Based on the HMPH of primary health care institutions in China, we explored the association between baseline BMI and weight change with CVD among patients with hypertension in a real-world medical setting. Our data revealed obesity might be a risk factor for CVD among patients with hypertension. This finding was consistent across different subgroups of sex and age. Patients with loss ≥ 4%, gain 1–4% and gain > 4% of body weight was significantly associated with increased risks of cardiovascular outcomes compared to those with stable weight, adjusting for confounding variables, including baseline BMI.
The relationship between BMI and CVD among patients with hypertension has been poorly studied. Our findings were in line with an 8-year follow-up study reported obesity was positively related to higher risk of CVD [16], and serval studies base on general population also reported similar findings [17–19]. The underlying mechanism between excessive body weight and CVD may be as follows. First, obesity increases the workload of the heart, thereby causes the progress of left ventricular hypertrophy [20, 21], which is associated with poor cardiovascular outcomes [22]. In addition, severe overweight and obesity are related to the activation of inflammatory response [23, 24], and thus increases vascular thromboxane receptor gene expression [25], which may be associated with prognosis of adverse cardiovascular outcomes [26]. Glitches in the innate autophagy and gut microbiome homeostasis networks may also serve as equally important elements among link obesity to atherosclerosis, which may contribute to CVD [27].
The relation of body weight and outcome was reported in most observational studies based on single-time assessment of body weight. Limited evidence addressed the association between weight change and CVD. In this study, we identified patients with weight gain was associated with higher risks of adverse cardiovascular events compared to those with stable body weight. The evidence for the association between weight gain and high risks of cardiovascular events among general population is compelling, and a recent meta–analysis of 23 prospective cohort studies suggested that weight gain could increase the risk of multiple cardiovascular events [28]. Several biological mechanisms may underlie the associations between weight gain and CVD. Weight gain intensifies the activities of sympathetic neural [29], which increases insulin resistance [30] and reduces endothelial, kidney, and heart function to accelerate the process of CVD [31]. Moreover, weight gain is associated with increased levels of multiple inflammation–sensitive plasma proteins [32], which could contribute to inflammation, metabolic syndrome, and CVD.
We found weight loss ≥ 4% during one year is a warning sign of harmful cardiovascular outcomes. Although limited evidence studied on impacts of weight loss on CVD among patients with hypertension, serval observational studies on weight change in patients with other chronic disease did not show a beneficial survival of weight reduction for improved prognosis. The PROactive study [33] and ORIGN study [34] reported that weight loss was associated with higher risks of negative cardiovascular outcomes. However, the mechanisms underlying the association weight loss and CVD remain unclear [35, 36]. The possible mechanisms are as follows. Weight loss may be related to disorder of nutrients intake or absorption and is a common sign of nutritional deficiencies [37], which causes electrolyte imbalances, cardiac arrhythmias, and thus promotes CVD [36].
We observed that patients over 60 had higher risks of CVD due to weight change. However, the underlying mechanism seems to be complex and remains unclear. Previous studies stated that aging is accompanied with deterioration of cardiovascular homeostasis and metabolic disorders, which are interconnected adverse vascular and cardiac phenotypes responsible for multiple CVD [38, 39]. Further research is needed to clarify if recommendations on weight management should differentiate more clearly between elder and younger patients with hypertension.
We believed that this study was one of the few studies conducted on weight change and CVD among Chinese patients with hypertension. However, there are several limitations. First, selection of study subjects who had received 12 months of follow-up service might have selection bias because patients with higher education level were more likely to participate in the regular health service (P < 0.0001). Second, with a mean follow-up of only 3.60 years, we may observe insufficient cardiovascular outcomes. Therefore, we might have underestimated the incidence of CVD.
In conclusion, this cohort study of community–dwelling adults with hypertension demonstrates that individuals with obesity generally exhibited more detrimental effects than normal weight patients. Moreover, patients with loss ≥ 4%, gain 1–4% and gain > 4% of body weight over 12 month had higher risks of CVD than patients with stable weight. Therefore, appropriate interventions aimed at achieving an optimal weight may be needed to prevent adverse health outcomes in patients with hypertension. Moreover, weight management strategies for patients with obesity and elderly patients need to be more personalized.