Citations

Abstract Introduction During the Coronavirus (COVID‐19) pandemic, healthcare providers have overcome difficult experiences such as workplace violence. Nurses are particularly vulnerable to workplace violence. The objective of this study was to characterize violence and aggression against nurses during the COVID‐19 pandemic in Latin America. Methods An electronic cross‐sectional survey was conducted in 19 Latin American countries to characterize the frequency and type of violent actions against front‐line healthcare providers. Results Of the original 3544 respondents, 16% were nurses ( n = 567). The mean age was 39.7 ± 9.0 years and 79.6% ( n = 2821) were women. In total, 69.8% ( n = 2474) worked in public hospitals and 81.1% ( n = 2874) reported working regularly with COVID‐19 patients. Overall, about 68.6% ( n = 2431) of nurses experienced at least one episode of workplace aggression during the pandemic. Nurses experienced weekly aggressions more frequently than other healthcare providers (45.5% versus 38.1%, p < .007). Nurses showed a trend of lower reporting rates against the acts of aggression suffered ( p = .076). In addition, nurses were more likely to experience negative cognitive symptoms after aggressive acts (33.4% versus 27.8%, p = .028). However, nurses reported considering changing their work tasks less frequently compared to other healthcare providers after an assault event ( p = .005). Conclusion Workplace violence has been a frequent problem for all healthcare providers during COVID‐19 pandemic in Latin America. Nurses were a particularly vulnerable subgroup, with higher rates of aggressions and cognitive symptoms and lower rate of complaints than other healthcare providers who suffered from workplace violence. It is imperative to develop strategies to protect this vulnerable group from aggressions during their tasks.

Cardiac structural and valve interventions have remained surgical procedures for several decades. The ability to directly visualize the region of interest during surgery made imaging of these structures pre- and postsurgery a secondary tool to compliment surgical visualization. The last two decades, however, have seen rapid advances in catheter-based percutaneous structural heart interventions (SHIs). Due to the “blind” nature of these interventions, imaging plays a crucial role in the success of these procedures. Fluoroscopy is used universally in all percutaneous cardiac SHIs and helps primarily in the visualization of catheters and devices. However, success of these procedures requires visualization of intracardiac soft tissue structures. Due to its portable nature and rapid ability to show cardiac structures online, transesophageal echocardiography (TEE) has become an integral tool for guidance for all percutaneous SHI. Transcatheter aortic valve replacement—one of the earliest catheter-based procedures—while initially dependent on TEE, has largely been replaced by preprocedural cardiac CT for accurate assessment of valve sizing. Developments in echocardiography now allow live three-dimensional (3D) visualization of cardiac structures mimicking surgical anatomy during TEE. Besides showing actual 3D intracardiac structures, 3D-TEE allows visualization of the interaction of intracardiac catheters and devices with soft tissue cardiac structures, thereby becoming a “second pair of eyes” for the operator. Real-time 3D-TEE now plays an important role complementing multiplane two dimensional and biplane TEE during such interventions. In this review, we discuss the incremental role of 3D-TEE during various SHIs performed today.

Objectives Lipoprotein(a) (Lp(a)) is associated with an increased incidence of native aortic stenosis, which shares similar pathological mechanisms with bioprosthetic aortic valve (bAV) degeneration. However, evidence regarding the role of Lp(a) concentrations in bAV degeneration is lacking. This study aims to evaluate the association between Lp(a) concentrations and bAV degeneration. Methods In this retrospective multicentre study, patients who underwent a bAV replacement between 1 January 2010 and 31 December 2020 and had a Lp(a) measurement were included. Echocardiography follow-up was performed to determine the presence of bioprosthetic valve degeneration, which was defined as an increase >10 mm Hg in mean gradient from baseline with concomitant decrease in effective orifice area and Doppler Velocity Index, or new moderate/severe prosthetic regurgitation. Levels of Lp(a) were compared between patients with and without degeneration and Cox regression analysis was performed to investigate the association between Lp(a) levels and bioprosthetic valve degeneration. Results In total, 210 cases were included (mean age 74.1±9.4 years, 72.4% males). Median time between baseline and follow-up echocardiography was 4.4 (IQR 3.7) years. Bioprostheses degeneration was observed in 33 (15.7%) patients at follow-up. Median serum levels of Lp(a) were significantly higher in patients affected by degeneration versus non-affected cases: 50.0 (IQR 72.0) vs 15.6 (IQR 48.6) mg/dL, p=0.002. In the regression analysis, high Lp(a) levels (≥30 mg/dL) were associated with degeneration both in a univariable analysis (HR 3.6, 95% CI 1.7 to 7.6, p=0.001) and multivariable analysis adjusted by other risk factors for bioprostheses degeneration (HR 4.4, 95% CI 1.9 to 10.4, p=0.001). Conclusions High serum Lp(a) is associated with bAV degeneration. Prospective studies are needed to confirm these findings and to investigate whether lowering Lp(a) levels could slow bioprostheses degradation.

