Prevalence and treatment of atrial fibrillation in older adults.

BACKGROUND: Atrial fibrillation (AF) is the most frequent cardiac arrhythmia with an impact on morbidity and mortality found in the geriatric population. OBJECTIVE: This retrospective study is the first to investigate the prevalence, treatment and comorbidities of AF in a large cohort of older adults. MATERIAL AND METHODS: Older adults with AF hospitalized between 2010 and 2018. The mean age of the 10,700 AF patients in 2018 was 83.2 ± 6.4 years. The frequency of anticoagulation in older adults with AF between 2010 and 2018 was analyzed. The relationship between comorbidities and anticoagulation in 2018 was examined. Logistic regression analysis was used to identify possible predictive factors for anticoagulation. RESULTS: The prevalence of AF in 35,887 hospitalized older adults was 29.8% in 2018. The mean CHA2DS2VASc score was 4.4 ± 1.3 (male 3.8 ± 1.3, female 4.7 ± 1.2). From 2010 to 2018, the frequency of anticoagulation for patients with AF rose from 32.1% to 64.2%. Statistically significant differences in the examined characteristics between anticoagulated and not anticoagulated patients were found. Furthermore, there were no predictive factors for anticoagulation in multivariate logistic analysis. CONCLUSION: Hospitalized older adults have an increased prevalence of AF compared to the general population. Despite the higher risk of bleeding, older adults were more frequently anticoagulated in the observation period, preferably with direct oral anticoagulants (DOACs). Patients without anticoagulation had more diagnoses and were worse in functional tests. This study suggests that the decision to give anticoagulants to older adults should be personalized.

Novel Genetic Triggers and Genotype-Phenotype Correlations in Patients With Left Ventricular Noncompaction.

BACKGROUND: Left ventricular noncompaction (LVNC) is a genetically and phenotypically heterogeneous disease and, although increasingly recognized in clinical practice, there is a lack of widely accepted diagnostic criteria. We sought to identify novel genetic causes of LVNC and describe genotype-phenotype correlations. METHODS AND RESULTS: A total of 190 patients from 174 families with left ventricular hypertrabeculation (LVHT) or LVNC were referred for cardiac magnetic resonance and whole-exome sequencing. A total of 425 control individuals were included to identify variants of interest (VOIs). We found an excess of 138 VOIs in 102 (59%) unrelated patients in 54 previously identified LVNC or other known cardiomyopathy genes. VOIs were found in 68 of 90 probands with LVNC and 34 of 84 probands with LVHT (76% and 40%, respectively; P<0.001). We identified 0, 1, and ≥2 VOIs in 72, 74, and 28 probands, respectively. We found increasing number of VOIs in a patient strongly correlated with several markers of disease severity, including ratio of noncompacted to compacted myocardium (P<0.001) and left ventricular ejection fraction (P=0.01). The presence of sarcomeric gene mutations was associated with increased occurrence of late gadolinium enhancement (P=0.004). CONCLUSIONS: LVHT and LVNC likely represent a continuum of genotypic disease with differences in severity and variable phenotype explained, in part, by the number of VOIs and whether mutations are present in sarcomeric or nonsarcomeric genes. Presence of VOIs is common in patients with LVHT. Our findings expand the current clinical and genetic diagnostic approaches for patients with LVHT and LVNC.

Tissue factor and tissue factor pathway inhibitor in chronically inflamed gallbladder mucosa.

We characterised a tissue factor (TF) and tissue factor pathway inhibitor (TFPI) expression in relation to severity of inflammatory infiltration of the gallbladder mucosa in a chronic cholecystitis. We prospectively studied the gallbladder specimens obtained from 54 patients who had undergone cholecystectomy due to chronic calculous cholecystitis and 16 calculosis-free gallbladder specimens obtained from patients who underwent cholecystectomy due to the polyp/polyps as well as in cases of gallbladder injury. To assess TF and TFPI immunoreactivity by immunohistochemistry, the monoclonal anti-human TF and TFPI antibodies were used. The inflammatory infiltration of the gallbladder mucosa was reflected by the number of CD3 and CD68 positive cells. The expression of TF and TFPI differed significantly between the cholecystitis and the control group. Most capillary endothelial cells of the cholecystitis group presented weak expression for TFPI. The mean number of CD3 positive lymphocytes in the cholecystitis group was 18.6 ± 12.2, but the mean number of CD68 positive cells was 29.7 ± 13.9. In the control sections, it was 3.1 ± 1.9 and 8.8 ± 3.9, respectively (P < 0.001). The results of the current study suggest that the tissue procoagulant state found may be engaged in the etiopathogenesis of the cholecystitis.