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Hostility is associated with increased platelet activation in coronary heart disease
1Division of Preventive Medicine, University of Alabama, Birmingham 35205, USA. jmarkovitz@cardia.dopm.uab.edu
Insights
Hostility is linked to platelet activation (PA) in coronary heart disease (CHD) patients. This study found a connection between hostility and PA markers in CHD patients, but not in healthy individuals.
Area of Science:
- Cardiology
- Psychosomatic Medicine
- Hematology
Background:
- Increased platelet activation (PA) is linked to adverse outcomes in coronary heart disease (CHD) patients.
- Psychological factors may influence cardiovascular health and disease progression.
Purpose of the Study:
- To investigate the relationship between Potential for Hostility and platelet activation (PA) in patients with CHD compared to healthy controls.
- To assess if hostility is associated with specific markers of platelet activation.
Main Methods:
- Whole blood flow cytometry was used to measure PA in 32 CHD patients and 23 healthy adults (aged 45-73).
- PA was assessed via wound-induced activation and in vitro stimulation, measuring fibrinogen receptor activation and binding.
- Potential for Hostility was evaluated using the Type A Structured Interview.
Main Results:
- Among CHD patients, all four indicators of wound-induced fibrinogen receptor activation were associated with hostility.
- Significant relationships were found between receptor activation at 2 minutes and binding at 1 minute (r=0.46, p=0.02) and hostility.
- Lipid-lowering medication use was associated with lower PA; healthy subjects showed higher PA than CHD patients before statistical adjustment.
Conclusions:
- Platelet activation is related to hostility in coronary heart disease patients.
- The study did not find increased PA in nonsmoking, nondepressed CHD patients compared to controls.
- Findings support the link between psychological factors and platelet activation in CHD.
Objective:
To determine whether Potential for Hostility is related to platelet activation (PA) among patients with coronary heart disease (CHD) and healthy controls. Increased PA has been associated with adverse secondary events after myocardial infarction or coronary angioplasty.
Methods:
We tested 32 CHD patients and 23 healthy men and women, aged 45 to 73 years, for PA by using whole blood flow cytometry. PA was measured in blood exiting a bleeding time wound (wound-induced platelet activation) and also in venous blood stimulated in vitro with collagen. Monoclonal antibodies were used to test for fibrinogen receptor activation and fibrinogen receptor binding. All subjects refrained from taking aspirin for at least 14 days before testing; CHD patients stopped nitrates and calcium channel blockers for 24 hours, while continuing to take lipid-lowering medications. Potential for Hostility was assessed, using the Type A Structured Interview.
Results:
Among the CHD patients only, all four of the wound-induced fibrinogen receptor activation indicators (activation and binding) were related to hostility; the relationships were significant for receptor activation at 2 minutes, and for receptor binding at 1 minute (r values = .46, p values = .02). Subjects on lipid-lowering medications had lower PA for most measures. Healthy subjects had higher wound-induced fibrinogen receptor activation at 2 minutes and fibrinogen receptor activation in vitro than the CHD patients (p = .04), but after statistical adjustment for lipid-lowering medications, there were no significant differences between the patients and controls.
Conclusions:
PA was related to hostility among CHD patients, consistent with previous studies indicating a relationship between PA and psychological factors among CHD patients. However, PA was not increased in nonsmoking, nondepressed CHD patients relative to controls.