What causes acute coronary syndrome (ACS)?

Updated: Sep 30, 2020
  • Author: David L Coven, MD, PhD; Chief Editor: Eric H Yang, MD  more...
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Answer

Acute coronary syndrome (ACS) is caused primarily by atherosclerosis. 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.

Elevated demand can produce ACS in the presence of a high-grade fixed coronary obstruction, due to increased myocardial oxygen and nutrition requirements, such as those resulting from exertion, emotional stress, or physiologic stress (eg, from dehydration, blood loss, hypotension, infection, thyrotoxicosis, or surgery).

ACS without elevation in demand requires a new impairment in supply, typically due to thrombosis and/or plaque hemorrhage.

The major trigger for coronary thrombosis is considered to be plaque rupture caused by the dissolution of the fibrous cap, the dissolution itself being the result of the release of metalloproteinases (collagenases) from activated inflammatory cells. This event is followed by platelet activation and aggregation, activation of the coagulation pathway, and vasoconstriction. This process culminates in coronary intraluminal thrombosis and variable degrees of vascular occlusion. Distal embolization may occur. The severity and duration of coronary arterial obstruction, the volume of myocardium affected, the level of demand on the heart, and the ability of the rest of the heart to compensate are major determinants of a patient's clinical presentation and outcome. (Anemia and hypoxemia can precipitate myocardial ischemia in the absence of severe reduction in coronary artery blood flow.)

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.

Baseline blood glucose levels appear to be an independent risk factor for a major adverse cardiac event (MACE) in emergency department (ED) patients with suspected ACS. [3, 4] In an analysis of data from 1708 Australian and New Zealand patients in a prospective observational study, investigators noted 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. [4] 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. [4] Other significant predictors of MACE included male sex, older age, family history, hypertension, dyslipidemia, ischemic findings on ECG, and positive troponintests. [3, 4]


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