Abstract
Non–ST-segment elevation (NSTE) acute coronary syndromes (ACS), encompassing NSTE myocardial infarction (NSTEMI) and unstable angina, lack the declarative electrocardiographic findings that readily identify patients with STEMI, yet comprise >70% of all ACS.1–3 Unlike STEMI patients who receive uniform treatment to restore flow in an occluded artery, NSTE-ACS patients (who often present first to an emergency department [ED]) have varying degrees of coronary obstruction, undergo more heterogeneous management, and have worse long-term outcomes.2, 4 Despite guidelines, there remains inconsistent use of routinely advocated medical therapies and invasive evaluation5 that reflect uncertainty in initial evaluation. Greater age and comorbidities plus varied coronary artery disease (CAD) severity further complicate decision making. In addition, although cardiogenic shock, heart failure, and arrhythmias may be less than in STEMI, NSTE-ACS patients suffer more recurrent events and worse long-term outcomes.1 As our understanding of NSTE-ACS pathophysiology has grown, several noninvasive imaging techniques have emerged that offer high-resolution characterization of relevant markers of pathophysiology such as coronary atherosclerotic plaque and salvageable myocardium. Incorporating such techniques into evaluating the ED patient with suspected or established NSTE-ACS promises improved outcomes by demonstrating patient-specific, mechanistically based targets for therapy. This review summarizes NSTE-ACS, current imaging approaches, and emerging imaging advances to improve diagnosis, treatment, and outcomes. NSTE-ACS is most commonly caused by disruption of a coronary artery atherosclerotic plaque, with myocardial ischemia and injury often resulting from partial or intermittent occlusion along the ischemic cascade.6 Other causes beyond the focus of this work include embolism and revascularization.7 Events in the coronary and downstream myocyte together offer targets for imaging in NSTE-ACS. ### Events in the Coronary Artery Coronary plaque formation has been well underway before NSTE-ACS presentation.8 The plaque prone to cause ACS has a thin fibrous cap, large lipid pool, and is susceptible to disruption via inflammation, metalloproteinases, …
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have