A nationwide cohort analysis to determine the prevalence of sinus node dysfunction and rates of pacemaker implantation in systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) has been known to have various degrees of cardiac involvement. However, limited evidence exists on prevalence of heart rhythm disorders in patients with SLE who have subsequent pacemaker (PM) implantation. The purpose of this study was to examine the prevalence of sinus node dysfunction (SND) in patients with SLE. The data was retrospectively analysed from the National Inpatient Sample database for the years 2010 to 2014 using the International Classification of Disease-9 diagnosis codes for SLE and SND in patients 18 years or older. We analysed data of 158,368 patients with SLE that were admitted from 2010 to 2014. The sample of patients ranged between 18 and 101 years of age (M = 52.13 ± 17.61), were primarily female (88.2%), and were Caucasian (50.6%). The prevalence of SND was 4.3%. In patients with both SLE and SND, the prevalence of PM implantation over the five-year period of analysis was 3.6% and the majority of these patients had a dual-chamber PM (85.6%). Prevalence rates of SND in patients with SLE increased for females over this five-year period (p = 0.023). Prevalence estimates of complications associated with PM in patients with SLE and SND were venous thromboembolism (2.1%), cardiac tamponade (0.4%), sepsis and severe sepsis (0.4%), septic shock (0%), pneumothorax (0%) and PM site hematoma (1.7%). The findings of this study revealed that the prevalence of SND and the prevalence of PM in patients with both SLE and SND have remained relatively consistent over the five years that our study analysed.

A population based analysis of trends, risk factors and outcomes associated with gastrointestinal bleeding in patients with left ventricular assist devices.

Introduction: Prior to the utilization of continuous flow (CF) devices in 2010, Gastrointestinal (GI) bleeding was a common adverse event related to left ventricular assist device (LVADs) that was found to be even more frequent when CF devices were first introduced. Objective: Given the drastic increase in the use of new CF-LVADs, we sought to determine if CF-LVADs are associated with an increased number of GI bleeds and higher mortality. Methods: We analysed the data from a national inpatient sample database using the ICD-9 procedure code for LVAD use in end-stage heart failure among patients > 18 years. The total sample consisted of 2,359 patients (M age=55 ± 13.7 years). A majority of the sample was male (77%) and Caucasian (59%). Results: The Incidence of GI bleeding from 2010 to 2014 was 7.46% with no significant change in yearly incidence over five-year period (P=.793). After controlling for age, sex, and length of stay, multivariate logistic regression revealed that significant predictors of GI bleed were acute kidney injury (AOR=1.87, 95% CI=1.26, 2.80), peripheral vascular disease (AOR=1.77, 95% CI=1.02, 2.94), body mass index ≥ 25 (AOR=.46, 95% CI=.22, .87), hemiplegia or paraplegia (AOR=3.01, 95% CI=1.17, 7.05), moderate or severe liver disease (AOR=2.40, 95% CI=.97, 5.34), peptic ulcer disease (AOR=18.13, 95% CI=7.86, 42.38), surgical aortic valve replacement (AOR=2.46, 95% CI=1.12, 5.15), and venous thromboembolism (AOR=2.58, 95% CI=1.57, 4.15). Conclusion: The results of the study show that GI bleeding is highly prevalent in patients with LVADs and there was no improvement in rates of GI bleed over five years since the CF-LVADs were initially introduced and is associated with an increased likelihood of mortality.

Mutations in SCN10A are responsible for a large fraction of cases of Brugada syndrome.

BACKGROUND: BrS is an inherited sudden cardiac death syndrome. Less than 35% of BrS probands have genetically identified pathogenic variants. Recent evidence has implicated SCN10A, a neuronal sodium channel gene encoding Nav1.8, in the electrical function of the heart. OBJECTIVES: The purpose of this study was to test the hypothesis that SCN10A variants contribute to the development of Brugada syndrome (BrS). METHODS: Clinical analysis and direct sequencing of BrS susceptibility genes were performed for 150 probands and family members as well as >200 healthy controls. Expression and coimmunoprecipitation studies were performed to functionally characterize the putative pathogenic mutations. RESULTS: We identified 17 SCN10A mutations in 25 probands (20 male and 5 female); 23 of the 25 probands (92.0%) displayed overlapping phenotypes. SCN10A mutations were found in 16.7% of BrS probands, approaching our yield for SCN5A mutations (20.1%). Patients with BrS who had SCN10A mutations were more symptomatic and displayed significantly longer PR and QRS intervals compared with SCN10A-negative BrS probands. The majority of mutations localized to the transmembrane-spanning regions. Heterologous coexpression of wild-type (WT) SCN10A with WT-SCN5A in HEK cells caused a near doubling of sodium channel current compared with WT-SCN5A alone. In contrast, coexpression of SCN10A mutants (R14L and R1268Q) with WT-SCN5A caused a 79.4% and 84.4% reduction in sodium channel current, respectively. The coimmunoprecipitation studies provided evidence for the coassociation of Nav1.8 and Nav1.5 in the plasma membrane. CONCLUSIONS: Our study identified SCN10A as a major susceptibility gene for BrS, thus greatly enhancing our ability to genotype and risk stratify probands and family members.