Background:Acute myocardial infarction (AMI) remains a leading cause of premature death (<65 years) in the United States, with a significant association with psychoactive substance use (PSU). However, long-term trends and future projections of this combined burden remain unclear. Methods:We conducted a retrospective observational study using the Centers for Disease Control and Prevention Wide-Ranging Online Data for Epidemiologic Research Multiple Cause of Death database to assess premature mortality (ages 25-65 years) related to AMI and PSU from 1999 to 2023. Age-adjusted mortality rates (AAMRs) were derived, and annual percentage changes (APCs) were calculated using joinpoint regression. An autoregressive integrated moving average (ARIMA) model was used to forecast mortality through 2035. Results:From 1999 to 2023, 176,641 premature deaths were attributed to AMI and PSU. The AAMR rose from 1.4 per 100,000 in 1999 to 4.16 in 2023. Mortality increased sharply from 1999 to 2005 (APC 19.04), continued rising through 2021 (APC 2.63), and declined between 2021 and 2023 (APC -9.13). Middle-aged adults (45-65 years) had substantially higher mortality than younger adults (25-45 years) (AAMR 9.63 vs 0.91, 2018-2023). Men had higher mortality than women (6.81 vs 2.53). American Indian/Alaska Native and White populations showed the higher racial burden. Nonmetropolitan areas had markedly higher mortality than metropolitan regions. South Dakota, Kentucky, and Arkansas had the highest state-level mortality. Forecasting predicts only a modest decline to 3.80 per 100,000 by 2035. Conclusion:Despite recent declines, premature mortality from AMI and PSU is projected to remain high through 2035, underscoring the need for targeted, evidence-based prevention strategies.
Background:Cardioplegia remains a cornerstone of myocardial protection during cardiac surgery; however, the configuration of its delivery circuit, particularly priming volume and blood-synthetic surface area, can exert a measurable influence on patient outcomes. Oversized or non-tailored circuits inherently increase hemodilution, inflammatory activation, and coagulation disturbances, effects that are especially pronounced in neonates and small children, whose circulating blood volume is limited. Advances in modular heart-lung machine (HLM) technology have introduced the possibility of tailoring cardioplegia circuits to patient size and procedural requirements, aligning mechanical design with physiological principles. Materials and Methods:A narrative review was conducted using PubMed, Scopus, and Google Scholar for studies published between January 1976 and July 2025. Search terms included "cardioplegia," "myocardial protection," "cardioplegia circuit," "priming volume," "modular heart-lung machine," "microplegia," "del Nido cardioplegia," and related keywords. The search identified 286 records; after duplicate removal and eligibility screening, 22 studies were included in the final qualitative synthesis. Evidence was analyzed according to four domains: priming volume and blood conservation, contact surface area and inflammation, modularity and circuit customization, and physiological implications of delivery strategy. Results:Cardioplegia delivery circuit design appears to be a clinically relevant but underrecognized component of myocardial protection. Modular HLM platforms provide a practical approach to reduce circuit complexity and adapt extracorporeal circulation to individual patient requirements. Further prospective multicenter studies are needed to define the impact of modular cardioplegia circuits on clinical outcomes. Conclusions:Modular HLM technology provides a flexible and physiologically grounded platform for tailoring cardioplegia delivery to individual patient profiles. Standardizing weight-banded modular configurations and implementing routine monitoring of priming volume-to-weight ratios could improve consistency in practice and serve as a foundation for prospective studies. The cumulative evidence suggests that extending modular principles to the cardioplegia circuit represents an underutilized but promising opportunity to enhance both pediatric and adult cardiac surgical outcomes.
Background:Pacemakers (PMs) are crucial for treating symptomatic bradyarrhythmias and improving patient health-related quality of life (HRQoL). While Chagas disease (ChD) is known to impair HRQoL, its specific impact on PM recipients, as measured by the AQUAREL questionnaire, is not well understood. This study aimed to compare HRQoL between pacemaker patients with and without ChD. Methods:This cross-sectional study included 57 adult patients with PM (29 with ChD and 28 without). HRQoL was evaluated using the AQUAREL questionnaire, which assesses three domains: Chest Discomfort, Arrhythmia, and Dyspnea. We used multivariate inflated beta regression models, adjusting for clinical and demographic covariates, to analyze the data. Results:Participants with ChD (median age 64 years, interquartile range [IQR], 56-72 years) reported significantly worse HRQoL than those without ChD (median age 57 years, IQR, 53-69 years). After multivariate adjustment, ChD remained significantly associated with poorer HRQoL scores in all domains: Chest discomfort (adjusted odds ratio [OR] 0.59; p = .044), Arrhythmia (adj. OR 0.38; p = .004), and Dyspnea (adj. OR 0.61; p = .049). An OR < 1 indicates worse outcomes for the ChD group. Conclusions:ChD is independently associated with a significantly poorer perception of HRQoL in pacemaker patients compared to those without ChD. This impairment spans the critical domains of chest discomfort, arrhythmia, and dyspnea, highlighting the distinct health burden imposed by ChD in this patient population.
