Key result
Acute mental stress provoked significant increases in multiple coagulation parameters (p<=0.019), and the magnitude of these responses did not habituate across repeated stress exposures.
Why the study?
Does natural habituation occur in coagulation responses to repeated acute mental stress in men?
Observational (n=24)
Does natural habituation occur in coagulation responses to repeated acute mental stress in men?
The coagulation system does not appear to habituate to repeated acute mental stress, which may contribute to increased coronary risk in susceptible individuals.
May sustain prothrombotic risk without habituation in men; leaves open whether stress interventions alter coronary outcomes.
Blood coagulation activation might be one mechanism linking acute mental stress with coronary events. We investigated the natural habituation of coagulation responses and recovery to short-term mental stress. Three times with one-week intervals, 24 men (mean age 47 +/- 7 years) underwent the same 13-min stressor (preparation, job interview, mental arithmetic). During each visit venous blood was obtained four times (baseline, immediately post-stress, 45 min of recovery, 105 min of recovery). Eight blood coagulation parameters were measured at weeks one and three. Acute stress provoked increases in von Willebrand factor antigen, fibrinogen, clotting factor FVII activity (FVII:C), FVIII:C, FXII:C (p's < or = 0.019), and D-dimer (N.S.). All coagulation parameters experienced full recovery except FVIII:C (p = 0.022). Stress did not significantly affect activated partial thromboplastin time and prothrombin time. At all time points FVIII:C and FXII:C levels were significantly higher at week one compared to week three (p's < or = 0.041). Before catheter insertion, systolic blood pressure (p = 0.001) and heart rate (p = 0.026) were relatively higher at week one. Unlike the magnitude of systolic blood pressure response to stress (p = 0.007) and of cortisol recovery from stress (p = 0.002), the magnitude of all coagulation responses to stress and the recovery from stress were similar in week one and week three. Sympathetic activation with anticipatory stress best explained increased baseline activity in FVIII and FXII at week one. An incapacity of the coagulation system to adapt to stress repeats is perhaps a consequence of evolution, but might also contribute to increased coronary risk in some individuals, particularly in those with cardiovascular diseases.
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Preckel et al. (2004) reported an observational. Acute mental stress vs. Baseline was evaluated on Coagulation parameters (von Willebrand factor antigen, fibrinogen, FVII:C, FVIII:C, FXII:C) (p=<=0.019). Acute mental stress provoked significant increases in multiple coagulation parameters (p<=0.019), and the magnitude of these responses did not habituate across repeated stress exposures.
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