A 72-year-old man with prior tobacco use, hypertension, and type 2 diabetes presented to the emergency department with prolonged chest pain (4 hours in duration). An electrocardiogram (ECG) showed evidence of ST-segment elevation in leads V₁ to V₄ (Figure 9-1).

ST-segment elevation myocardial infarction (STEMI) patients present with ischemic symptoms, ST-segment elevation on ECG, and subsequent release of biomarkers of myocardial necrosis. Most of these patients will progress to Q-wave myocardial infarction (MI), representing transmural infarction.^1,2 The incidence of STEMI is approximately 80 cases per 100,000 people-years, and it composes 25% to 40% of MIs. Of note, the incidence of STEMI appears to be declining, whereas the incidence of non-STEMI is increasing. In-hospital mortality for STEMI ranges between 6% and 14%.

It is incredibly important to make the diagnosis of STEMI at the time of first medical contact (FMC). When suspected, guidelines advocate for a time from FMC to ECG of ≤10 minutes. A history of chest pain lasting more than 20 minutes and not responsive to nitroglycerine is frequent, with possible radiation to the left arm, jaws, and neck. However, up to 30% of patients have atypical symptoms such as nausea/vomiting, shortness of breath, fatigue, and palpitations. These patients, more commonly women and elderly, tend to present later and are less likely to receive reperfusion therapy. An early ECG is of paramount importance.^1,2 ST-segment elevation (1 mm, >0.1 mV) should be apparent in 2 contiguous leads, although elevation of 2 mm (>0.2 mV) in V₂-V₃ is the standard for anterior MI.³ In the setting of suspected inferior wall MI, V₃R and V₄R should be assessed to determine potential right ventricular involvement. In addition, it should be realized that ST-segment depression in V₁-V₃ may be representative of posterior STEMI, in which case V₇-V₉ should be placed to corroborate. Left ventricular hypertrophy, left bundle branch block, and paced rhythms may obscure the interpretation of the ECG. If STEMI is identified on the ECG, biomarkers should not delay access to reperfusion therapy. Diagnosis is confirmed by angiography, which often displays a totally occluded vessel (Figure 9-2).

STEMI is caused by an abrupt thrombotic occlusion of a coronary artery. Two mechanisms tend to precede this: plaque rupture and plaque erosion^4,5 (Figure 9-3). Plaque rupture is characterized by disruption of the thin fibrous cap overlying a lipid-rich plaque. Plaque rupture is likely preceded by macrophage infiltration which thins the cap due to release of metalloproteinases. Once the thrombogenic subendothelium is exposed, the release of thrombin stimulates platelet and coagulation activation.⁶ Coronary erosion, in turn, often develops over moderate fibrotic plaques that are more common in young women and smokers. Detachment of endothelial cells causes exposure of prothrombotic substances. In particular, local accumulation of hyaluronan has been described, leading to activation of neutrophils and coagulation pathways.^4,5

The use of an emergency medical system is the preferred mode of initial care for patients with STEMI; however, patients often self-present to the hospital. Ambulance transport is preferred, as earlier diagnostics and therapies can be employed; moreover, the possibility of cardiac arrest during transportation is approximately 1 in 300.^1,2

Once STEMI is suspected, aspirin (non–enteric-coated aspirin up to 325 mg) should be administered to disrupt platelet activation. Nitroglycerin is often provided, along with opioids (virgola), to relieve pain, but these interventions are not accompanied by a mortality benefit. The primary mortality benefit for STEMI therapies is early aspirin and reperfusion; accordingly, features that delay reperfusion are of importance.

Minimizing the delay from symptom onset to presentation has been a focus of multiple educational campaigns in both the United States and Europe. The system delay, in turn, is due to the sum of the delay between FMC and diagnosis and that between diagnosis and reperfusion therapy. The sum of the patient delay and system delay is the total time to reperfusion. Guidelines suggest a goal of FMC to primary percutaneous coronary intervention (PCI) of ≤90 minutes, and ≤30 minutes if fibrinolysis is performed. Door-to-balloon time should be ≤60 minutes in PCI capable hospitals. All efforts to minimize delays are based on the concept that “time is muscle,” and irreversible myocardial necrosis begins early after thrombotic epicardial vessel occlusion.

When patients present to a PCI-capable hospital either due to self-presentation or by ambulance, primary PCI should be performed within 60 minutes. There is general consensus that patients with low bleeding risk, who present early after symptoms onset (<2 hours) and with a transfer delay of <120 minutes, are best suited for initial fibrinolysis. Of note, after thrombolysis is delivered, patients should be transferred to a PCI-capable hospital in the event of vessel re-occlusion. Moreover, any patient suffering a cardiac arrest should be transferred to a PCI-capable hospital for emergency angiography.