Explore the vast range of titles available.

Background: Ultrasound (US)-guided axillary vein puncture (AVP) is an established technique for cardiac implantable electronic device (CIED) implantation. Yet real-world data concerning shifting from conventional venous access into US-guided AVP are not widely available. Methods: This is a single-center prospective registry reporting safety (complications) and efficacy (success rate: i.e., accomplishment of the vein access utilizing only the initially employed approach) of self-taught US-guided AVP integration into the standard workflow of CIED procedures. Results: A total of 539 patients (mean age 71.5 ± 12.4 years old, 78.7% males) were treated in our institution over a three-year period. Regarding CIED type and lead number, 58.3% used an implantable cardioverter defibrillator, 32% used permanent pacemakers, and two leads were involved in 65.8% of the cases and three leads in 8.9%. Before integration of US-guided AVP, the venous access success rate was 93.5%. The US-guided AVP success rate was 377/400 procedures (94.2%). After the first semester of US-guided AVP utilization, a pattern of increased success rate was observed (p = 0.002) and remained stable over the following semesters. No major complication (periprocedural or 30-day mortality, hemothorax, pneumothorax and tamponade) occurred after US AVP integration in our workflow. Conclusions: The integration of US-guided AVP in a self-taught manner is feasible among electrophysiologists with experience in US-guided vascular access. A high success rate can be reached quickly and safely.

Isolated coronary artery ectasia (CAE) is a relatively rare clinical entity, the pathogenesis of which is poorly understood. More and more evidence is accumulating to suggest a critical inflammatory component. We aimed to elucidate any association between neutrophil to lymphocyte ratio and coronary artery ectasia. A systematic MEDLINE database, ClinicalTrials.gov, medRxiv, Scopus and Cochrane Library search was conducted: 50 studies were deemed relevant, reporting on difference in NLR levels between CAE patients and controls (primary endpoint) and/or on high-sensitive CRP, IL-6, TNF-a and RDW levels (secondary endpoint), and were included in our final analysis. (PROSPERO registration number: CRD42021224195). All inflammatory biomarkers under investigation were found higher in coronary artery ectasia patients as compared to healthy controls (NLR; SMD = 0.73; 95% CI: 0.27–1.20, hs-CRP; SMD = 0.96; 95% CI: 0.64–1.28, IL-6; SMD = 2.68; 95% CI: 0.95–4.41, TNF-a; SMD = 0.50; 95% CI: 0.24–0.75, RDW; SMD = 0.56; 95% CI: 0.26–0.87). The main limitations inherent in this analysis are small case-control studies of moderate quality and high statistical heterogeneity. Our findings underscore that inflammatory dysregulation is implicated in coronary artery ectasia and merits further investigation.

The prevalence of atrial fibrillation (AF) is bound to increase globally in the following years, affecting the quality of life of millions of people, increasing mortality and morbidity, and beleaguering health care systems. Increasingly effective therapeutic options against AF are the constantly evolving electroanatomic substrate mapping systems of the left atrium (LA) and ablation catheter technologies. Yet, a prerequisite for better long-term success rates is the understanding of AF pathogenesis and maintenance. LA electrical and anatomical remodeling remains in the epicenter of current research for novel diagnostic and treatment modalities. On a molecular level, electrical remodeling lies on impaired calcium handling, enhanced inwardly rectifying potassium currents, and gap junction perturbations. In addition, a wide array of profibrotic stimuli activates fibroblast to an increased extracellular matrix turnover via various intermediaries. Concomitant dysregulation of the autonomic nervous system and the humoral function of increased epicardial adipose tissue (EAT) are established mediators in the pathophysiology of AF. Local atrial lymphomononuclear cells infiltrate and increased inflammasome activity accelerate and perpetuate arrhythmia substrate. Finally, impaired intracellular protein metabolism, excessive oxidative stress, and mitochondrial dysfunction deplete atrial cardiomyocyte ATP and promote arrhythmogenesis. These overlapping cellular and molecular alterations hinder us from distinguishing the cause from the effect in AF pathogenesis. Yet, a plethora of therapeutic modalities target these molecular perturbations and hold promise in combating the AF burden. Namely, atrial selective ion channel inhibitors, AF gene therapy, anti-fibrotic agents, AF drug repurposing, immunomodulators, and indirect cardiac neuromodulation are discussed here.

