A 74-year-old male patient with history of heavy smoking, hypertension, and hyperlipidemia presented to our emergency department with unstable angina. The patient was given sublingual nitroglycerin, aspirin, clopidogrel, and heparin drip, which resolved his chest pain. His cardiopulmonary exam was unremarkable. The electrocardiogram on presentation didn't show acute ST/T wave abnormalities. Echocardiography revealed preserved left ventricular function with no abnormal wall motion. Lexiscan stress test demonstrated ischemia involving anterior, anteroseptal, and apical ischemia. The patient was started on tirofiban infusion while undergoing coronary angiography. The left coronary system was engaged via Judkins Left 4.0 catheter, demonstrating critical mid-left anterior descending artery (LAD) lesion with a hazy lesion suggesting local thrombus burden (Figure 1). Following balloon inflation for 8 sec @ 10 atm, mid-LAD had no reflow (Figure 2). Intracoronary nitroglycerine of 200 mcg was given to exclude coronary spasm. Activated clotting time was then checked and determined to be therapeutic.
Figure 1
Figure 2
What is the best next step in management of this patient?
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The correct answer is: C. Intracoronary adenosine bolus
This case represents a no-reflow to mid-LAD despite triple antiplatelet therapy. Although the etiology of the no-reflow phenomenon is not well-established, suggested hypotheses include microvascular ischemia, endothelial dysfunction, and distal thromboembolism.1 Coronary perforation or dissection should be considered in the differential diagnosis of no-reflow phenomenon. A small intracoronary injection of contrast can help differentiate between the former entities. Intracoronary nitroglycerin should be administered to exclude coronary spasm as well. Clinicians should try to prevent no-reflow by decreasing door-to-balloon time in ST-segment elevation myocardial infarction settings and avoiding deployment of long or high-pressure stents. Nevertheless, no-reflow can still occur regardless of preventive measures. Pharmacological therapy including intracoronary adenosine, nicardipine, or nitroprusside, preferably via infusion catheters, form the mainstay of treatment of no-reflow, with no significant difference between various agents.1 Intracoronary adenosine, both in a bolus and 50 mcg/kg/min infusion, have been found to decrease infarct size and no-reflow.2 Distal protection devices and intracoronary thrombectomy can be used only if angiographic evidence of a thrombus burden is present.1 Other answers, including intravenous unfractionated heparin bolus or intracoronary tenecteplase, have no role in managing no-reflow phenomenon. Failure to manage no-reflow can have detrimental effects on the patient's outcome including infarct expansion, ventricular arrhythmias, and pathological left ventricular remodeling.1
References
Rezkalla SH, Stankowski RV, Hanna J, Kloner RA. Management of No-Reflow Phenomenon in the Catheterization Laboratory. JACC Cardiovasc Interv 2017;10:215-23.
Yetgin T, Uitterdijk A, te Lintel Hekkert M, et al. Limitation of Infarct Size and No-Reflow by Intracoronary Adenosine Depends Critically on Dose and Duration. JACC Cardiovasc Interv 2015;8:1990-9.
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