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The importance of optimal blood pressure control for preventing or reducing the impairment of vascular and cognitive functions is well known. However, the reversibility of early alterations in vascular and cognitive functions through antihypertensive agents is under-investigated. In this study, we evaluated the influence of 3 months of angiotensin-converting enzyme (ACE) inhibition treatment on the morphological and functional arterial wall and cognitive performance changes in 30 newly diagnosed primary hypertensive patients. Common carotid intima-media thickness (IMT) and brachial artery flow-mediated dilatation (FMD) were detected by ultrasonography. Arterial stiffness indicated by augmentation index (AIx) and pulse wave velocity (PWV) was assessed by arteriography. Cognitive functions were assessed by neuropsychological examination. The executive function overall score was significantly higher at 3-month follow-up than at baseline (median, 0.233 (IQR, 0.447) vs –0.038 (0.936); P = .001). Three-month ACE inhibition did not produce significant improvement in IMT, FMD, AIx and PWV values. Significant negative associations were revealed between IMT and complex attention (r = –0.598, P = .0008), executive function (r = –0.617, P = .0005), and immediate memory (r = –0.420, P = .026) overall scores at follow-up. AIx had significant negative correlations with complex attention (r = –0.568, P = .001), executive function (r = –0.374, P = .046), and immediate memory (r = –0.507, P = .005). PWV correlated significantly and negatively with complex attention (r = –0.490, P = .007). Timely and effective antihypertensive therapy with ACE inhibitors has significant beneficial effects on cognitive performance in as few as 3 months. Early ACE inhibition may have an important role in the reversal of initial impairments of cognitive function associated with hypertension-induced vascular alterations.

Beside the well-known complications of poorly controlled, long-standing hypertension, milder abnormalities induced by early-stage hypertension have also been described. In our study, the authors examined the reversibility of changes induced by early-stage hypertension. The authors performed laboratory testing, ambulatory blood pressure monitoring, carotid intima-media thickness (IMT) measurement, evaluation of stiffness parameters, assessment of various cardiac and cerebral hemodynamic parameters during head-up tilt table (HUTT) testing, and neuropsychological examinations in 49 recently diagnosed hypertensive patients. Following baseline assessment, antihypertensive therapy was commenced. After one year of therapy, lower IMT values were found. Pulse wave velocity showed a borderline significant decrease. During HUTT, several hemodynamic parameters improved. The patients performed better on neuropsychological testing and reached significantly lower scores on questionnaires evaluating anxiety. The present study shows that early vascular changes and altered cognitive function observed in newly diagnosed hypertensive patients may improve with promptly initiated antihypertensive management.

In this observational study we investigated whether levels of factor XIII (FXIII) and its major polymorphisms affect the outcome of thrombolysis by recombinant tissue plasminogen activator (rtPA) in acute ischemic stroke (AIS) patients. Study cohort included 132 consecutive AIS patients undergoing i.v. thrombolysis within 4.5 h of symptom onset. Blood samples taken on admission, immediately after and 24 h after therapy were analyzed for FXIII activity and antigen levels. FXIII-A p.Val34Leu, p.Tyr204Phe, FXIII-B p.His95Arg and intron K(IVS11 + 144) polymorphisms were genotyped. Neurological deficit was assessed using the National Institutes of Health Stroke Scale. Intracranial hemorrhage was classified according to ECASSII criteria. Long-term functional outcome was defined at 3 months post-event by the modified Rankin scale. FXIII levels showed a gradual decrease immediately after thrombolysis and 24 h later, which was not related to therapy-associated bleeding. In a multiple logistic regression model, a FXIII level in the lowest quartile 24 h post-lysis proved to be an independent predictor of mortality by 14 days post-event (OR:4.95, 95% CI:1.31–18.68, p

Introduction. Mannose-binding lectin (MBL) activates complement system and has been suggested to play a role in vascular complications in diabetics. Carotid intima-media thickness (cIMT) detects subclinical atherosclerosis. We evaluated the association of MBL and IMT in type 2 diabetic (T2DM) patients.Methods. Serum MBL levels and cIMT were measured in a total of 103 diabetics and in 98 age-matched healthy controls.Results. There was no significant difference in MBL level in T2DM versus controls. As expected, IMT was significantly higher in T2DM patients than in controls (P=0.001). In T2DM, the lowest cIMT was seen in patients with normal MBL level (500–1000) while cIMT continuously increased with both high MBL and absolute MBL deficiency states. This was especially significant in high MBL versus normal MBL T2DM patients (P=0.002). According to multiple regression analysis the main predictors of IMT in T2DM are age (P<0.003), ApoA level (P=0.023), and the MBL (P=0.036).Conclusions. Our results suggest a dual role of MBL as a risk factor for cIMT in T2DM. MBL may also be used as a marker of macrovascular disease, as both low and high levels indicate the susceptibility for atherosclerosis in T2DM.

Background Alcohol is a known triggering factor for orthostatic dysfunction, increasing the risk of neurally-mediated syncope. Since orthostatic tolerance may be affected by both systemic and cerebral hemodynamic changes, our aim was to investigate the acute effects of alcohol on cerebral vasoreactivity measured during the head-up tilt (HUT) test in 20 healthy subjects. Methods Mean arterial blood pressure (mBP), heart rate, and flow parameters in both middle cerebral arteries (MCAs) were continuously recorded in the supine and during a 10-minute HUT positions before and after alcohol intake. Results The HUT test resulted in a more prominent decline of adjusted mBP at the level of MCAs (mBPMCA) and a significantly larger decrease of MCA mean flow velocities (MFVMCA) in the post-alcohol period than before alcohol intake. During the HUT phase, the relative decrease in MFVMCA was significantly smaller than the reduction in mBPMCA before drinking alcohol, while these changes were similar after alcohol ingestion. The cerebrovascular resistance index (CVRi) decreased during the HUT phase in the control period, however, it increased after alcohol intake. Conclusion The similar decrease in mBPMCA and MFVMCA during orthostatic stress after alcohol ingestion together with the increased CVRi indicated the impairment of the compensatory vasodilation of cerebral resistance vessels, i.e. impaired cerebral autoregulation. These findings suggest that alcohol may contribute to impaired orthostatic tolerance not only by a hypotensive response but also by the alteration of cerebral blood flow regulation.

Hypertension is one of the most important modifiable risk factors of cardioand cerebrovascular diseases, responsible for the development of severe target organ damages. It has been shown that hypertension is associated with an increased prevalence of cognitive decline. It negatively affects the cognitive battery and accelerates dementia. Beside the known detrimental effects of senile hypertension on cognitive performance in the elderly population, previous studies pointed out that young, hypertensive individuals may also suffer from hypertension related changes in their cognitive capacity. Given the high prevalence of hypertension in a wide range of the age pyramid (young individuals, middle aged adults, elderly people), specific cognitive deficits may be present in a large portion of the population putting a heavy burden on society. Better understanding of the underlying mechanisms of hypertension induced cognitive impairment may contribute to the identification of its initiating pathophysiological factors, and serve an earlier diagnosis, intervention at an early stage and prevention of further deficits. Our aim with the current review was to summarize some of the previous findings regarding altered cognitive performance of individuals with hypertension and of those with the most common co-existing risk factors. Furthermore, efforts to explore effects of various antihypertensive medications on cognition and to survey proposed pathophysiological mechanisms of hypertension induced cognitive changes have been made.