Which one of the following statements is true regarding trends in incidence of acute coronary syndrome (ACS) in the United States?
All of the above. Based on data from national heart disease stroke statistics, while the incidence of overall ACS, STEMI, and NSTEMI has declined with time, the incidence of UA has been increasing in the last decade. The observed decline in the rate of UA is largely attributable to the availability of sensitive troponin assays that detect myocardial necrosis.
Which of the following processes represents the dominant initiating event in the pathogenesis of an ACS?
Plaque rupture. Plaque rupture is the dominating initiating event of acute MI. Rupture of the fibrous cap of the coronary atheroma exposes the underlying subendothelial matrix eventually leading to activation of platelets, thrombin generation, and final thrombus formation. While erosion of the plaque without rupture can lead to thrombus formation, it is not as frequent an event as plaque rupture and accounts for a third of MIs.
What is the most important clinical predictor of 30-day mortality in a patient presenting with acute STEMI?
Age. Based on results of the large GUSTO-I trial the strongest predictor of mortality following STEMI is advanced age. In addition to age, other major predictors of poor prognosis on presentation include systolic BP <100 mmHg, heart rate >100 per minute, higher Killip classification stage, and anterior infarction.
Which of the following is a prodrug and requires bioactivation?
Both b and c. Aspirin, clopidogrel, prasugrel, and ticagrelor are all antiplatelet agents. Aspirin irreversibly blocks the formation of thromboxane A2 in platelets, producing an inhibitory effect on platelet aggregation. While clopidogrel and prasugrel are prodrugs that require hepatic bioactivation to their pharmacologically active metabolite, ticagrelor is phenotypically active and is not affected by hepatic metabolism.
Which of the following statements regarding prasugrel is true?
All of the above are correct. Prasugrel has faster onset of action and potency of platelet inhibition when compared with clopidogrel. Unlike clopidogrel, prasugrel is not influenced by P-450 genetic polymorphisms. In the large, randomized TRITON-TIMI-38 trial, investigators compared prasugrel with clopidogrel in patients with ACS initiated following coronary angiography. While there was no difference in mortality, there was a reduction in composite of major adverse cardiovascular events primarily driven by reduction in nonfatal MI. A higher incidence of bleeding with prasugrel when compared with clopidogrel was noted. Post hoc analysis showed net harm in patients with prior history of TIA/stroke and prasugrel should be avoided in these patients.
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