Background:Ultrathin bioresorbable-polymer sirolimus-eluting stents (BP-SES), including bioresorbable scaffolds (BRS), were developed to mitigate adverse events associated with durable-polymer everolimus-eluting stents (DP-EES). This study aims to compare the efficacy and safety of BP-SES versus DP-EES in patients undergoing percutaneous coronary intervention for de novo coronary artery lesions. Methods:We searched PubMed, Embase, ScienceDirect and ClinicalTrials.gov from inception to May 2026 for randomised controlled trials (RCTs) comparing BP-SES or BRS with DP-EES. Random-effects models were used to pool risk ratios (RRs) or mean differences with 95% confidence intervals (CIs). Results:Nineteen RCTs involving 18,501 patients were included. No significant differences were observed between BP-SES and DP-EES for target lesion failure (RR 1.15, 95% CI 0.74-1.79; I2 = 94%), target vessel failure (RR 0.93, 95% CI 0.84-1.03; I2 = 10%), cardiac death (RR 0.96, 95% CI 0.78-1.18), target vessel myocardial infarction (RR 0.89, 95% CI 0.77-1.03), clinically indicated target lesion revascularisation (RR 0.99, 95% CI 0.80-1.22). Binary restenosis was significantly higher in the BP-SES arm overall (RR 2.46, 95% CI 1.41-4.29; p = 0.001). Conclusions:Metallic BP-SES and DP-EES showed similar rates for most clinical endpoints. However, extreme heterogeneity and accrual of only 5.7% of the required information size render the evidence for target lesion failure inconclusive. Higher binary restenosis increased target lesion revascularisation with fully BRS indicate that these platforms are not interchangeable with contemporary metallic stents. Further large, long-term trials are required.
Since the first implant over two decades ago, transcatheter aortic valve implantation (TAVI) has become the standard treatment for patients with severe aortic stenosis at high and intermediate risk, with mounting evidence to support its use in the younger lower-risk patient. Increasing operator experience and ongoing technological advances have both refined the procedure and reduced overall risk. However, important challenges remain, including coronary access after TAVI, conduction disturbance following implantation, the long-term consequences of paravalvular leak, cost-effectiveness and broader implications on healthcare systems. This review is timely following publication of the latest European Society of Cardiology guidelines on the management of valvular heart disease and recent landmark trials. We aim to provide an update on key areas of development including patient selection, imaging, management of coronary disease, valve durability and lifetime management.
Tricuspid regurgitation (TR) has a community prevalence of 3%, which increases with age and affects up to 7% of elderly patients. TR is secondary (functional) in 90% of cases (usually resulting from left heart disease and/or pulmonary hypertension), although atrial dilatation is an increasingly recognised cause. Awareness of the poor prognosis associated with increasing TR severity has refocused the quest for effective treatments. Surgical intervention has been hindered by high in-hospital mortality (up to 10%), even in carefully selected cases, and transcatheter tricuspid valve interventions (TTVIs) have emerged as a low-risk alternative for this high-risk cohort. Increasing data demonstrate the clinical safety and efficacy of TTVIs, but uncertainties remain concerning optimal case selection and procedural timing. Herein, we review newly established techniques alongside emerging clinical and procedural outcome data.
