Endothelial function in the stress echocardiography laboratory

Abstract

Endothelial dysfunction is an early stage of atherosclerotic disease [1], characterized mainly by reduced NO availability. In this early stage, no structural lesions are present, but the functional alteration may progress at the cardiac level to impairment in coronary flow reserve in the intermediate stage and then to stress-induced dysfunction in the advanced stages (Fig. 26.1). A direct evaluation of endothelial function is hardly possible, due to NO extremely short half-life. Mirroring endothelial physiology, in vascular reactivity tests, non-pharmacological or pharmacological stimuli for NO release, and thus for endothelium-dependent vasodilatation, are administered. Different techniques have been developed to assess endothelial function in humans, both invasive and noninvasive, exploring endothelial function in different districts (). Some of them, such as flow-mediated dilation (FMD), employ the same basic echocardiography hardware of stress echocardiography testing [1]. The additional technological and cultural burden required to implement the technique is high for a hypertension specialist or a cardiologist without cardiovascular ultrasound training and only modest for a cardiologist already skilled in cardiovascular ultrasound. The study of endothelial function is attractive for a cardiologist because of the potential it has to supply important pathophysiological, diagnostic, and prognostic information currently missed by our noninvasive testing modalities. Endothelial dysfunction is a key factor in the onset and development of atherosclerosis, hypertension, and heart failure, as it is also a serious candidate to bridge the gap between hemodynamic atherosclerotic burden and occurrence of clinical events [2]. It is placed exactly in the physiological blind spot of stress echocardiography, which somewhat measures the functional or hemodynamic impact of a coronary stenosis but is unable to assess the status of endothelial function, allegedly responsible for many catastrophic cardiovascular events.