OBJECTIVES: To evaluate the associations of high awake blood pressure (BP), high asleep BP, and nondipping BP, determined by ambulatory BP monitoring (ABPM), with left ventricular hypertrophy (LVH) and geometry. METHODS: Black and white participants (n = 687) in the Coronary Artery Risk Development in Young Adults study underwent 24-h ABPM and echocardiography at the Year 30 Exam in 2015-2016. The prevalence and prevalence ratios of LVH were calculated for high awake SBP (≥130 mmHg), high asleep SBP (≥110 mmHg), the cross-classification of high awake and asleep SBP, and nondipping SBP (percentage decline in awake-to-asleep SBP < 10%). Odds ratios for abnormal left ventricular geometry associated with these phenotypes were calculated. RESULTS: Overall, 46.0 and 49.1% of study participants had high awake and asleep SBP, respectively, and 31.1% had nondipping SBP. After adjustment for demographics and clinical characteristics, high awake SBP was associated with a prevalence ratio for LVH of 2.79 [95% confidence interval (95% CI) 1.63-4.79]. High asleep SBP was also associated with a prevalence ratio for LVH of 2.19 (95% CI 1.25-3.83). There was no evidence of an association between nondipping SBP and LVH (prevalence ratio 0.70, 95% CI 0.44-1.12). High awake SBP with or without high asleep SBP was associated with a higher odds ratio of concentric remodeling and hypertrophy. CONCLUSION: Awake and asleep SBP, but not the decline in awake-to-asleep SBP, were associated with increased prevalence of cardiac end-organ damage.
OBJECTIVES: To evaluate the associations of high awake blood pressure (BP), high asleep BP, and nondipping BP, determined by ambulatory BP monitoring (ABPM), with left ventricular hypertrophy (LVH) and geometry. METHODS: Black and white participants (n = 687) in the Coronary Artery Risk Development in Young Adults study underwent 24-h ABPM and echocardiography at the Year 30 Exam in 2015-2016. The prevalence and prevalence ratios of LVH were calculated for high awake SBP (≥130 mmHg), high asleep SBP (≥110 mmHg), the cross-classification of high awake and asleep SBP, and nondipping SBP (percentage decline in awake-to-asleep SBP < 10%). Odds ratios for abnormal left ventricular geometry associated with these phenotypes were calculated. RESULTS: Overall, 46.0 and 49.1% of study participants had high awake and asleep SBP, respectively, and 31.1% had nondipping SBP. After adjustment for demographics and clinical characteristics, high awake SBP was associated with a prevalence ratio for LVH of 2.79 [95% confidence interval (95% CI) 1.63-4.79]. High asleep SBP was also associated with a prevalence ratio for LVH of 2.19 (95% CI 1.25-3.83). There was no evidence of an association between nondipping SBP and LVH (prevalence ratio 0.70, 95% CI 0.44-1.12). High awake SBP with or without high asleep SBP was associated with a higher odds ratio of concentric remodeling and hypertrophy. CONCLUSION: Awake and asleep SBP, but not the decline in awake-to-asleep SBP, were associated with increased prevalence of cardiac end-organ damage.
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