Atrial fibrillation (AF) prevalence has increased markedly over the past two decades, underscoring the need for personalized approaches to diagnosis, risk stratification, and therapy. Computational modeling provides a framework to integrate patient-specific anatomy and electrophysiology, offering mechanistic insights into arrhythmia susceptibility. We analyzed a virtual population of 160 bi-atrial models to investigate how structural and electrophysiological markers contribute to AF vulnerability and patterns. Each virtual patient incorporated geometries with varying enlargement, structural (conduction velocity, CV), and electrical (action potential duration, APD) remodeling. Virtual patients were characterized through anatomical markers, defined as inter-landmark distances, and electrophysiological markers, such as total activation time. AF vulnerability was tested by programmed stimulation from multiple atrial sites in 800 simulations. Lower CV and APD increased arrhythmic incidence, consistent with prior work. Larger atrial lateral extent and longer Bachmann's bundle length raised AF initiation likelihood by ∼20% ( p < 0.05), while total activation time did not distinguish inducible from non-inducible anatomies ( p > 0.05). Anatomical features, including superior-to-inferior vena cava distance, distinguished organized from disorganized patterns, while electrophysiological biomarkers alone did not. Combined high anatomical and electrophysiological marker values were linked to greater inducibility during AF progression (+20%). These findings provide mechanistic evidence for the role of atrial biomarkers in AF initiation and maintenance, highlighting the value of virtual populations in capturing inter-patient variability. By linking structural and electrophysiological characteristics to arrhythmic risk, this approach supports improved patient stratification and the design of individualized therapeutic strategies for AF.
Objective:The study aimed to investigate which anthropometric indicator are most associated with cardiovascular risk (CVR) in low-income women with short stature and to determine the cut-off point that best determined CVR. Methods:This cross-sectional study was conducted with meticulous attention to detail. We evaluated a comprehensive range of sociodemographic and anthropometric data, including body mass index (BMI), waist circumference, waist-to-hip ratio, waist-to-height ratio, and body adiposity index. Additionally, dietary and biochemical data such as glucose and lipid profile, ultrasensitive C-reactive protein (CRP), and blood pressure were assessed in 83 women. Body composition was measured using dual-energy X-ray absorptiometry. Results:Approximately 85% had excess total body fat, 70% had low levels of high-density lipoprotein and increased levels of ultrasensitive CRP, 29.3% were hypercholesterolemic, and 13.4% were hypertensive. Multivariate logistic regression analyses indicated that BMI was the most associated factor of CVR (ultrasensitive CRP) (OR: 1.31, 95% CI: 1.10-1.56). The area under the receiver operating characteristic curve was 0.64 for cholesterol (95% CI 0.517-0.766; p = 0.04) and 0.72 for ultrasensitive CRP (95% CI 0.601-0.840; p = 0.002). BMI cut-off points with the best balance of sensitivity and specificity were 24.0 kg/m2 for identifying hypercholesterolemia and 23.8 kg/m2 for identifying elevated high-sensitivity CRP levels. Conclusion:BMI was the most associated factor of CVR in low-income women with short stature. The results indicate that more sensitive BMI cut-off points should be considered to detect CVR in this population group.
Objectives Functional mitral regurgitation (FMR) remains challenging to repair surgically, as highlighted by the Cardiothoracic Surgical Trials Network (CTSN) trial, which showed limited durability of mitral annuloplasty. We previously demonstrated in vivo and experimentally that papillary muscle approximation (PMA) can improve mitral valve (MV) function, with or without annuloplasty. In this study, we assessed valve biomechanics after PMA, mitral annuloplasty, and their combination in imaging-derived computational models.Methods 3D echo images were obtained in three pigs with heart failure, dilated ventricles, and FMR. Each echo dataset was segmented, and a subject-specific computational model of the MV was created. Virtual FMR repair was performed on each valve using PMA, annuloplasty with true-sized (40 mm) and downsized (38 mm and 36 mm) rings, and a combination of both techniques. For each repair strategy, leaflet closure was simulated, and MV geometry and biomechanics at peak systole were evaluated.Results Isolated PMA improved valve coaptation, reduced leaflet stresses and chordal tension forces, but failed to completely eliminate FMR. Isolated mitral annuloplasty also improved coaptation, but overall provided only limited geometric and biomechanical benefits. Combining annuloplasty and PMA resulted in the most favorable outcomes, eliminating FMR, increasing coaptation length (up to 97.7%), and reducing leaflet stresses (up to 43.7%) and chordal forces (up to 43.0%).Conclusions While both PMA and annuloplasty independently improved MV function, neither technique fully resolved FMR on its own. Their combination yielded the most favorable repair outcomes, eliminating FMR and significantly improving valve geometry and biomechanics without the need for excessive annular downsizing.
