Related Experiment Video
Updated: Jul 30, 2026

An Alternative to the Traditional Cold Pressor Test: The Cold Pressor Arm Wrap
Published on: January 16, 2014
Platelet release of beta-thromboglobulin within the coronary circulation during cold pressor stress
Insights
Cold stress increases platelet activation and beta-thromboglobulin release in coronary blood, potentially contributing to acute coronary events in patients with and without coronary artery disease.
Area of Science:
- Cardiology
- Hematology
- Physiology
Background:
- Cold stress can increase circulating catecholamines, potentially sensitizing platelets.
- Platelet activation and aggregation are implicated in acute coronary syndromes.
Purpose of the Study:
- To investigate the effect of cold stress on beta-thromboglobulin release in coronary venous blood.
- To compare these effects in patients with coronary artery disease (CAD) and those with normal coronary arteries (NCA).
Main Methods:
- Measured beta-thromboglobulin levels in arterial and coronary venous blood before and during cold pressor stress.
- Assessed platelet counts and systolic arterial pressure.
- Correlated beta-thromboglobulin release with systolic pressure and platelet cyclic adenosine monophosphate generation.
Main Results:
- Cold stress increased systolic arterial pressure more in CAD patients than NCA subjects.
- Arterial beta-thromboglobulin was higher in CAD patients at rest.
- Coronary venous beta-thromboglobulin increased significantly during cold stress in both NCA and CAD groups, despite no change in arterial levels.
- Beta-thromboglobulin release correlated with systolic pressure and inversely with platelet cyclic adenosine monophosphate generation.
Conclusions:
- Cold stress provokes the release of platelet constituents into the coronary circulation.
- This release may contribute to stress-induced acute coronary occlusion in patients with and without angiographically apparent atherosclerotic disease.
Abstract:
Cold stress by increasing circulating catecholamines may sensitize blood platelets to aggregate and release their constituents. This study investigates the effect of cold stress on the release of the platelet-specific protein beta-thromboglobulin into the coronary venous blood of 12 subjects with atherosclerotic coronary artery disease (CAD) and 7 subjects with angiographically normal coronary arteries (NCA). Cold pressor stress caused a greater increase in systolic arterial pressure in patients with CAD than in subjects with NCA (p less than 0.05). There was no significant difference between the platelet counts in the arterial or coronary venous blood either before or during cold stress. Arterial beta-thromboglobulin was higher in the group with CAD (77 +/- 18 ng/ml) than in subjects with NCA (49 +/- 12 ng/ml, p less than 0.01). Although there was no arteriovenous difference of beta-thromboglobulin at rest in either group, during cold stress, coronary venous beta-thromboglobulin increased in both the NCA (53 +/- 16 to 95 +/- 26 ng/ml, p less than 0.05) and CAD groups (76 +/- 13 to 117 +/- 53 ng/ml, p less than 0.025) despite no change in arterial beta-thromboglobulin. Release of beta-thromboglobulin, although not related to the presence of angiographic arterial disease, correlated with the systolic arterial pressure during cold stress (r = 0.66) and inversely with the platelet's ability to generate cyclic adenosine monophosphate (r = 0.69). The release of platelet constituents in the coronary circulation is provoked by cold stress and may play a role in stress-induced acute coronary occlusion in patients with atherosclerotic disease and in those with apparently normal vessels.
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