Neonatal and infant aortic arch reconstruction remains a high-risk cardiovascular procedure requiring effective cerebral and myocardial protection. Variability in perfusion strategies may influence early hemodynamic stability and postoperative recovery. This study aimed to evaluate the early and short-term cardiovascular outcomes of a standardized beating-heart aortic arch reconstruction strategy incorporating simultaneous antegrade selective cerebral and continuous coronary perfusion. In this retrospective single-center cohort study, 31 consecutive neonates and infants undergoing aortic arch reconstruction between November 2022 and December 2025 were analyzed. A standardized surgical protocol was applied, consisting of extensive ductal tissue resection, interdigitating posterior end-to-end anastomosis, anterior autologous pericardial patch augmentation, and moderate hypothermic antegrade selective cerebral perfusion combined with continuous coronary perfusion via innominate artery cannulation. Early postoperative outcomes and short-term echocardiographic follow-up results were assessed. The cohort included 31 patients, 22.6% of whom had complex associated cardiac anomalies requiring concomitant procedures. Median cardiopulmonary bypass and aortic cross-clamp times were 119 and 64 min, respectively. There was no in-hospital mortality. Major complications were infrequent, and median intensive care unit stay was 5 days. During a median follow-up of 6.8 months, one patient (3.2%) developed recoarctation requiring reintervention. No late mortality was observed. A fully standardized beating-heart aortic arch reconstruction strategy incorporating simultaneous cerebral and coronary perfusion demonstrated favorable early cardiovascular and short-term outcomes, even in anatomically complex cases. Preservation of continuous coronary perfusion may be associated with improved myocardial stability and early postoperative recovery; however, these findings should be interpreted as observational and hypothesis-generating given the absence of a control group. Larger multicenter studies with longer follow-up are warranted to confirm these findings.

Cardiogenic shock is a life-threatening condition caused by the heart's sudden inability to pump sufficient blood to maintain adequate tissue perfusion, most commonly occurring following a myocardial infarction or acute decompensated heart failure. The resultant hypoperfusion can quickly progress to end-organ failure and ultimately death if not treated urgently. This review explores the management of cardiogenic shock, highlighting current treatments, their effectiveness, and the challenges faced by healthcare providers. It looks at both pharmacological therapies and devices used for cardiac support, including mechanical circulatory support and emergency revascularisation procedures to restore blood flow. We also examine how different stages of shock affect survival and how new technologies including artificial intelligence and wearable monitors could help detect and treat this condition earlier. In addition, this review discusses the significant pressure that cardiogenic shock places on healthcare provision, including the typical financial cost of treatment in the UK, resource utilisation and regional disparities. Finally, we outline future directions for trial design, better prevention, more rapid diagnosis and improved treatments that could improve morbidity and mortality.

Cardiometabolic diseases remain the leading cause of morbidity and mortality worldwide, despite major advances in pharmacological and lifestyle interventions. Exercise training is a cornerstone of prevention and treatment; however, adherence to traditional aerobic programs remains suboptimal. Isometric handgrip (IHG) training has emerged as a simple, time-efficient, and potentially effective strategy for improving cardiovascular and metabolic outcomes. This state-of-the-art review synthesizes current evidence on the physiological mechanisms underlying IHG training, including autonomic modulation, vascular function improvement, endothelial adaptation, and metabolic regulation. We summarize clinical data regarding its effects on blood pressure, arterial stiffness, endothelial function, insulin sensitivity, and inflammatory markers. Special attention is given to its applicability in specific populations, including hypertensive patients, individuals with metabolic syndrome, heart failure patients, and cancer survivors. We also discuss methodological heterogeneity across studies, safety considerations, and knowledge gaps. Finally, we outline future research directions needed to define optimal protocols and clarify long-term cardiometabolic benefits. IHG training represents a promising adjunctive strategy within cardiometabolic prevention and rehabilitation programs.

