• Critical Care
• Myocardial Infarction

• Critical Care
• Myocardial Infarction
• Emergency Medicine

Acute coronary syndromes (ACSs) affect > 780 000 individuals in the United States each year, 70% of which cases will be NSTEMI [Amsterdam EA et al. Circulation. 2014]. Tarlan Hedayati, MD, Cook County Health and Hospitals System, Chicago, Illinois, USA, discussed updates in the treatment of NSTE-ACS based on the 2014 American Heart Association / American College of Cardiology guideline for the management of patients with NSTE-ACS [Amsterdam EA et al. Circulation. 2014].

NSTE-ACS includes NSTEMI and unstable angina (UA). The difference between the 2 is the myocardial necrosis that occurs in NSTEMI, which can be identified by an increase in biomarkers caused by myocyte death. However, troponin levels are elevated not only in patients with myocardial infarction (MI) but also in those with other conditions, such as tachycardia, trauma, heart failure, pulmonary embolism, burns, drug toxicity, respiratory failure, and neurologic diseases. Therefore, a history and clinical exam are important in the diagnosis of NSTEMI. Elevated troponin levels may be present for up to 2 weeks after the index event, but a > 20% increase over prior troponin levels may indicate reinfarction.

Patients with NSTEMI should receive initial treatment of 162 to 325 mg of aspirin or a loading dose of clopidogrel if they cannot tolerate aspirin. In addition, patients should receive nitrates and may require oxygen if their oxygen saturation is < 90%. Patients expected to undergo early invasive therapy should receive a P2Y₁₂ receptor inhibitor, such as clopidogrel or ticagrelor, in addition to aspirin [Amsterdam EA et al. Circulation. 2014]. For patients with UA or NSTEMI who will receive conservative therapy, P2Y₁₂ receptor inhibition should be administered upon admission.

Clopidogrel is a prodrug that requires a 2-step process to produce the active metabolite that elicits antiplatelet activity. Some patients harbor a polymorphism in 1 of the metabolic enzymes required for this transformation, and in these patients, the benefit of clopidogrel therapy is attenuated. In contrast, ticagrelor is the active agent and does not require biotransformation.

The PLATO trial [Wallentin L et al. N Engl J Med. 2009] evaluated ticagrelor in > 18 000 patients with ACS, with a primary end point of cardiovascular death, MI, and stroke at 12 months. Patients treated with ticagrelor experienced a lower rate of cardiovascular death, MI, and stroke, without an increase in major bleeding. However, patients with a body weight < 60 kg and normal biomarker levels did not experience a benefit from ticagrelor when compared with clopidogrel. Patients in North America who received ticagrelor also did not demonstrate an improvement regarding the primary end point when compared with clopidogrel; however, it is believed that the higher aspirin dose that is administered in North America may have negated the advantage of ticagrelor.

In addition to dual antiplatelet therapy (DAPT), patients with UA or NSTEMI who are expected to undergo invasive therapy should receive glycoprotein IIb/IIIa inhibition with intravenous eptifibatide or tirofiban [Amsterdam EA et al. Circulation. 2014]. Anticoagulation should also be initiated. In patients who are undergoing an invasive strategy, bivalirudin, unfractionated heparin (UFH), or enoxaparin should be administered, whereas in patients who are undergoing conservative therapy, enoxaparin or fondaparinux is preferred over UFH.

An early invasive strategy is typically performed in patients with UA or NSTEMI if they are high risk according to the TIMI criteria. In the TIMACS study [Mehta SR et al. N Engl J Med. 2009], early vs delayed percutaneous coronary intervention (PCI) was evaluated in > 3000 patients with NSTEMI with a primary outcome of death, MI, and stroke. There was no significant difference in the primary outcome among the 2 arms of the study (P = .15). However, early PCI was associated with a significant decrease in the secondary outcome of death, MI, and refractory ischemia (HR, 0.72; 95% CI, 0.58 to 0.89; P = .003). In this study, high-risk patients experienced a benefit from early PCI, but medium- to low-risk patients did not.

In conclusion, once NSTEMI is diagnosed, all patients should be treated with DAPT and anticoagulation. Beyond that, risk stratification should be performed to determine if an early invasive therapy should be initiated.

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