Oxidative modification of apolipoprotein B-100 (apoB) containing particles and subsequent immune responses contribute to the pathogenesis of atherosclerosis. Circulating IgG and IgM apoB-containing immune complexes (apoB-IC) and autoantibodies to a malondialdehyde mimotope (anti-MDA-mimotope) serve as biomarkers of oxidative stress and immune activation in atherosclerotic cardiovascular disease. Elevated lipoprotein(a) [Lp(a)] is associated with increased oxidative burden and immune activation. To investigate the effect of lipid-lowering medications on IgG and IgM apoB-IC and IgG and IgM autoantibodies to an MDA-mimotope in individuals with elevated lipoprotein(a) [Lp(a)] concentrations. In this prospective study, patients (n = 70) with Lp(a) levels ≥ 75nmol/L were assigned to 3 treatment regimens according to current guidelines: high-intensity statin monotherapy (n = 28), ezetimibe added to high-intensity statin (n = 31) and proprotein convertase subtilisin/kexin type 9 inhibitor (PCSK9i) added to high-intensity statin plus ezetimibe (n = 11). IgG and IgM apoB-IC and IgG and IgM anti-MDA-mimotope were measured at baseline and 3months after treatment initiation. Patients had a mean age of 51 ± 15years and 40% were male. Significant reductions in IgG apoB-IC levels were observed following treatment with high-intensity statins, add-on ezetimibe and add-on PCSK9i (by 18.3%, 17.5% and 25.5%, respectively, all p < 0.05). No significant changes in IgM apoB-IC, or IgG and IgM anti-MDA-mimotope levels were observed in any treatment group. In individuals with Lp(a) levels ≥ 75nmol/L, high-intensity statins, add-on ezetimibe and add-on PCSK9i reduced IgG apoB-IC but did not affect IgM apoB-IC, or IgG and IgM anti-MDA-mimotope levels. The clinical significance of these findings warrants further investigation.

Tricuspid regurgitation (TR) is associated with increased morbidity and mortality. Since surgical treatment of tricuspid regurgitation in elderly, multimorbid patients is associated with high risk, less invasive therapies such as tricuspid transcatheter edge-to-edge repair (T-TEER) and transcatheter tricuspid valve replacement (TTVR) have been developed. This study aimed to compare 30-day clinical and echocardiographic outcomes of T-TEER and TTVR in high-risk patients with severe TR. T-TEER was performed in 104 patients and TTVR in 10 patients based on anatomical suitability. All procedures were guided by transesophageal echocardiography and fluoroscopy. Primary endpoints included TR reduction, NYHA functional class, and safety events according to TVARC criteria. At 30days, TR reduction to grade 0/I was achieved in 44.9% of T-TEER and 80% of TTVR patients (p < 0.001). NYHA class I/II was present in 63.2% after T-TEER and 70% following TTVR (p = 0.69). Major bleeding occurred more frequently in the TTVR group (20%) than in the T-TEER group (1.96%; p = 0.041). One patient in the TTVR group required a new pacemaker. No deaths, strokes, or surgical conversions occurred in either group. T-TEER and TTVR are effective for treating severe TR in high-risk patients. TTVR achieved greater TR reduction but was associated with more access site bleeding. T-TEER demonstrated a favorable safety profile. Careful patient selection remains essential to optimize outcomes.

Management of aortic stenosis, particularly with preserved left ventricular ejection fraction (LVEF) and discordant or borderline echocardiographic findings, remains challenging, both in assessing the true severity of stenosis and in isolating the valvular contribution to symptoms amidst comorbid conditions. This study evaluates the feasibility and physiological insight obtained from invasive pressure measurements across the aortic valve at rest and during exercise in symptomatic patients with aortic stenosis (AS). This prospective cross-sectional study included patients with symptomatic high-gradient severe, low-gradient severe, and moderate aortic stenosis. They underwent invasive pressure gradient measurements across the aortic valve (pressure catheters in the left ventricle and ascending aorta) with concurrent right heart catheterization at rest and during peak supine bicycle exercise. Of 28 patients included, invasive measurements during exercise were feasible in 25 patients. Overall, exercise induced increases in aortic valve gradient, flow, and opening area, but there was considerable heterogeneity in individual hemodynamic responses. Notably, of the 14 patients in the low-gradient severe group based on echocardiography, nine demonstrated divergent physiological responses consistent with either moderate or high-gradient severe during exercise. All patients - irrespective of stenosis severity - had differential causes of symptoms during exercise with at least one of the following: chronotropic incompetence, abnormal increase in pulmonary artery or left ventricular end-diastolic pressures, or peripheral impairment of oxygen extraction or utilization. These findings demonstrate the safety and feasibility of invasive hemodynamic exercise testing in patients with aortic stenosis and highlight heterogeneity in pressure-flow responses during exercise. Invasive hemodynamic assessment during exercise may help elucidate alternative contributing mechanisms to exertional dyspnea, particularly in patients with aortic stenosis and discordant symptoms and findings.