(1) Background: Out-of-hospital cardiac arrest (OHCA) remains a major public health issue, with survival largely determined by the initial rhythm and timeliness of resuscitation. Comprehensive population-based data are essential for guiding prevention, emergency medical services (EMS) planning, and improving outcomes. (2) Methods: We performed a retrospective observational study of all adult OHCA cases managed by EMS in Lecce (Italy) between January 2013 and March 2025. Demographics, arrest circumstances, initial rhythm, time intervals, and return of spontaneous circulation (ROSC) were analyzed across age, sex, temporal, and pandemic-related strata. Rhythm classification followed European Resuscitation Council guidelines. (3) Results: A total of 11,653 cases were analyzed (mean age 76.8 ± 15.5 years, 56.6% male). Asystole (AS) was the predominant rhythm (88.7%), followed by ventricular fibrillation (VF, 7.6%), pulseless electrical activity (PEA, 1.3%), and pulseless ventricular tachycardia (pVT, 0.08%). VF was more common in younger and male patients, while AS increased with age. Hour-level analysis revealed circadian peaks: VF in late afternoon and AS in early morning. Pandemic analysis showed reduced VF and increased AS during COVID-19, with partial recovery post-pandemic. ROSC occurred in 3.47% overall, strongly associated with shockable rhythms. EMS response times were stable across day-night and pandemic phases. (4) Conclusions: AS dominates OHCA presentations, especially among the elderly, whereas VF remains the strongest predictor of ROSC. Circadian variation at the hourly level suggests potential for EMS optimization. Pandemic-related shifts in rhythm highlight the vulnerability of the chain of survival to societal disruptions. Strengthening bystander CPR, expanding AED availability, and tailoring EMS strategies remain key priorities for improving OHCA outcomes.

Long-term transthoracic echocardiogram (TTE) follow-up guidelines after muscular ventricular septal defect (mVSD) device closure are vague. The primary goal of this study was to perform a literature search to characterize the type and timing of complications that occur after mVSD device placement. The search was performed in Medline (PubMed) with English language and publication date (1983 to 2024) filters applied. Studies were included if they reported on patients who underwent mVSD device closure. Studies were excluded if they reported on other types of ventricular septal defect (VSD) device closures, were review papers, or did not report outcomes after the device procedure. A total of 139 articles met the criteria (retrospective, n = 63; prospective, n = 10; case reports, n = 66), encompassing 1668 patient cases. Age at the time of mVSD closure was 10.6 + 2.7 years. Incidence of complications was 17.9% (299/1668). Maximum follow-up was 160 months. Most complications were residual shunts (40.8%, 122/299), followed by valve dysfunction (13.7%, 41/299) and arrhythmias (13.7% 41/299). The vast majority of complications occurred ≤12 months post-device placement 98.0% (293/299). Only 1.3% (4/299) of complications occurred at >12 months (mild tricuspid regurgitation, n = 2; left bundle branch block, n = 1; atrial fibrillation, n = 1). Time until complication was not reported in 0.7% (2/299) of patients (residual shunts, n = 2). All clinically significant complications diagnosed via TTE occurred <12 months post-mVSD device procedure. The utility of repeat TTE beyond one year after mVSD device closure should be reassessed if no clinical concerns are present.

The objective of this study is to evaluate the safety, feasibility, and mid-term outcomes of using the left axillary artery (AXA) as an alternative inflow source for the proximal anastomosis of the saphenous vein graft (SVG) in MICS-CABG, focusing on intraoperative graft haemodynamics, early patency, and clinical outcomes. We retrospectively analyzed consecutive patients who underwent MICS-CABG between April 2020 and August 2025 at a single center. Patients were divided into two groups based on the inflow source: the ascending aorta (n = 292) or the left axillary artery (n = 90). After propensity score matching, 80 matched pairs were analyzed. Intraoperative graft haemodynamics were assessed. Early graft patency was evaluated using coronary angiography or CT angiography. Mid-term outcomes, including overall survival and major adverse cardiac and cerebrovascular events (MACCEs), were compared between groups. Both groups demonstrated comparable intraoperative hemodynamic performance. The AXA group demonstrated an early graft occlusion rate comparable to that of the AOR group (1.32% vs. 3.16%, RR = 0.42, 95% CI = 0.08-2.11, and p = 0.45). Overall survival (93.2% vs. 100%, p = 0.06) and the MACCE-free metric (91.9% vs. 92.1%, p = 0.83) showed no significant difference between groups. The left axillary artery is a safe and feasible alternative inflow source in MICS-CABG. This approach provides acceptable intraoperative flow dynamics, early patency, and mid-term outcomes to conventional ascending aortic inflow.

