Citations

Background: Cardiac arrest is a major global health concern, contributing significantly to mortality rates. While conventional cardiopulmonary resuscitation (CPR) has long been the standard care approach, emerging research indicates that extracorporeal cardiopulmonary resuscitation (ECPR) may provide superior survival advantages. Studies suggest that timely application of ECPR can lead to improved outcomes, particularly in terms of survival rates and neurological recovery. The comparative efficacy of ECPR is further corroborated by various randomized controlled trials (RCTs), as well as retrospective and prospective studies. Search Methods: We conducted a comprehensive search of databases including PubMed, Google Scholar, Cochrane Library, PLOS One, ClinicalTrials.gov, and ScienceDirect from 2014 to 2025. Our analysis included 3 RCTs, 3 prospective, and 5 retrospective studies (n=154,216). Inclusion criteria involved patients undergoing cardiac arrest managed in inpatient or outpatient settings. Meta-analysis was performed using Review Manager (RevMan) version 5.4, calculating safety endpoints as odds ratios for ROSC, favorable neurological outcomes , and survival rates. Results: Findings indicated that ECPR was associated with a significantly higher rates of ROSC (OR 0.36, 95% CI [0.24–0.54], p<0.00001) and favorable neurological outcome (OR 0.47 , 95% CI [0.37–0.60], p<0.00001). The Survival at 6 months was significantly better in the ECPR group (OR 0.21, 95% CI [0.12–0.36], p<0.00001). Although CCPR showed higher odds for survival to ICU (OR 1.31, 95% CI [0.86–2.00], p=0.21) and discharge (OR 1.42, 95% CI [0.90–2.25], p=0.13), these did not reach statistical significance. Conclusion: ECPR shows improved ROSC and neurological outcomes over conventional CPR, with higher six-month survival rates, emphasizing the need to adopt ECPR in cardiac arrest management.

Background: Cardiac disease is the leading cause of premature mortality in Friedreich Ataxia (FA). However, validated prognostic indicators or early imaging biomarkers that can reliably predict cardiac events are lacking. To address this gap, we created a multicenter FA cardiac registry to characterize disease progression and identify early echocardiographic (echo) predictors of major adverse cardiac events (MACE). Methods: FA subjects from 6 North American centers with at least two echos performed ≥5 years apart were included. Demographics, FA-specific disease characteristics, and MACE (a composite of death, heart failure hospitalization, aborted sudden cardiac death, and/or life-threatening arrhythmia) were abstracted. Digital echo images were re-read at a centralized core lab. Paired T tests were utilized for comparison of the normally distributed first and second echo parameters, and logistic regression models were utilized to evaluate for predictors of MACE. Results: Of 115 subjects, 52 (45%) were female. Mean age at diagnosis was 10 ± 3 years, median GAA1 repeat length (a marker of genetic severity) was 700 (range 66–1200), and median age at first analyzed echo was 12 years (range 4-36). MACE occurred in 35 (30%) of the cohort. Serial echocardiograms demonstrated progressive worsening of multiple cardiac parameters over time, including markers of ventricular thickness and hypertrophy, chamber size, systolic function, and novel markers of atrial and ventricular strain (Table 1). On univariate analysis, several markers of hypertrophy and systolic function from the earliest analyzed echo predicted MACE. However, after adjusting for age of diagnosis, GAA1 repeat length, and collinearity among variables, only posterior wall thickness in diastole (PWTd) remained an independent predictor of MACE (odds ratio 1.8 per mm increase, 95% CI 1.1–3.3, p = 0.028). Conclusions: This multicenter FA registry identifies early posterior wall thickness as a significant and independent predictor of major adverse cardiac events in FA. Each millimeter increase in PWTd on early echo is associated with nearly double the odds of MACE. This commonly acquired parameter is often overlooked and may serve as a powerful early marker of cardiac risk. Further investigation of PWTd as a potential surrogate endpoint for therapeutic trials in FA is warranted.

Background: Adults with congenital heart disease (CHD) face ongoing physical, emotional, and psychosocial challenges that impact long-term outcomes. Research is limited on how their health topic interests vary by levels of empowerment. The 15-item Gothenburg Empowerment Scale (GES) assesses CHD patient empowerment across five domains. Objective: Examine the association between patient empowerment levels and patient-prioritized health education topics among adults with CHD. Methods: This cross-sectional study included adults (≥18) with self-reported CHD enrolled in the Empower My Congenital Heart digital study. Participants completed the GES survey and responded to open-ended questions regarding information of interest to them in managing their healthcare. GES scores were divided into tertiles, and responses were grouped into patient-prioritized topics. Descriptive analysis examined associations between empowerment levels and topic preferences. Results: Of 292 eligible patients, mean age was 45.6 ± 14.7 years, 91.4% were Caucasian, and 66.4% were female. The median (25th, 75th) GES score was 62 (57, 68). The most frequently observed patient prioritized topic was CHD health knowledge (73%), followed by interest in building CHD community (52.7%), lifestyle management (23.6%), health care navigation (7.2%), research and representation (5.1%). Participants in the lower and middle GES tertiles more frequently expressed interest in foundational sub-topics such as understanding CHD and surgical history, finding ACHD specialists, exercise and nutrition. In contrast, participants in the highest GES tertile prioritized sub-topics related to aging with CHD, managing menopause, CHD research and legislative activities. Peer support was a common topic across all groups (Figure 1). Patient quotes were stratified by tertile and patient prioritized health topics and subtopics as summarized in table 1. Conclusion: Adults with CHD prioritized varied health education topics depending on their baseline empowerment levels. Those with lower GES scores prioritized foundational information and guidance, while those with higher scores prioritized community-oriented and research-related topics. These findings could help tailor CHD patient-centered education strategies based on individual empowerment profiles.

Background: Kounis syndrome (allergic angina syndrome) is triggered commonly by drugs, insect bites and even ice cream, causing myocardial infarction (MI). Treating this with the typical acute coronary syndrome (ACS) protocol may be clinically detrimental. We present a case of suspected type 2 Kounis syndrome in a low-resource setting. Case Description: A 45-year-old man presented to the emergency room with chest pain for the past 6 hours. He had history of multiple bee stings 14 hours ago. Review of systems was negative for rash, dizziness, palpitations or shortness of breath. He was a chronic smoker and alcoholic with no comorbidities and no history of allergies. He was conscious, oriented and his vitals were stable. ECG showed ST segment elevation in leads II, III and aVF (Figure 1). Echocardiogram showed mild left ventricular systolic dysfunction. Acute inferior wall MI and Kounis syndrome were suspected, and he was treated with routine ACS protocol, steroids and anti-histaminics. Coronary angiography showed mild, clinically insignificant atherosclerotic changes in the proximal right coronary artery (Figure 2), but absence of thrombus occluding the vessel. Patient was admitted in the cardiac intensive care unit and recovered well. Discussion: Common triggers for Kounis are antibiotics and insect bites. Insect venom contains phospholipase A2&5-HT, which can be allergic or directly toxic to cardiac tissue. They activate mast cells and induce vasospasm, leading to acute MI. Most patients present immediately with anaphylaxis and ACS, but some, like our patient, present with delayed, subclinical symptoms, presenting a diagnostic challenge. Tryptase and IgE levels as diagnostic tools are still under investigation considering the short half-life and lack of sensitivity respectively, and non-availability in low-resource settings. A therapeutic oxymoron has been described - the need for systemic vasoconstrictors and myocardial vasodilators. This warrants cautious use of beta blockers and epinephrine. The use of steroids and antihistaminics are under evaluation. A consensus is yet to be reached regarding diagnosis and treatment guidelines. Conclusion: Kounis syndrome must be considered high on differential in a case of acute MI if supporting history is positive. More research needs to be done on the long-term outcomes of the empiric treatment of suspected Kounis syndrome in low-resource settings, where advanced diagnostic tests are unavailable.

Background: We have previously reported that Sorbs2 (sorbin and SH3 domain 2) knockout mice have significant cardiac structural and electrical remodeling, including atrial enlargement and fibrosis. The mechanisms of such changes were unknown. Hypothesis: We hypothesized that loss of Sorbs2 in cardiac fibroblasts promotes profibrotic signaling pathways and alters the balance between matrix metalloproteinases (MMPs), and their inhibitors (TIMPs) resulting in excessive collagen deposition in the atria. Methods: We used Sorbs2 global knockout ( Sorbs2 KO) mice and age-matched wild-type (WT) controls at 4 to 5 months of age. Left atrial fibrosis was quantitated by Masson's trichrome staining in serial sections. Scratch wound healing assays and transwell migration assays were performed in isolated Sorbs2 KO and WT atrial fibroblasts. Protein expression was determined by Western blots. Interleukin-6 (IL-6) production in cultured fibroblast supernatants was measured by ELISA. Results: Sorbs2 KO mice showed significant increase in atrial diameter (16.6 ± 1.5 mm vs 12.0 ± 1.1 mm in WT; n=3, p < 0.05) and atrial fibrosis (fraction of fibrotic areas: 18.6± 2.9 % vs. 7.6 ± 0.9 % in WT; p < 0.01). Collagen 1 and collagen 3 protein levels in Sorbs2 KO mouse atria were 1.8-fold and 1.7-fold higher than those of WT respectively. Sorbs2 KO atrial fibroblasts showed impaired function with significantly reduced migration and slower scratch-wound closure (migration area after 24h: 18.5 ± 3.8 % vs 70.1 ± 6.7 % in WT; n=6, p < 0.01).Moreover, transforming growth factor β1 (TGF-β1), α-smooth muscle actin, and periostin expression levels were significantly reduced in isolated fibroblasts and atrial myocardia from Sorbs2 KO mice, suggesting that fibrosis is not caused by TGF-b1-dependent mechanisms or from myofibroblast transformation. Analysis of ECM proteins showed significant downregulation of MMP1 and MMP3 but upregulation of TIMP1, while TIMP3 was unchanged. Consistent with a pro-inflammatory phenotype, Sorbs2 KO atrial fibroblasts secreted higher IL-6 levels at baseline (3303± 463 pg/mL vs. 2075 ± 731 pg/mL in WT; n=6, p < 0.01) and with LPS stimulation (7791 ± 604 pg/mL vs. 5588 ± 763 pg/mL in WT; n=6, p < 0.01). Conclusion: Sorbs2 deficiency is associated with abnormal atrial fibroblast function showing impaired migration and scratch wound healing, as well as increased IL-6 production and imbalanced MMP/TIMP. These changes result in collagen accumulation and enhanced fibrosis.

Background: Valve-in-valve transcatheter aortic valve replacement (ViV-TAVR) is an increasingly preferred strategy for managing failed surgical bioprosthetic valves, especially in high-risk patients. However, limited data exist comparing outcomes between balloon-expandable (BE) and self-expandable (SE) transcatheter heart valves (THVs) in this setting. The influence of aortic annular area on outcomes by valve type remains poorly understood. This study evaluated the impact of annular area on clinical outcomes following ViV-TAVR with BE vs. SE valves. Methods: We conducted a retrospective, single-center analysis of 353 patients who underwent ViV-TAVR between 2012 and 2024. All had prior surgical bioprosthetic AVR and received either BE (n=267) or SE (n=86) valves. Preprocedural multidetector CT was used to quantify aortic annular area. Transthoracic echocardiography was performed before and after the procedure to assess transvalvular gradients and hemodynamics. The primary endpoint was all-cause mortality. Penalized spline regression was used to model the nonlinear relationship between annular area and mortality and assess interaction by valve type. Results: Median age was 79 (IQR: 72–83) in the BE group and 80 (IQR: 76–85) in the SE group (p=0.07). Female sex was more common in the SE group (32% vs. 22%, p=0.047). Median annular area was 374 mm2 (IQR: 316–440) for BE and 365 mm2 (IQR: 308–432) for SE (p=0.081). Preprocedural gradient and effective orifice area index were 36 mm Hg (IQR: 28–46) and 0.6 cm2/m2 (IQR: 0.5–0.9), respectively, with no significant differences. Median hospital stay was 2 vs. 3 days (p=0.68). Thirty-day mortality was low (1 per group, p=0.36). Median follow-up was 4.0 years (IQR: 1.6–6.4). One- and 5-year survival rates were 94.75% and 61.7%, respectively (p=0.20). Penalized spline analysis showed a nonlinear association between annular area and mortality. The hazard ratio for BE valves declined with increasing annular area and fell below SE valves beyond ~400 mm2. Conclusion: ViV-TAVR is a safe and effective treatment for failed surgical bioprostheses. Smaller annular areas were associated with higher mortality. Outcomes with BE valves improved in larger annuli, suggesting annular area could guide valve selection. Further studies are warranted to validate these observations.

Background: Lung cancer is classified into small cell lung cancer (SCLC) and non-small cell lung cancer (NSCLC – including adenocarcinoma, squamous cell, and large cell carcinoma). The incidence of major adverse cardiovascular events (MACE)—defined as acute myocardial infarction, acute coronary syndrome/ischemic heart disease requiring revascularization, stroke, and cardiovascular death—have not been well defined in lung cancer patients following treatment. Coronary artery calcifications (CAC) and aortic calcifications (CA) are known cardiovascular risk markers in non-cancer populations. Purpose: To determine whether the presence of CAC or CA, as identified on baseline PET-CT (Positron Emission Tomography–Computed Tomography) or chest CT imaging, is predictive of MACE and all-cause mortality (ACM) in patients with lung cancer. Methods: We conducted a retrospective cohort study of patients diagnosed with SCLC or NSCLC who received chemotherapy, between January 1, 2010, and December 31, 2024. The baseline PET-CT or chest CT scans were reviewed for the presence of CAC and/or CA. Patients were excluded if they lacked baseline imaging or had experienced a MACE before treatment. Univariate and multivariate adjusted Cox regression models were employed to assess associations between CAC/CA and MACE or ACM. The Kaplan-Meier survival analyses was performed to evaluate event-free survival. Results: A total of 385 patients were included (mean age: 74 years, IQR: 67–79), predominantly female (158 [55%]) and white (279 [96.2%]). NSCLC was found in 255 (88%) and SCLC in 35 (12%). CAC was identified in 172 (60%) and CA in 87 (30%). Among patients with NSCLC, the presence of CAC was significantly associated with MACE (HR: 2.84 [95% CI: 1.6–4.8], p=0.0001) (Fig. a), particularly in those with adenocarcinoma (Fig. b). In SCLC, (HR: 1.56 [95% CI: 0.1–14.0], p=ns). On multivariable analysis, CAC remained the strongest predictor of MACE after adjusting for age, hypertension, diabetes, dyslipidemia, and smoking status (HR: 2.6 [95% CI: 1.5–4.4], p=0.0008) (Fig. d). No significant association was found between CA and MACE in either group (p>0.05). ACM was similar for SCLC, squamous cell, and NSCLC (Fig. c). Conclusion: In patients with NSCLC especially lung adenocarcinoma, the presence of CAC in the baseline PET/CT was an independent predictor of MACE. This finding supports the value of CAC as a non-invasive cardiovascular risk marker.

Background: Journal editors influence the visibility and direction of scientific research and should have adequate gender and geographic representation. Research Question: Are there disparities in gender and institutional country affiliation among editors of highly cited cardiology and cardiovascular disease journals? Methods: In May 2025, we used Scimago Journal Rankings to identify the 50 top-cited cardiology and cardiovascular disease journals worldwide from 2022 to 2024. Due to the large volume of members, general editorial board listings without defined roles were excluded. Editors’ genders and country of institutional affiliation were extracted independently and in duplicate by eight sub-investigators. An additional sub-investigator resolved any discrepancies. Gender was determined using institutional profiles and publicly available pronouns on academic or professional platforms. Country affiliation was based on the editor’s primary institution and categorized by World Bank income classification 2025, which divides countries into high-income (HIC), upper-middle income (UMIC), lower-middle income (LMIC), and low-income countries (LIC). Key journal characteristics, such as country, impact factor, and article processing charges, were also extracted in duplicate. Results: All 50 top-cited cardiology and cardiovascular disease journals identified were based in HICs. A total of 1,762 editors were included. Most editorial positions were held by men (67%), with women accounting for 28%. One editor was identified as non-binary, and the gender of 91 editors (5%) could not be determined based on publicly available information (Table 1). Pronouns were identifiable for all EIC (n=52), out of which 87% were men (n=45) and 13% were women (n=7). Ninety-five percent of editors were affiliated with institutions based in HIC, while only 5% were based in UMIC (n=71), LMIC (n=16), or LIC (n=5). The most represented countries were the US (41%), Italy (8%), and the UK (7%) (Figure 2). All EICs (100%) were affiliated with institutions based in HICs, mainly the US (52%) and the UK (10%) (Figure 3). Conclusion: Editors of top-cited cardiology journals are predominantly men affiliated with HICs. Diverse editorial leadership in academic cardiology journals is needed to reflect global perspectives in research.

Background: The growing epidemiologic burden of heart failure (HF) poses a significant public health challenge. The development of conduction abnormalities influences HF outcomes, with left bundle branch block (LBBB) established as an independent mortality predictor. However, the impact of right bundle branch block (RBBB) on HF mortality is still controversial. The aim of this study is to compare survival in HF patients with and without RBBB. Methods: A comprehensive search was conducted on PubMed, Scopus, Web of Science, and Cochrane Library from inception to 12 October 2024. Raw data coordinates were extracted from Kaplan–Meier curves and merged into one dataset to reconstruct individual patient data. Hazard ratios (HR) with 95% confidence intervals (CI) were estimated using the Cox regression model. Dichotomous outcomes were pooled as risk ratios (RR) with 95% confidence interval (CI) using a random-effects model. Results: 13 studies incorporating 25714 HF patients were included in our analysis. Patients with RBBB had a significantly lower median survival of 41.0 months (95% CI: 39.0 – 44.8) compared to 51.2 months (95% CI: 49.2 – 52.8) in patients without RBBB. Survival at 1,3, and 5 years in RBBB patients was 74.2%, 54.0%, and 39.4%, respectively, compared to 77.2%, 58.1%, and 45.4% in patients without RBBB. The HR for mortality was 0.87 (95% CI: 0.83 – 0.91, p < 0.001), indicating a 13% lower risk of death in patients without RBBB compared to those with RBBB. There was no significant difference in cardiovascular mortality between groups (RR: 1.34; 95% CI: 0.88 – 2.05; p = 0.17). Conclusion: RBBB was associated with an increased risk of mortality in HF patients. These findings support the use of RBBB as a potential marker for risk stratification in HF. Further research with stricter inclusion criteria is warranted to better understand how the observed association is influenced by preserved versus reduced ejection fraction.

Introduction: Semaglutide 2.4 mg has been shown to reduce the risk and severity of cardiometabolic comorbidities (CMCs) and to improve cardiometabolic biomarkers in patients with overweight or obesity in clinical trials. However, real-world evidence in these areas is limited. Research Question: This study compared the incidence rates of CMCs and 12-month changes in biomarkers between adults with overweight/obesity with and without once-weekly subcutaneous semaglutide 2.4 mg use. Methods: A retrospective cohort study using a large U.S. claims database linked with clinical data evaluated patients with semaglutide 2.4 mg use for ≥12 months (June 2021–June 2023) and those without. For each CMC, including hypertension, T2D, dyslipidemia, HF, prediabetes, ASCVD, and CVD, patients were excluded from analysis of each individual CMC if they had claims indicating the corresponding CMC during the 12-month baseline. For each biomarker, patients were required to have the corresponding biomarker measurements at both baseline and 12-month follow-up. For each CMC and biomarker, propensity score weighting was used to balance patient characteristics between semaglutide 2.4 mg users and non-users. Time to CMCs were compared using weighted Cox proportional hazards models and biomarker changes were compared using weighted linear regression. Results: Sample sizes ranged from 14,067 to 25,490 in semaglutide 2.4 mg users and 4,271,926 to 8,578,948 in non-users across CMCs. After balancing, baseline characteristics were similar between users and non-users. Mean age ranged from 44.4 to 47.2 years among users and 44.4 to 47.4 years among non-users; 77%–83% of users and 75%–82% of non-users were women. Compared to non-users, semaglutide 2.4 mg users had significantly lower risk of incident hypertension (Hazard ratio [HR]: 0.62, 95% confidence intervals [CI]: 0.57; 0.68), T2D (HR: 0.45, 95% CI: 0.39; 0.51), HF (HR: 0.48, 95% CI: 0.38; 0.61), prediabetes (HR: 0.75, 95% CI: 0.70; 0.80), ASCVD (HR: 0.65, 95% CI: 0.58; 0.72), and CVD (HR: 0.69, 95% CI: 0.64; 0.75) (all p<0.001). The risk of dyslipidemia was similar between users and non-users (HR: 1.05, 95% CI: 1.00; 1.11, p=0.05). Semaglutide 2.4 mg use was also associated with significant improvements in cardiometabolic biomarkers specified in Table 1 and slower decline in eGFR. Conclusion: In adults with overweight/obesity, semaglutide 2.4 mg was associated with lower risk of specified CMCs and greater improvements in cardiometabolic biomarkers.