Background:The 12-lead electrocardiogram (ECG) records body-surface potentials that represent cardiac electrical activity filtered through the torso. Recovering the original cardiac sources from these surface signals-the inverse problem of electrocardiography-is mathematically ill-posed: multiple distinct source configurations produce identical tracings. This constraint is seldom discussed in clinical practice, yet it underlies many recognized ECG diagnostic limitations. Methods:This narrative review provides a clinician-oriented summary of the forward and inverse formulations, and then organizes ECG interpretive pitfalls into five mechanistic categories: volume-conductor filtering, source-model ambiguity, cardiac motion during repolarization, patient-specific anatomy and lead-placement variability, and signal noise and filtering. Each category is linked to quantitative clinical data and to practical reporting recommendations. Results:Volume-conductor attenuation limits VA localization accuracy to 38.9% at the AHA-segment level. Source ambiguity allows 59% of combined anterior-inferior ST elevation to originate from RCA rather than LAD occlusion, and permits unrelated diseases (pulmonary embolism, arrhythmogenic cardiomyopathy) to produce identical repolarization patterns. Cardiac motion during repolarization introduces time-variant geometric distortion independent of pathology. The Mason-Likar lead system erases established inferior infarctions and shifts QRS axes by up to 60°. Fragmented QRS detects scar (sensitivity 68%, specificity 80%) but fails territorial localization (sensitivity 1.7%). Electrocardiographic imaging reduces localization error but cannot recover spatial detail lost to the torso filter. Conclusions:The inverse problem imposes identifiability limits on every 12-lead ECG. Territorial labels should be treated as probabilistic and corroborated with imaging or hemodynamics when localization carries therapeutic consequences.
Lowering low-density lipoprotein cholesterol (LDL-C) is a cornerstone of atherosclerotic cardiovascular disease (ASCVD) prevention, with robust evidence supporting the principle that "the lower, the better," particularly in secondary prevention. Contemporary guidelines recommend intensive LDL-C lowering to <70 mg/dL in high-risk patients and <55 mg/dL in very high-risk populations, including those with acute coronary syndrome and familial hypercholesterolemia. In addition to statins, proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors, including monoclonal antibodies and small interfering RNA, have emerged as highly effective therapies, demonstrating substantial LDL-C reduction and cardiovascular event risk reduction, as exemplified by the Further Cardiovascular Outcomes Research with PCSK9 Inhibition in Subjects with Elevated Risk (FOURIER) trial. Patients with peripheral arterial disease, including lower extremity arteriosclerosis obliterans, represent a particularly high-risk population in whom PCSK9 inhibition provides marked absolute risk reduction. Despite intensive LDL-C lowering, considerable residual cardiovascular risk persists. Accumulating evidence indicates that elevated triglyceride (TG) levels are independently associated with cardiovascular events. However, clinical trials targeting TG reduction, including fibrate-based therapies such as pemafibrate, have not consistently demonstrated cardiovascular benefit, highlighting the complexity of lipid metabolism and the limitations of TG lowering alone. Lipoprotein(a) [Lp(a)] has recently gained recognition as a genetically determined, independent risk factor for ASCVD. Emerging antisense and RNA-targeted therapies have shown profound Lp(a)-lowering effects and are currently being evaluated in large-scale outcome trials. Future lipid management strategies will require a comprehensive approach that integrates LDL-C lowering, residual risk modification, and novel therapeutic targets such as Lp(a), with personalized risk stratification to optimize clinical benefit and cost-effectiveness.
Hypertrophic cardiomyopathy (HCM) stands as the most common monogenic cardiac disease, with an estimated prevalence historically reported as 1:500, but likely closer to 1:200 based on contemporary population studies in the general population. The past decade has marked a fundamental shift in therapeutic strategy: from symptomatic relief toward interventions directly targeting pathological sarcomeric hypercontractility. Conventional therapy relies on beta-blockers and non-dihydropyridine calcium channel antagonists, which provide symptomatic benefits through negative inotropic effects. For refractory left ventricular outflow tract obstruction, disopyramide constitutes an effective third-line option, although its anticholinergic profile requires cautious administration. Cardiac myosin inhibitors, mavacamten and aficamten, have introduced a novel therapeutic paradigm through direct modulation of actin-myosin cross-bridge formation. Pivotal clinical trials have demonstrated significant improvements in exercise capacity, reduction in obstruction severity, and enhancement of functional status, validating for the first time a therapeutic strategy that directly targets the underlying sarcomeric mechanism of hypercontractility. The therapeutic horizon includes next-generation myosin modulators, metabolic pathway interventions, and gene-based strategies. Current challenges involve accessibility to these therapies, substantial costs, and the requirement for mandatory regular echocardiographic monitoring. Future perspectives are oriented toward precision personalized medicine, integrating molecular therapeutics with genetic profiling to enable increasingly individualized risk stratification and therapeutic decision making.
