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Updated: May 17, 2026

Cooling or Warming the Esophagus to Reduce Esophageal Injury During Left Atrial Ablation in the Treatment of Atrial Fibrillation
Published on: March 15, 2020
Aspirin and clopidogrel alter core temperature and skin blood flow during heat stress
Rebecca S Bruning1, Jessica D Dahmus, W Larry Kenney
1Noll Laboratory, Department of Kinesiology, The Pennsylvania State University, University Park, PA 16802, USA.
Unlabelled:
Antithrombotic therapy with oral aspirin (ASA) or clopidogrel (CLO) (Plavix; Bristol-Myers Squibb, Bridgewater, NJ) is associated with an attenuated skin vasodilator response and a greater rate of rise in core temperature in healthy, middle-age individuals during passive heating in a water perfused suit.
Purpose:
The present double-blind, crossover study examined the functional consequences of 7 d of low-dose ASA (81 mg·d) versus CLO (75 mg·d) treatment in 14 healthy, middle-age (50-65 yr) men and women during passive heating in air (40 min at 30°C, 40% relative humidity) followed by exercise (60% V˙O2peak).
Methods:
Oral temperature (Tor) was measured in the antechamber (23.0°C ± 0.1°C) before entering a warm environmental chamber. After 40 min of rest, subjects cycled on a recumbent cycle ergometer for up to 120 min. Esophageal temperature (Tes) and laser Doppler flux were measured continuously, and the latter was normalized to maximal cutaneous vascular conductance (%CVCmax).
Results:
Before entry into the environmental chamber there were no differences in Tor among treatments; however, after 40 min of rest in the heat, Tes was significantly higher for ASA and CLO versus placebo (37.2°C ± 0.1°C, 37.3°C ± 0.1°C, vs 37.0°C ± 0.1°C, both P < 0.001), a difference that persisted throughout exercise (P < 0.001 vs placebo). The mean body temperature thresholds for the onset of cutaneous vasodilation were shifted to the right for both ASA and CLO during exercise (P < 0.05).
Conclusion:
ASA and CLO resulted in elevated core temperatures during passive heat stress and shifted the onset of peripheral thermoeffector mechanisms toward higher body temperatures during exercise heat stress.
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