IntrOductIOnDipyridamole is a nucleoside transport inhibitor that augments endogenous adenosine [1]. Moreover, it inhibits phosphodiesterases and causes an increase in cellular content of cyclic Adenosine Monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP) [2]. Dipyridamole is indicated for the induction of stress in myocardial scintigraphy [3].Adenosine plays an important role as a paracrine and/ or an autocrine hormone in a variety of physiological or pathophysiological processes including cardiovascular diseases and diabetes [4,5]. It acts by binding to adenosine receptors and influences glucose disposal, carbohydrate metabolism, lipolysis and insulin sensitivity [6,7], local blood flow [8], mean arterial pressure and heart rate [9]. Four adenosine receptors (A1, A2a, A2b, and A3) have been cloned and characterized in mammalian species. While A1 and A3 receptors are preferentially coupled to inhibitory G-proteins (Gi/o), the A2 receptors interact with stimulatory G-protein (Gs) [10]. Adenosine A3 receptors were found to produce cardioprotective effects during myocardial ischemia/ischemic reperfusion [10]. On the other hand, blockade of adenosine A1 receptors improves glucose tolerance in obese Zucker rats; these rats show a better profile of peak serum insulin level and areas under glucose curves, compared to untreated rats [11]. Yet, adenosine is not the sole mediator of dipyridamole pharmacological effects [12].It is noteworthy that the concentration of dipyridamole required to produce a significant effect on glycolytic rate (2µM) is much less than that required to exert a significant rise in intracellular and interstitial adenosine concentration in muscles (50µM) [12]. Dipyridamole reduces glucose-induced osteopontin expression in arterial vasculature, thereby decreasing the medial artery calcification and stiffness. This effect is mediated through inhibition of phosphodiesterase, and Reactive Oxygen Species (ROS) [2]. However, a net effect of dipyridamole in blood sugar during cardiac scintigraphy has been not investigated.Cardiovascular stress test using exercise or pharmacological agents has long been established as a diagnostic procedure in cardiovascular scintigraphy. In this regard, pharmacological stress is produced by dobutamine, dipyridamole, adenosine or regadenoson [13]. Dipyridamole inhibits intracellular reuptake and deamination of adenosine, thereby producing a vasodilatory effect on coronary arteries. Such an effect on coronary vasodilation is attenuated in diseased coronary arteries, showing a reduced coronary flow reserve and failure of dilation in response to the drug [14].The aim of this study was to evaluate the acute effect of dipyridamole on blood glucose in patients undergoing myocardial rest/stress scintigraphy using 99mTc-sestamibi. In addition, a potential alteration of the outcome of a radionuclide scan was explored. MAterIAls And MethOdsThis cross-sectional study was performed on 299 patients who were recruited from the Department of Nuclear Medicine of
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