We hypothesized that body surface area (BSA)-weighted left ventricular ejection fraction (LVEF) (bLVEF) would represent a superior predictor of mortality in off-pump coronary artery bypass grafting (OPCABG) patients than standard predictors. LVEF is associated with worse outcomes upon OPCABG, while referring left ventricular measurements to BSA should improve predictability.
The bLVEF was calculated by multiplying the LVEF by the BSA. The primary endpoint was all-cause mortality within 30 days of hospitalization, while secondary endpoints included major postoperative complications.
A total of 7927 patients from five leading cardiac centers participating in the Chinese Cardiac Surgery Registry were included in the final analysis, of which 7093 (89.48%) had normal LVEF, 639 (8.06%) presented heart failure with mid-range ejection fraction (HFmrEF), and 195 (2.46%) exhibited heart failure with reduced ejection fraction (HFrEF). The average bLVEF in the cohort was 109.63 ± 18.16. Both the mortality (odds ratio (OR) 0.97) and secondary endpoints (OR 0.97) followed a similar trend with increasing bLVEF, indicating that bLVEF is a more reliable predictor of adverse outcomes. The individual components of bLVEF, including BSA (area under the curve (AUC) 0.63) and LVEF (AUC 0.64), made minor contributions to mortality risk with relatively low AUC values. However, these components were less impactful than bLVEF (AUC 0.70). Notably, patients with a bLVEF less than 85 had an increased mortality risk relative to those whose bLVEF was 85 or higher (adjusted OR 4.65 (95% confidence interval (CI): 3.81–5.83; p < 0.01)).
The bLVEF serves as a key predictor of mortality in OPCABG patients, effectively eliminating BSA-related bias and demonstrating a strong capacity to predict mortality.
NCT02400125, https://www.clinicaltrials.gov/study/NCT02400125.
Tricuspid valve replacement (TVR), particularly as an isolated procedure, is historically associated with high perioperative risk and poor outcomes. This study aimed to evaluate in-hospital and long-term outcomes of isolated versus concomitant TVR and identify predictors of morbidity/mortality in patients with severe tricuspid regurgitation (TR).
This retrospective study included 245 consecutive adult patients who underwent surgical TVR at Beijing Anzhen Hospital between 1993 and 2019. Primary outcomes were in-hospital mortality and long-term survival. Univariate and multivariate logistic regression analyses were conducted to determine factors associated with in-hospital mortality, adjusting for chronic kidney disease (CKD) and TRI-SCORE. Additionally, univariate and multivariate Cox regression analyses were performed to identify factors associated with long-term mortality, adjusting for age, CKD, TRI-SCORE, and previous cardiac surgery history. Propensity score matching (PSM) and inverse probability of treatment weighting (IPTW) were utilized to adjust for baseline differences.
Patients were categorized into two groups: isolated TVR (n = 128) and concomitant TVR (n = 117). The mean age was 47 ± 13 years, 58.4% were male, and the mean left ventricular ejection fraction was 62 ± 10%. Isolated TVR patients had lower in-hospital mortality (7.8% vs. 17.9%; p = 0.017) compared to concomitant TVR patients. At 1, 5, and 10 years, the survival rates for isolated TVR were 89.1%, 83.3%, and 77.7%, respectively. For concomitant TVR, the corresponding rates were 72.6%, 68.9%, and 60.5%, respectively. Multivariate analysis identified isolated TVR as protective against in-hospital death (odds ratio (OR) = 0.40, 95% confidence interval (CI): 0.17–0.95; p = 0.037) and overall mortality (hazard ratio (HR) = 0.49, 95% CI: 0.30–0.81; p = 0.005). Additionally, TRI-SCORE and CKD were associated with in-hospital mortality, and both remained significant predictors of long-term mortality. IPTW and PSM analyses confirmed the results.
Isolated TVR is associated with lower in-hospital and long-term mortality compared to concomitant TVR. Early referral before multivalve disease progression and meticulous patient selection—particularly avoiding advanced right-sided heart failure or renal dysfunction—may optimize outcomes. These findings advocate for timely isolated TVR in select TR patients to mitigate the compounding risks of delayed intervention.
