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Its subsequent release is prolonged with degradation of actin and myosin filaments. Isoforms of the protein, T and I, are specific to myocardium. Differential diagnosis of troponin elevation includes acute infarction, severe pulmonary embolism causing acute right heart overload, heart failure, myocarditis.
The cardiac troponins T and I which are released within 4–6 hours of an attack of MI and remain elevated for up to 2 weeks, have nearly complete tissue specificity and are now the preferred markers for assessing myocardial damage. [14] Heart-type fatty acid binding protein is another marker, used in
Ischemic heart disease, which results from an occlusion of one of the major coronary arteries, is currently still the leading cause of morbidity and mortality in western society. [14] [15] During ischemia reperfusion, ROS release substantially contribute to the cell damage and death via a direct effect on the cell as well as via apoptotic ...
Treatment aims to preserve as much heart muscle as possible, and to prevent further complications. [28] Treatment depends on whether the myocardial infarction is a STEMI or NSTEMI. [72] Treatment in general aims to unblock blood vessels, reduce blood clot enlargement, reduce ischemia, and modify risk factors with the aim of preventing future ...
Hence, blood-thinning medications can be prescribed to reduce the risk of cardiovascular diseases led by blood clots, such as myocardial infarction (heart attack), ischemic stroke, and venous thromboembolism. [35] Haemorrhage (internal bleeding) is the most prominent side effect of blood-thinning therapy. [36]
This enzyme is responsible for breaking down a molecule called cAMP, which is the key signalling molecule in our body. [31] When PDE3 is inhibited, the breakdown of cAMP is prevented, leading to increased levels of cAMP in our cells. [32] In our heart muscle cells, when the levels of cAMP rise, it activates a protein called protein kinase A ...
Heart-type Fatty Acid-Binding Protein (H-FABP) is a small cytoplasmic protein (15 kDa) released from cardiac myocytes following an ischemic episode. [7] Like the nine other distinct FABPs that have been identified, H-FABP is involved in active fatty acid metabolism where it transports fatty acids from the cell membrane to mitochondria for oxidation. [7]
Streptokinase is a thrombolytic medication activating plasminogen by nonenzymatic mechanism. [1] As a medication it is used to break down clots in some cases of myocardial infarction (heart attack), pulmonary embolism, and arterial thromboembolism. [2]
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