Pathophysiology of Acute Coronary Syndrome

* in most of ACS cases syndrome occurs when an atherosclerotic plaque ruptures, fissures or ulcerates and precipitates thrombus formation. This results in sudden total or near-total arterial occlusion. Alternatively thrombus may break off from a ruptured plaque and occlude smaller vessels like coronary arteries.
    * systemic factors and inflammation also play role  in changing haemostatic and coagulation pathways and may play a part in the initiation of the intermittent thrombosis that is a characteristic of unstable angina. Inflammatory acute phase proteins, cytokines, chronic infections and catecholamine surges may enhance production of tissue factor, procoagulant activity or platelet hyperaggregability.
    * in the case of Q wave Mycardial infarction results in a spreading area of necrosis that reaches epicardium in 4-6 hours – full thickness infarction
    * in rare cases may be due to coronary artery occlusion by embolism, congenital abnormalities, coronary artery spasm and a wide variety of systemic (particularly inflammatory) diseases
    * initially infarcted muscle is softened leading to an increase in ventricular compliance but, as fibrosis takes place, compliance of heart muscles decreases
    * poor correlation between angiographic severity of coronary stenosis and chance of acute occlusion
    * Other causes of reduced myocardial blood flow include mechanical obstruction (e.g. air embolus), dynamic obstruction (e.g. vessel spasm), and infection or inflammation.

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