The coronary sinus reducer (CSR) is a percutaneous device designed to improve coronary blood flow and alleviate symptoms of refractory angina in patients with severe coronary artery disease (CAD) who are unsuitable for revascularization therapy. CSR originated from earlier surgical techniques, such as coronary sinus ligation (CSL), and functions by narrowing the coronary sinus to enhance perfusion in ischemic myocardial territories—particularly in the subendocardial regions—while also reducing microvascular resistance and increasing capillary recruitment. CSR is currently recognized as an effective treatment for patients with chronic refractory angina, especially those deemed ineligible for revascularization according to current European Society of Cardiology (ESC) guidelines. Moreover, emerging studies are expanding the understanding of the mechanism of action involved in CSR, demonstrating that this technique may also improve microvascular function, particularly in patients with coronary microvascular dysfunction. These trials have shown significant improvements in coronary microcirculation and reductions in angina symptoms, suggesting that CSR may have therapeutic potential beyond obstructive CAD. Thus, CSR may represent a promising treatment option for microvascular ischemia, thereby broadening its clinical applicability to patients with angina/ischemia and non-obstructive coronary arteries (ANOCA/INOCA).
Current evidence suggests that multiple arterial grafting improves long-term survival following coronary artery bypass grafting (CABG). Sequential radial artery (RA) grafting is known to be a safe approach for maximizing arterial revascularization. This study aimed to compare RA conduit patency between sequential and individual grafting.
A total of 274 CABG patients who received at least one RA graft between January 2017 and June 2021 were included in our retrospective study. The occlusion of RA anastomoses was assessed by postoperative computed tomography angiography or coronary angiography at follow-up. Group comparisons for long-term outcomes were conducted using adjusted Cox regression models.
The median image follow-up time was 1.8 years. Among the 278 total RA grafts, 208 were individual and 70 were sequential. Multivariable Cox analysis found that sequential anastomoses were an independent risk factor for RA graft occlusion (adjusted hazard ratio = 2.45, 95% confidence interval (CI): 1.15–5.22; p = 0.020). However, the observed rate of occlusion was low (2.9%) when all the target vessels for a sequential graft had a quantitative flow ratio of ≤0.71.
Sequential RA grafting is associated with graft occlusion compared with individual grafting. For each RA graft, the selection of only one target vessel with significant functional stenosis may be preferable to achieve superior long-term patency.
The low-density lipoprotein cholesterol (LDL-C)/(high-density lipoprotein C (HDL-C) + direct bilirubin (DBIL)) ratio has been linked to the development of atherosclerosis. However, the association of this ratio with clinical outcomes in patients with prior coronary artery bypass grafting (CABG) undergoing percutaneous coronary intervention (PCI) remains unclear. Therefore, this study aimed to explore whether the LDL/(HDL + DBIL) ratio is predictive of clinical outcomes in this patient group.
We retrospectively reviewed 1352 patients who underwent re-PCI after CABG surgery and categorized the patients into three groups based on the third quartile of the ratio levels. The primary endpoint was major adverse cardiovascular and cerebrovascular events (MACCE), defined as a composite of all-cause death, stroke, myocardial infarction, or target vessel revascularization.
During the follow-up period, the occurrence rate of MACCE in the high ratio group was significantly higher than that in the low to moderate ratio groups (9.9% vs. 11.4% vs. 20.1%; p < 0.001). This trend was consistent for cardiac death (6.2% vs. 6.2% vs. 9.8%; p = 0.021) and non-fatal myocardial infarction (3.2% vs. 4.0% vs. 7.4%; p = 0.003). After adjusting for other risk factors, Cox multiple regression analysis suggested that LDL-C/(HDL-C + DBIL) remained significantly correlated with MACCE (hazard ratio (HR) = 1.33, 95% confidence interval (CI): 1.186–1.193; p < 0.001) with the high ratio group having the highest risk (HR = 2.331, 95% CI: 1.585–3.427; p < 0.001). According to the subgroup analysis, the selection of bypass graft or native vascular PCI did not affect the relationship between the ratio and the occurrence of MACCE.
