Abstract

Objectives: Patients with atherosclerotic cardiovascular diseases (ASCVDs) are predisposed to atherothrombosis and ischemic phenomena. Antiplatelets mitigate this but not consistently, as these ischemic events still occur despite their administration. This is called antiplatelet resistance. We sought to see how much of this occurs in our patients since its rate is bound to differ from place to place. The burden of antiplatelet resistance has not been determined in our environment. Material and Methods: Patients at risk of ASCVD who were receiving antiplatelet treatments were invited to participate in this study. They were enrolled first into a two week wash out phase, after which baseline aggregometry and full blood count were done. They were then given either Aspirin or Clopidogrel for four weeks and had the same blood work-up repeated. The Aggregometer was used to determine the platelet aggregability at these different times. If the second set showed >10% reduction from baseline, such patients were adjudged sensitive. A reduction <10% of the first value defined resistance. Results: Twenty patients (15 F/5 M) were in Group 1 and received a low dose of Aspirin (75 mg), the age range of 42–76 years, with a mean (standard deviation [SD]) of 60.75 (10.45). Twenty-six were in Group 2 (18 F/8 M) and received low dose clopidogrel (75 mg), with an age range of 23–87 years and a mean (SD) of 58.08 (14.18). Fifteen (75%) were sensitive in Group 1 (Aspirin) with 25% resistant. For Clopidogrel, 14 (53.85%) were sensitive and 12 (46.15%) resistant. In a few cases, the aggregability actually increased paradoxically on treatment. Conclusion: Antiplatelet resistance also occurs in our environment; it is worse for Clopidogrel than for Aspirin. These are people who, despite being on antiplatelets, would go on to develop these atherothrombotic ischemic phenomena. Efforts to identify the predictors of this phenomenon of resistance and work out effective counteractions should be encouraged.

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