The systemic inflammatory response index (SIRI)-an inflammatory index derived from neutrophil, monocyte, and lymphocyte counts-has shown potential in predicting cardiovascular risk. However, its prognostic value in patients with acute coronary syndrome (ACS) treated with primary percutaneous coronary intervention (pPCI) remains unclear. This study was aimed at evaluating the prognostic significance of SIRI in this specific high-risk population. We conducted a systematic search of PubMed, Embase, and The Cochrane Library up to June 2025 to identify all relevant studies about SIRI applied to patients with ACS after pPCI. The primary outcome was all-cause mortality. Among major adverse cardiovascular events (MACE), new-onset acute myocardial infarction (AMI), revascularization, and stroke were included as secondary outcomes. Risk estimates were pooled as odds ratios (OR) with 95% confidence intervals (CI). A total of nine studies involving 7679 patients were included. The pooled analysis demonstrated that an elevated SIRI was a significant predictor for both all-cause mortality (OR 3.32; 95% CI 1.29 to 8.54; p = 0.01), MACE (OR 2.45; 95% CI 1.74 to 3.45; p = 0.001), new-onset AMI (OR 1.86; 95% CI 1.25 to 2.77; p = 0.001), and myocardial revascularization (OR 1.64; 95% CI 1.35 to 1.98; p = 0.001). Our meta-analysis demonstrates that an elevated SIRI is a useful predictor of all-cause mortality, MACE, new-onset AMI, and revascularization in patients with ACS undergoing PCI. As a simple and cost-effective index, SIRI shows significant potential for early risk stratification and may help guide clinical management in this patient population.

The increasing prevalence of heart failure with preserved ejection fraction (HFpEF) is often accompanied by mitral regurgitation (MR). Transcatheter edge-to-edge repair (M-TEER) is established for treating MR in heart failure with reduced ejection fraction (HFrEF), but its impact in patients with HFpEF phenotype is unclear. To investigate the effect of M-TEER in patients with HFpEF phenotype and concomitant MR based on diagnostic criteria according to current ESC guidelines and established HFpEF scores. 181 patients with severe MR underwent M-TEER at our center with HFpEF phenotype. Echocardiography, symptom burden (NYHA class), quality of life (MLWHFQ, SF-PCS, and functional capacity (6MWD) were assessed before and 30 days after M-TEER. Survival and rehospitalisation rates were assessed at long-term follow-up. M-TEER in patients with HFpEF phenotype significantly reduced MR grade and improved symptom burden, quality of life, and exercise capacity. Patients with either primary or secondary MR experienced clinically relevant symptomatic improvement for MLWHFQ (69%) and SF-PCS (60%) as well clinically relevant increase (44%) of the 6MWD. The clinical outcome between patients with primary or secondary MR was comparable. Severe tricuspid regurgitation (TR) complicating HFpEF was independently linked to an increased mortality risk (HR 3.66, 95%CI 1.32-10.15, p = 0.013). M-TEER is an effective treatment for both severe primary and secondary MR in patients with HFpEF phenotype, significantly reducing MR and improving symptoms. The independent association of severe TR with increased all-cause mortality highlights the importance of timely intervention to prevent right heart failure and worse outcomes.

