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Stress echocardiography is the combination of 2D echocardiography with physical, pharmacological or electrical stress. The diagnostic endpoint of the detection of myocardial ischemia is the induction of a transient change in regional function during stress.1 Myocardial ischemia results in a typical “cascade” of events in which the various markers are hierarchically ranked in a well-defined time sequence. Flow heterogeneity between subendocardial and subepicardial perfusion is the forerunner of ischemia, followed by metabolic changes, alteration in regional mechanical function, and only at a later stage by electrocardiographic (ECG) changes, global left ventricular dysfunction (LV) and pain.2 Wall motion and perfusion or coronary flow reserve (CFR) changes are highly accurate, and more accurate than ECG changes for detection and location of underlying coronary artery disease. However, wall motion is more specific and requires ischemia; perfusion changes are more sensitive and may occur in the absence of true ischemia (microvascular disease, or LV hypertrophy).1 The three most common ischemic stressor are exercise, dobutamine, and vasodilators (dipyridamole, adenosine). They are equally potent for inducing wall abnormalities in the presence of a critical epicardial coronary artery stenosis. Dobutamine and exercise manly act through increased myocardial oxygen demand. Vasodilators act by stimulating A2 adenosinergic receptors present on the endothelial and smooth muscle cells of coronary arterioles and induce ischemia due to reduced subendocardial flow supply subsequent to inappropriate arteriolar vasodilatation and steal phenomena.1 Dipyridamole was the first pharmacological stress agent used for the diagnosis of coronary artery disease, with a pioneering indication proposed in Europe for the identification of ischemia during 12-lead ECG3, and later in the USA by Lance Gould as hyperemic stress perfusion imaging.4 Dipyridamole stress echocardiography pioneered in the year of 1985 (Picano et al). The safety record of high dose dipyridamole is well established on the basis of large scale multicentric studies with data from thousands of patients. The incidence of major complications, i.e. myocardial infarction, atrioventricular block, cardiac asystole, sustained ventricular tachycardia, is about 1/1500 cases. The mortality rate is about 1/10000 cases, similar to that of the exercise stress test. Dipyridamole has a better safety profile than when stress testing with dobutamine, where the incidence of major adverse reactions is about 1/300 studies.5 Many centers from 1988 until today, have used high doses administered in a short time (syringe-based infusion of 0.84 mg/kg). Later, some studies were reproduced with these doses, and today, most centers worldwide use high dose delivered in 4-6 min.6 Center experience: In 2017 we started to perform stress echocardiography in Čakovec County Hospital. The first method was exercise echocardiography using treadmill protocol, with imperative do accomplish postexercise imaging as soon as possible (<1 min from the cessation of exercise) where patient moved immediately from treadmill to imaging bed. With this method we have information from exercise stress testing combined with echocardiographic wall motions analysis to make final interpretation. The second method and most used until recently in our echo lab is standard dobutamine stress protocol, starting with 5 ug/kg/min and increasing 10, 20, 30 and 40 ug/kg/min. If no endpoint is reached, atropine, usually in dose 0.25 mg, is added to maximal dobutamine dose infusion. We are using this method for coronary disease detection, but also low dose protocol, to asses myocardial viability, valvular pathology (low-flow aortic stenosis) and other indications. rECEIvEd: february 28, 2019

Dipyridamole stress echo – the next step in evolution of stress imaging in the Echocardiography Laboratory at the Čakovec County Hospital