A 56-year-old man with hypercholesterolemia was rushed to the hospital with crushing chest pain radiating to his left arm and a probable heart attack. Which of the following treatments should be considered?
A. A platelet transfusion
B. Heparin transfusion
C. Thrombin transfusion
D. Fibrinogen infusion
E. Tissue plasminogen activator infusion
The correct answer is- E- Tissue plasminogen activator infusion.
Tissue plasminogen activator (tPA) causes activation of plasminogen (zymogen form) to plasmin (active form). Plasmin hydrolyzes fibrin to form soluble degradation products (Figure-1).
Figure-1- Mechanism of action of tPA
The main goals of medical therapy of acute myocardial infarction are- rapid intravenous thrombolysis and/or rapid referral for PCI (Percutaneous coronary intervention), optimizing oxygenation, decreasing cardiac workload, and controlling pain.
1) Antithrombotic agents
These agents prevent the formation of thrombus associated with myocardial infarction and inhibit platelet function. Low dose Aspirin, Heparin and Low-molecular-weight heparins (LMWH) are used as antithrombotic agents.
These agents oppose coronary artery spasm, which augments coronary blood flow and reduce cardiac work by decreasing preload and after load.
Nitrates are useful for preload reduction and symptomatic relief but have no apparent impact on mortality rate in MI.
3) Beta-adrenergic blockers
These agents inhibit chronotropic, inotropic, and vasodilatory responses to beta-adrenergic stimulation and reduce blood pressure, which decreases myocardial oxygen demand. Greatest benefit is achieved when given within 8 hours of symptom onset.
4) Thrombolytic agents
These agents prevent recurrent thrombus formation and rapid restoration of hemodynamic disturbances. In addition, they remove pathologic intraluminal thrombus or embolus not yet dissolved by the endogenous fibrinolytic system. When given within 12 h of symptom onset, they restore patency of occluded arteries, salvage myocardium, and reduce morbidity and mortality rates of AMI. Thrombolytic treatment should be started within 30 min of arrival (door-drug time). Maximum benefit occurs when administered within 1-3 h of symptom onset in patients with ST-segment elevation.
These agents are-
- Alteplase-Tissue plasminogen activator(tPA)
- Tenecteplase –Modified version of alteplase (tPA)
- Reteplase – (figure-2).
Figure-2- Mechanism of action of thrombolytic agents
5) Platelet aggregation inhibitors
These agents inhibit platelet aggregation and reduce mortality.
These agents reduce pain, which decreases sympathetic stress. They may provide some preload reduction.
Thus for immediate restoration of circulation the treatment of choice is tissue plasminogen activator. Adjunctive therapy with IV heparin is necessary to maintain patency of arteries recanalized by tPA, especially during the first 24-48 h.
Platelets, thrombin and fibrinogen promote clotting through the intrinsic pathway and are contraindicated in the treatment of Acute MI. Platelets form a plug at the site of bleeding and bind prothrombin to facilitate its conversion to thrombin. Fibrinogen is the substrate acted upon by thrombin to yield the fibrin mesh of blood clots.
Heparin is a mucopolysaccharide that activates antithrombin and prevents the conversion of Prothrombin to thrombin. Heparin can inhibit the clot formation but cannot dissolve the clot that has already formed.Please help Biochemistry for Medics by "CLICKING ON THE ADVERTISEMENTS" every time you visit us. Thank you!