A study of platelet aggregation in patients with acute myocardial infarction at presentation and after 48 hrs of initiating standard anti platelet therapy.

ABSTRACT

AIMS & OBJECTIVES: Platelet aggregation is a key factor behind coronary artery disease. Various complications after an attack of acute coronary syndrome are often related to the platelet hyperactivity in the early hours following the event. There is a growing concern regarding aspirin & clopidogrel resistance, which has put the time-tested therapies under scrutiny. Time has come to address the issue of platelet hyperactivity in the early hours & whether to individualize therapy and drug doses in different patients. MATERIALS & METHODS: We prospectively enrolled 41 patients with a diagnosis of acute myocardial infarction (AMI) between July 2009 and July 2010 admitted to the cardiology ward and ICCU of Medical College, Kolkata, after fulfillment of inclusion & exclusion criteria. The study was reviewed and approved by the Institutional Ethical Committee. Platelet Aggregation (PA) with 10 microM epinephrine, 2 microg/ml collagen and 10 microM ADP was performed with light transmittance aggregometry in all patients according to the standard protocol. Tests were done within 3 hours of sampling with platelet-rich plasma (PRP) by the turbidometric method in a 2-channel aggregometer (Chrono-Log 490 Model, Chrono-Log Corp, Havertown, Pa). Aspirin & clopidogrel resistance were defined as per ACC/AHA guidelines. Platelet aggregation studies were done at presentation (zero hour) and 48 hours after instituting dual antiplatelet therapy in standard doses. RESULTS: Patients with first attack of AMI showed a high mean platelet aggregation at 0 hours of 77.4% +/- 18.8% with ADP, 77.5% +/- 26% with Epinephrine & 73.5% +/- 24.9% with Collagen. With all three agonists, the initial hyperactivity of platelets at 0 hours was significantly higher among diabetics & obese. Though reduced, significant platelet hyperactivity remained at 48 hours after initiating standard antiplatelet therapy; 50.3% +/- 14.3% with ADP, 56.5% +/- 21.6% with epinephrine & 38.4% +/- 22% with collagen. CONCLUSION: In the early hours after AMI there is a fairly high degree of platelet aggregation. Even after 48 hours of standard antiplatelet therapy the platelet aggregation though reduced, still remains significantly high. Since recurrent ischemic episodes frequently occur in this vulnerable period, time has come to assess platelet aggregation status in high risk groups, if not in all patients of acute coronary syndrome during this period so that therapy may be individualized. Further researches are required in this area.