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Additional info for Antiplatelet Therapy In Ischemic Heart Disease (American Heart Association Clinical Series)
Platelets, 2nd edn. Elsevier/Academic Press, San Diego, 2007; 519–534. 21 Frossard M, Fuchs I, Leitner JM et al. Platelet function predicts myocardial damage in patients with acute myocardial infarction. Circulation 2004; 110: 1392–1397. 22 Campo G, Valgimigli M, Gemmati D et al. Value of platelet reactivity in predicting response to treatment and clinical outcome in patients undergoing primary coronary intervention: insights into the STRATEGY Study. J Am Coll Cardiol 2006; 48: 2178–2185. 23 Lanza GA, Sestito A, Iacovella S et al.
Postulated mechanisms include reduced prostacyclin synthesis, elevated blood pressure, abnormal vascular remodeling, inhibition of protective mechanisms against ischemia–reperfusion injury, and inhibition of lipoxin A4 production, which has a wide range of anti-inflammatory effects . The relationship between COX-2 inhibition and prostacyclin inhibition appears linear , and marked suppression of COX-2 (70–80%) may significantly reduce the cardioprotective effect of prostacyclin. Renal effects COX-2 inhibitors have a similar renal risk profile to non-selective NSAIDs.
Circulation 2004; 110: 1392–1397. 22 Campo G, Valgimigli M, Gemmati D et al. Value of platelet reactivity in predicting response to treatment and clinical outcome in patients undergoing primary coronary intervention: insights into the STRATEGY Study. J Am Coll Cardiol 2006; 48: 2178–2185. 23 Lanza GA, Sestito A, Iacovella S et al. Relation between platelet response to exercise and coronary angiographic findings in patients with effort angina. Circulation 2003; 107: 1378–1382. 24 Linden MD, Furman MI, Frelinger III AL et al.