Background: Severe mitral regurgitation (MR) in cardiogenic shock (CS) presents unique therapeutic challenges, especially in patients with prohibitive surgical risk. Transcatheter edge-to-edge repair (TEER) with MitraClip offers a less invasive alternative, yet optimal strategies for hemodynamic support in this setting remain unclear. Methods: We conducted a retrospective study of patients undergoing MitraClip implantation for severe MR and CS between 2018 and 2024 at a tertiary academic center. Of 440 screened cases, 47 met CS criteria and were stratified based on receipt of periprocedural Impella support. Clinical, procedural, and survival outcomes were compared between Impella-supported and unsupported cohorts using appropriate statistical methods. Results: Among the 47 patients, 24 received Impella support and 23 did not. The Impella group had greater illness severity, including higher rates of preprocedural intubation (75.0% vs. 43.5%) and SCAI stage D shock (50.0% vs. 13.0%). Despite these differences, procedural success was 100% in both groups. In-hospital (8.3% vs. 8.7%), 30-day (12.5% vs. 8.7%), and 1-year mortality (25.0% vs. 26.0%) were similar between Impella and non-Impella patients, respectively. Impella recipients had longer hospital stays (median 18 vs. 11 days; p=0.032) and higher 1-year readmission rates (55.0% vs. 21.7%; p=0.024), reflecting baseline acuity. There were no differences in major procedural complications or re-intervention rates. Conclusions: MitraClip implantation in CS patients supported with Impella is feasible and safe. Despite significantly worse hemodynamic profiles, outcomes were comparable to those without mechanical support. These findings suggest a potential role for tailored Impella use in expanding TEER to critically ill patients and underscore the need for prospective studies to guide support strategies in high-risk MR intervention.
Abstract 4345595: Five-Year Outcomes of Glucagon-Like Peptide-1 Agonists in Obstructive Hypertrophic Cardiomyopathy: A Population-Based Retrospective Study
Background: Glucagon-like peptide-1 (GLP-1) agonists have been shown to improve outcomes across various cardiovascular diseases. However, data regarding the effects of GLP-1 agonists in obstructive hypertrophic cardiomyopathy (HCM) is limited. Objective: This study aimed to evaluate the 5-year outcomes of GLP-1 agonists in patients with HCM. Methods: Using TriNetX Analytics Network, we identified patients aged ≥18 years with a diagnosis of obstructive hypertrophic cardiomyopathy between 1/1/2014 and 1/1/2019. Patients were divided into two groups: those treated with GLP-1 agonists for ≥ 1 year and those who were not. Propensity score matching (PSM) was performed using demographics, cardiac medications, and comorbidities. The study outcomes were 5-year all-cause mortality and cardiac adverse events. Results: A total of 52,978 patients with HCM were identified, including 2,654 (5.0%) patients treated with GLP-1 agonists. After PSM, 2,588 patients in each group were analyzed. Patients on GLP-1 agonists were associated with lower odds of all-cause mortality (5.0% vs. 15.6%, p<0.01), all-cause hospitalization (46.3% vs. 67.8%, p<0.01), acute decompensated heart failure ((9.4% vs. 21.4%, p<0.01), cardiac arrest (3.6% vs. 5.4%, p<0.01), cerebrovascular accidents (9.5% vs. 14.1%, p<0.01), and cardiogenic shock (1.4% vs. 3.6%, p<0.01). Additionally, reduced rates of new ICD implantation (3.5% vs. 7.9%, p<0.01) and septal reduction therapy (1.7% vs. 3.5%, p<0.01) were observed in the GLP-1 agonists group. Conclusion: The use of GLP-1 agonists in HCM was associated with improved cardiovascular outcomes. Future clinical trials are needed to validate these potential benefits.
The relative risk of ischemic cerebrovascular accident in patients with Von Willebrand disease
Cerebrovascular accident (CVA) is one of the leading causes of death in the United States. Von Willebrand factor plays an important role in platelet activation and adhesion. It remains unclear whether Von Willebrand disease (vWD) is associated with a decreased risk of developing CVA. The study aimed to compare the relative risk (RR) of CVA in patients with and without vWD. We queried the National Inpatient Sample from 2009 to 2014 for discharge data and records for vWD and CVA using International Classification of Diseases, Ninth-Revision codes. The unadjusted and adjusted RR of CVA in patients with and without vWD were estimated using log-binomial model. Descriptive measures including means, medians, standard deviations, and range were presented based on normality test of continuous data. The prevalence of CVA was lower in patients with vWD than in those without vWD (1.31% vs 2.04%), with a RR of 0.64 (95% confidence interval (CI): 0.60–0.68). After adjusting for common CVA risk factors, the RR remained lower in vWD patients: 0.81 (95% CI: 0.76–0.86). vWD is associated with a lower RR of developing CVA. This suggests that deficiency of Von Willebrand factor is potentially protective against the development of CVA. To the best of our knowledge, this is the first study in humans to compare the RR of CVA in patients with and without vWD. Future studies are needed to explore causal relationships and therapeutic benefits.