Most cases of ACS occur from disruption of a previously nonsevere lesion (an atherosclerotic lesion that was previously hemodynamically insignificant yet vulnerable to rupture). The vulnerable plaque is typified by a large lipid pool, numerous inflammatory cells, and a thin, fibrous cap.
Baseline blood glucose levels appear to be an independent risk factor for a MACE in patients with suspected ACS. In an analysis of data from 1708 Australian and New Zealand patients in a prospective observational study, investigators noted that a MACE occurred within 30 days of presentation in 15.3% of patients whose ED admission blood glucose levels were below 7 mmol/L (about 126 mg/dL); however, in the same time period, a MACE occurred in twice as many patients (30.9%) whose blood glucose levels were above 7 mmol/L. After controlling for various factors, patients who had admission blood glucose levels of 7 mmol/L or higher were at 51% higher risk of experiencing a MACE compared with patients who had lower baseline blood glucose levels.
ACS without elevation in demand requires a new impairment in supply, typically due to thrombosis and/or plaque hemorrhage. A syndrome consisting of chest pain, ischemic ST-segment and T-wave changes, elevated levels of biomarkers of myocyte injury, and transient left ventricular apical ballooning (Takotsubo syndrome) has been shown to occur in the absence of clinical CAD, after emotional or physical stress. The etiology of this syndrome is not well understood but is thought to relate to a surge of catechol stress hormones and/or high sensitivity to those hormones.
For more on the etiology of ACS, read here.
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Cite this: Yasmine S. Ali. Fast Five Quiz: Test Your Knowledge of Acute Coronary Syndrome - Medscape - Apr 26, 2017.
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