Weight and Blood Pressure Changes in High Vascular Risk Patients

In the present issue of The Journal of Clinical Hypertension, Tyson and colleagues1 evaluated, through secondary analysis of the Weight Loss Maintenance Randomized Controlled Trial,2 the relationship between weight and blood pressure (BP) changes in a cohort of overweight or obese patients with hypertension and/or dyslipidemia. All studied patients before inclusion in the analysis experienced a weight reduction of ≥4 kg through behavioral weight loss intervention during a 6-month period (phase 1). Subsequently, patients were followed for 5 years and were divided into 3 groups according to an additional change in weight of >3% observed at the end follow-up: positive (weight gain), negative (weight loss), and no weight change (weight stable). During this 5-year period they were randomized 2 times (at baseline and after 2.5 years from baseline) according to the implemented strategy for sustaining weight loss. The first randomization (phase 2) was made through a personal contact maintenance weight loss program, an internet-based interactive technology maintenance weight loss program or no further treatment, while the second randomization (phase 3) was made through a personal contact maintenance weight loss program or no further treatment. Tyson and colleagues1 demonstrated a modest positive association between body weight and BP change over a period of 5 years and that after an initial weight loss of ≥4 kg, regain of body weight compared with body weight maintenance was associated with the same extent of systolic BP increase; by contrast, weight loss was not accompanied by systolic BP changes. The authors also suggested that advancing age might be a potential promoter of BP increase beyond weight changes in the stable-weight group. Since an increase in pulse pressure can partially reflect a vascular aging process, throughout phase 3 it can be observed that the weight-loss group demonstrated a mean change in pulse pressure of 0.4 mm Hg, the stable-weight group of 0.7 mm Hg, and the weight-gain group of 1.6 mm Hg. Thus, we can identify an almost 2- and 4-fold increased change in pulse pressure over a 2.5-year period when comparing the weight-loss group with both the stable-weight and the weight-gain groups, respectively. This observation raises the hypothesis that vascular aging would be more attenuated in the weight-loss group compared with the others. However, it is unclear whether this phenomenon would be more or less evident at different ages. An analysis of the results in young, middle-aged, and older patients would be of importance to clarify this issue. With respect to crude BP changes, we should underline the following issues. First, BP was not measured at the beginning of phase 1 and thus the extent of BP lowering with body weight reduction during the intensive weight–lowering strategy (phase 1) remains unknown. As pointed out by the authors,1 a plateau effect possibly took place for BP during this investigational period. Second, BP was curiously measured by an automated device not validated for clinic BP use.3 However, since the outcome was “changes in BP” along with the changes of body weight, we feel that this shortcoming did not affect the results in a meaningful way. Third, the duration of hypertension at baseline might be important to modulate BP changes through lifestyle interventions, because patients with an onset of hypertension close to baseline and mild vascular damage may be more responsive to BP reduction compared with those with long-lasting hypertension and more pronounced vascular damage. This is also the case for patients with and without overt cardiovascular disease, as well as for patients with hyperlipidaemia alone compared with those with hypertension or with the combined phenotype of hyperlipidemia and hypertension. Additional important confounders that could entail significant consequences on the investigating dynamic relationship are related to sodium intake and sleep habits. Indeed, sleep disruption associated with underlying sleep apnea4 and time asleep5 both promote weight and BP changes beyond daytime attitudes including exaggerated sodium consumption and increased salt sensitivity, especially in postmenopausal women.6 Finally, we should point out that the implemented strategies for lifestyle modification were assessed “on top” of ongoing pharmacologic treatment. Thus, the type and changes in antihypertensive agents might also contribute to different changes in body weight. Beyond the previous comments, the study by Tyson and colleagues1 provides enough evidence that weight-loss strategies associated with continued reduction of body size may be beneficial for BP stability over long periods. It could also be hypothesized that continued weight reduction may delay the aging-related hemodynamic deterioration. However, more studies are needed to clarify this complex issue at different ages, possibly complemented by measurement of arterial stiffness and further controlling for hidden confounders that modulate this relationship.