Life expectancy is reduced by 13.2 years in male smokers compared with nonsmokers, and this trend is stronger in female smokers, with a 14.5-year decrease in life expectancy.32 Cigarette smoking independently predicts increased risk of cardiac arrest in patients with CAD,33 and even exposure to secondhand smoke increases the risk of develop- ing CAD by 25% to 30%.34 As with other risk factors, there is a synergistic increase in cardiovascular risk in smokers who have other, concurrent, cardiovascular risk factors. Elevated cholesterol confers a higher risk of cardiovascular events in smokers than in nonsmokers, and smokers disproportionately tend toward unfavorable lipoprotein profiles.35 In patients with hypertension, smokers are 5 times more likely to develop severe hypertension than nonsmokers, and smokers with severe hyper- tension have higher mortality rates than nonsmokers.36 It is encouraging that studies of smoking cessation dem- onstrate significant long-term reduction (15% over 14 years) in mortality in patients who participate in smoking cessation The prevalence of obesity, defined as a body mass index 30 , has increased in recent years, with 30% of the adult US population falling into this category.38 The positive rela- tionship between obesity and BP is well documented.39 41 Obese adults are 3 times more likely to be hypertensive compared with nonobese adults,40 42 and increased adiposity may explain >60% of hypertension in adults.40 Furthermore, obesity is considered a major risk factor for poor BP control in hypertensive patients.3 Although the mechanisms of obesity-related hypertension are numerous, including activation of the sympathetic nervous system, sodium retention, activation of the renin-angiotensin- aldosterone system (RAAS), insulin resistance, and altered there is no acceptable guideline on the antihypertensive drug of choice for the management of hyper- tension among obese patients.3,44 Some investigators consider ACE inhibitors the drugs of choice for adequate BP control in obesity-related hyperten- sion because of their capacity to increase insulin sensitivity and thus reduce the risk of diabetes mellitus.45 This is in con- trast to thiazide diuretics, which are associated with increased risk of diabetes mellitus.46 That said, the efficacy of thiazide diuretics in lowering BP and improving cardiovascular out- comes in obese hypertensive patients is well established.47 -Blockers also have adverse effects on glucose metabo- lism but have led to significant improvement in BP in obese hypertensive patients because they decrease renin activity and cardiac output, which are often elevated in obese patients.48 However, enthusiasm for the use of -blockers as initial ther- apy is largely dampened by their negative profile on stroke outcomes compared with placebo and other antihypertensive There is abundant evidence in support of the effectiveness of lifestyle interventions in improving BP control among obese hypertensive patients. 