Acute coronary syndrome
Acute coronary syndromes (ACSs) include all syndromes compatible with acute myocardial ischemia resulting from imbalance between myocardial oxygen demand and supply.
• ACSs are classified according to electrocardiographic (ECG) changes into
(1)ST-segment-elevation (STE) myocardial infarction (MI)
(2) non–ST-segmentelevation (NSTE) ACS, which includes NSTE MI and unstable angina (UA)
Endothelial dysfunction, inflammation, and formation of fatty streaks contribute to development of atherosclerotic coronary artery plaques. The cause of ACS in more than 90% of patients is rupture, fissuring, or erosion of an unstable atheromatous plaque. A clot forms on top of the ruptured plaque. Exposure of collagen and tissue factor induces platelet adhesion and activation, which promote release of adenosine diphosphate (ADP) and thromboxane A2 from platelets producing vasoconstriction and platelet activation. A change in the conformation of the glycoprotein (GP) IIb/IIIa surface receptors of platelets occurs that cross-links platelets to each other through fibrinogen bridges.
Simultaneously, activation of the extrinsic coagulation cascade occurs as a result of exposure of blood to the thrombogenic lipid core and endothelium, which are rich in tissue factor. This leads to formation of a fibrin clot composed of fibrin strands, cross-linked platelets, and trapped red blood cells. Ventricular remodeling occurs after MI and is characterized by left ventricular dilation and reduced pumping function, leading to cardiac failure
Predominant symptom is midline anterior chest discomfort (usually at rest), severe new-onset angina, or increasing angina that lasts at least 20 minutes. Discomfort may radiate to the shoulder, down the left arm, to the back, or to the jaw. Accompanying symptoms may include nausea, vomiting, diaphoresis, and shortness of breath. No specific features indicate ACS on physical examination. However, patients with ACS may present with signs of acute HF or arrhythmias.
(1) early restoration of blood flow to the infarct-related artery to prevent infarct expansion (in the case of MI) or prevent complete occlusion and MI (in UA)
(2) prevention of death and other complications
(3) prevention of coronary artery re-occlusion
(4) relief of ischemic chest discomfort
(5) resolution of ST-segment and T-wave changes on ECG.
Long-term goals include control of cardiovascular (CV) risk factors, prevention of additional CV events, and improvement in quality of life.