Lipoprotein(a) [Lp(a)] is a lipid molecule with atherogenic, inflammatory, thrombotic, and antifibrinolytic effects, whose concentrations are predominantly genetically determined. The association between Lp(a) and cardiovascular diseases (CVDs) has been well-established in numerous studies, and the ability to measure Lp(a) levels is widely available in the community. As such, there has been increasing interest in Lp(a) as a therapeutic target for the prevention of CVD. The impact of the currently available lipid-modifying agents on Lp(a) is modest and heterogeneous, except for the monoclonal antibody proprotein convertase subtilisin/kexin type 9 inhibitors (PCSK9i), which demonstrated a significant reduction in Lp(a) levels. However, the absolute reduction in Lp(a) to significantly decrease CVD outcomes has not been definitely established, and the magnitude of the effect of PCSK9i seems insufficient to directly reduce the Lp(a)-related CVD risk. Therefore, emerging therapies are being developed that specifically aim to lower Lp(a) levels and the risk of CVD, including RNA interference (RNAi) agents, which have the capacity for temporary and reversible downregulation of gene expression. This review article aims to summarize the effects of Lp(a) on CVD and to evaluate the available evidence on established and emerging therapies targeting Lp(a) levels, focusing on the potential reduction of CVD risk attributable to Lp(a) concentrations.

Abstract Funding Acknowledgements Type of funding sources: Private hospital(s). Main funding source(s): Mayo Clinic Background/Introduction Syncope is a common presentation in heart failure (HF) patients. However, the associations between syncope and prognosis in HF patients with the cardiac implantable electronic device (CIED) have not been demonstrated. It is unclear whether syncope increases all-cause mortality in HF patients with CIED. Purpose We aimed to examine the association between syncope and all-cause mortality in the largest cohort of HF with reduced ejection fraction (HFrEF), mid-ranged ejection fraction (HFmEF), and preserved ejection fraction (HFpEF) patients with and without CIED. Methods A retrospective cohort of patients with HF and syncope at our hospital between 2010 and 2015 were identified, and 1:1 propensity was matched with a control group of HF patients without syncope. A chart review was conducted. The multivariate Cox regression model was applied to estimate the association between syncope and the all-cause mortality endpoint. Results 3,449 HF patients were diagnosed with syncope (mean age, 72.8±14.5 years; 41.5% women), and the propensity-matched control HF patients without syncope (n=3,449) aged 72.8±14.3 years, and 42.5% women were selected. Cardiac implantable electronic devices were implanted more in HF patients with syncope (32.5% versus 13.7%, p&lt;0.001). Implantable cardioverter defibrillators were implanted more in HF patients with syncope (15.6% versus 8.3%, p&lt;0.001) as well as pacemakers (16.9% versus 7.5%, p&lt;0.001) and cardiac resynchronization therapy devices (6.9% versus 4.8%, p=0.015). Among HF patients with CIED, syncope significantly increased the risk of all-cause mortality in HFrEF patients (hazard ratio [HR]=1.479, 95% confidence interval [CI]: 1.197-1.828, p&lt;0.001) but not in HFpEF (HR=0.980, 95%CI: 0.793-1.210, p=0.849)(Figure 1). Syncope also tended to increase the risk of all-cause mortality in HFmEF patients with CIED but was not significant (HR=1.193, 95%CI: 0.762-1.865, p=0.762)(Figure 1). Among HF patients without CIED, syncope did not increase the risk of all-cause mortality in HFrEF (HR=0.923, 95%CI: 0.806-1.057, p=0.247), HFmEF (HR=1.074, 95%CI: 0.848-1.360, p=0.554), or HFpEF (HR=0.964, 95%CI: 0.883-1.052, p=0.406). Conclusions Syncope significantly increased the risk of all-cause mortality in HFrEF patients but not in HFmEF or HFpEF patients with CIED. The association of syncope and increased mortality in HFrEF patients with CIED suggests that syncope may be a marker and a factor of mortality and warrants further investigation.

AbstractBackgroundAortic stenosis (AS) is associated with myocardial ischemia through different mechanisms and may impair coronary arterial flow. However, data on the impact of moderate AS in patients with acute myocardial infarction (MI) is limited.AimsThis study aimed to investigate the impact of moderate AS in patients presenting with acute myocardial infarction (MI).MethodsWe conducted a retrospective analysis of all patients who presented with acute MI to all Mayo Clinic hospitals, using the Enterprise Mayo PCI Database from 2005 to 2016. Patients were stratified into two groups: moderate AS and mild/no AS. The primary outcome was all cause mortality.ResultsThe moderate AS group included 183 (13.3%) patients, and the mild/no AS group included 1190 (86.7%) patients. During hospitalization, there was no difference between both groups in mortality. Patients with moderate AS had higher in‐hospital congestive heart failure (CHF) (8.2% vs. 4.4%, p = 0.025) compared with mild/no AS patients. At 1‐year follow‐up, patients with moderate AS had higher mortality (23.9% vs. 8.1%, p < 0.001) and higher CHF hospitalization (8.3% vs. 3.7%, p = 0.028). In multivariate analysis, moderate AS was associated with higher mortality at 1‐year (odds ratio 2.4, 95% confidence interval [1.4–4.1], p = 0.002). In subgroup analyses, moderate AS increased all‐cause mortality in STEMI and NSTEMI patients.ConclusionThe presence of moderate AS in acute MI patients was associated with worse clinical outcomes during hospitalization and at 1‐year follow‐up. These unfavorable outcomes highlight the need for a close follow‐up of these patients and for timely therapeutic strategies to best manage these coexisting conditions.