Treatment of hypertension in patients taking sibutramine

Cardiology Review® Online, December 2007, Volume 24, Issue 12

Obesity is a growing epidemic in the United States and around the world.

Obesity is a growing epidemic in the United States and around the world. Obese patients are more likely to have hypertension, diabetes, and hyperlipidemia. Even though lifestyle modification is the cornerstone of therapy for obesity, as well as hypertension, the majority of patients need both medication and lifestyle modification for effective control.

In their study, Patschan and Scholze asked the important question of whether there is an optimal blood pressure treatment regimen for obese hypertensive patients who are currently taking sibutramine (Meridia) for weight loss. Sibutramine is a selective serotonin and norepinephrine uptake inhibitor that has been shown to be effective for weight loss. A potential side effect of sibutramine is increased blood pressure. In a prospective, 16-week double-blind, placebo-controlled, randomized, multicenter study of 171 obese hypertensive subjects, they found that sibutramine treatment resulted in decreased body weight, body mass index, and waist circumference. There was a significant increase in diastolic blood pressure during 24-hour ambulatory blood pressure monitoring, however. Interestingly, they found that weight loss and reduction in visceral obesity were markedly diminished in patients receiving metoprolol/ hydrochlorothiazide therapy compared with calcium channel blocker/angiotensin-converting enzyme (ACE) inhibitor therapy. Even though this was a very small study without a control group, it makes an interesting contribution regarding the effective treatment of the obese hypertensive patient.

Until recently, beta blockers were recommended as first-line therapy for patients with essential uncomplicated hypertension. Recent data, however, have shown that initiating therapy with a beta blocker did not reduce cardiovascular risk to the same degree as starting with thiazide diuretics or ACE inhibitors. Also, patients on beta blocker therapy were more likely to develop diabetes, especially when beta blockers were combined with thiazide-type diuretics. Beta blockers are still the mainstay therapy, however, when additional therapy is warranted and when hypertension is associated with heart failure or occurs after myocardial infarction or in patients with coronary artery disease.

Beta blockers most likely promote weight gain and metabolic disturbances due to a reduction in basal metabolic rate and energy expenditure. It is important to note, however, that all beta blockers are not the same. Beta blockers are a diverse group of agents with varying pharmacologic properties. First-generation beta blockers include propranolol (Inderal), timolol (Blocadren), and nadolol (Corgard). These are nonselective beta blockers, which have similar binding affinity to both ß-1 and ß-2 receptors. At higher doses, however, the selectivity is decreased. Second-generation beta blockers include atenolol (Tenormin), bisoprolol (Zebeta), and metoprolol. The third generation of beta blockers includes carvedilol (Coreg) and labetalol (Normodyne, Trandate), which combine nonselective beta blockade with peripheral vasodilator activity. Whether the weight gain seen in this study can be generalized to other beta blockers is unknown. In the meantime, Patschan and Scholze have added an important finding to the growing literature about the treatment of obese uncomplicated hypertensive patients.