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The influence of baseline diastolic blood pressure on the effects of intensive blood pressure lowering on cardiovascular outcomes and all-cause mortality in type 2 diabetes mellitus

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posted on 04.05.2020 by Olesya L. Ilkun, Tom Greene, Alfred K. Cheung, Paul K. Whelton, Guo Wei, Robert E. Boucher, Walter Ambrosius, Glenn M. Chertow, Srinivasan Beddhu
Objective: To examine whether low baseline diastolic blood pressure (DBP) modifies the effects of intensive systolic blood pressure (SBP) lowering on cardiovascular outcomes in type 2 diabetes mellitus (T2DM).

Research Design and Methods: The Action to Control Cardiovascular Risk in Diabetes Blood Pressure trial (ACCORD BP),a 2X2 factorial randomized controlled trial, examined effects of SBP (<120 vs. <140 mmHg) and glycemic (HbA1C < 6% vs. 7.0–7.9% (<42 vs 53-63 mmol/mol)) control on cardiovascular events in T2DM (N=4731). We examined whether effects of SBP control on cardiovascular composite was modified by baseline DBP and glycemic control.

Results: Intensive SBP lowering decreased the risk of the cardiovascular composite (HR 0.76, 95% CI 0.59 to 0.98) in the standard glycemic arm but not in the intensive glycemic arm (HR=1.06, 95% CI 0.81 to 1.40). Spline regression models relating the effects of the intervention on the cardiovascular composite across the range of baseline DBP did not show evidence of effect modification by low baseline DBP for the cardiovascular composite in the standard or intensive glycemic arms. The relation between the effect of the intensive SBP intervention and baseline DBP was similar between glycemic arms for the cardiovascular composite (3-way interaction p-value = 0.83).

Conclusions: in persons with T2DM, intensive SBP lowering decreased the risk of cardiovascular composite endpoint irrespective of baseline DBP in the setting of standard glycemic control. Hence, low baseline DBP should not be an impediment to intensive SBP lowering in T2DM patients treated with guidelines recommended standard glycemic control.


Statistical analyses and preparation of this manuscript were supported by grants from the National Heart, Lung and Blood Institute (R21HL145494) and National Institute of Diabetes and Digestive and Kidney Diseases (R01 DK091437) and the University of Utah Study Design and Biostatistics Center (funded in part from the Public Health Services research grant numbers UL1- RR025764 and C06-RR11234 from the National Center for Research Resources). ACCORD BP was funded by NHLBI. This manuscript was prepared using ACCORD Research Materials obtained from the NHLBI Biologic Specimen and Data Repository Information Coordinating Center and does not necessarily reflect the opinions or views of the ACCORD or the NHLBI.