TY - JOUR
T1 - Relation of Season and Temperature to Endothelium-Dependent Flow-Mediated Vasodilation in Subjects Without Clinical Evidence of Cardiovascular Disease (from the Framingham Heart Study)††Conflict of interest
T2 - Dr. Mitchell is president of Cardiovascular Engineering, Inc.
AU - Widlansky, Michael E.
AU - Vita, Joseph A.
AU - Keyes, Michelle J.
AU - Larson, Martin G.
AU - Hamburg, Naomi M.
AU - Levy, Daniel
AU - Mitchell, Gary F.
AU - Osypiuk, Ewa W.
AU - Vasan, Ramachandran S.
AU - Benjamin, Emelia J.
PY - 2007/8/1
Y1 - 2007/8/1
N2 - Multiple studies have documented an increased incidence of cardiovascular events in the winter, but the pathophysiologic mechanisms remain incompletely understood. It was hypothesized that brachial flow and flow-mediated dilation (FMD) would vary by season and temperature. Season and temperature were related to ultrasonic brachial artery endothelium-dependent FMD% (n = 2,587), baseline flow velocity, and maximal reactive hyperemia (n = 1,973) in the Framingham Offspring Cohort (mean age 61 ± 10 years, 53% women). Outdoor temperatures were obtained from National Climate Data Center records for Bedford, Massachusetts (about 14 miles from the testing site), and the examination room temperature was measured. In multivariate models, FMD% was highest in summer and lowest in winter (3.01 ± 0.09% vs 2.56 ± 0.10%, respectively, p = 0.02 for differences across all 4 seasons). FMD% was highest in the warmest and lowest in the coldest outdoor-temperature quartiles. In stepwise models adjusting for risk factors and selecting among season, outdoor temperature, and room temperature, FMD% was associated with season (p = 0.02); temperature did not enter the model. In contrast, hyperemic flow velocity was significantly lower for cooler and higher for warmer room temperatures (p = 0.02 overall); season did not enter the model. Season and outdoor and room temperature were each retained in a stepwise model of baseline flow velocity (p <0.0001, p = 0.02, and p <0.0001, respectively). In conclusion, a significant association was observed between season and FMD%. Microvascular vasodilator function, as reflected by hyperemic flow velocity, was more strongly related to temperature than season. Endothelial dysfunction may be 1 of the mechanisms influencing seasonal variation in cardiovascular events.
AB - Multiple studies have documented an increased incidence of cardiovascular events in the winter, but the pathophysiologic mechanisms remain incompletely understood. It was hypothesized that brachial flow and flow-mediated dilation (FMD) would vary by season and temperature. Season and temperature were related to ultrasonic brachial artery endothelium-dependent FMD% (n = 2,587), baseline flow velocity, and maximal reactive hyperemia (n = 1,973) in the Framingham Offspring Cohort (mean age 61 ± 10 years, 53% women). Outdoor temperatures were obtained from National Climate Data Center records for Bedford, Massachusetts (about 14 miles from the testing site), and the examination room temperature was measured. In multivariate models, FMD% was highest in summer and lowest in winter (3.01 ± 0.09% vs 2.56 ± 0.10%, respectively, p = 0.02 for differences across all 4 seasons). FMD% was highest in the warmest and lowest in the coldest outdoor-temperature quartiles. In stepwise models adjusting for risk factors and selecting among season, outdoor temperature, and room temperature, FMD% was associated with season (p = 0.02); temperature did not enter the model. In contrast, hyperemic flow velocity was significantly lower for cooler and higher for warmer room temperatures (p = 0.02 overall); season did not enter the model. Season and outdoor and room temperature were each retained in a stepwise model of baseline flow velocity (p <0.0001, p = 0.02, and p <0.0001, respectively). In conclusion, a significant association was observed between season and FMD%. Microvascular vasodilator function, as reflected by hyperemic flow velocity, was more strongly related to temperature than season. Endothelial dysfunction may be 1 of the mechanisms influencing seasonal variation in cardiovascular events.
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U2 - 10.1016/j.amjcard.2007.03.055
DO - 10.1016/j.amjcard.2007.03.055
M3 - Article
C2 - 17659939
AN - SCOPUS:34547122236
SN - 0002-9149
VL - 100
SP - 518
EP - 523
JO - American Journal of Cardiology
JF - American Journal of Cardiology
IS - 3
ER -