Atrial fibrillation and mild cognitive impairment: what correlation?

AIM: Atrial fibrillation (AF), in addition to macroembolic complications, may also produce multiple cerebral ischemic areas due to microembolic phenomena and transient hypoperfusion, eventually leading to a progressive cognitive impairment and even to acclaimed vascular dementia. The aim of this study was to evaluate the prevalence of cognitive impairment in patients with AF. The reported results concern data obtained at the moment of recruitment. METHODS: The authors studied 42 patients with a history of non valvular AF (paroxysmal, persistent, recurrent or permanent) and 40 homogenous controls in sinus rhythm without previous AF. All subjects underwent anamnesis, physical examination, biochemical and instrumental tests. To investigate the cognitive status, subjects underwent the following neuropsychological rating scales: Mini Mental State Examination (MMSE), Clinical Dementia Rating Scale (CDR),Activity of Daily Living (ADL), Instrumental Activity of Daily Living (IADL) Global Deterioration Scale (GLDS), Geriatric Depression Scale (GDS) and Hachinski Ischemic Score (HIS). RESULTS: AF Patients had worse scores versus controls at GLDS (P=0.0001), HIS (P=0.001), CDR (P=0.07) and GDS (P=0.07); no significant differences were found for MMSE even after correction for age and education. AF patients treated with warfarin showed better scores at CDR (P=0.04),GLDS (P=0.03) and GDS (P=0.007), compared to those in aspirin-treatment. Corrected MMSE scores did not differ. CONCLUSIONS: The authors identified a slight cognitive impairment in the AF group; patients with paroxysmal, persistent or recurrent AF showed worse cognitive performances than permanent ones, suggesting a possible microembolic pathogenesis. Anticoagulation therapy could play a protective role, however more evidence is needed.

Non invasive evaluation of endothelial function in patients with Anderson-Fabry disease.

AIM: Fabry's disease is an X-linked recessive abnormality of glycosphingolipid metabolism. Increased levels of endothelial prothrombotic factors have recently been demonstrated in Fabry's disease, whereas endothelial function has not been studied using high resolution ultrasound. METHODS: We enrolled 6 patients (4 male, 2 female; mean age, 37 years) and 12 sex matched control subjects (mean age, 37 years). Patients' exclusion criteria included a prior history of cardiac disease, diabetes and treated or untreated hypertension. Patients underwent: anamnesis, physical examination, EKG, 2-dimensional echocardiography with tissue Doppler, measurement of body weight and height, blood pressure. Biochemistry variables were also considered: fasting blood sugar, total cholesterol, HDL-C, LDL-C, triglycerides, fibrinogen, C reactive protein and homocysteine. Using high resolution ultrasound, we assessed the brachial vasodilator response to reactive hyperemia (endothelium-dependent) and sublingual nitroglycerin (NTG) (endothelium-independent). Flow-mediated dilatation (FMD) was expressed as percentage change in post-stimulus diameter in comparison with the baseline. RESULTS: In baseline condition, there was no significant difference between patients and controls in the brachial artery diameter (3.5+/-0.55 vs 3.1+/-0.4). After reactive hyperemia, the FMD change was significantly higher in controls than in patients (16.5+/-6.3% vs 9.3+/-6.2%, P<0.05). After NTG, endothelium-independent vasodilation did not show a significant difference between cases and controls (15+/-7.7% vs 13.8+/-7.1%). CONCLUSIONS: Our study demonstrated the presence of endothelial dysfunction in patients with Fabry's disease in comparison to controls. We hypothesized that endothelial dysfunction may contribute to the pathogenesis of ischemic events in patients with Fabry's disease.