Prediction of conduction disturbances in patients undergoing transcatheter aortic valve replacement

Aim Transcatheter aortic valve replacement (TAVR) can cause intraventricular conduction disturbances (ICA), particularly left bundle branch block (BBB) and high-degree atrioventricular block (HAVB). The aim of this study was to investigate clinical, anatomical, procedural, and electrophysiological parameters predicting ICA after TAVR. Methods Patients with severe aortic stenosis (n=203) without pacing devices undergoing TAVR with a self-expanding (n=103) or balloon-expanding (n=100) valve were enrolled. Clinical and anatomical parameters, such as length of the membranous septum (MS) and implantation depth, were assessed. His-ventricular interval (HVi) before and after implantation was determined. 12-lead-electrocardiograms (ECG) before, during and after 3 and 30 days after TAVR were analyzed for detection of any ICA. Results Among 203 consecutive patients (aortic valve area 0.78±0.18 cm2 , age 80±6 years, 54% male, left ventricular ejection fraction 52±10%), TAVR led to a signifcant prolongation of infranodal conduction in all patients from 49±10 ms to 59±16 ms (p=0.01). The HVi prolongation was independent of valve types, occurrence of HAVB or ICA. Fifteen patients (7%) developed HAVB requiring permanent pacemaker (PPM) implantation and 63 patients (31%) developed ICA within 30 days. Pre-existing BBB (OR 11.64; 95% CI 2.87–47.20; p=0.001), new-onset left BBB (OR 15.72; 95% CI 3.05–81.03; p=0.001), and diabetes mellitus (OR 3.88; 95% CI 1.30–15.99; p=0.02) independently predicted HAVB requiring PPM. Neither pre-existing right BBB, a prolonged postHVi, increases in PR duration, any of the TAVR implantation procedural and anatomic nor echocardiographic characteristics were predictive for later HAVB. Conclusions New-onset left BBB and diabetes mellitus independently predicted HAVB requiring PPM after TAVR and helped to identify patients at risk. Electrophysiologic study (EPS) of atrioventricular conduction was neither specifc nor predictive of HAVB and can be skipped. Trial registration number NCT04128384 (https://www.clinicaltrials.gov)

E. coli Nissle 1917 Affects Salmonella Adhesion to Porcine Intestinal Epithelial Cells

BACKGROUND: The probiotic Escherichia coli strain Nissle 1917 (EcN) has been shown to interfere in a human in vitro model with the invasion of several bacterial pathogens into epithelial cells, but the underlying molecular mechanisms are not known. METHODOLOGY/PRINCIPAL FINDINGS: In this study, we investigated the inhibitory effects of EcN on Salmonella Typhimurium invasion of porcine intestinal epithelial cells, focusing on EcN effects on the various stages of Salmonella infection including intracellular and extracellular Salmonella growth rates, virulence gene regulation, and adhesion. We show that EcN affects the initial Salmonella invasion steps by modulating Salmonella virulence gene regulation and Salmonella SiiE-mediated adhesion, but not extra- and intracellular Salmonella growth. However, the inhibitory activity of EcN against Salmonella invasion always correlated with EcN adhesion capacities. EcN mutants defective in the expression of F1C fimbriae and flagellae were less adherent and less inhibitory toward Salmonella invasion. Another E. coli strain expressing F1C fimbriae was also adherent to IPEC-J2 cells, and was similarly inhibitory against Salmonella invasion like EcN. CONCLUSIONS: We propose that EcN affects Salmonella adhesion through secretory components. This mechanism appears to be common to many E. coli strains, with strong adherence being a prerequisite for an effective reduction of SiiE-mediated Salmonella adhesion

The evolution and nomenclature of GnRH-type and corazonin-type neuropeptide signaling systems

The work of the authors reported in this review was supported by grants from the BBSRC (BB/M001644/1; BB/M001032/1), the Leverhulme Trust (RGP-2013-351) and the China Scholarship Council

Microalbuminuria independently correlates to cardiovascular comorbidity burden in patients with hypertension

Microalbuminuria (MAU) is a marker for endothelial dysfunction and a predictor of cardiovascular events. Cardiovascular risk and mortality are mainly influenced by associated morbidities and risk factors. The present analysis aimed to investigate the relationship between the number of cardiovascular comorbidities and both the prevalence of MAU and the extent of albuminuria (measured as urinary albumin excretion, UAE) in 21,867 high-risk hypertensive patients included in the I-SEARCH study. A total of 6,945 patients (32 %) suffered from at least one comorbidity, out of which 5,437 patients (25 %) had one cardiovascular comorbidity, 1,163 (5 %) patients had two, and 345 (2 %) had a parts per thousand yen3. The prevalence of MAU increased from 54 % in patients without cardiovascular comorbidity to 74 % in the presence of a parts per thousand yen3 comorbidities (p < 0.01). In a multivariate analysis, the presence of a parts per thousand yen3 cardiovascular comorbidities nearly doubled the risk for MAU (HR 1.79, CI 1.07-2.68, p = 0.025). Compared to other comorbidities, patients with left ventricular hypertrophy had the highest prevalence of MAU (68 %, p < 0.01). The extent of UAE was related to the number of concomitant disease and increased significantly in patients with a parts per thousand yen3 comorbidities compared to patients with no comorbidity (UAE of 80 mg/L: 12-22 %, p < 0.01; UAE of 150 mg/L: 8-19 %, p < 0.01). In hypertensive patients at high cardiovascular risk, both the prevalence of MAU and the extent of albuminuria increase with the number of comorbidities

Proceedings from the 3rd European Clinical Consensus Conference for clinical trials in device-based hypertension therapies

Sin financiación22.673 JCR (2019) Q1, 2/138 Cardiac & Cardiovascular Systems5.883 SJR (2019) Q1, 4/362 Cardiology and Cardiovascular MedicineNo data IDR 2019UE

Renal artery anatomy assessed by quantitative analysis of selective renal angiography in 1,000 patients with hypertension

AIMS With increasing attention to renovascular causes and targets for hypertension there arises a critical need for more detailed knowledge of renal arterial anatomy. However, a standardised nomenclature is lacking. The present study sought to develop a standardised nomenclature for renal anatomy considering the complexity and variation of the renal arterial tree and to assess the applicability of the nomenclature. METHODS AND RESULTS One thousand hypertensive patients underwent invasive selective renal artery angiography in nine centres. Further, renovasography was performed in 249 healthy swine as a surrogate for normotensive anatomy. Anatomical parameters were assessed by quantitative vascular analysis. Patients' mean blood pressure was 168/90±26/17 mmHg. The right main renal artery was longer than the left (41±15 mm vs. 35±13 mm, p<0.001), but the left had a greater diameter (5.4±1.2 vs. 5.2±1.2 mm, p<0.001). Accessory renal arteries and renal artery disease were documented in 22% and 9% of the patients, respectively. Other than exhibiting a longer left main renal artery in uncontrolled hypertensives (+2.7 mm, p=0.034) there was no anatomical difference between patients with controlled and uncontrolled hypertension. Main renal artery mean diameter was smaller in patients with impaired kidney function (GFR <90 ml/min, left -0.5 mm, right -0.4 mm, both p<0.001). CONCLUSIONS Renal arterial anatomy differs between sides but shows no difference between patients with and without blood pressure control. Impaired GFR was associated with small main renal artery diameter