Choice of drug treatment for obesity-related hypertension: where is the evidence?

Sharma, Arya M.; Pischon, Tobias; Engeli, Stefan; Scholze, J.

doi:10.1097/00004872-200104000-00001

Cited by 86 publications

(56 citation statements)

References 91 publications

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“…3,44 Some investigators consider ACE inhibitors the drugs of choice for adequate BP control in obesity-related hypertension because of their capacity to increase insulin sensitivity and thus reduce the risk of diabetes mellitus. 45 This is in contrast 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 outcomes in obese hypertensive patients is well established.…”

Section: Obesitymentioning

confidence: 99%

Treatment of Hypertension in Patients With Coronary Artery Disease

Rosendorff¹,

Lackland²,

Allison³

et al. 2015

Hypertension

111

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Section: Obesitymentioning

confidence: 99%

Treatment of Hypertension in Patients With Coronary Artery Disease

Rosendorff¹,

Lackland²,

Allison³

et al. 2015

Hypertension

111

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“…7 This comprises actions that support concomitant weight-reducing therapy and positive effects on associated metabolic disorders, such as insulin resistance, glucose intolerance, and dyslipidemia. 7 Correspondingly, weightreducing medication should enhance antihypertensive treatment.…”

Section: Editorial P 1973 Clinical Perspective P 1998mentioning

confidence: 99%

Optimal Treatment of Obesity-Related Hypertension

et al. 2007

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Background-Current guidelines for the treatment of hypertension do not provide specific recommendations for obese hypertensive patients. To identify an optimal treatment regimen for obese hypertensive patients, we studied the interactions between a drug-based weight loss approach by sibutramine and different antihypertensive drug regimens. Methods and Results-This was a prospective, 16-week double-blind placebo-controlled randomized multicenter study in 171 obese hypertensive patients. After a 2-week run-in period, patients receiving 1 of the 3 antihypertensive combination therapies (felodipine 5 mg/ramipril 5 mg [nϭ57], verapamil 180 mg/trandolapril 2 mg [nϭ55], or metoprolol succinate 95 mg/hydrochlorothiazide 12.5 mg [metoprolol/hydrochlorothiazide; nϭ59]) were assigned randomly to sibutramine (15 mg) or placebo. Sibutramine treatment resulted in a significantly greater decrease in body weight, body mass index, and waist circumference and a significant increase in diastolic blood pressure during 24-hour blood pressure monitoring compared with placebo treatment. Sibutramine-induced weight loss and reduction of visceral obesity were markedly attenuated in the metoprolol/hydrochlorothiazide group compared with the other groups. Consistently, improvement in glucose tolerance and hypertriglyceridemia by sibutramine was abrogated in the cohort treated with metoprolol/ hydrochlorothiazide compared with the other groups. Conclusions-The present study demonstrates for the first time that an antihypertensive combination therapy regimen with angiotensin-converting enzyme inhibitors and calcium channel blockers is more advantageous than a ␤-blocker/diuretic-based regimen in supporting the weight-reducing actions and concomitant metabolic changes induced by sibutramine in obese hypertensive patients. These data may help to develop future comprehensive treatment strategies and guidelines for this high-risk patient population.

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“…␣-Adrenoreceptor antagonists are effective antihypertensive agents and improve insulin sensitivity, 18 but there are concerns about their safety profile. In the ALLHAT Trial, the ␣-blocker doxazosin arm was stopped prematurely because of an increased risk of cardiovascular events, particularly heart failure.…”

Section: Does It Matter What Antihypertensive Agents We Use As Long Amentioning

confidence: 99%

Should We Target the Sympathetic Nervous System in the Treatment of Obesity-Associated Hypertension?

Biaggioni

2008

Hypertension

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A n estimated 60% to 70% of hypertension may be attributed to obesity. 1 As our population increases in weight and girth, obesity-associated hypertension will be an increasing medical problem, contributing to greater health care costs and reversing the gains that we have achieved in the treatment of hypertension. Considering that 30% of hypertensive subjects are undiagnosed, 40% remain untreated, and, of those being treated, 65% do not meet treatment goals, 2 the opening of the spigot of obesityassociated hypertension will result in an ever-growing number of patients with uncontrolled hypertension, particularly because obesity is a predictor of poor blood pressure control. 3 It is important, therefore, to understand the pathophysiology of obesity-associated hypertension. This commentary focuses on the role that the sympathetic nervous system plays in this condition and its relevance to treatment. Sympathetic Activity and Obesity-Associated HypertensionLandsberg 4 postulated that obesity induces sympathetic activation as a compensatory mechanism to increase resting energy expenditure and restore energy balance; sympathetically mediated hypertension is the price to pay for this beneficial metabolic effect. A competing MONA LISA (Most Obesities kNown Are Low In Sympathetic Activity) hypothesis postulates that lower sympathetic activity is an initiating event leading to decreased energy expenditure and obesity. 5 In white populations, in whom most of the studies have been done, the preponderance of evidence supports the concept that sympathetic activation accompanies obesity-associated hypertension. There is less agreement about the cause of sympathetic activation; potential culprits include the increase in insulin, leptin, and angiotensin II; the decrease of adiponectin; and the sleep apnea 6,7 associated with obesity. Despite the disparity of these mechanisms, it is interesting that all of them act in the central nervous system to increase sympathetic outflow. This central sympathetic activation is not generalized; rather, it is selectively increased in organs relevant to blood pressure regulation, including the kidney, heart, and skeletal muscle vasculature. 6,8 To determine whether sympathetic activation indeed contributed to obesity-associated hypertension, Wofford et al 9 used combined ␣-and ␤-blockade with doxazosin and atenolol and showed a greater decrease in blood pressure in obese compare with lean hypertensive subjects. We recently used a similar approach, inducing complete but transient autonomic withdrawal with the ganglionic blocker trimethaphan, and showed that most of the increase in blood pressure observed in obese subjects was mediated by the autonomic nervous system. 10 As expected, resting energy expenditure was higher in obese subjects but, in contrast to blood pressure, it remained significantly elevated after autonomic blockade. We found that the increase in energy expenditure was likely because of the increase in muscle mass that usually companies obesity 10 ; in our patients, a 30-kg increa...

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Choice of drug treatment for obesity-related hypertension: where is the evidence?

Cited by 86 publications

References 91 publications

Treatment of Hypertension in Patients With Coronary Artery Disease

Treatment of Hypertension in Patients With Coronary Artery Disease

Optimal Treatment of Obesity-Related Hypertension

Should We Target the Sympathetic Nervous System in the Treatment of Obesity-Associated Hypertension?

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