Relation of season and temperature to endothelium-dependent flow-mediated vasodilation in subjects without clinical evidence of cardiovascular disease (from the Framingham Heart Study).

Relation of season and temperature to endothelium-dependent flow-mediated vasodilation in subjects without clinical evidence of cardiovascular disease (from the Framingham Heart Study). Research Abstract Details 

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Relation of season and temperature to endothelium-dependent flow-mediated vasodilation in subjects without clinical evidence of cardiovascular disease (from the Framingham Heart Study). Abstract Text:

Michael E Widlansky,Joseph A Vita,Michelle J Keyes,Martin G Larson,Naomi M Hamburg,Daniel Levy,Gary F Mitchell,Ewa W Osypiuk,Ramachandran S Vasan,Emelia J Benjamin,

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.

Relation of season and temperature to endothelium-dependent flow-mediated vasodilation in subjects without clinical evidence of cardiovascular disease (from the Framingham Heart Study). Publishing Authors By Initials

ME Widlansky,JA Vita,MJ Keyes,MG Larson,NM Hamburg,D Levy,GF Mitchell,EW Osypiuk,RS Vasan,EJ Benjamin,

For similar vasodilation research abstracts see: vasodilation research

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Relation of season and temperature to endothelium-dependent flow-mediated vasodilation in subjects without clinical evidence of cardiovascular disease (from the Framingham Heart Study). Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: The American journal of cardiology

VOLUME: 100

Page Numbers: 518-23

Journal Abbreviation: Am. J. Cardiol.

ISSN: 0002-9149

DAY: 18

MONTH: 06

YEAR: 2007

Relation of season and temperature to endothelium-dependent flow-mediated vasodilation in subjects without clinical evidence of cardiovascular disease (from the Framingham Heart Study). Information

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LANGUAGE: eng

NlmUniqueID: 207277

Relation of season and temperature to endothelium-dependent flow-mediated vasodilation in subjects without clinical evidence of cardiovascular disease (from the Framingham Heart Study). Keywords Mesh Terms:

KEYWORDS: Vasodilation

MESH TERMS: physiology

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Grant and Affiliation Information for Relation of season and temperature to endothelium-dependent flow-mediated vasodilation in subjects without clinical evidence of cardiovascular disease (from the Framingham Heart Study).

AFFILIATION: Cardiology Department, Boston University School of Medicine, Boston, Massachusetts, USA.

Country: United States

AGENCY: United States NHLBI

GRANT: R01 HL077447-01A1

ACRONYM: HL

MEDLINETA: Am J Cardiol

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