Tumor Necrosis Factor-a and Interleukin-10 Genotypes in Congestive Heart Failure

7. Montgomery HE, Clarkson P, Dollery CM, Prasad K, Losi M-A, Hemingway H, Statters D, Jubb M, Girvain M, Varnava A, World M, Deanfield J, Talmud P, McEwan JR, McKenna WJ, Humphries S. Association of angiotensin-converting enzyme gene I/D polymorphism with change in left ventricular mass in response to physical training. Circulation. 1997;96:741–747. Increased Membrane and Soluble P-Selectin in Atrial Fibrillation To the Editor: Inappropriate platelet activation and thrombus formation are frequent findings in many cardiovascular disorders and are believed to have an important pathogenic role. P-selectin, the membrane of the component of a-granule and membrane of the Weibel-Palade body, aids the adhesion of leukocytes bearing its ligand. Increased expression of P-selectin at the surface of the platelet, as defined by flow cytometry, is therefore a likely marker of the activation of these cells.1 The recent article by Minamino and colleagues2 reporting increased expression of P-selectin by platelets in subjects with atrial fibrillation (AF) is therefore in keeping with platelet activation and a prothrombotic state in AF, leading to the high risk of stroke and thromboembolism in this common condition. Nevertheless, a soluble form of P-selectin (sP-selectin) is also present in the plasma, and increasing evidence points toward elevated plasma levels among patients with thrombotic disorders, stroke, and atherosclerosis, thus providing an additional tool to study platelet activation.3,4 Similar to Minamino and colleagues,2 we hypothesised that patients with AF would have raised levels of sP-selectin. To investigate this further, we recruited 52 consecutive patients (45 males, mean age 66 years) with chronic AF who were not taking any antithrombotic therapy and 60 ageand sexmatched healthy controls. sP-selectin was measured in citrated plasma by commercial ELISA (R&D Systems). Mean6SD levels in the patients with AF were 2326181 ng/mL compared with 161682 ng/mL in the controls (unpaired t test P50.015). Like Minamino and colleagues,2 we would interpret our preliminary data showing raised sP-selectin in AF as evidence of increased platelet activation in our patients. Our findings may be applicable to other forms of atherothrombotic disorders, such as stroke, and warrant further attention in larger groups of patients with more diverse disease(s). If raised sP-selectin levels are truly a marker of platelet activation, this may possibly provide a new rationale for developing and using therapy targeting platelets. sP-selectin would also be an easily measurable index of platelet activation, allowing large-scale epidemiological and prognostic studies in AF and other disorders to be performed without encountering the limitations imposed by complex flow cytometry. Andrew D. Blann Foo Li-Saw-Hee Gregory Y.H. Lip Hemostasis, Thrombosis and Vascular Biology Unit University Department of Medicine City Hospital Birmingham, UK 1. Wu KK. Platelet activation mechanisms and markers in arterial thrombosis. J Intern Med. 1996;239:17–34. 2. Minamino T, Kitakaze M, Sanada S, Asanuama A, Kurotobi T, Koretsune Y, Fukunami M, Kuzuya T, Hoki N, Hori M. Increased expression of P-selectin on platelets is a risk factor for silent cerebral infarction in patients with atrial fibrillation: role of nitric oxide. Circulation. 1998;98: