Citations

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.

Introduction: Anthracycline-induced left ventricular dysfunction is well documented in lymphoma patients. However, the impact of cardiovascular risk factors (CVRF) and obesity on the right ventricle (RV) remains poorly characterized. Hypothesis: How does baseline CVRF burden—including obesity—affect RV structure and function over time in lymphoma patients treated with doxorubicin-based chemotherapy? Methods: A prospective cohort of patients with Hodgkin or non-Hodgkin lymphoma treated with doxorubicin-based chemotherapy at Mayo Clinic between March 1, 2013, and December 31, 2024, underwent echocardiography prior to chemotherapy initiation (T0), at 3–6 months (T1) and 6-18 months (T2) after treatment completion. A dedicated RV 4-Chamber view was used for all measurements. Patients were stratified into five groups: BMI>30, BMI>35, no CVRF, 1 CVRF (hypertension, diabetes, dyslipidemia, or smoking status), and ≥2 CVRF. RV parameters included end-diastolic/systolic area, FAC, TAPSE, S′ velocity, TRV, RVSP, and RV free wall strain. Group and time differences were analyzed using the Kruskal–Walli’s test due to non-normal distribution. Results: Among of 356 lymphoma patients (mean age 59.2 years, IQR:46-69) predominantly male (63.7%), 39.3% met criteria for obesity. At T0, patients with BMI >35 had greater RV end-diastolic (20.4 ± 4.4 vs. 18.7 ± 3.5 mm; p=0.009) and end-systolic diameters (11.0 ± 2.1 vs. 9.9 ± 2.6 mm; p=0.024), higher TRV (2.5 ± 0.4 vs. 2.2 ± 0.3 m/s; p<0.001) vs. no CVRFs. TAPSE was reduced vs. >2 CVRF group (23.7 ± 4.2 vs. 22.1 ± 4.8 mm; p=0.032). At T1, BMI >35 patients showed increased RV end-diastolic (22.3 ± 3.6 mm; p<0.001) and end-systolic areas (12.8 ± 2.9 mm; p<0.001), and worsened RVFWS (−24.0 ± 4.7% vs. −26.1 ± 2.98%; p=0.001) vs. no CVRF. RVSP was higher in those with >2 CVRFs (32.3 ± 5.4 mmHg; p=0.001). At T2, RVFWS was reduced in obese patients (−22.9 ± 3.5% vs. −27.1 ± 4.0%; p<0.001). RVSP stayed elevated in BMI >35 (33.0 mmHg) and >2 CVRFs (30.7 mmHg) vs. no CVRFs (23.7 mmHg; p<0.001). FAC and S′ did not differ significantly. Conclusion: In lymphoma patients treated with anthracyclines, isolated obesity was associated with the most pronounced RV changes—greater than those seen in non-obese patients with other CVRFs. These early and persistent alterations underscore the need for dedicated cardio-oncology care regardless of additional risk factors.

Introduction: In patients with type 2 diabetes (T2D) at high cardiovascular risk, glucagon-like peptide-1 receptor agonists (GLP1-RAs) have been shown to reduce major adverse cardiovascular events. However, patients with valvular heart disease, including those undergoing transcatheter aortic-valve implantation (TAVI), have been largely excluded from randomized trials. Hypothesis: We investigated whether GLP1-RA use is associated with improved one-year cardiovascular outcomes in patients with T2D undergoing TAVI. Methods: We conducted a retrospective cohort study using the TriNetX network. Adults (≥18 years) with T2D who underwent TAVI between 2015 and 2023 were included and stratified based on GLP1-RA initiation within 14 days post-TAVI. Baseline characteristics, comorbidities, medications, and laboratory data were balanced using 1:1 propensity score matching (PSM). The primary outcome was a composite of all-cause mortality or hospitalization at 1 year. Secondary outcomes included acute heart failure (HF) exacerbation, acute myocardial infarction (AMI), cardiac arrest, and ischemic stroke. Outcomes were assessed from 1 month to 1 year after TAVI. Survival probabilities were estimated using Kaplan-Meier analysis, and hazard ratios (HRs) were calculated with Cox proportional hazards models. Results: Among 20,454 patients with T2D undergoing TAVI from 2015-2023, 937 received GLP1-RAs. After PSM, 930 patients were included in each cohort, with a mean age of 73 years and 37% female. The mean follow-up duration was 342 days for GLP1-RA users and 325 days for non-users. GLP1-RA cohort exhibited a higher 1-year survival probability (93.8%) compared to non-users (89.5%) (HR 0.573 [95% CI, 0.410-0.801]; p=0.001). GLP1-RA use was also associated lower rates of all-cause hospitalization (HR 0.762 [95% CI, 0.652-0.891]; p=0.001), acute HF exacerbation (HR 0.687 [95% CI, 0.566-0.834]; p<0.001), and cardiac arrest (HR 0.452 [95% CI, 0.213-0.960]; p=0.034). No differences were observed in AMI (HR 1.033 [95% CI, 0.750-1.423]; p=0.844), or ischemic stroke (HR 0.875 [95% CI, 0.659-1.162]; p=0.356). Conclusions: In patients with T2D undergoing TAVI, GLP1-RA use is associated with significant survival benefits and improved cardiovascular outcomes, including reductions in acute HF exacerbation, all-cause hospitalization, and cardiac arrest. These findings highlight the need for prospective clinical trials to confirm these results.

Background: Muscular dystrophies (MDs) may cause heart failure (HF), but outcomes specific to MD-related HF are not well characterized. Research Question: Do the outcomes of HF hospitalizations differ between patients with underlying MDs (MD-HF) vs. patients without MDs (non-MD-HF) in the United States? Methods: Discharge data from HF hospitalizations were abstracted from the Nationwide Readmissions Database (2016-2022) and stratified by the presence or absence of MD (MD-HF vs. non-MD-HF). Logistic regression and lognormal models were estimated to assess differences in inpatient mortality, length of stay (LOS), total costs, complications, and 30-day and 90-day all-cause readmissions. Propensity-score matching (PSM) was used to control baseline differences between the MD-HF and non-MD-HF cohorts. Odds ratios (OR) with associated 95% Confidence intervals (CI) and p-values were reported. Analyses were conducted via SAS v. 9.4, with statistical significance indicated by two-tailed p<.05. Results: 8,466,806 HF hospitalizations were included in the analysis, of which 3688 (0.04%) involved patients with MD. MD-HF hospitalizations involved younger patients (mean age 55.3 vs. 71.3 years, p<0.001) with higher rates of HF with reduced ejection fraction (HFrEF) compared to non-MD-HF hospitalizations (48.1% vs. 34.9%, p<0.001). Compared to non-MD-HF hospitalizations (2.01%), MD-HF hospitalizations (5.82%) were associated with significantly higher odds of inpatient mortality (OR 3.01, 95% CI: 2.03, 4.45); higher complications rate (OR 2.11, 95% CI, 1.77, 2.52) including cardiogenic shock (OR 2.61, 95% CI, 1.90, 3.59), cardiac arrest (OR 2.27, 95% CI, 1.17, 4.41), use of mechanical ventilation (OR 2.23, 95% CI, 1.82, 2.73); higher palliative care consultation (OR 4.52, 95% CI, 3.21, 6.36); as well as more extended hospital LOS (OR 1.18, 95% CI, 1.09, 1.29), higher total costs (OR 1.32, 95% CI, 1.24, 1.41), and higher odds of discharge to rehab facility (OR 2.46, 95% CI, 1.99, 3.03) and home healthcare (OR 1.85, 95% CI, 1.55, 2.21) (all p<0.001). MD was not associated with a significant difference in 30-day (OR 0.94, 95% CI, 0.78, 1.12) and 90-day (OR 0.98, 95% CI, 0.82, 1.17) all-cause readmission rates. Conclusion: MD-HF hospitalizations were associated with higher inpatient mortality, complication rates, resource utilization, discharge to rehab facility and home healthcare, and no difference in readmission rates compared to non-MD-HF hospitalizations.