Current guidelines support dual antiplatelet therapy with aspirin and clopidogrel (Plavix) in a number of clinical scenarios:
- ST-segment-elevation myocardial infarction (SEMI),
- Non-ST-elevation MI,
- Percutaneous Coronary Intervention.
The guidelines are based on strong evidence from several large randomized clinical trials over the last 10 years.
- Dual antiplatelet therapy is recommended after ST-elevation MI or non-ST-elevation acute coronary syndromes, with aspirin indefinitely and clopidogrel for up to 1 year.
- Dual antiplatelet therapy is recommended for at least 1 month after placement of a bare-metal stent and for at least 1 year (or possibly indefinitely) after placement of a drug-eluting stent.
- There is no compelling indication for clopidogrel in patients with chronic coronary artery disease.
Antiplatelet drugs
The most important antiplatelet drugs are:
- Cyclooxygenase inhibitors
- Adenosine diphosphate (ADP) receptor inhibitors
- Clopidogrel (Plavix)
- Prasugrel (Effient)
- Ticlopidine (Ticlid)
- Phosphodiesterase inhibitors
- Cilostazol (Pletal)
- Glycoprotein IIB/IIIA inhibitors(intravenous use only)
- Abciximab (ReoPro)
- Eptifibatide (Integrilin)
- Tirofiban (Aggrastat)
- Adenosine reuptake inhibitors
- Dipyridamole (Persantine)
Prevention and treatment of arterial thrombosis
Treatment of established arterial thrombosis includes the use of Antiplatelet drugs and thrombolytic therapy. Antiplatelet drugs alter the platelet activation at the site of vascular damage crucial to the development of arterial thrombosis.
- Aspirin irreversibly inhibits the enzyme COX, resulting in reduced platelet production of TXA2 (thromboxane – powerful vasoconstrictor which lowers cyclic AMP and initiates the platelet release reaction).
- Dipyridamole inhibits platelet phosphodiesterase, causing an increase in cyclic AMP with potentiation of the action of PGI2 – opposes actions of TXA2
- Clopidogrel affects the ADP-dependent activation of IIb/IIIa complex
- Glycoprotein IIb/IIIa receptor antagonistsblock a receptor on the platelet for fibrinogen and von Willebrand factor. 3 classes:
- Murine-human chimeric antibodies (e.g. abciximab)
- Synthetic peptides (e.g. eptifibatide)
- Synthetic non-peptides (e.g. tirofiban)
- Epoprostenol is a prostacyclin which is used to inhibit platelet aggregation during renal dialysis (with or without heparin) and is also used in primary pulmonary hypertension.
Thrombolytic therapy is used in myocardial infarction, cerebral infarction and occasionally in massive pulmonary embolism. The main risk is bleeding. Treatment should not be given to patients who have had recent bleeding, uncontrolled hypertension or a hemorrhagic stroke, or surgery or other invasive procedures within the previous 10 days.
- Streptokinase forms a complex with plasminogen, resulting in a conformational change which activates other plasminogen molecules to form plasmin.
- Plasminogen activators (PA), tissue-type plasminogen activators (alteplase, tenecteplase) are produced by recombinant technology.
Comments 3
I had a stent in April 2018. Now I am perfectly fine with. How is future life ?
Why would a doctor put a stent on top of a stent ? The doctor then said the drug plavix is the only drug that works with this stent. Why ??
I had two stents in my right descending coranary Artery butter up against each other that became 98% blocked after a few years after placement, my Dr. Just Roto Rudered the two stents out with a razor blade tipped ballon Cathater !
Stuck it up in them stents inflated it and twisted that Cath ! And cleaned most of the Plaque out of both stents, at the same time the plaque was being scraped from the wall of the stents, it was being sucked out of the Artery ! So it wouldn’t float up to my brain and give me a stroke. As years passed by I had to have 5 stents placed in my Widow maker Artery the LAD. All butted up against each other. So my next trip will be to the Operating Room for Bypass surgery.