Procoagulant stress reactivity and recovery in apparently healthy men with systolic and diastolic hypertension

Association of vital exhaustion and depressive symptoms with changes in fibrin D-dimer to acute psychosocial stress

“…A procoagulant milieu promotes coronary thrombus formation in the hours after coronary plaque disruption [16]. Therefore, stressinduced hypercoagulability, which in relation to increased VE and depression carries over to a critically long period after stress cessation, might enhance atherothrombotic risk [51]. Notably, such reasoning seems of clinical significance in that effects were medium to large with VE and depression accounting for 8% and 9%, respectively, of the variance in D-dimer change over time.…”

Effects of depressive and anxious symptoms on norepinephrine and platelet P-selectin responses to acute psychological stress among elderly caregivers

“…Blood was drawn using an indwelling 22-gauge venous forearm catheter at 3 points: baseline (following 20-minutes of quiet rest), speech (immediately following the stress test), and recovery (14-minutes following the speech task). This recovery period was selected based on the balance of two factors: 1. minimizing participant burden associated with asking elderly participants to sit for extended periods, and 2. recent research demonstrating that the hemostatic factors D-dimer and fibrinogen returned to baseline in less than 20 minutes in the absence of hypertension (Wirtz et al, 2007). The first 2 ml of blood was discarded to control for the potential effects of artificial platelet activation evoked by drawing blood.…”

Hemoconcentration and Hemostasis During Acute Stress: Interacting and Independent Effects

“…These effects remained when controlling for age, body mass index, resting mean arterial pressure, and resting coagulation factor levels. The findings of this study suggest that acute psychological stress causes a prothrombotic state that is greater in hypertensive than in normotensive individuals [163]. Thus, hypertensive individuals may be at a greater risk for developing premature atherosclerosis because of the magnified bursts of hypercoagulability that occur during times of stress and builds over a person's lifetime.…”

“…Exaggerations of stress reactivity of blood coagulation could provide one possible mechanism for the increased risk of atherothrombotic complications in individuals with essential hypertension. As such, Wirtz and colleagues [163] examined coagulant stress reactivity and recovery to the TSST in otherwise healthy middle-aged men with systolic and diastolic hypertension. FVII, FVIII, fibrinogen, and D-dimer were assessed from blood drawn immediately before stress, immediately after stress, and 20 and 60 min after stress.…”