Surgical bailout during transcatheter aortic valve replacement (TAVR) is rare but highly critical. We evaluated the impact of hospital infrastructure, procedural setting, timing metrics, and haemodynamic stability on patients requiring emergent surgical bailout. A single-centre analysis was conducted on consecutive TAVR cases requiring emergent surgical bailout between 2009 and 2024. Two eras were compared: Era 1 (2009-2016), with procedures performed in a conventional catheterisation laboratory (CCL) requiring transfer to a distant operating room, and Era 2 (2017-2024), using a purpose-built hybrid operating room (HOR) with all disciplines on site. The primary endpoint was in-hospital mortality. Secondary endpoints included time to extracorporeal life support (ECLS) initiation and surgical incision. Of 3039 TAVR procedures, 16 patients (0.53%) required surgical bailout (10 in Era 1, 6 in Era 2). In-hospital mortality was 100% in the CCL group versus 33.3% in the HOR group (P < 0.01). While time to ECLS was similar, time to surgical intervention was significantly shorter in the HOR group. All HOR patients received definitive surgical treatment, whereas 60% of CCL patients died before surgery could be initiated. Haemodynamic instability prior to conversion differed significantly between groups. Surgical bailout during TAVR is rare, but associated mortality remains high. Bailout performed in a HOR was associated with shorter delays to surgical incision and improved outcomes, with haemodynamic stability at the time of conversion emerging as an important factor associated with survival. These findings highlight the potential relevance of minimising time to surgery through optimised infrastructure, such as a HOR.

SELUTION Sustained Limus Release (SEL, Cordis, Miami, Florida, USA) is a novel biodegradable polymer microsphere sirolimus-coated balloon (SCB) characterized by sustained coronary drug retention. A head-to-head comparison to currently available paclitaxel-coated balloons (PCB) is lacking. To compare clinical outcomes after percutaneous coronary intervention (PCI) with SEL SCB and iopromide-based SeQuent Please/NEO (SEQ, B. Braun, Melsungen, Germany) PCB. Consecutive all-comer patients undergoing PCI with SEL SCB or SEQ PCB for both de novo lesions and in-stent restenosis between January 2021 and December 2024 at two Italian centers were included in this observational, retrospective, cohort study. The primary endpoint was target lesion failure (TLF), defined as the composite of cardiac death, target vessel myocardial infarction (MI), and target lesion revascularization (TLR) at 12-month follow-up. Inverse probability of treatment weighting was applied to adjust for baseline differences. A total of 487 patients (589 lesions) were included: 250 patients (302 lesions) treated with SEL SCB and 237 patients (287 lesions) with SEQ PCB. At a median follow-up of 403 [223-617] days, the 12-month rate of TLF was similar between SEL SCB and SEQ PCB (4.3% vs. 4.0%; adjusted hazard ratio [aHR]: 0.97; 95% confidence interval [CI]: 0.37-2.52). No significant differences were observed in cardiac death, target vessel MI, or TLR (aHR: 1.23; 95% CI: 0.21-7.19). Results were consistent across prespecified subgroups and sensitivity analyses. The SELSEQ study suggests comparable outcomes at 12-month follow-up among patients undergoing PCI with the biodegradable polymer microsphere SEL SCB and the iopromide-based SEQ PCB.

Fabry disease (FD) is a multisystemic disease affecting the heart and the kidneys of affected patients. In addition to FD-specific treatment, patients require concomitant medication for cardio- and nephroprotection. Sodium-dependent glucose transporter 2 inhibitors (SGLT2i) are recommended for patients with heart failure and/or kidney disease, but efficacy data for FD are scarce. In this multicenter study (n = 8), the effects of SGLT2i therapy after 12months of treatment in 48 patients (12 females) on FD-specific therapy were examined. Patients were retrospectively analyzed at three time points (before SGLT2i: T-1; SGLT2i start: T0; and end of observation: T+1). Patients showed advanced cardiac manifestations with a high frequency of left ventricular hypertrophy (LVH) (females: 81.8% and males: 90.0%) at T0. Males presented with a significantly lower left ventricular ejection fraction LVEF (56 [29-73]% versus 65 [38-78]%; p = 0.0113). There were no treatment-related adverse events or Fabry-associated clinical events (FACEs) between T0 and T+1. Females showed a stable disease course independent of the concomitant treatment with SGLT2i. Males showed an eGFR decrease of 3.7ml/min/1.73 m2 per year (p = 0.0018) before and an ameliorated decrease of 2.7ml/min/1.73 m2 per year (p = 0.0182) after SGLT2i initiation. Importantly, a slight but significant improvement of LVEF by 0.6% per year (p = 0.0319) was observed, which was more prominent in males with a reduced LVEF (< 50%) at baseline. Treatment with SGLT2i of FD patients was safe and patients presented with stable disease courses. Especially males with reduced LVEF might benefit from SGLT2i treatment.