The LDL-C/(HDL-C + DBIL) ratio level is closely related to the risk of long-term MACCE in patients undergoing PCI after CABG surgery, and the LDL-C/(HDL-C + DBIL) level can be an important indicator for post-PCI risk assessment.
Coronary artery bypass grafting (CABG) remains a cornerstone in the treatment of advanced ischemic heart disease, offering durable and effective revascularization. Despite surgical success, long-term patient outcomes are often shaped by the progression of native coronary disease and the development of comorbid conditions. This narrative review explores seven critical domains in secondary prevention following CABG: Early recognition of postoperative complications, evidence-based pharmacotherapy, management of atrial fibrillation, lifestyle modification, psychological well-being, preservation of ventricular function, and collaboration within the multidisciplinary team. Effective secondary prevention can significantly reduce the risk of further cardiovascular events and support the longevity of the graft. Interventions such as lipid management, smoking cessation, and structured cardiac rehabilitation promote both physiological recovery and emotional resilience. Timely treatment of arrhythmias and ventricular dysfunction further reduces the risk of heart failure and recurrent ischemia. Primary care practitioners are uniquely positioned to lead the delivery of long-term secondary prevention. By integrating evidence-based strategies into routine care, these strategies can play a pivotal role in improving quality of life and long-term outcomes for post-CABG patients.
Drug-coated cardiovascular devices (DCCDs), including drug-eluting stents (DESs) and drug-coated balloons (DCBs), have significantly advanced interventional cardiology by reducing restenosis and improving long-term outcomes. However, their effectiveness is limited by challenges such as patient-device mismatch, variability in drug delivery kinetics, and dependence on operator experience. Traditional strategies for device selection and performance evaluation are often inadequate to address patient-specific complexities. This narrative review aims to explore how artificial intelligence (AI) can improve the design, deployment, and monitoring of DCCDs, focusing on personalized treatment strategies, regulatory implications, and future innovations in interventional cardiology. A targeted literature search was conducted in PubMed, Scopus, and Web of Science between 2020 and 2025 using keywords such as “artificial intelligence”, “drug-eluting stents”, “cardiovascular devices”, “machine learning”, and “intravascular imaging”. Studies were included based on their relevance to AI applications in DCCD design, procedural support, or post-procedural monitoring. AI has demonstrated significant potential throughout the DCCD lifecycle. In design, machine learning models enable optimization of drug release kinetics and device geometry. During procedures, AI improves real-time intravascular imaging interpretation and provides guidance for precise device placement. Post-intervention, predictive analyses using patient data can aid in the early detection of complications such as in-stent restenosis. Furthermore, technical, regulatory, and ethical challenges remain, including model validation, data bias, and the need for transparency in decision-making algorithms. AI-driven approaches offer a promising paradigm for advancing cardiovascular device technology toward more adaptable, personalized, and efficient care. Integrating explainable, clinically validated AI systems with DCCDs can improve outcomes, reduce procedural variability, and support value-based care. Future research should prioritize real-time intraoperative feedback systems, adaptive AI models based on longitudinal patient data, and regulatory compliance and fairness strategies.
Previous studies have shown a strong link between sleep and cardiovascular disease. However, the association of sleep duration and quality with coronary atherosclerotic plaque vulnerability remains unclear. This study aimed to investigate the correlation between sleep duration, sleep quality, and coronary plaque vulnerability using optical coherence tomography (OCT).
A total of 260 patients with stable angina who completed an OCT examination were included. Patients were divided into a thin-cap fibroatheroma (TCFA) group and a non-TCFA group according to the presence of TCFA on OCT. The sleep duration of the patients was recorded by questionnaire, and the sleep quality was evaluated using the Pittsburgh Sleep Quality Index (PSQI).
The TCFA group had significantly shorter sleep duration and higher PSQI values (p < 0.05). A multivariable logistic regression analysis revealed that sleep duration and PSQI were independent predictors of TCFA (p < 0.05). A receiver operating characteristic (ROC) study demonstrated that the area under the curve values for sleep duration and PSQI were 0.698 and 0.721, respectively, in predicting the presence of TCFA. Patients with a sleep duration ≤5.5 hours or a PSQI value >9 had a thinner fibrous cap thickness, a larger maximal lipid pool arc, and a higher incidence of TCFA and macrophage deposition (p < 0.05). Sleep duration was positively correlated with the thinnest fibrous cap thickness (r = 0.451; p < 0.001), and negatively correlated with the radian of the maximum lipid pool (r = –0.470; p < 0.001). The PSQI was negatively correlated with the thinnest fibrous cap thickness (r = –0.477; p < 0.001), and positively correlated with the radian of maximum lipid pool (r = 0.340; p < 0.001).
Both sleep duration and sleep quality were significantly associated with coronary plaque vulnerability. Patients with either insufficient sleep duration or poor sleep quality exhibited significantly greater plaque vulnerability.
Peripheral arterial disease (PAD) is a global atherosclerotic disease which can lead to acute limb ischemia, chronic limb-threatening ischemia, and limb amputation. It has similar risk factors to coronary artery disease (CAD). Elevated lipoprotein A (Lp[a]) is associated with CAD, myocardial infarction, and PAD. Patients with PAD can have CAD and polyvascular disease. An extensive PubMed and Cochrane library search was performed in April 2025 using the words “Lipoprotein A and PAD”, “Elevated lipoprotein A and PAD”, and “High Lipoprotein A and PAD” to obtain relevant English articles for this systematic review. An elevated Lp(a) may enhance the risk of PAD. Elevated Lp(a) can amplify the risk of CAD, PAD, and polyvascular disease. It may portend worse outcomes in patients with CAD and PAD. It can increase the risk of acute limb ischemia, coronary revascularization, peripheral revascularization, cardiovascular death, and all-cause mortality. Hence, elevated Lp(a) may serve as a risk factor for patients with CAD who could potentially develop PAD. No currently approved medical therapy aimed at Lp(a) reduction exists; only lipoprotein apheresis is approved to lower Lp(a) levels in these patients. This systematic review discusses the role of an elevated Lp(a) in PAD, clinical research in PAD with elevated Lp(a), and the current treatment for PAD and elevated Lp(a).
While sinus bradycardia and atrioventricular (AV) block in athletes have traditionally been viewed as benign consequences of enhanced vagal tone, recent evidence suggests that, in some individuals, nodal dysfunction may be intrinsic and potentially mediated by epigenetic mechanisms. Therefore, differentiating between these mechanisms is crucial for guiding appropriate clinical management.
Among 550 elite athletes undergoing routine cardiovascular evaluation, 72 were referred for a transesophageal electrophysiological study (EPS): 58 with significant sinus bradycardia or suspected AV node dysfunction (cases) and 14 athletes with symptoms consistent with supraventricular tachyarrhythmias but no bradyarrhythmia (controls). All participants underwent an EPS to assess corrected sinus node recovery time (CSNRT) and AV nodal Wenckebach point. In the case group, 24 athletes exhibited abnormal parameters at baseline and underwent a repeat EPS following complete autonomic blockade with intravenous propranolol and atropine, aimed at suppressing extrinsic autonomic influences.
The corrected sinus node recovery time exceeded 550 ms in 18 (31%) cases, and the Wenckebach point was greater than 500 ms in 8 (14%) cases. In all eight athletes with baseline AV conduction abnormalities, they normalized after autonomic blockade, consistent with a functional vagal mechanism. In contrast, the mean sinus rate remained unchanged after autonomic blockade, and in 12/18 (67%) of the athletes with prolonged CSNRT, continued to exhibit abnormal values despite autonomic suppression, indicating a probable intrinsic origin. Control subjects showed normal EPS parameters.
