This absence of benefit on nonstroke out- comes was not attributable to obesity because effects were simi- lar across levels of obesity. A meta-analysis of 31 trials with 73913 individuals with diabetes mellitus demonstrated that more intensive BP reduction significantly reduced the risk of stroke but not MI.248 For every 5-mmHg reduction in SBP, the risk of stroke decreased by 13% (95% CI, 5 20). In a secondary analysis of the Losartan Intervention for Endpoint Reduction in Hypertension (LIFE) trial, however, among 9193 hyperten- sive patients with left ventricular hypertrophy by ECG criteria, achieving intensive BP control to <130 mmHg was not associ- ated with a reduction in stroke after multivariable adjustment, and there was a significant increase in all-cause mortality (HR, The target for BP reduction, there- fore, may differ by patient characteristics and comorbidities. Pharmacogenomics may contribute to improving individu- alized selection of antihypertensive medications for stroke prevention. For example, in genetic studies ancillary to the Antihypertensive and Lipid Lowering to Prevent Heart Attack Trial (ALLHAT), individuals with the stromelysin (matrix metalloproteinase-3) genotype 6A/6A had higher stroke rates on lisinopril than on chlorthalidone, and those with the 5A/6A genotype had lower stroke rates on lisinopril.250 homozygotes had the lowest stroke rates compared with those taking chlorthalidone (HR for interaction=0.51; 95% CI, 0.31 0.85). The effect was not seen for other medications. Carriers of mutations of the fibrinogen- gene also had a lower risk of stroke on lisinopril compared with amlodipine than those who were homozygous for the usual allele, potentially because ACEIs lower fibrinogen levels and this effect is more clinically important among those with mutations associated with higher The role of genetic testing in hypertension management remains undefined at present, however. 