Therapeutic Considerations in the Treatment of Obesity Hypertension

Treatment of Obesity Hypertension

The sixth report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC VI) recommends nonpharmacologic therapies, such as weight loss, increased physical activity, and sodium restriction, as the initial approach to treating most patients with high-normal blood pressure and stages 1 and 2 essential hypertension.^[28] The objective of identifying and treating obesity-related high blood pressure is the same as for all patients: to reduce the risk of CVD and associated morbidity and mortality. Goals for treatment and therapeutic decisions should be based on a constellation of factors, including the actual level of blood pressure. There are currently no specific guidelines for pharmacologic treatment of hypertension in obesity.^[28]

The National Heart, Lung, and Blood Institute (NHLBI) guidelines for weight loss recommend that a combination of increased physical activity and dietary modification be attempted for at least 6 months before consideration of the addition of Food and Drug Administration (FDA)-approved antiobesity pharmacotherapy for individuals with obesity associated with other risks for CVD, including hypertension.^[7]

Lifestyle modifications should be strongly recommended for the entire population. Even more far-reaching than their value in the treatment of established hypertension is the potential for disease prevention. Lifestyle modifications are effective in lowering blood pressure and can reduce other cardiovascular risk factors. A systematic team approach utilizing health care professionals and community resources when possible can assist in providing the necessary education, support, and follow-up needed to achieve successful lifestyle changes. Although the difficulty in achieving and maintaining lifestyle changes is recognized, all patients should be encouraged to adopt and maintain healthier lifestyles.

Nonpharmacologic interventions, including weight reduction, a low-fat diet, and increased physical activity, have a primary role in the treatment of hypertension. Weight reduction should be addressed with every overweight or obese hypertensive patient. Education regarding the risks associated with increasing weight, assessment of body fat distribution, and treatment strategies should be discussed with the patient. Individuals with concomitant risks may not realize the impact that body weight has on the risk for CVD and the benefits of weight reduction.

The most practical method for clinical assessment and classification of overweight and obesity is the BMI (body weight in kilograms/[height in meters]²). A BMI exceeding 25 kg/m² is considered overweight, while a BMI greater than 30 kg/m² is classified as obese.^[7] Limitations of BMI as an index of total body fat include overestimates of body fat in persons who are very muscular and underestimates of body fat in persons who have lost muscle mass. The waist-to-hip ratio allows a determination of upper- and lower-body obesity and has been shown in epidemiologic studies to predict the correlation between obesity and hypertension and risk for CVD.^[29] The presence of excess abdominal fat that is disproportionate to the total body fat is an independent predictor of risk factors and morbidity. Upper-body obesity, as compared to lower-body obesity, is most closely associated with obesity hypertension. Waist circumference (greater than measurement of hip circumference or more than 38 inches in a man or 34 inches in a woman) is positively correlated with abdominal fat and provides a clinically useful measure of abdominal fat. The BMI and the waist circumference should be measured in all hypertensive subjects. The NHLBI guidelines for assessment of body weight and associated risk are illustrated in Table I .^[7]

Weight reduction remains the cornerstone of treatment for obesity hypertension and is the most effective method of risk reduction, particularly if it reduces visceral or abdominal fat. Weight reduction has been shown to decrease blood pressure in normotensive and hypertensive subjects in clinical trials implementing low-calorie dietary interventions.^[30,31] In a 5-year study of obese adults with high-normal blood pressure,^[32] modest weight reduction was associated with a significantly lower incidence of hypertension, compared to the control group. Weight reduction by dietary modification has also been shown to decrease the dose and quantity of antihypertensive medications required to control blood pressure in overweight individuals.^[33]

The mean effect of a 10-kg (22-lb) decrease in body weight is an associated reduction in systolic and diastolic pressures of 7 and 3 mm Hg, respectively.^[34] Decreased intravascular volume and reduced cardiac output and left ventricular work are seen with moderate weight loss (20 lb) in obese hypertensives. Left ventricular mass decreases after weight loss. The effects of weight reduction appear to be independent of sodium restriction.^[35] Weight reduction has been shown to result in a decrease in sympathetic activity and alteration in sodium metabolism, possibly related to a decrease in plasma renin activity and aldosterone.^[36]

Although the benefits of weight reduction on blood pressure are obvious in short- and long-term studies, maintenance of weight with dietary intervention alone is difficult. Maintenance of a modest weight loss -- 10% reduction in body weight for individuals with mild, moderate, and severe obesity -- would yield substantial lifetime health and economic benefits. Controlled clinical trials of weight reduction have shown that hypertensive subjects who have lost weight but regained the weight over time maintain lower blood pressures^[37] and require fewer antihypertensive agents^[33] than control subjects.

