PS-C17-9: RELEVANT BLOOD PRESSURE REDUCTION WITH ORAL SEMAGLUTIDE IN PATIENTS WITH TYPE 2 DIABETES AND OBESITY, INDEPENDENT OF PREVIOUS ANTIHYPERTENSIVE TREATMENT

Abstract

Objective: The antihypertensive effect of oral semaglutide is apparently modest in published trials but it has not been explored in uncontrolled hypertensive patients. We sought to assess whether oral semaglutide may elicit a clinically relevant reduction of systolic blood pressure (SBP) in patients with type 2 diabetes (T2D), obesity and uncontrolled hypertension, and whether the attained SBP reduction is diluted by the previous antihypertensive treatment. Design and Methods: Retrospective analysis of the SBP and antihypertensive medication data were performed in consecutive patients with T2D and obesity who started therapy with oral semaglutide. Data were obtained from a baseline visit in which oral semaglutide was initiated, and a second visit after 3–4 months. Patients who initiated or changed antihypertensive medication simultaneously with oral semaglutide were excluded. Consent for anonymous analysis and reporting of data were obtained from all included subjects. Results: 50 patients with T2D (by usual clinical criteria) and obesity (BMI < 30 kg/m2) were included; their age was 56 ± 11 years. 32 (64%) were female, and their diabetes duration was 6.9 ± 2.9 years. 41 (82%) of them were diagnosed with hypertension (sitting office SBP > 140 and/or taking antihypertensive drugs). Globally there was a significant but modest reduction in SBP (149.8 ± 11.7 to 146.7 ± 12.4 mmHg, p = 0.041, paired t-test), but this reduction was strongly correlated with the baseline SBP (Pearson's r 0.39, p < 0.001). In the Figure (A) the reductions in SBP for patients with controlled SBP (< 140 mmHg), stage 1 (SBP 140–159 mmHg), stage 2 (160–179 mmHg) and stage 3 hypertension (> 180 mmHg) are shown (p = 0.0056 for differences among SBP categories, one-way ANOVA). The Figure (B) also shows the reductions in SBP for patients taking 0, 1, 2 or > 3 different antihypertensive drugs, but there are no significant differences (p = 0.2312, one-way ANOVA). In the second visit the number of patients with SBP < 140 mmHg had increased from 19 (38%) to 25 (50%). Conclusions: Treatment with oral semaglutide in patients with T2D, obesity and uncontrolled hypertension elicits a clinically significant decrease in SBP, enough to bring about acceptable SBP control in a relevant fraction. As expected, the reduction in SBP was strongly dependent on the baseline SBP. Interestingly, this reduction does not seem to be diluted by the use of multiple antihypertensive drugs, suggesting that oral semaglutide could be considered as an add-on in patients with apparent resistant hypertension.