Background Left atrium changes are implicated in atrial fibrillation (AF) substrate and are predictive of AF outcomes. Left atrial appendage (LAA) is an integral component of left atrial structure and could be affected by atrial cardiomyopathy. We aimed to elucidate the association between LAA indices and late arrhythmia recurrence after atrial fibrillation catheter ablation (AFCA). Methods The MEDLINE database, ClinicalTrials.gov, medRxiv and Cochrane Library were searched for studies evaluating LAA and late arrhythmia recurrence in patients undergoing AFCA. Data were pooled by meta-analysis using a random-effects model. The primary endpoint was pre-ablation difference in LAA anatomic or functional indices. Results A total of 34 studies were found eligible and five LAA indices were analyzed. LAA ejection fraction and LAA emptying velocity were significantly lower in patients with AF recurrence post-ablation [SMD = − 0.66; 95% CI (− 1.01, − 0.32) and SMD = − 0.56; 95% CI (− 0.73, − 0.40) respectively] as compared to arrhythmia free controls. LAA volume and LAA orifice area were significantly higher in patients with AF recurrence post-ablation (SMD = 0.51; 95% CI 0.35–0.67, and SMD = 0.35; 95% CI 0.20–0.49, respectively) as compared to arrhythmia free controls. LAA morphology was not predictive of AF recurrence post-ablation (chicken wing morphology; OR 1.27; 95% CI 0.79–2.02). Moderate statistical heterogeneity and small case–control studies are the main limitations of our meta-analysis. Conclusions Our findings suggest that LAA ejection fraction, LAA emptying velocity, LAA orifice area and LAA volume differ between patients suffering from arrhythmia recurrence post-ablation and arrhythmia free counterparts, while LAA morphology is not predictive of AF recurrence.

There is substantial evidence that the autonomic system plays an important part in the pathogenesis of atrial fibrillation (AF). It appears that, although some patients have a preponderantly sympathetic or vagal overactivation leading to AF, a combined sympathovagal drive is most commonly responsible for AF triggering. The purpose of this hypothesis-generating study was to test whether moxonidine, a centrally acting sympathoinhibitory agent, on top of optimal antihypertensive treatment, can lead to a decrease in AF burden in hypertensive patients with paroxysmal AF. This was a prospective, double-blind, 1-group, crossover study. Hypertensive patients with paroxysmal AF sequentially received treatment with placebo and moxonidine for two 6-week periods, respectively. The change in AF burden (measured as minutes of AF per day in three 48-hour Holter recordings) between the 2 treatment periods was the primary outcome measure. Fifty-six patients (median age 63.5 years, 35 men) were included. During moxonidine treatment, AF burden was reduced from 28.0 min/day (interquartile range [IQR] 15.0 to 57.8) to 16.5 min/day (IQR 4.0 to 36.3; p <0.01). European Heart Rhythm Association symptom severity class decreased from a median of 2.0 (IQR 1.0 to 2.0) to 1.0 (IQR 1.0 to 2.0; p = 0.01). Systolic blood pressure levels were similar in the 2 treatment periods, whereas diastolic blood pressure was lower (p <0.01) during moxonidine treatment. The most frequent complaint was dry mouth (28.6%). No serious adverse events were recorded. In conclusion, treatment with moxonidine, a centrally acting sympathoinhibitory agent, results in reduction of AF burden and alleviation of AF-related symptoms in hypertensive patients with paroxysmal AF.

Background Placement of an electrode catheter in the coronary sinus (CS) through the jugular or subclavian vein, as part of electrophysiology (EP) procedures, increases patient discomfort and the possibility of adverse events. We studied the hypothesis that peripheral venous access for CS cannulation, as part of EP procedures, is feasible and can reduce patient discomfort, eliminating central venous access-associated risks. Methods Consecutive patients submitted to EP procedures were randomly assigned to peripheral or central venous access for CS cannulation. If after 30 min from initial needle insertion the CS was still not catheterized, the attempt was considered unsuccessful. Patient level of discomfort was assessed with a visual analog scale (VAS). Results Success rate was 90% in the peripheral versus 95% in the central venous access group ( p  = 1.00). No complications related to venous access were observed in the peripheral venous access group, whereas one case of pneumothorax and one case of extensive hematoma in the anterior cervical area were recorded in the central venous access group. Patients submitted to central vein catheterization reported higher VAS scores, 46.8 ± 16.3 versus 36.8 ± 12.9 ( p  = 0.04). No significant difference was observed in fluoroscopy time needed for CS cannulation (51.1 ± 9.2 s versus 51.4 ± 7.9 s; p  = 0.71) between the two groups. Conclusion This small, randomized study indicates that peripheral venous access for CS catheter placement during EP procedures is feasible, with equivalent success rate to the central venous access approach, and associated with lower levels of self-reported patient discomfort.