Congestion drives symptoms and adverse outcomes in heart failure (HF), and loop diuretics remain the cornerstone of decongestion. Yet randomized trials of diuretic strategies and other acute decongestive approaches have not shown mortality benefit, while mechanistic studies demonstrate rapid neurohormonal activation after acute loop diuretic administration. In chronic HF, observational data consistently associate higher loop diuretic requirements-particularly above ∼40 mg/day furosemide equivalent or with dose escalation-with worse prognosis across HF phenotypes, though confounding by disease severity is likely. Decongestion needs vary across the HF trajectory: early guideline-directed therapy provides intrinsic decongestive effects, whereas advanced HF is marked by diuretic resistance and renal vulnerability. Preload-dependent states (notably cardiac amyloidosis and selected HFpEF phenotypes) require especially careful titration to avoid hypovolemia and low output, and robust protocol-level trial evidence is lacking. Contemporary randomized data do not demonstrate superiority of torsemide over furosemide. Small trials and systematic reviews suggest that in carefully selected, stable, non-congested patients, diuretic withdrawal or reduction can be feasible, with ∼25-35% requiring re-initiation within 1-3 months and consistent lowering of renin activity; however, clinical outcome benefit remains unproven. Overall, evidence supports maintaining euvolemia with the lowest effective diuretic dose and considering monitored deprescribing in appropriate low-risk patients.
Atrial fibrillation and venous thromboembolism cause significant morbidity and mortality worldwide. Therefore, anticoagulation therapy (even chronic) is mandatory for the broad majority of affected persons. Warfarin therapy has been, for decades, the best oral anticoagulant alternative for venous thromboembolism, as well as for stroke prevention in atrial fibrillation. However, modern oral direct oral anticoagulants (DOACs) are consolidated drugs for these purposes with well-designed pivotal randomized clinical trials, and with long data bases of clinical posterior experience which demonstrate better efficacy, safety, or both than warfarin. However, since DOACs also present some limitations, there are diverse emergent agents and strategies in anticoagulation. This manuscript reviews the available anticoagulation strategies for both clinical entities and presents new rational therapeutic targets in the hemostatic system.
The saga of antiarrhythmic drug (AAD) therapy reflects a field shaped by empiricism and burdened by challenges related to safety. The Singh-Vaughan-Williams classification was a timely necessity that eventually slowed pharmacological innovation by prioritizing electrophysiologic properties over arrhythmogenic mechanisms. The present, limited pharmacological armamentarium demands efforts to reassess legacy antiarrhythmics, repurpose non-antiarrhythmic agents as upstream or downstream therapy, and develop novel compounds. Flecainide, propafenone, and dronedarone have demonstrated their reliable efficacy and safety, even in patients with structural heart disease, which should allow clinicians to reduce their reliance on amiodarone. Previous concerns regarding the proarrhythmic risk of dofetilide and ibutilide are currently managed through careful patient selection and adequate QT interval monitoring. Novel targeted AADs are advancing through the development pipeline, of which etripamil and landiolol have already been approved. Other emerging drugs, such as SK channel blockers (AP30663 and AP31969), RyR2 blockers, CaMKII inhibitors, and TASK-1 blockers (doxapram), are aligned with the new paradigm of atrial fibrillation that focuses on triggers and re-entry. Once triggered, arrhythmias are perpetuated by the underlying substrate, which could be directly targeted by antifibrotic therapy. Developing concepts such as atrial cardiomyopathy allows clinicians to characterize substrate objectively, in order to assess disease severity and individualize antiarrhythmic treatment. The future of antiarrhythmic therapy will be reshaped by artificial intelligence and digital twinning, which allow precise phenotyping and a tailored approach based on individual patient profiles, complemented by rhythm monitoring through wearables.
