Immediate P2Y12 Inhibition in the Current Era of Percutaneous Intervention

An 86-year-old man with a history of coronary artery disease, hypertension, and hyperlipidemia presented with chest pain and acute dyspnea. His home medications included aspirin and valsartan.

His initial examination was notable for hypoxia on room air (89%) that improved with 2 liters oxygen supplementation. His blood pressure was 95/78 mmHg, and his heart rate was regular at 92 beats per minute. The chest had bilateral inspiratory crackles, and there was 1+ peripheral edema. The electrocardiogram showed normal sinus rhythm with a right bundle branch block and anterior ST-segment elevation (Figure 1). Chest radiograph showed pulmonary vascular congestion, edema, and cardiac enlargement. The troponin I was 10.0 ng/mL (normal is 0.00-0.50 ng/mL), platelet was 160 K/mm3 (normal is 150-450), creatinine was 4.0 mg/dL, and pro-NT brain natriuretic peptide was 2,649 pg/mL (normal is ≤125 pg/mL). The patient was thought to be in cardiogenic shock. The patient underwent emergent cardiac catheterization. Coronary angiography revealed a 95% calcified lesion in the ostial, proximal, and mid-left anterior descending artery with Thrombolysis in Myocardial Infarction 2 flow and a 30% lesion in the ostial left main coronary (Videos 1-2). The left ventricular ejection fraction was ~20%, and end-diastolic pressure 15 mmHg. An intra-aortic balloon pump was placed, and cardiothoracic surgery was consulted due to the high-risk anatomy. The patient was declined for emergent coronary artery bypass grafting by cardiothoracic surgery, and percutaneous coronary intervention (PCI) was recommended.

Figure 1

Figure 1

Video 1

Video 2

Prior to attempting PCI on this patient, which of the following next steps would provide the most rapid inhibition of platelets and would also not be influenced by concomitant renal insufficiency?

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