The EPS with a pharmacological autonomic blockade represents a useful approach for distinguishing extrinsic, functional bradycardia from intrinsic nodal disease in athletes. While AV node dysfunction appears exclusively vagally mediated and reversible, a subset of sinus node dysfunction cases may reflect early, possibly epigenetically driven, intrinsic alterations.
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease caused by the production of autoantibodies, which form pathogenic immune complexes that deposit in multiple organs, leading to the multisystem involvement characteristic of SLE. Cardiovascular complications contribute substantially to the morbidity and mortality associated with SLE. Thus, this review discusses the cardiac manifestations of SLE, including the epidemiology, risk factors, pathogenesis, clinical features, diagnosis, and treatment options. Furthermore, we discuss the role of autoantibodies, endothelial dysfunction, and immune complex-mediated injury in the pathogenesis of SLE. Finally, we discuss emerging therapies and future research directions aimed at mitigating cardiac complications in SLE.
Sex-specific disparities in the pathogenesis and outcomes of cardiovascular diseases (CVDs) highlight critical gaps in current clinical paradigms, particularly regarding endothelial dysfunction as a pivotal mediator of such differences. Males have a higher incidence of atherosclerosis-related CVD, while postmenopausal females experience microvascular dysfunction due to estrogen loss and androgen dominance. Estrogen confers cardioprotective effects via nitric oxide (NO)-mediated vasodilation and antioxidant pathways. In contrast, androgens exert dual pathological effects by promoting inflammation and oxidative stress in a concentration-dependent manner. Clinically, men develop obstructive coronary disease, whereas women present with underdiagnosed microvascular ischemia due to sex-neutral thresholds. Sex-specific risks (e.g., smoking/diabetes in women) and treatment disparities persist in CVDs, meaning sex-stratified diagnostics/therapeutics and trial reforms are needed to advance precision cardiology. Unlike traditional reviews that focus on mechanisms, this study aims to link molecular insights with translational strategies by proposing endothelial-targeted therapies, sex-adjusted diagnostic algorithms, and policy-driven trial reforms. By prioritizing the endothelial–sex hormone crosstalk as the nexus of pathophysiology and clinical translation, this synthesis advances precision cardiology beyond conventional symptom-focused paradigms.
Hypertrophic cardiomyopathy (HCM) and left ventricular hypertrophy (LVH) from other causes present similar features on transthoracic echocardiography (TTE), making an accurate differentiation challenging. Recent advancements in radiomics and deep transfer learning (DTL) have shown promise; however, no studies have combined these techniques to diagnose HCM and LVH resulting from other causes. Therefore, we developed a fusion model that integrates radiomic features from the left ventricular myocardium in the four-chamber view of TTE with DTL features to differentiate HCM from other causes of LVH, providing more reliable diagnostic support.
This multicenter study included 971 patients (303 with HCM, 668 with hypertensive heart disease and uremic cardiomyopathy). Patients from Institution 1 were split into a training set and an internal validation set, while patients from Institution 2 served as an external validation set. Radiomic features were extracted using pyradiomics, and DTL features were obtained via DenseNet121. Features were selected using least absolute shrinkage and selection operator (LASSO) and input into ten machine learning algorithms, with support vector machine (SVM) as the classifier. Model performance was assessed using receiver operating characteristic (ROC) curves and decision curve analysis (DCA) and compared with the diagnostic results of two ultrasound physicians.
The fusion model demonstrated excellent diagnostic performance: the area under the curve (AUC) values were 0.966 (training set), 0.945 (internal validation), and 0.934 (external validation), thereby outperforming models that used only radiomic or DTL features. DCA indicated superior clinical effectiveness, surpassing the diagnostic performance of two ultrasound physicians.
A fusion model combining radiomics and DTL features significantly improves the ability to distinguish HCM from other causes of LVH and has strong potential for clinical applications.
