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Published on: November 8, 2024
Exaggerated platelet and hemodynamic reactivity to mental stress in men with coronary artery disease
Philip C Strike1, Kesson Magid, Lena Brydon
1Psychobiology Group, Department of Epidemiology and Public Health, University College London, London, UK. p.strike@public-health.ucl.ac.uk
Insights
Acute mental stress causes greater cardiovascular and prolonged platelet activation in coronary artery disease (CAD) patients compared to controls. These responses may increase the risk of acute coronary syndromes in individuals with CAD.
Area of Science:
- Cardiology
- Psychophysiology
- Hematology
Background:
- Coronary artery disease (CAD) poses significant health risks.
- Mental stress is a known trigger for cardiovascular events.
Purpose of the Study:
- To compare cardiovascular, subjective, and platelet activation responses to acute mental stress in male CAD patients and healthy controls.
Main Methods:
- Seventeen male CAD patients and 22 healthy male controls underwent stress-inducing tasks (color/word, mirror tracing).
- Cardiovascular parameters (blood pressure, heart rate, cardiac index) and platelet activation (platelet-leukocyte aggregates) were measured before, during, and after stress.
- Subjective stress and depression ratings were also collected.
Main Results:
- CAD patients exhibited significantly greater increases in systolic blood pressure, heart rate, and cardiac index during stress compared to controls.
- Platelet-leukocyte aggregates increased in both groups but remained elevated longer in CAD patients.
- Cardiovascular and platelet responses correlated with subjective stress, depression, and task difficulty ratings.
Conclusions:
- Acute mental stress elicits exaggerated cardiovascular and prolonged platelet activation in CAD patients.
- These psychophysiological responses may contribute to plaque instability and thrombosis, potentially triggering acute coronary syndromes.
Objective:
This study compared the effects of acute mental stress on cardiovascular and subjective responses and platelet activation in male patients with established coronary artery disease (CAD) and age-matched controls.
Methods:
We assessed 17 male CAD patients aged 44 to 59 years and 22 healthy male controls. Blood pressure, heart rate, and hemodynamics were assessed before, during, and up to 2 hours after administration of color/word and mirror tracing tasks. Blood was sampled at baseline, after tasks, and at 30 and 75 minutes after stress, and platelet activation was assessed by measuring platelet-leukocyte aggregates (PLAs) using flow cytometry.
Results:
CAD patients showed significantly greater systolic blood pressure stress responses than controls (mean increases of 43.9 and 28.3 mm Hg, adjusted for income, body mass index, waist/hip ratio, and medication), together with larger increases in heart rate (14.1 and 4.7 bpm) and cardiac index. Total peripheral resistance increased during the poststress recovery period in CAD patients but not in controls. PLAs increased with stress in both groups, but remained elevated at 75 minutes in CAD patients, returning to baseline in controls. Heart rate and cardiac index responses were correlated with increases in subjective stress and with depression ratings, whereas PLA responses were associated with ratings of task difficulty.
Conclusion:
Acute mental stress stimulated heightened cardiovascular responses in CAD patients, coupled with more prolonged platelet activation. These factors may contribute to plaque rupture and thrombogenesis, and partly mediate stress-induced triggering of acute coronary syndromes.
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