@article {1068, title = {Platelet count and the risk for thrombosis and death in the elderly.}, journal = {J Thromb Haemost}, volume = {7}, year = {2009}, month = {2009 Mar}, pages = {399-405}, abstract = {

AIM: Our aim was to examine the association between platelet count and the incidence of myocardial infarction, ischemic stroke, hemorrhagic stroke, venous thrombosis, and mortality.

METHODS AND RESULTS: Platelet count was measured at baseline in 1989-1990 and at 3 years follow-up, or at baseline (for a newly recruited group) in 1992-1993 in 5766 community-dwelling individuals aged 65 years and older (mean age at baseline, 73 years). During 12-15 years of follow-up, there were 821 incident myocardial infarctions, 807 ischemic strokes, 161 hemorrhagic strokes, 159 venous thrombotic events, and 3413 participants died. Platelet count was not associated with the occurrence of myocardial infarction, ischemic or hemorrhagic stroke, venous thrombosis, or cardiovascular mortality. Non-cardiovascular mortality was higher among both participants with low and with high platelet count. Adjusted non-cardiovascular mortality rates for platelet counts below 100, 100-199, 300-399, and above 400 x 10(9) L(-1) relative to the reference mortality rate in participants with platelet count values between 200 and 299 x 10(9) L(-1) were 1.89 (1.21-2.96), 1.08 (0.98-1.20), 1.20 (1.06-1.37), and 1.47 (1.14-1.90), respectively.

CONCLUSION: Platelet counts were not associated with vascular outcomes but low and high platelet counts were associated with non-cardiovascular mortality, including cancer mortality.

}, keywords = {Aged, Aged, 80 and over, Cause of Death, Cerebral Hemorrhage, Female, Humans, Male, Myocardial Infarction, Platelet Count, Risk, Stroke, Survival Analysis, Thrombosis, Venous Thrombosis}, issn = {1538-7836}, doi = {10.1111/j.1538-7836.2008.03267.x}, author = {van der Bom, J G and Heckbert, S R and Lumley, T and Holmes, C E and Cushman, M and Folsom, A R and Rosendaal, F R and Psaty, B M} } @article {7491, title = {Pharmacogenomics study of thiazide diuretics and QT interval in multi-ethnic populations: the cohorts for heart and aging research in genomic epidemiology.}, journal = {Pharmacogenomics J}, year = {2017}, month = {2017 Jul 18}, abstract = {

Thiazide diuretics, commonly used antihypertensives, may cause QT interval (QT) prolongation, a risk factor for highly fatal and difficult to predict ventricular arrhythmias. We examined whether common single-nucleotide polymorphisms (SNPs) modified the association between thiazide use and QT or its component parts (QRS interval, JT interval) by performing ancestry-specific, trans-ethnic and cross-phenotype genome-wide analyses of European (66\%), African American (15\%) and Hispanic (19\%) populations (N=78 199), leveraging longitudinal data, incorporating corrected standard errors to account for underestimation of interaction estimate variances and evaluating evidence for pathway enrichment. Although no loci achieved genome-wide significance (P<5 {\texttimes} 10(-8)), we found suggestive evidence (P<5 {\texttimes} 10(-6)) for SNPs modifying the thiazide-QT association at 22 loci, including ion transport loci (for example, NELL1, KCNQ3). The biologic plausibility of our suggestive results and simulations demonstrating modest power to detect interaction effects at genome-wide significant levels indicate that larger studies and innovative statistical methods are warranted in future efforts evaluating thiazide-SNP interactions.The Pharmacogenomics Journal advance online publication, 18 July 2017; doi:10.1038/tpj.2017.10.

}, issn = {1473-1150}, doi = {10.1038/tpj.2017.10}, author = {Seyerle, A A and Sitlani, C M and Noordam, R and Gogarten, S M and Li, J and Li, X and Evans, D S and Sun, F and Laaksonen, M A and Isaacs, A and Kristiansson, K and Highland, H M and Stewart, J D and Harris, T B and Trompet, S and Bis, J C and Peloso, G M and Brody, J A and Broer, L and Busch, E L and Duan, Q and Stilp, A M and O{\textquoteright}Donnell, C J and Macfarlane, P W and Floyd, J S and Kors, J A and Lin, H J and Li-Gao, R and Sofer, T and M{\'e}ndez-Gir{\'a}ldez, R and Cummings, S R and Heckbert, S R and Hofman, A and Ford, I and Li, Y and Launer, L J and Porthan, K and Newton-Cheh, C and Napier, M D and Kerr, K F and Reiner, A P and Rice, K M and Roach, J and Buckley, B M and Soliman, E Z and de Mutsert, R and Sotoodehnia, N and Uitterlinden, A G and North, K E and Lee, C R and Gudnason, V and St{\"u}rmer, T and Rosendaal, F R and Taylor, K D and Wiggins, K L and Wilson, J G and Chen, Y-DI and Kaplan, R C and Wilhelmsen, K and Cupples, L A and Salomaa, V and van Duijn, C and Jukema, J W and Liu, Y and Mook-Kanamori, D O and Lange, L A and Vasan, R S and Smith, A V and Stricker, B H and Laurie, C C and Rotter, J I and Whitsel, E A and Psaty, B M and Avery, C L} }