Heart Attack Medication, Drugs to Treat a Myocardial Infarction

A heart attack (myocardial infarction) is death of a portion of the muscular heart wall as a result of severely reduced blood supply. It is most commonly due to a blockage in the coronary artery which supplies oxygen-rich blood to the heart wall. An occlusion that causes injury but not death to the heart wall over a period of time is known as ischemic heart disease (IHD). With a myocardial infarction, the already occluded coronary artery is suddenly blocked almost completely most often by the formation of a blood clot at the site of the narrowing. Severe pain arises which is not relived by rest or nitrates as is used for the relief of angina. There are prominent ST changes in the ECG and the incident is more accurately described as ST elevation myocardial infarction (STEMI). Other indicators may include significantly elevated cardiac markers (enzymes) of ischemia which can be found in the blood

STEMI is a medical emergency. Patients are treated with aspirin, beta blockers, nitrates, low molecular weight heparin and glycoprotein IIb/IIIa inhibitor. Other symptoms and complications are also treated appropriately. Strong opioid analgesics like morphine are used to control the pain of myocardial infarction. Fear and apprehension of the patients are also reduced with use of morphine. Some patients may require additional sedation to calm them. Patients in cardiac failure or having cardiac arrhythmias are treated appropriately. PCI (usually with stenting) may be performed immediately in the early invasive approach. The PCI treatment may be delayed till patient is stabilized in the conservative approach. In places where facility for PCI is not available, STEMI patients are managed medically with ‘clot buster’ or thrombolytic therapy.


Anti-platelet drugs are drugs that inhibit aggregation of platelets that lead to blood clot formation. The platelet aggregation is inhibited by targeting various agents involved in the normal regulation of platelet function. It includes prostaglandins, ADP, thrombin, collagen etc. The prominent anti-platelet drugs currently in clinical use exert its action by inhibition of prostaglandin synthesis (aspirin), inhibition of ADP-induced aggregation of platelets (ticlopidine, clopidogrel and prasugrel), and inhibition of the glycoprotein IIb/IIIa receptors on platelets (abciximab, and tirofiban).

Prostaglandin Synthesis Inhibitors

Thromboxane A2 is a prostaglandin that causes platelets to aggregate. Aspirin inhibits the synthesis of thromboxane A2 by inhibiting cyclooxygenase enzyme irreversibly. Thereby aspirin prevents platelet aggregation and clot formation. This property of aspirin is unique. The other drugs related to aspirin (salicylates) do not inhibit cycloxygenase irreversibly and hence the anti-platelet effect is not strong like aspirin. Low dose aspirin (less than 325 mg/day) is used for prevention of myocardial infarction in people at risk. Use of aspirin is associated with gastric irritation, profuse bleeding following trivial injuries and precipitation of asthma attacks in sensitive individuals.

Platelet ADP-Receptor Inhibitors

Clopidogrel, prasugrel and ticlopidine irreversibly block the ADP receptor on platelets. This reduces the platelet aggregation and formation of clots. These drugs prevent ischemic events among patients with unstable angina pectoris. These drugs are also used to prevent thrombus formation in patients undergoing coronary stenting. Prevention of stroke in patients at risk is another important use for these drugs. Ticlopidine is associated with more adverse effects and is less preferred than clopidogrel. Ticlopidine is known to cause dyspepsia and diarrhea in large number of patients. It can occasionally cause serious reduction in white blood count. Clopidogrel is associated with fewer adverse effects than ticlopidine. The white blood count reduction with clopidogrel is a rare occurrence. Prasugrel is relatively a new drug and has been associated with higher incidence of bleeding.

Glycoprotein IIb/IIIa Receptor Inhibitors

Activation of the glycoprotein IIb/IIIa receptor is an important step for platelet aggregation. Inhibition of this receptor reduces platelet aggregation. The glycoprotein IIb/IIIa inhibitors are of use in patients with acute coronary syndromes and following PCI. Abciximab is a monoclonal antibody against the glycoprotein IIb/IIIa complex. It has been approved for use in percutaneous coronary intervention and in acute coronary syndromes. Tirofiban is another drug that targets glycoprotein IIb/IIIa receptor. These drugs are available only as injections.

Thrombolytics (Clot Busters)

Thrombolytics (clot busters or fibrinolytics) are drugs that break down the thrombus. Myocardial infarction results from blockade of one or more of the major vessels supplying blood to the heart muscles. The blockade is usually by a thrombus and immediate break down of the thrombus can restore the blood supply to the ischemic area. This can minimize the damage of the cardiac muscles caused by the ischemic event. Thrombolytics break down thrombus by enhancing formation of plasmin from plasminogen.

Thrombolytics are administered intravenously and are most beneficial if administered with in 6 hours of onset of the myocardial infarction. The various available thrombolytics are :

  • streptokinase
  • urokinase
  • alteplase
  • reteplase
  • tenecteplase

Streptokinase is a protein produced by b-hemolytic streptococci. Streptokinase is associated with allergic reactions and is known to produce antibodies against it. A repeat use of streptokinase in same individual is likely to be less effective due to antibody formation. Streptokinase is less commonly used at present due to availability of newer and safer drugs. Urokinase is synthesized by the kidney that directly converts plasminogen to active plasmin. Alteplase, reteplase and tenecteplase are human tissue plasminogen activators (tPAs) produced by recombinant DNA technology. Human tPAs are more selective in its action and hence its actions are localized to the formed thrombus. This minimizes the tendency for bleeding complications. The thrombolytic therapy is indicated in patients with acute myocardial infarction which is confirmed on ECG. Streptokinase, urokinase and alteplase are given by intravenous infusion while reteplase and tenecteplase are given in bolus injections.

Thrombolytics are also of use in patients with acute ischemic stroke, pulmonary embolism and severe deep vein thrombosis. Thrombolytic use is associated with increased risk of bleeding. Bleeding is more common with streptokinase than with tissue plasminogen activators. Thrombolytic therapy is not indicated in patients who have undergone any major surgeries in last 10 days, suffering from bleeding disorders or major gastrointestinal bleeding in the past 3 months. It should also be avoided in patients with any active bleeding or history of hemorrhagic stroke.

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