1604-P: Glucose Intolerance Modifies the Association between Diastolic Blood Pressure Variability and All-Cause Mortality

Purpose: There is growing literature on the association between blood pressure variability (BPV) and mortality. We sought to determine whether the association between BPV and all-cause mortality was modified by glucose intolerance (GI). Methods: A total of 12,256 non-pregnant adults from the National Health and Nutrition Examination Surveys-III (1988-1994) were linked to the National Death Index through 2015. The primary predictors were systolic and diastolic BPV, defined as the standard deviation of 3-6 BP readings taken consecutively. Systolic and diastolic BPV were categorized into quintiles ( 15 mmHg). We used Cox proportional hazards modeling to assess the risk of all-cause mortality, adjusting for confounders (age, sex, race/ethnicity, mean BP, BMI, lipids, kidney and liver function, c-reactive protein) and the survey design. Analyses were stratified by GI status (yes/no), defined as either a fasting glucose ≥100 mg/dl, HbA1c ≥5.7%, or diabetes medication use. Results: Of the 12,256 participants, 28% had GI. The mean follow-up time was 22.1 years, with a total 3,632 deaths (2,096 [46%] among GI and 1,536 [20%] among non-GI) from all causes. Among those with GI, the highest quintile of diastolic BPV had 60% higher risk of mortality relative to the lowest quintile (unadjusted HR [95% CI] = 1.51 [1.04, 2.23], adjusted HR = 1.60 [1.12, 2.28]). This association did not exist among those without GI (unadjusted HR [95% CI] = 0.87 [0.60, 1.26], adjusted HR = 0.80 [0.58, 1.10]). Those in the highest quintile of systolic BPV had an insignificant increase in risk of all-cause mortality among both GI and non-GI participants (GI: adjusted HR = 1.41 [0.98, 2.01], non-GI: adjusted HR = 1.09 [0.78, 1.51], interaction p=0.34). Conclusion: Only those with GI had a significant positive association between diastolic BPV and all-cause mortality. GI may play a role in modifying this association through changes in vascular autonomic regulation due to autonomic neuropathy. Disclosure A. Visaria: None. T. Dharamdasani: None. D. Lo: None. K. Wickramasinghe: None. R. Malhotra: None.