Congenital heart disease (CHD) is increasingly detected in cardiac imaging. Effective management of CHD requires thorough imaging of the heart and circulation, extending beyond simple anatomical identification. Cardiovascular computed tomography angiography (CCTA) provides rapid imaging, high spatial resolution, and precise visualization of three-dimensional vascular structures, while offering strong multi-planar reconstruction capabilities at sub-millimeter resolution and a wide field of view. These features enable CCTA to overcome the challenges faced by other imaging modalities. Thus, this review highlights the advantages of CCTA in evaluating simple cardiac shunts in adult congenital heart disease pre- and post-intervention.
The coexistence of type 2 diabetes (T2D), metabolic dysfunction-associated steatotic liver disease (MASLD), and cardiovascular disease (CVD) defines a clinical profile that is frequently observed in clinical practice. In addition to being highly prevalent, patients with this triad of diseases experience accelerated vascular aging and poor prognosis. Insulin resistance remains the common symptom; however, the systemic impact of this extends far beyond glucose handling, shaping inflammation, oxidative stress, and endothelial dysfunction. In this review, we highlight how these intertwined conditions challenge current diagnostic frameworks and therapeutic approaches. Moreover, we discuss under-recognized aspects, such as the contribution of gut-derived metabolites and adipose dysfunction, which often remain neglected in routine care despite strong mechanistic evidence. We also summarize the potential of noninvasive tools, biomarkers, and cardioprotective agents, such as sodium–glucose cotransporter-2 (SGLT2) inhibitors, glucagon-like peptide-1 (GLP-1) receptor agonists, and tirzepatide. While promising, these agents still face gaps in translation to everyday hepatology and cardiology clinics. Our message is that prevention and care should not be compartmentalized. Instead, an integrated, patient-centered approach, with early screening and multidisciplinary management, is needed to address this complex interplay. Moreover, recognizing the shared pathways of T2D, MASLD, and CVD may help clinicians anticipate potential complications and design more effective and sustainable strategies for long-term outcomes.
Angiography remains the standard imaging modality during cardiac catheterization; however, this technique provides only a two-dimensional representation of the coronary lumen, which limits the assessment of vessel wall pathology. In comparison, intravascular imaging techniques, such as intravascular ultrasound (IVUS) and optical coherence tomography (OCT), provide high-resolution cross-sectional and two-dimensional reconstructions of the coronary arteries. Thus, these modalities complement angiographic findings, enable detailed evaluation of underlying pathology, and facilitate precise procedural guidance. Advancements in imaging technologies, including near-infrared spectroscopy and virtual histology intravascular ultrasound, further enhance lesion characterization and procedural planning. An increasing body of evidence from registries, randomized controlled trials, and meta-analyses supports the use of intravascular imaging-guided percutaneous coronary interventions, demonstrating improved procedural success rates and superior long-term clinical outcomes. In the context of acute coronary syndromes (ACS), OCT offers critical diagnostic insights that enhance accuracy and inform optimal treatment strategies. This review highlights the evolving role of OCT in the management of ACS and the favorable impact of this technique on patient outcomes.
This study aimed to identify risk factors for contrast-induced nephropathy (CIN) following rotational atherectomy (RA) in patients with severely calcified coronary lesions to facilitate the prevention of CIN.
A retrospective analysis was performed on 111 patients who underwent RA in Wuhan Fourth Hospital from July 2021 to June 2023. The creatinine levels of the patients were detected within 48–72 hours after RA, and the patients were divided into a CIN (n = 16) and a non-CIN group (n = 95). Propensity score matching was applied with a caliper value set at 0.02, resulting in 13 matched patient pairs. The risk factors for CIN after RA in these patients were analyzed.
