Purpose: “No reflow” is defined as suboptimal myocardial reperfusion through a part of coronary circulation without angiographic evidence of mechanical vessel obstruction in the setting of percutaneous coronary intervention (PCI). Distal atherothrombotic embolization, ischemic or reperfusion injury, and exposure of the coronary microcirculation to injury are held responsible for etiopathogenesis of the phenomenon. Thus, mechanical and pharmacologic strategies to treat no reflow target these mechanisms. In the medical treatment of no reflow, local antiplatelet and local vasodilator drugs have been tried largely. Epinephrine has potent beta2 receptor agonist properties and beta1 agonist properties that mediate vasodilatation of the arteriolar circulation and increase inotropic and chronotropic stimulation of the myocardium.
Materials and Methods: A 68-year-old man with paroxysmal atrial fibrillation and hypertension presenting with fatigue and intermittent chest pain scheduled an elective coronary investigation. Electrocardiography showed biphasic T waves in inferolateral leads. Echocardiography showed ejection fraction of 50%, LVDd of 50 mm, a left atrium of 41 mm, and no significant valvular abnormalities. Diagnostic coronarography showed the right coronary artery without stenosis, Cx with 95% to 99% stenosis, the proximal and mid left anterior descending artery (LAD) with 90% (tandem lesion), and Dg2 with 80% stenosis. A decision was made to perform PCI on the LAD. The first stent was a Resolute Integrity 3.0- ´ 38-mm stent. After the stenting, the clinical and hemodynamical condition of the patient started to deteriorate. He promptly went into a cardiogenic shock, with severe reduction of the blood pressure (TA 50/3040/20 mm Hg) and bradycardia (heart rate ~30 beats/min). Intravenous noradrenalin was administered, and the patient was intubated and placed on mechanical ventilation. The second stent was a Resolute Integrity 3.5- ´ 15-mm stent. After the second stenting, there was not any improvement in the patient’s condition. TIMI (Thrombolysis In Myocardial Infarction) 0 flow was seen in the LAD. A decision was made to administrate intracoronary adrenalin.
Results: Intracoronary epinephrine was relative well tolerated and resulted in prompt recovery of flow and significant improvement of hemodynamics followed by general condition stabilization.
Conclusions: Intracoronary epinephrine may exert encouraging effects in patients developing refractory no reflow after elective PCI. Prospective randomized studies will be necessary to determine whether intracoronary epinephrine should be used primarily or in combination with other medications for the treatment of patients with no reflow.