A 69-year-old African gentleman with a medical history of coronary artery disease after percutaneous coronary intervention to his right coronary artery in 2014 for a non-ST-segment elevation myocardial infarction and prior contrast-media allergy presented to the emergency department with atypical angina.\nShortly after his arrival, he was seen by the emergency medicine physician who initiated an acute coronary syndrome antiplatelet regimen comprising both oral aspirin 325 mg and ticagrelor 180 mg. Vital signs revealed mild hypertension with a blood pressure of 147/94 mmHg, normal pulse rate of 74 beats per minute, and an oxygen saturation of 99% on pulse oximetry on room air. His physical examination was significant for left-sided chest wall tenderness only. A 12-lead electrocardiogram (EKG) revealed sinus rhythm with a 1st degree atrioventricular block and a left anterior fascicular block with prior inferior myocardial infarction. There were no acute ischemic changes. His cardiac biomarkers were normal (peak serum levels of creatine phosphokinase-MB fraction (CK-MB) and troponin T were 1.5 ng mL−1 (normal range, 1–5 ng mL−1) and 0.034 ng mL−1 (normal range, 0-0.1 ng mL−1), respectively) and did not reflect a myocardial infarction.\nApproximately 1 hour after ticagrelor administration, the patient reported a constellation of symptoms which included worsening chest pain, sudden-onset respiratory distress, and generalized urticaria. His repeat physical examination revealed new-onset periorbital edema and angioedema (). He was immediately administered 200 mg intravenous hydrocortisone, 100 mg intravenous ranitidine, and 10 mg intravenous chlorphenamine with nebulized albuterol and ipratropium, and his symptoms resolved shortly thereafter (within an hour).\nBased on the clinical scenario, the patient's tentative diagnosis was ticagrelor-induced hypersensitivity reaction with angioedema as this was the only new medication he was given (he was on daily maintenance aspirin for his CAD and previously tolerated a 1-year course of clopidogrel after drug-eluting stent implantation). It was also noted that he was not on an angiotensin-converting enzyme inhibitor or angiotensin receptor blocker. He was subsequently transferred to cardiac care unit for further observation and supportive care. The following day, a 2D transthoracic echocardiogram revealed a preserved left ventricular ejection fraction of 60% without regional wall motion abnormalities. He reported that his symptoms were much improved and was hemodynamically stable. His clinical angioedema completely resolved. The patient's atypical angina completely abated, and subsequent cardiac biomarkers and electrocardiograms were unremarkable. As a result, inpatient coronary angiography was not pursued as his TIMI risk stratification was considered low to moderate risk, and outpatient exercise stress echocardiography was the preferred management strategy to assess for ischemia. He was safely discharged on guideline-recommended, optimal medical therapy comprising aspirin, clopidogrel (which he previously tolerated as DAPT for his prior stent implantation without any adverse effects), beta-blocker, mineralocorticoid receptor antagonist with high-intensity statin, and a tapered course of oral steroid therapy.
A 41-year-old male visited the EMC of our hospital complaining of a sharpening chest pain of his mid sternum lasting for 1 hour. He had previously been diagnosed with ankylosing spondylitis and had been treated with oral meloxicam, sulfasalazine, and methylprednisolone for 10 years. The patient had also been diagnosed with hypertension for 8 years, but did not take any anti-hypertensive medications. EKG revealed ST-segment elevations in the V 2-4 precordial leads. A chest X-ray revealed mild pulmonary congestion and laboratory tests revealed elevated leukocytes, cardiac enzymes, and N-terminal b-natriuretic peptide levels. The patient was subsequently diagnosed with ST elevation myocardial infarction, which we addressed by performing an emergent PCI. Before a coronary angiography was performed, we administrated a loading dose of clopidogrel 600 mg, aspirin 300 mg, and carvedilol. Coronary angiography revealed subtotal occlusion in the proximal left anterior descending artery (LAD). PCI using drug-eluting stents (DESs; Xience prime, Abbott Vascular, Santa Clara, CA, USA, 3.0×38 in proximal to mid LAD lesion, 2.5×15 in the 1st diagonal branch lesion) was performed successfully without any significant complications. A rheumatologist confirmed that the patient was not in the course of active disease, and thus we decided to withhold rheumatologic medications in order to focus on treating the myocardial infarction. The treatment plan for the patient consisted of continued oral methylprednisolone to control ankylosing spondylitis, and we switched clopidogrel to prasugrel, which is known as a more potent thrombus inhibitor, on the 3rd day of admission considering the increased risk of stent thrombosis. Prasugrel was administered with a loading dose of 50 mg daily maintenance dose of 10 mg. The patient was discharged taking aspirin, carvedilol, rosuvastatin, candesartan, furosemide, spironolactone and prasugrel; however, he revisited our outpatient clinic after 5 days complaining of a worsened whole body skin rash with pruritic symptoms (). Blood tests and chest X-rays showed no abnormal findings, and vital signs were within normal limits. Because aspirin was administered without any evidence of skin hypersensitivity or reaction prior to admission, we suspected prasugrel as the cause of the skin reaction. Accordingly, we discontinued prasugrel and switched the patient to clopidogrel (75 mg/d). A punch biopsy of the abdominal skin revealed mild perivascular lymphocytic infiltrations that were compatible with a hypersensitivity skin reaction (). The patient was followed through the outpatient clinic without further complaint of hypersensitivity skin reaction.