A total of 16 cases of CIN occurred among the 111 patients with coronary heart disease who underwent RA. Following propensity score matching, 13 patients were included in both the CIN and non-CIN groups. The rates of heart failure were significantly higher in the CIN group than those in the non-CIN group before RA (all p < 0.05). However, there was no significant difference in preoperative mean arterial pressure (MAP) between the two groups. Nonetheless, the rate of patients with preoperative MAP <80 mmHg was higher in the CIN group than in the non-CIN group (53.8% vs. 7.7%; p < 0.05). The coronary artery lesion characteristics and interventional treatment strategies were comparable between the two patient groups. Moreover, no statistically significant difference was observed in 1-year major adverse cardiovascular and cerebrovascular events (MACCEs) or secondary endpoint events between the two groups. Logistic regression analysis showed that among the risk factors for CIN after RA, preoperative MAP <80 mmHg (odds ratio (OR) = 17.865, 95% confidence interval (CI): 1.135–281.246) was a risk factor for CIN (p < 0.05).
Patients with a preoperative MAP below 80 mmHg are at increased risk of CIN following RA. This cohort requires intensive monitoring to prevent CIN, ensuring prompt implementation of management strategies to avert CIN onset and mitigate the adverse effects of CIN post-RA treatment.
While a potential relationship between red cell distribution width (RDW) and cardiac arrest (CA) prognosis has been raised, the question of whether there is robust data to support this connection remains open. To examine the association of red blood cell distribution width with prognosis in patients with cardiac arrest.
This study strictly followed the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. Relevant studies were identified from searches conducted in the PubMed, Web of Science, the Cochrane Library, and Embase electronic databases up to March 12, 2025. The Newcastle–Ottawa scale was used to assess the quality of the included studies. The combined effect size was determined utilizing standardized mean differences (SMDs), hazard ratios (HRs), and 95% confidence intervals (CIs). Subgroup analyses were also performed to elucidate the sources of heterogeneity. Simultaneously, we also pooled sensitivity (SEN), specificity (SPE), diagnostic odds ratios (ORs), and the area under the summary receiver operating characteristic curve (AUROC).
This meta-analysis encompassed eight studies involving CA patients with CA. Our results suggested that patients who died after CA exhibited higher RDW levels than those who survived (SMD = 0.45; 95% CI: 0.30–0.60). There was a 1.63-fold higher risk of death in CA patients with high RDW levels versus those with low levels (95% CI: 1.27–2.08). The SEN, SPE, and AUC for using the RDW to predict mortality were 0.82 (95% CI: 0.74–0.88), 0.49 (95% CI: 0.23–0.74), and 0.80 (95% CI: 0.76–0.83), respectively.
RDW is a relatively accurate predictor of prognosis in patients after CA. Thus, using RDW can provide some insights into patient outcomes, enabling healthcare professionals to make informed decisions in advance.
CRD420251023018, https://www.crd.york.ac.uk/PROSPERO/view/CRD420251023018.
Brugada syndrome (BrS) is an inherited cardiac arrhythmia disorder associated with sudden cardiac death (SCD), primarily due to ventricular tachycardia (VT) or ventricular fibrillation (VF). Meanwhile, atrial fibrillation (AF) is becoming increasingly recognized in BrS cases, with a higher prevalence noted among individuals harboring Sodium Voltage-Gated Channel Alpha Subunit 5 (SCN5A) variants. However, the prognostic value and management implications of AF in BrS remain unclear. Therefore, this narrative review aims to summarize current evidence on the prevalence, clinical significance, pathophysiological mechanisms, and management of AF in BrS. Relevant studies were identified through systematic searches in the PubMed, EBSCOhost, and Google Scholar databases from inception to July 2025 using Boolean operators with keywords such as “Brugada Syndrome” AND “Atrial Fibrillation”, “Brugada” AND “AF” AND “Management”, and “Brugada” AND “SCN5A” AND “Atrial Arrhythmia”. The bibliographies of the selected articles were further reviewed to identify additional relevant studies. The prevalence of AF among patients with BrS ranged from 6% to 39% across various cohorts. Observational studies demonstrated a higher incidence of SCN5A-positive BrS, suggesting that overlapping atrial and ventricular arrhythmogenic substrates exist. Unrecognized BrS in patients presenting with AF may result in inappropriate administration of sodium channel-blocking agents, potentially triggering malignant ventricular arrhythmias. Management strategies include the careful selection of antiarrhythmic drugs, consideration of pulmonary vein isolation (PVI), and implantation of an implantable cardioverter-defibrillator (ICD) device in high-risk cases. Quinidine remains a potential pharmacological option for recurrent ventricular arrhythmias. AF is a relatively common but understudied arrhythmia in BrS. While the direct association of AF with SCD remains uncertain, AF may serve as a marker of a more arrhythmogenic phenotype in BrS. Nonetheless, current guidelines provide limited recommendations for managing AF in this population, underscoring the need for individualized treatment strategies and further research.