Physical inactivity is associated with obesity hypertension. Increased physical activity contributes to weight loss, singularly and when combined with dietary therapy. The NHLBI guidelines^[7] recommend that physical activity be an integral part of weight loss therapy and weight maintenance. The JNC VI guidelines^[28] also recommend regular exercise in the management of hypertension.

An inverse relation between physical fitness and blood pressure levels, independent of all other risk factors for hypertension, is shown in population studies.^[37,38,39] Sedentary individuals with normal blood pressure have an increased risk of developing hypertension when compared with more active and fit peers.^[38] In studies looking at the effects of aerobic exercise training in hypertensive patients, average blood pressure reduction ranges from 4 mm Hg-10 mm Hg.^[39] Mechanisms proposed for the hypotensive efficacy of regular exercise include reduction in sympathetic activity and improved vasodilatation and arterial compliance.^[40]

Adding regular physical activity to caloric restriction can accelerate weight loss and increase the overall amount of weight lost by 4-7 lb. Physical activity is also beneficial for maintenance of weight loss. In studies comparing long-term weight loss and maintenance, individuals who combined exercise and diet were much less likely to regain weight.^[7] The combination of an exercise program with weight reduction has additive effects on blood pressure reduction in hypertensives.

Sustained blood pressure reduction in hypertensives has been reported with aerobic activities, such as swimming, cycling, brisk walking for 40 minutes three times a week, and jogging. Initially, moderate levels of physical activity should be encouraged. Both NHLBI obesity and JNC VI hypertension guidelines recommend a goal for all adults to accumulate at least 30 minutes or more of moderately intense physical activity on most, and preferably all, days of the week.

In addition to the direct effects of regular exercise on blood pressure, increased physical activity may also alter other factors that influence blood pressure, such as diet, body weight, smoking, and alcohol consumption.

Sleep apnea is much more common than previously recognized, and an important but often overlooked risk factor for life-threatening disorders. Sleep apnea can exacerbate underlying disease or cause problems for those who are otherwise healthy. All patients with obesity hypertension should be questioned regarding the symptoms of this sleep disturbance, including snoring, choking or gasping during sleep, daytime somnolence, and morning headaches.

Obstructive sleep apnea (OSA) has numerous adverse effects, including increased systemic and pulmonary hypertension, increased sympathetic activity, hypoxia, cardiac arrhythmias, and sleep disturbance.^[41] The hemodynamic changes associated with OSA that result in hypertension are not clearly understood, but there is a dose-response association between the severity of OSA and hypertension. Individuals with mild to moderate OSA had a 42% greater probability of having hypertension than did persons with normal sleep patterns. Those with more severe OSA had two to three times the probability of hypertension than those without evidence of OSA.^[41]

Sympathetic control of vascular tone and modification of peripheral vascular resistance could be related to increased systemic blood pressure. Studies measuring serum and urinary catecholamines and muscle sympathetic nerve activity provide partial but inconclusive explanations.^[42] Other investigations have explored the role of nitric oxide and other modifiers of endothelial cells.^[43] An understanding of the physiologic changes in OSA that result in hypertension may provide noninvasive treatment modalities that effect blood pressure control.

Identification of the patient with OSA and effective treatment with weight loss, continuous positive airway pressure, or surgical intervention may be necessary to achieve blood pressure control. Reduction in cardiovascular events and hypertension and improvements in quality of life may result from management of this frequently overlooked disorder.

© 2002 Le Jacq Communications, Inc.

Cite this: Therapeutic Considerations in the Treatment of Obesity Hypertension - Medscape - May 01, 2002.