Dr.Armughan Riaz
M.B.B.S, Dip Card
Consultant Cardiologist


Pathophysiology of Acute Coronary Syndrome

Here is information about pathophysiology of Acute coronary syndrome

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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