Myocardial infarction (MI), commonly termed "heart attack", occurs when the blood supply to part of the heart muscle (the myocardium) is severely reduced or blocked. 70% of MI cases are the result of Vulnerable Plaque (VP). Vulnerable Plaque is characterized by fatty buildup leading to the development of a substantial necrotic core within the artery wall with a thin fibrous cap covering it and significant extent of macrophage infiltration (inflammation). Vulnerable plaques characteristically contain a lipid pool of more than 40% of volume, while the thin, fibrous cap is less than 100 microns. When vulnerable plaque lesions rupture, the content of the lesion spills into the bloodstream. The cytokines on the artery wall capture blood cells (mainly platelets) that rush to the site of injury and create a thrombus which can become large enough to block the artery. Thus, it is the aggregation of platelets inside the blood vessel which blocks the artery. Therefore, an effective evaluation of the patient's platelet function, following by timely preventive treatment with anti-aggregatory (antiplatelet) drugs may be crucial to saving the lives of patients in the event of MI.

The treatment with platelet aggregation inhibitors (antiplatelet drugs) which help to prevent the formation of potentially harmful blood clots has become a cornerstone of cardiovascular medicine. Aspirin and clopidogrel have emerged as critical therapies in the treatment of cardiovascular disease.

Aspirin

According to the World Health Organization, the most immediate improvements in cardiovascular health can be achieved with drugs, including aspirin, given to people at elevated risk of heart attack and stroke. It is estimated that aspirin therapy can reduce the risk of a first heart attack by 32% and the combined risk of heart attack, stroke and vascular death by 15%.

Mechanism of Action: Acetylsalicylic acid (ASA) - which is the major active ingredient of Aspirin - interferes with the formation of Thromboxane A2 by irreversibly inhibiting the key enzyme cyclo-oxygenase. Thromboxane A2, a prostaglandin, intensifies platelet aggregation and constriction of blood vessels. Once platelets have been in contact with ASA they become unable to produce Thromboxane A2 for the rest of their lifetime of 7 to 10 days, while the endothelial cells regain their ability to produce prostacyclin after a few hours. Therefore, ASA helps to ensure the vessel's integrity and to prevent the formation of platelet-rich clots.

Clopidogrel (Plavix®)

Clopidogrel is a potent oral antiplatelet agent often used in the treatment of coronary artery disease, peripheral vascular disease, and cerebrovascular disease. It is marketed by Bristol-Myers Squibb and Sanofi-Aventis under the trade name Plavix. It is also marketed in the generic form by Apotex, a Canadian generic pharmaceutical company. In 2005, it was the world's second highest selling pharmaceutical with sales of $5.9 billion.

Mechanism of Action: The mechanism of action of clopidogrel is irreversible blockade of the adenosine diphosphate (ADP) receptor on platelet cell membranes. This receptor named P2Y12 plays an important role in platelet aggregation, and specifically in the cross-linking of platelets by fibrin. The blockade of this receptor inhibits platelet aggregation by blocking activation of the glycoprotein IIb/IIIa pathway. Plavix is an expensive drug costing approximately $3 a day or about $100 a month.

The treatment of coronary artery disease with platelet aggregation inhibitors (anti-platelet drugs) which help to prevent the formation of potentially harmful blood clots has become a cornerstone of cardiovascular medicine. Consequently, evaluation of the pharmacological response to anti-platelet drugs is becoming an important part of cardiovascular diagnostics. The Impact Analyzer meets the need for wide-scale testing of platelet response to these drugs.