Objectives:To identify patient factors associated with poor transthoracic echocardiographic image quality and to evaluate whether a simple pre-test triage model could improve imaging efficiency. Design:Retrospective cohort study with derivation and independent validation cohorts, together with a model-based cost-effectiveness analysis. Setting:Single large UK tertiary centre using routinely collected data from 2010 to 2020. Participants:70,597 adult transthoracic echocardiograms, divided into a derivation cohort (n = 40,000) and an independent validation cohort (n = 30,597). Main outcome measures:Poor image quality (limited or non-diagnostic vs good or adequate), model discrimination, sensitivity, specificity and comparative imaging costs. Results:Of 70,597 studies, 24,213 (34.3%) were poor quality, including 8582 (12.2%) non-diagnostic and 15,631 (22.1%) limited studies. Lung disease was the strongest predictor (OR 2.04, 95% CI 1.59 to 2.61), followed by suspected heart failure, inpatient status, arrhythmia, prior cardiac surgery and permanent pacemaker (all p < 0.01). Validation performance was modest (AUC 0.58; sensitivity 67.3%; specificity 45.7%). In a model-guided simulation using 2024/25 NHS tariffs, total imaging costs were lower than with standard care (£11.85 million vs £12.16 million), yielding an estimated saving of £317,331. Conclusions:Several routinely available clinical factors influence transthoracic echocardiographic image quality. Although individual-level prediction is modest, pre-test triage may help direct higher-risk patients to contrast echocardiography or alternative imaging, reducing repeat testing and improving efficiency.
Purpose Computed tomography angiography (CTA) is a key component of preprocedural planning for transcatheter aortic valve implantation (TAVI). Although current guidelines recommend electrocardiogram (ECG)-gated acquisition of the aortic root, non-ECG-gated CTA protocols are still used in clinical practice. The present study aimed to evaluate the clinical feasibility and safety of a non-ECG-gated CTA protocol for TAVI planning.Methods We conducted a retrospective, single-centre observational study including 194 consecutive patients who underwent TAVI between January 2012 and December 2024 and were planned using a non-ECG-gated, single-phase CTA protocol. CTA-derived anatomical measurements were used to guide prosthesis selection and vascular access planning. Clinical outcomes were assessed during the index hospitalization and up to 30 days.Results CTA measurements were successfully used to guide prosthesis sizing in all patients. Thirty-day all-cause mortality was 3.6%, stroke or transient ischaemic attack occurred in 1.5% of patients, and vascular complications were observed in 6.7%. Conduction disturbances occurred in 38.1% of patients, while new permanent pacemaker implantation was required in 3.1%. Paravalvular leak (PVL) was predominantly mild; no cases of severe PVL were observed, and no patient required surgical or interventional correction for PVL.Conclusion This study demonstrates that a non-ECG-gated CTA protocol appears feasible and may support TAVI planning in selected centres with experienced teams. In this single-centre experience, a non-ECG-gated CTA protocol provided sufficient anatomical information for TAVI planning, with acceptable short-term clinical outcomes. While ECG-gated CTA remains the reference standard, this approach may represent a pragmatic alternative when integrated into a structured workflow.
Background:Nearly 500,000 open-heart operations are performed annually in the United States, with complications such as postcardiotomy cardiogenic shock (PCCS) occurring in 2-9% of cases. Extracorporeal membrane oxygenation (ECMO) is a critical salvage therapy for patients unable to wean from cardiopulmonary bypass (CPB). This study aims to review our institution's experience with ECMO in managing PCCS and to analyze patient outcomes. Methods:Following IRB approval, a retrospective observational study was conducted on adult patients aged 32-84 years who underwent open-heart procedures with the use of CPB requiring ECMO support due to failed wean from CPB from 1 April 2014 to 31 December 2022. Data were analyzed from electronic medical records for demographics, procedural details, ECMO therapy duration, and outcomes. Results:Of 45 patients identified from 6346 open-heart procedures, 33 were male, and 12 were female, with an average age of 59.9 years. The majority of patients were Caucasian (88.8%, n = 40). Extracorporeal membrane oxygenation was initiated using venoarterial configurations in 100% (n = 45) of cases, with three patients transitioning to venovenous configurations. The median ECMO duration for all patients in the study was 4 days. In-hospital mortality was 51.1% (n = 23), while 48.9% (n = 22) of patients survived to discharge. Survivors were discharged to rehabilitation facilities (54.5%, n = 12), home (31.8%, n = 7), long-term acute care hospitals (9.1%, n = 2), or detention centers (4.5%, n = 1). Conclusions:Extracorporeal membrane oxygenation remains a valuable rescue therapy for PCCS, achieving a 48.9% survival rate. This study highlights the importance of timely intervention and underscores the need for future research into optimizing patient selection and perioperative management.