The global burden of atrial fibrillation (AF) is constantly increasing, necessitating novel and effective therapeutic options. Sodium glucose co-transporter 2 (SGLT2) inhibitors have been introduced in clinical practice as glucose-lowering medications. However, they have recently gained prominence for their potential to exert substantial cardiorenal protection and are being evaluated in large clinical trials including patients with type 2 diabetes and normoglycemic adults. In this review we present up-to-date available evidence in a pathophysiology-directed manner from cell to bedside. Preclinical and clinical data regarding a conceivable antiarrhythmic effect of SGLT2 inhibitors are beginning to accumulate. Herein we comprehensively present data that explore the potential pathophysiological link between SGLT2 inhibitors and AF. With regard to clinical data, no randomized controlled trials evaluating SGLT2 inhibitors effects on AF as a pre-specified endpoint are available. However, data from randomized controlled trial post-hoc analysis as well as observational studies point to a possible beneficial effect of SGLT2 inhibitors on AF. Meta-analyses addressing this question report inconsistent results and the real magnitude of AF prevention by SGLT2 inhibition remains unclear. Still, while (i) pathophysiologic mechanisms involved in AF might be favorably affected by SGLT2 inhibitors and (ii) emerging, yet inconsistent, clinical data imply that SGLT2 inhibitor-mediated cardiorenal protection could also exert antiarrhythmic effects, the argument of whether these novel drugs will reduce AF burden is unsettled and mandates appropriately designed and adequately sized randomized controlled studies.

Invasive hemodynamic monitoring with Swan-Ganz catheterization to guide treatment decisions in heart failure may be hazardous and may lack prognostic value. We assessed the clinical utility of B-type natriuretic peptide (BNP) in estimating left ventricular filling pressures in patients with inconclusive tissue Doppler indexes. In this study, 50 patients with systolic heart failure and an early transmitral velocity to early diastolic mitral annular velocity ratio (E/Ea) between 8 and 15 were studied. Among them, 25 had been admitted for acutely decompensated heart failure (group A) and the remainder were clinically stable outpatients (group B). All patients underwent simultaneous invasive pulmonary capillary wedge pressure (PCWP) determination, BNP measurement, and echocardiography. In group A, BNP correlated with PCWP ( r = 0.803, P < 0.001), deceleration time (DT, r = −0.602, p = 0.001), and end-systolic wall stress (SWS, r = 0.565, P = 0.003). In multivariate analysis, BNP was the only parameter independently associated with PCWP ( P = 0.023). In group B, no correlation was found between BNP and PCWP or SWS, while DT correlated significantly with both PCWP ( r = −0.817, P < 0.001) and BNP ( r = −0.8, P < 0.001). We conclude that BNP may be a useful noninvasive tool for the assessment of left ventricular filling pressures in patients with acutely decompensated heart failure and inconclusive tissue Doppler indexes.

BackgroundEvidence shows that the soluble tumour necrosis factor-related apoptosis-inducing ligand (sTRAIL) may play a protective role against atherosclerosis. This study sought to investigate the potential association of sTRAIL levels with intravascular ultrasound (IVUS) and virtual histology characteristics of coronary plaques.MethodsPatients with stable angina or positive for ischaemia non-invasive test were submitted to left cardiac catheterisation. Coronary blood samples were collected and sTRAIL was measured. Coronary arteries with at least one 50% or greater stenosis were studied with IVUS.Results56 coronary arteries were studied with significant coronary artery disease. Plaque volume per unit of arterial length was 63±5 mm3/cm in arteries at the lower quartile of sTRAIL concentration versus 30±4 mm3/cm at the upper quartile (p<0.001; 95% CI of the difference 19.7 to 46.3 mm3/cm). The necrotic core and fibrofatty content of atheromatous plaques were inversely associated with sTRAIL (p<0.001). Thin-cap fibroatheromas (TCFA) were discovered in 16 of the 56 arterial segments. The mean sTRAIL concentration in these segments was 56.8±7.5 pg/ml versus 99.9±5.7 pg/ml in those without TCFA (p<0.001; 95% CI of the difference 22.7 to 63.5 pg/ml). The association of sTRAIL with the presence of TCFA remained significant in the logistic multivariate analysis (p=0.009).ConclusionAccording to the findings of the present study, in addition to coronary artery disease burden, the sTRAIL concentration is also related to the composition of atheromatous plaques. A significant association is demonstrated between low sTRAIL levels and the presence of TCFA, the IVUS–virtual histology prototype of the vulnerable plaque.

In 2020, SARS-COV-2 put health systems under unprecedented resource and manpower pressure leading to significant number of deaths. Expectedly, researchers sought to shed light on the pathophysiologic background of this novel disease (COVID-19) as well as to facilitate the design of effective therapeutic modalities. Indeed, early enough the pivotal role of inflammatory and thrombotic pathways in SARS-COV-2 infection has been illustrated. The purpose of this article is to briefly present the epidemiologic and clinical features of COVID-19, analyze the pathophysiologic importance of immunologic dysregulation and hypercoagulability in developing disease complications and finally to present an up-to-date systematic review of colchicine’s immunomodulating capacity in view of hindering coronavirus complications.