moreover, nuclear magnetic resonance spectroscopy studies, demonstrated transient myocardial ischaemia in 20% of women with syndrome X. Microvascular endothelial dysfunction appears to be responsible for at least some of the abnormalities detected in the coronary circulation of patients with syndrome X («microvascular angina»). ET-1, a potent vasoconstrictor, is synthesised by endothelial cells and may be responsible for coronary flow abnormalities inmicrovascular angina. Plasma levels of ET-1 are significantly raised in patients with syndrome X, compared to normal controls and a significant relationship has been found between baseline ET levels and abnormal coronary vascular responses in patients with syndrome X. Several investigators, however, have questioned the existence of myocardial ischaemia in patients with cardiac syndromeX. Their arguments are mainly based on the fact that prognosis is good in these patients and that studies with stress echocardiography have consistently failed to show regional wall motion abnormalities, even in patients with typical ischaemic ECG changes. Controversy exists as to the causes of syndrome X and this article reviews the evidence in relation to myocardial ischaemia as a pathogenic mechanism in this syndrome (AU)