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Medical Author:

Daniel Lee Kulick, MD, FACC, FSCAI

Daniel Lee Kulick, MD, FACC, FSCAI

Dr. Kulick received his undergraduate and medical degrees from the University of Southern California, School of Medicine. He performed his residency in internal medicine at the Harbor-University of California Los Angeles Medical Center and a fellowship in the section of cardiology at the Los Angeles County-University of Southern California Medical Center. He is board certified in Internal Medicine and Cardiology.

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Medical Editor:

Jay W. Marks, MD

Jay W. Marks, MD

Jay W. Marks, MD, is a board-certified internist and gastroenterologist. He graduated from Yale University School of Medicine and trained in internal medicine and gastroenterology at UCLA/Cedars-Sinai Medical Center in Los Angeles.

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In this Article

• What is a heart attack?
• How is a heart attack treated?
• Antiplatelet agents
• Aspirin
• Thienopyridines
• Glycoprotein IIb/IIIa inhibitors
• Anticoagulants
• Clot-dissolving drugs
• Coronary angiography and percutaneous transluminal coronary angioplasty (PTCA)
• Coronary artery stents
• Nitrates
• Angiotensin converting enzyme (ACE) inhibitors
• Beta blockers
• Oxygen
• Coronary artery bypass
• What can a patient expect during recovery from a heart attack?
• How can a second heart attack be prevented?
• Find a local Cardiologist in your town
• Heart Attack Treatment Index

The glycoprotein IIb/IIIa inhibitors such as abciximab (Reopro) and eptifibatide (Integrilin) prevent aggregation of platelets by inhibiting the glycoprotein receptors on the platelets. They are the most potent antiplatelet agents, approximately 9 times more potent than aspirin, and 3 times more potent than the thienopyridines. The glycoprotein IIb/IIIa inhibitors are also the most expensive antiplatelet agents. The currently FDA-approved glycoprotein IIb/IIIa inhibitors have to be given intravenously. They usually are given along with aspirin and heparin. They are quick acting; their maximal antiplatelet effects are achieved within minutes of infusion. These inhibitors have become important in the treatment of patients with heart attacks, patients with unstable angina, and patients undergoing PTCA with or without stenting. Numerous studies have shown that glycoprotein IIb/IIIa inhibitors:

• Decrease the size of the blood clot blocking the coronary arteries, thus improving blood flow, limiting damage to heart muscle, and improving survival among patients with heart attacks
• Decrease the incidence of heart attacks and improve survival among patients with unstable angina
• Prevent the formation of blood clots inside coronary stents and in coronary arteries unblocked by PTCA, thus decreasing the incidence of heart attacks and improving survival, specifically, when given intravenously at the time of PTCA and stenting and followed by oral aspirin and clopidogrel

The major risk of glycoprotein IIb/IIIa inhibitors is bleeding. Therefore, patients on heparin, aspirin, and glycoprotein IIb/IIIa inhibitors have to be monitored closely for bleeding. Recent studies have demonstrated equal efficacy of abciximab and eptifibatide. Eptifibatide is shorter acting than abciximab. In the event of major bleeding, the antiplatelet effect of eptifibatide can be reversed within hours of stopping the intravenous infusion, while the antiplatelet effect of abciximab will last much longer. Sometimes, transfusions of platelets are necessary to treat major bleeding due to abciximab.

An uncommon side effect of glycoprotein IIb/IIIa inhibitors is the development of low platelet counts (thrombocytopenia). Thrombocytopenia can increase the risk for bleeding and, in rare instances, may actually cause blood to clot. Thus, patients receiving glycoprotein IIb/IIIa inhibitors should have their platelet counts monitored closely.