OBJECTIVE: Increased blood pressure (BP) variability is suggested to be a risk factor for cardiovascular disease. Although a postprandial decline in BP is a frequently observed phenomenon in the elderly, little attention has been paid to the clinical and diagnostic significance of postprandial BP change. Here, we aimed to clarify the possible association between postprandial BP dysregulation and arteriosclerosis. METHODS: The study subjects were 1339 apparently healthy middle-aged to elderly persons (66 ± 9 years old). Postprandial changes in BP were calculated by two readings on the same day, one just before lunch with a standardized Japanese meal and the second 30 min after lunch. Arteriosclerosis was assessed by carotid intima-media thickness and brachial-to-ankle pulse wave velocity. RESULTS: Mean preprandial and postprandial systolic BP was 127 ± 18 and 123 ± 18 mmHg respectively. One hundred and twelve subjects (8.4%) showed a greater than 20-mmHg postprandial decline in systolic BP, while 129 (9.6%) showed a greater than 10-mmHg increase. Arteriosclerosis was significantly higher in both postprandial hypotensive and hypertensive subjects. The postprandial changes in systolic BP were strongly associated with preprandial systolic BP (r = 0.335, p < 0.001). The association between postprandial hypotension and increased arteriosclerosis was therefore lost after adjustment for basal systolic BP. Multiple linear regression analysis adjusted for possible covariates, including basal BP, identified a postprandial increase in BP as an independent determinant of insulin resistance as assessed by HOMA-IR (β = 0.093, p < 0.001), carotid thickness (β = 0.086, p = 0.001) and pulse wave velocity (β = 0.170, p < 0.001). CONCLUSION: Postprandial increase in BP is a novel risk marker for arteriosclerosis.
OBJECTIVE: Increased blood pressure (BP) variability is suggested to be a risk factor for cardiovascular disease. Although a postprandial decline in BP is a frequently observed phenomenon in the elderly, little attention has been paid to the clinical and diagnostic significance of postprandial BP change. Here, we aimed to clarify the possible association between postprandial BP dysregulation and arteriosclerosis. METHODS: The study subjects were 1339 apparently healthy middle-aged to elderly persons (66 ± 9 years old). Postprandial changes in BP were calculated by two readings on the same day, one just before lunch with a standardized Japanese meal and the second 30 min after lunch. Arteriosclerosis was assessed by carotid intima-media thickness and brachial-to-ankle pulse wave velocity. RESULTS: Mean preprandial and postprandial systolic BP was 127 ± 18 and 123 ± 18 mmHg respectively. One hundred and twelve subjects (8.4%) showed a greater than 20-mmHg postprandial decline in systolic BP, while 129 (9.6%) showed a greater than 10-mmHg increase. Arteriosclerosis was significantly higher in both postprandial hypotensive and hypertensive subjects. The postprandial changes in systolic BP were strongly associated with preprandial systolic BP (r = 0.335, p < 0.001). The association between postprandial hypotension and increased arteriosclerosis was therefore lost after adjustment for basal systolic BP. Multiple linear regression analysis adjusted for possible covariates, including basal BP, identified a postprandial increase in BP as an independent determinant of insulin resistance as assessed by HOMA-IR (β = 0.093, p < 0.001), carotid thickness (β = 0.086, p = 0.001) and pulse wave velocity (β = 0.170, p < 0.001). CONCLUSION: Postprandial increase in BP is a novel risk marker for arteriosclerosis.
Authors: Bert Bond; Craig A Williams; Carly Isic; Sarah R Jackman; Keith Tolfrey; Laura A Barrett; Alan R Barker Journal: Eur J Appl Physiol Date: 2014-12-11 Impact factor: 3.078