(1) Background: Functional pulmonary atresia (FPA) and pulmonary atresia with intact ventricular septum (PA/IVS) are rare neonatal congenital heart diseases with similar early clinical manifestations but distinct pathophysiology and treatment strategies, making early and accurate differentiation clinically important. (2) Methods: This single-center retrospective study included 43 neonates diagnosed with FPA (n = 12) or PA/IVS (n = 31) between December 2016 and March 2025. Echocardiographic parameters and clinical data were compared between groups, and receiver operating characteristic curve analysis was performed to evaluate the usefulness of selected echocardiographic indices for differentiation in clinical practice. (3) Results: Compared with PA/IVS, neonates with FPA exhibited significantly larger right atrial area, relatively better preserved right ventricular development, larger patent ductus arteriosus diameter, and lower peak tricuspid regurgitation velocity. Several parameters, including right atrial area and the right-to-left ventricular ratio, demonstrated strong between-group discrimination in this cohort. Clinically, most FPA neonates were managed conservatively with favorable outcomes, whereas PA/IVS neonates required surgical intervention and experienced higher perioperative mortality. (4) Conclusions: FPA and PA/IVS differ significantly in right heart morphology, hemodynamic characteristics, and management strategies. A comprehensive multi-parameter echocardiographic evaluation demonstrated discriminatory ability in this cohort, facilitating appropriate treatment decisions and potentially helping to avoid unnecessary high-risk surgical interventions.

The global disease burden of aortic valve disease is already substantial and is projected to rise significantly in the coming decades. Aortic valve replacement (AVR) with a biological prosthesis has become highly popular and commonly used. This study aims to assess long-term outcomes after biological AVR with regard to structural and non-structural deterioration. In this single-centre retrospective study, 918 patients undergoing surgical AVR with a biological prosthesis at the University Hospital Frankfurt from January 2006 to July 2009 were included. The primary endpoints were freedom from reoperation and from structural and non-structural deterioration, and the secondary was long-term survival. Follow-up was completed in 95.6% with a median of 7.6 years, accounting 6610 patient-years. The mean age was 74.9 years and a median EuroSCORE II (range) was 3.34 (0.77-62.4). Twenty-two percent of surgeries were either emergent or urgent. Many patients had concomitant surgery, while coronary artery bypass grafting in 45.3% of patients was the most common. Three prosthetic valve models were used in our patient population: Carpentier Edwards Perimount (CEP) Model 2900, Model 3000 and Medtronic Mosaic (MM). Reoperation occurred in 36 patients (3.9%) due to endocarditis (2.0%), aortic root aneurysm (0.1%), isolated or combined aortic stenosis or aortic regurgitation (1.9%). Freedom from reoperation at 5, 10 and 15 years was 97 ± 0.6%, 95.6 ± 0.8% and 90.3 ± 2.3%, respectively. Freedom from major stroke at 5, 10 and 15 years was 97.9 ± 0.0%, 96.4 ± 0.8%, and 96.1 ± 0.08%, and freedom from major bleeding event at 5, 10 and 15 years was 98.5 ± 0.4%, 95.7 ± 0.9% and 92.7 ± 2.2%, respectively. A subgroup analysis of the Carpentier Edwards (CEP) valves and the Medtronic Mosaic (MM) valves showed no significant differences regarding the primary endpoints. The overall survival at 5, 10 and 15 years was 67 ± 1.7%, 39.8 ± 1.8%, and 15.1 ± 2.2% respectively. The Kaplan-Meier survival estimator was 96 ± 2.2 months. This study showed a good long-term survival of surgical AVR with biological prostheses in relatively high-risk and elderly patient population. All biological prosthetic valves showed good long-term durability with low levels of complications and reoperations. The different models did not show any significant differences. Surgical AVR remains a valuable therapeutic option even though transcatheter aortic valve implantation has been greatly expanded since its introduction.

