The potential usage of epinephrine in the treatment of no-reflow was evaluated in a previous study in which some promising results were showed. Although epinephrine has been used clinically to treat cardiopulmonary arrest, there is a paucity of published data regarding its effectiveness in coronary no-reflow. Epinephrine has potent beta-2 receptor agonist properties that mediate vasodilatation of the arteriolar circulation, as well as the better known beta-1 agonist properties that increase inotropic and chronotropic stimulation of the myocardium. In the medical treatment of no-reflow, local vasodilator and local antiplatelet drugs have been tried extensively. Thus, pharmacologic and mechanical strategies to treat no reflow target these mechanisms. Distal atherothrombotic embolization, ischemic or reperfusion injury, and susceptibility of coronary microcirculation to injury are held responsible for etiopathogenesis of the phenomenon. The reduction of the beneficial effects of PCI is the main adverse consequence of no-reflow phenomenon. But, it may be observed in up to 50% of primary PCI cases. For elective PCIs, the frequency of no-reflow can be reported as 0.6–5%. No-reflow is defined as the lack of myocardial perfusion despite opening up the epicardial coronary vessels in the setting of percutaneous coronary intervention (PCI). Intracoronary epinephrine may become an effective alternative in patients suffering refractory no-reflow following primary PCI. One patient (8%) died despite all therapeutic measures. During the procedure, intra-aortic balloon pump counterpulsation was required in two (17%) patients, transvenous pacing in 2 (17%) cases, and both intra-aortic balloon counterpulsation and transvenous pacing in one (8%) patients. Hypotension associated with no-reflow developed in 5 (42%) patients. Intracoronary epinephrine resulted in significant but tolerable increase in heart rate (68 ± 13 to 95 ± 16 beats/min p < 0.001) and systolic blood pressure (94 ± 18 to 140 ± 20 p < 0.001). Epinephrine administration was well tolerated without serious adverse hemodynamic or chronotropic effects. There was an improvement in coronary flow of at least one TFG in 11 (93%) patients, two TFG in 5 (42%) cases. No-reflow was successfully reversed with complete restoration of TIMI 3 flow in 9 of 12 patients (75%). ResultsĪ mean of 333 ± 123 mcg of intracoronary epinephrine was administered. TFG, TIMI frame count (TFC), and TIMI myocardial perfusion grade (TMPG) were recorded before and after intracoronary epinephrine administration. Refractory no-reflow was defined as persistent TIMI flow grade (TFG) ≤2 despite intracoronary administration of at least one other pharmacologic intervention. Among those, 12 patients which received intracoronary epinephrine to treat a refractory no-reflow phenomenon were evaluated. MethodsĪ total of 248 consecutive STEMI patients who had undergone primary PCI were retrospectively evaluated. The goal of this study was to evaluate the safety and efficacy of intracoronary epinephrine in reversing refractory no-reflow during primary PCI. Despite the advances in medical and interventional treatment modalities, some patients develop epicardial coronary artery reperfusion but not myocardial reperfusion after primary percutaneous coronary intervention (PCI), known as no-reflow.
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