Current antithrombotic drugs reduce the risk of stroke, heart attack and deathfrom vascular causes by 25 % in patients with cerebral ischemic events resulting from disease of small or large cerebral arteries. In the primary prevention, Acetylsalicylic acid (ASA) reduces the risk of stroke by 19 % in women but not in men. In patients with nonvalvular atrial fibrillation the risk of stroke treating with ASA is reduced by 20 %. Oral anticoagulants significantly reduce stroke risk due to nonvalvular atrial fibrillation by 65-70 % compared with placebo and by 40% compared with ASA alone. At the same time they cause more major bleedings. Recently studied new antiplatelet drugs and anticoagulants might alter the current course of stroke prevention treatment. Research is also needed on the benefits and risks of combination antiplatelets and anticoagulants in patients with nonvalvular atrial fibrillation in combination with arterial cerebral disease.
COBISS.SI-ID: 29586905
We investigated the hypothesis that during tonic pain stimulus, neurovascular coupling (NVC) decreases, measuring visually evoked cerebral blood flow velocity response (VEFR) during cold pressor test (CPT) in healthy human subjects as a test. VEFR was calculated as a relative increase in blood flow velocity in the posterior cerebral artery from average values during the last 5 s of the stimulus-OFF period to average values during the last 10 s of the stimulus-ON period. Three consecutive experimental phases were compared: basal, CPT and recovery. During CPT, end-diastolic and mean VEFR increased from 20.2 to 23.6% (p ( 0.05) and from 17.5 to 20.0% (p ( 0.05), respectively.In recovery phase, end-diastolic and mean VEFR decreased to 17.7%and 15.5%, respectively. Both values were statistically significantly different from CPT phase (p ( 0.05). Compared with the basal phase, only end-diastolic VEFR was statistically significantly different in the recovery phase (p ( 0.05). Our results are consistent with the assumption that there isa change in the activity of NVC during CPT because of the modulatory influence of subcortical structures activated during tonic pain. Contrary to our expectations, the combined effect of such influences increases rather thandecreases NVC.
COBISS.SI-ID: 29112537
It seems that migraine patients might suffer from localized and not systemic endothelial dysfunction. However, the probability whether impaired endothelialfunction in the posterior cerebral circulation, and intact endothelial function elsewhere is associated with migraine is not known. This is a post hoc study based on two of our previous published studies that evaluated cerebral and systemic endothelial function in 40 migraine patients (20 with (MwA) and 20 without aura (MwoA)) without comorbidities, and 20 healthy subjects. Cerebrovascular reactivity (CVR) to l-arginine in the middle(MCA) and posterior (PCA) cerebral artery as well as flow mediated vasodilatation (FMD) were used for this purpose. The logistic regression analysis was used to evaluate the association between CVR to l-arginine, FMD and migraine. We found a significant association between CVR to l-arginine in the PCA and migraine (OR: 0.38; CI 95%: 0.19-0.79; p = 0.01), but not between CVR to l-arginine in the MCA and migraine (OR: 0.74; CI 95%: 0.34-1.59; p = 0.44). Similar results were obtained in MwA and MwoA. We did not find any significant association between FMD and migraine (OR: 0.99; CI 95%: 0.83-1.19;p = 0.96). The same conclusion was reached in both migraine groups (MwA OR: 1.0; CI 95%: 0.83-1.19; p = 0.99, MwoA OR: 0.99; CI 95%: 0.81-1.21; p= 0.99). We could conclude that impaired endothelial function in the posterior cerebral circulation is associated with migraine, both MwA and MwoA,while intact endothelial function in the anterior cerebral and systemic circulation is not associated only with migraine.
COBISS.SI-ID: 275116