Fariña, Juliana

Abstract Background Sodium-glucose cotransporter 2 inhibitors (SGLT2-Is) have emerged as a vital component in the management of heart failure (HF), demonstrating significant improvements in cardiac function. However, their impact on outcomes in patients with acute myocardial infarction (AMI) remains poorly characterized. This study aimed to evaluate the long-term outcomes of SGLT2-Is among patients with AMI. Methods We conducted a retrospective cohort study using data from the TriNetX Banner Health Network platform in the United States, including patients aged ≥18 years with AMI identified through ICD-10 codes. Patients were categorized into two cohorts based on SGLT2-I use. Propensity score matching (PSM) was performed to balance baseline demographics, comorbidities (e.g., hypertension, diabetes, chronic kidney disease, heart failure, and hyperlipidemia), and medication use (e.g., heart failure therapies, antiplatelet agents, anticoagulants). Risk ratios (RRs) and 95% confidence intervals (95% CIs) were estimated for the following cardiovascular outcomes: acute HF hospitalizations, stroke, all-cause hospitalizations, recurrent AMI, cardiac arrest, and new-onset atrial fibrillation (AF). Kaplan-Meier analysis was completed to estimate survival probability from all-cause hospitalizations. Results After PSM, 2,440 patients were analyzed (1,220 SGLT2-I users; 1,220 non-users). Both cohorts had similar characteristics without any residual imbalance: mean age 67.7 years in the SGLT2-I group vs. 67.5 years in non-users, and both groups included 85.2% White and 33.6% female patients. Mean follow-up duration was 608 days for SGLT2-I users and 1,013.5 days for non-users. SGLT2-I use was associated with significantly lower rates of all-cause hospitalizations (RR: 0.712; 95% CI: 0.652–0.777), HF-related hospitalizations (RR: 0.878; 95% CI: 0.781–0.987), recurrent AMI (RR: 0.821; 95% CI: 0.703–0.959), and cardiac arrest (RR: 0.500; 95% CI: 0.345–0.725). No significant differences were observed in stroke (RR: 0.909; 95% CI: 0.702–1.178) or new-onset AF (RR: 0.889; 95% CI: 0.782–1.010) between the cohorts. Conclusions SGLT2-Is are associated with improved cardiovascular outcomes in patients with AMI, including reductions in all-cause and HF-related hospitalizations, recurrent AMI, and cardiac arrest. While these findings are hypothesis-generating, they emphasize the need for prospective clinical trials to confirm these results.Kaplan-Meier Analysis.

Abstract Introduction Lipoprotein(a) [Lp(a)] is associated with an increased incidence of aortic stenosis. Bioprosthetic aortic valve degeneration and native aortic stenosis share similar pathological mechanisms. Evidence regarding the role of serum Lp(a) concentrations in bioprosthetic aortic valve degeneration is lacking. Purpose To evaluate the association between serum Lp(a) concentrations and bioprosthetic aortic valve degeneration. Methods In this retrospective multicenter study, consecutive patients who underwent a bioprosthetic aortic valve replacement between Jan-2010 and Dec-2020 and had a preoperatory serum Lp(a) measurement were included. A baseline transthoracic echocardiography (TTE) was performed following the aortic valve replacement and a follow-up TTE was performed at least 24 months after the baseline study to determine the presence of bioprosthetic valve degeneration. Significant degeneration was defined as: (a) an increase >10 mmHg in mean bioprosthetic aortic valve gradient from baseline status + a decrease in effective orifice area + a decrease in Doppler velocity index + exclusion of clinically thrombotic leaflet thickening, OR (b) new moderate or severe prosthetic aortic regurgitation (if the main component was periprosthetic, then it was not considered). Lp(a) concentrations were compared between patients with and without degeneration and regression analysis was conducted to investigate the association between bioprosthetic valve degeneration and Lp(a) levels. Results In total, 211 cases were included (mean age 74.1 ±9.4 years, 72.0% males, 29.9% transcatheter aortic valve replacements) (Figure 1). Median time between baseline and follow-up TTE was 5.0 (IQR 3.7) years. Bioprostheses degeneration was observed in 33 (15.6%) patients at follow-up. Median serum levels of Lp(a) were significantly higher in the patients affected by degeneration versus non-affected cases (50.0 vs 15.7 mg/dl, p=0.003). In the regression analysis, high Lp(a) levels (≥30 mg/dl) were associated with degeneration both in a univariate analysis (OR 4.8, 95%CI 2.2-10.9, p<0.001) and multivariate analysis adjusted by other risk factors for bioprostheses degeneration (age, sex, hypertension, smoking, patient prosthesis mismatch, creatinine levels, and body surface area) (OR 5.2, 95%CI 2.1-12.8, p<0.001). Conclusion Serum Lp(a) concentrations seem to be a risk factor for bioprosthetic aortic valve degeneration (Figure 2). There is an increasing need to accurately predict bioprosthetic aortic valve degeneration and to develop novel methods and treatments to increase their durability. Prospective studies are needed to confirm these findings and to investigate whether lowering Lp(a) could slow bioprostheses degradation.Population characteristicsLp(a) and bioprostheses degeneration

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<0.001). Implantable cardioverter defibrillators were implanted more in HF patients with syncope (15.6% versus 8.3%, p<0.001) as well as pacemakers (16.9% versus 7.5%, p<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<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.