Subclinical coronary atherosclerosis is common but its biological aggressiveness and interplay with extracoronary disease in asymptomatic individuals remain unclear. We evaluated the prevalence of high-risk coronary plaques (HRPs) and their relationship with mild carotid atherosclerosis and coronary calcium in a cardiovascular (CV) high-risk cohort in primary prevention. This retrospective multicenter study enrolled 269 asymptomatic adults with multiple CV risk factors who underwent Coronary Computed Tomography Angiography (CCTA) after prior carotid duplex ultrasound (CDUS). Coronary artery disease (CAD) was graded as absent, non-obstructive (<50% stenosis) or obstructive (≥50%), and HRPs were identified by ≥1 adverse morphological feature (low attenuation, positive remodeling, napkin-ring sign, spotty calcification). Carotid disease was classified as CDUS 0 (no plaque), CDUS 1-49% (mild), or CDUS ≥ 50% (significant). Pre-specified analyses explored prevalence of HRPs across CDUS-calcium-score strata (cut-off 100 Agatston) and independent predictors within the CDUS 1-49% subgroup. CAD was absent in 31%, non-obstructive in 41%, and obstructive in 28%. HRPs were present in 30.9% of all cases, in 26.6% of non-obstructive and in 64.6% of obstructive CAD. HRPs prevalence rose step-wise from 10.0% (CDUS 0 + Ca < 100) to 27.7% (CDUS 1-49% + Ca < 100), 41.2% (CDUS 0 + Ca ≥ 100) and 59.4% (CDUS 1-49% + Ca ≥ 100). In patients with CDUS 1-49%, current smoking independently predicted HRPs (OR 2.1, 95% CI 1.0-4.5; p = 0.049). Nearly one-third of asymptomatic adults with high CV risk already showed HRPs. Mild carotid atherosclerosis synergized with a calcium score ≥ 100 to identify a subgroup in which six of ten individuals exhibited HRPs. Smoking was the only independent clinical correlate identified of plaque vulnerability. Combined carotid ultrasound, calcium scoring and CCTA may substantially refine primary prevention risk stratification beyond traditional factors.

Atherosclerosis is a chronic, progressive disease of the arterial wall and the principal pathological substrate underlying most cardiovascular diseases, including ischemic heart disease, stroke, and peripheral arterial disease. Despite advances in prevention, imaging, and therapy, atherosclerosis remains the leading cause of cardiovascular morbidity and mortality worldwide. From a pathological perspective, the disease represents a dynamic and heterogeneous process characterized by endothelial dysfunction, lipid retention and modification, chronic inflammation, immune activation, smooth muscle cell phenotypic modulation, extracellular matrix remodeling, and thrombogenic surface alterations. This review provides a comprehensive overview of atherosclerosis from a pathologist's perspective, integrating classical morphological concepts with contemporary insights into immunopathology, plaque classification, and mechanisms of plaque instability. We summarize the structure and function of the arterial wall, the stepwise pathogenesis of lesion initiation and progression, and the histopathological classification systems established by the American Heart Association and subsequently refined through Virmani's framework. Particular emphasis is placed on plaque instability, highlighting the qualitative features-such as fibrous cap thinning, necrotic core expansion, macrophage-driven inflammation, plaque erosion, and calcification patterns-that determine clinical outcomes rather than luminal stenosis alone. Furthermore, the review discusses the expanding role of immunohistochemical markers in defining plaque biology, including lineage markers and functional indicators of inflammation, matrix integrity, osteogenic signaling, and local anticoagulant balance. These pathological insights are integrated with contemporary risk assessment tools, imaging modalities, preventive strategies, and therapeutic interventions, including emerging lipid-lowering and RNA-based therapies. In conclusion, pathology remains central to understanding atherosclerosis as a biologically active disease and to refining concepts of plaque instability. Integrating histopathology with molecular profiling, imaging, and clinical data is essential for advancing precision prevention and targeted treatment strategies in atherosclerotic cardiovascular disease.