The relationship between regional brain volumes and the extent of coronary artery disease in mild cognitive impairment.

BACKGROUND: There are conflicting reports regarding the association between coronary artery disease (CAD) and mild cognitive impairment (MCI). Volumetric Magnetic resonance imaging (MRI) investigations have been considered as an objective biomarker for MCI. In this study, we determined the relationship between the regional brain volumes and the extent of CAD in MCI patients and cognitively normal controls. MATERIALS AND METHODS: In a case-control study a subset of MCI patients (n = 20) and cognitively normal controls (n = 20), aged 66.4 ± 4.6 and 65.3 ± 3.9 respectively, from subjects who were recently admitted to cardiac catheterization facilities in two general hospitals were selected. All subjects underwent a clinical interview, biochemical measures, neuropsychological testing and Neuropsychiatry Unit COGnitive assessment tool. Video records of coronary angiography were scored with the Gensini method. For volumetric evaluation of regions of interest, brain MRI scans was processed using the FreeSurfer software package the relationship between the regional brain volumes and the extent of CAD in MCI patients and cognitively normal controls were compared. RESULTS: We have found that, there were significant differences between the two groups in volumes of left fusiform (P = 0.039), left pars triangularis (P = 0.003) and left superior temporal gyrus (P = 0.009), after controlling for intracranial volumes. Higher Gensini scores were associated with reduced volumes of total cortical volume (P = 0.047, R = -0.4), left precuneus (P = 0.022, R = -0.5), right inferior parietal lobule (P = 0.011, R = -0.5) and left supra marginal gyrus (P = 0.035, R = -0.04) in MCI. CONCLUSION: In MCI, a greater degree of coronary stenosis correlates with greater loss of gray matter in specific brain regions relevant to cognitive function. This, however, was not the case for cognitively normal subjects.

P wave duration and dispersion in Holter electrocardiography of patients with obstructive sleep apnea.

PURPOSE: The underlying mechanisms of the association between obstructive sleep apnea (OSA) and atrial fibrillation (AF) remained unclear. We investigated P wave parameters as indicators of atrial conduction status among OSA patients. METHODS: We studied 42 untreated OSA patients, categorized into mild (6), moderate (18), and severe (18) OSA based on the apnea/hypopnea index (AHI) and 18 healthy controls. Twenty-four-hour Holter electrocardiography was applied to measure P wave parameters including P wave duration and P wave dispersion; difference between the maximum (P-max) and minimum (P-min) measured P wave duration. RESULTS: Mean P wave duration ranged from 110.2 ± 9.3 ms in mild OSA patients to 121.1 ± 15.4 ms in severe OSA patients and was 113.4 ± 10.0 ms in controls with no significant difference among the groups, P = 0.281. P wave dispersion and P-max were significantly longer in those with moderate OSA (68.0 ± 9.3 and 154.2 ± 9.3 ms) and those with severe OSA (71.6 ± 13.7 and 157.2 ± 13.3 ms) than controls (52.6 ± 15.3 and 142.1 ± 15.4 ms), P < 0.05. AHI was significantly correlated with P-max (r = 0.407, P = 0.012) and P wave dispersion (r = 0.431, P = 0.008). With linear regression analysis controlling for age, gender, and BMI, the AHI was independently associated with P wave dispersion (ß = 0.482, P = 0.002). CONCLUSIONS: Using Holter monitoring for measurement of P wave parameters, this study showed an association of OSA with prolonged P-max and P wave dispersion. These results indicate that patients with OSA have disturbances in atrial conduction associated with OSA severity. Repeating this study in a larger sample of patients is warranted.

Association between heme oxygenase-1 gene promoter polymorphisms and metabolic syndrome in Iranians.

Heme oxygenase-1 (HO-1) which is a rate-limiting enzyme in heme degradation processes shows a dinucleotide GT repeat in the promoter that alters the level of gene transcription. This study is aimed to assess the association of HO-1 gene promoter polymorphism and metabolic syndrome (MetS). A hundred and fifty two individuals, who were followed in Isfahan Cohort Study since 2001, were enrolled in this study. They consisted of 78 MetS patients and 74 controls without MetS. Blood samples were obtained from all participants and after extracting the genomic DNA, promoter sequence was determined by PCR-based genotyping. The serum levels of iron, ferritin and bilirubin were also measured in all subjects. The proportion of short and long allele frequency did not significantly differ in patients with metabolic syndrome compared to control group. In conclusion, the results showed that there is no significant difference between two groups in (GT)n repeat of HO-1 gene promoter. These findings suggest the insignificant role of genetic risk factors compared to environmental risk factors in the development of MetS.