Renal dysfunction might affect outcomes in patients with ST-segment elevation myocardial infarction (STEMI) and multivessel coronary artery disease (MVD) undergoing percutaneous coronary intervention (PCI). In MULTISTARS AMI, patients with STEMI and MVD were randomized to immediate or staged PCI of non-culprit lesions. In this pre-specified analysis, patients were stratified according to the presence of renal dysfunction at baseline, defined at an estimated glomerular filtration rate (eGFR) of 60ml/min/1.73 m2. Patients with an eGFR < 30ml/min/1.73 m2 were excluded from the trial. The primary endpoint was a composite of death, non-fatal myocardial infarction, stroke, unplanned revascularization, or hospitalization for heart failure at 1year. In MULTISTARS AMI, 108 (13%) of 832 patients had renal dysfunction. The primary endpoint occurred more frequently in patients with renal dysfunction (19.4% vs. 11.2%, unadjusted HR 1.82, 95% CI 1.13-2.94), primarily driven by higher rates of death. Among patients with renal dysfunction, the rates of the primary end point were 14.5% and 24.5% in the immediate and staged PCI groups (unadjusted HR 0.55, 95% CI 0.23-1.33). There was no interaction between renal dysfunction and the randomized treatment assignment with respect to the primary end point (adjusted HR 1.30, 95% CI 0.8-2.20, pint 0.82). The occurrence of acute renal insufficiency was statistically similar in patients with renal dysfunction who underwent immediate and staged PCI (10.9% vs. 18.9%, unadjusted HR 0.61, 95% CI 0.22-1.72, pint 0.09). Renal dysfunction at baseline emerged as a strong risk factor for the development of acute renal insufficiency (adjusted HR 5.0, 95% CI 2.30-10.70, p < 0.01). Outcomes with immediate compared to staged multivessel PCI did not appear significantly altered by the presence of renal dysfunctionat baseline. (Supported by Boston Scientific; MULTISTARS AMI ClinicalTrials.gov number, NCT03135275).

This study investigated the safety and tolerability of regadenoson for pharmacologic stress testing in the context of myocardial scintigraphy under routine clinical conditions in a cardiology practice in 5780 consecutive patients. The drug regadenoson was approved in Germany in 2010 for pharmacological stress testing in myocardial scintigraphy for patients who are unable to undergo adequate physicalexercise. Previously, only dipyridamole or adenosine were available for diagnostic pharmacological vasodilation, but they were not approved for this indication. Data on safety and tolerability were prospectively collected from consecutive patients referred for the assessment of myocardial ischemia using myocardial scintigraphy. Data were immediately entered into a dedicated computer program. After injection of regadenoson, there was a significant mean increase in heart rate from 70.2 ± 12.3 to a maximum of 94.6 ± 17.3bpm. Systolic blood pressure dropped from 128.9 ± 16.2 to a minimum of 123.3 ± 20.3mmHg. 86% of patients experienced any adverse effects, with the most frequent being dyspnea (64.2%), followed by headaches (20.7%), a sensation of warmth (20.2%), and numerous other, less frequent sensations. Bronchospasms were not observed, notably not in the 508 patients with COPD/bronchialasthma. Asystole of > 6s occurred in 2 patients (0.03%), which were both successfully terminated immediately with theophylline and atropine. There were no fatalities. Overall, regadenoson demonstrated very good tolerability. The development of the selective A2A adenosine receptor agonist regadenoson, compared to classical non-selective adenosine, represents a significant advancement in non-invasive imaging diagnostics of myocardial ischemia, using myocardial scintigraphy and other modalities such as MRI. Since adenosine is contraindicated in patients with bronchialasthma/COPD, regadenoson has become the diagnostic agent of choice in these cases, although it must be considered that very rare instances (< 0.1%) of life-threatening events can occur, necessitating that antidotes such as theophylline and atropine be readily available.