Clinical meaning
Contemporary understanding of unstable angina has evolved with high-sensitivity troponin assays. The traditional classification of UA as troponin-negative ACS is being challenged: hs-cTn detects myocardial injury previously below detection limits, reclassifying approximately 25% of former UA patients as NSTEMI. True troponin-negative UA now represents a smaller, lower-risk cohort. Pathologically, UA involves superficial plaque erosion (more common than rupture in younger women and smokers) or plaque rupture with non-occlusive, platelet-rich white thrombus. Endothelial erosion exposes basement membrane collagen and von Willebrand factor, triggering platelet adhesion via GPIb-IX-V, activation through collagen-GPVI interaction and thrombin-PAR1/PAR4 signaling, and aggregation via GPIIb/IIIa-fibrinogen cross-linking. The non-occlusive nature reflects a balance between thrombosis and endogenous fibrinolysis (tissue plasminogen activator from endothelial cells). The clinician applies the 0/1-hour hs-cTn algorithm for rapid rule-out (hs-cTnT below 5 ng/L at 0h excludes MI with NPV above 99%), calculates HEART score for discharge decision-making, prescribes guideline-directed therapy, and determines invasive vs conservative strategy using GRACE score and clinical features. The clinician also differentiates type 1 ACS from type 2 MI (demand ischemia from tachycardia, anemia, sepsis) and addresses Takotsubo cardiomyopathy in...