Since the beginning of the percutaneous coronary intervention (PCI) era, periprocedural myocardial infarction (PMI) has been recognized as a potential source of impaired outcomes in patients undergoing revascularization. Subsequently, several different definitions of PMI have been provided, coming from trial research groups or international consensus. Despite these efforts, the debate over the prognostic value or PMI in terms of mortality risk, as well as its role in defining composite ischemic endpoints in clinical investigations, has been extremely active. Currently, three international definitions of PMI are available: the Universal Definition of Myocardial Infarction (UDMI), the Academic Research Consortium (ARC)-2 definition, and the definition by the Society for Cardiovascular Angiography and Interventions (SCAI). These definitions differ significantly in terms of sensitivity and prognostic relevance, which has led to heterogeneous findings in clinical studies investigating this topic. Thus, this review aims to provide an overview of the main features of these definitions, their association with the risk of mortality, and how different definitions can influence the results of major investigations in the research setting.
Despite the established concordance between core temperature and brain temperature (BT) in out-of-hospital cardiac arrest (OHCA) patients, the relationship between BT and neurological outcomes in those who received targeted temperature management (TTM) has yet to be elucidated. Thus, this study aimed to explore the relationship between BT and neurological outcome in OHCA patients who received TTM.
This observational study involved adult patients (≥18 years) with OHCA who received TTM at 33 °C between April 2021 and December 2023. We recorded BTs at the initiation of TTM (BTINI) and during the maintenance phase of TTM (BTMAIN). A neurological outcome at 6 months was the primary outcome. Poor outcome was considered as Cerebral Performance Categories 3, 4, and 5.
Of the 149 included patients with OHCA, 109 (73.2%) patients exhibited poor outcomes. Compared with the good outcome group, the BTINI (35.8 °C [interquartile range (IQR), 33.4–36.3 °C] vs. 33.4°C [IQR, 32.6–35.4 °C]) and BTMAIN (33.1 °C [IQR, 32.8–33.2 °C] vs. 32.6 °C [IQR, 32.2–32.9 °C]) were lower in the poor outcome group. Multivariate analysis after adjusting for confounders revealed that BTINI (odds ratio (OR), 0.223; 95% confidence interval (CI), 0.054–0.917; p = 0.038) and BTMAIN (OR, 0.078; 95% CI, 0.019–0.322; p < 0.001) were associated with poor outcomes.
BTs at the initiation of TTM and during the maintenance phase of TTM at 33 °C are associated with poor outcomes.
The clinical value of remnant cholesterol (RC) in patients with in-stent restenosis (ISR) who undergo percutaneous coronary intervention (PCI) is unknown. Therefore, this study aimed to clarify the association between increased RC levels and clinical prognosis in patients with ISR.
This retrospective study enrolled 836 patients diagnosed with ISR. The study population was divided into four quartiles (Q1–Q4) according to median RC levels. Using a multivariate Cox proportional hazards model and Kaplan–Meier (KM) curve, the association between RC levels and the study endpoint, defined as target-vessel failure (TVF) within 3 years after PCI, was investigated. A discordance analysis was also performed with several definitions.
The KM curve showed an increased risk of TVF with elevated RC levels (p < 0.001). After adjustment, the RC level was identified as an independent predictor of TVF, regardless of whether the metric was considered as a continuous or categorical variable (hazard ratio (HR) = 1.37, 95% confidence interval (CI): 1.16–1.62; p < 0.001; HR = 3.43, 95% CI: 1.85–6.36; p < 0.001). Subgroup analysis showed that the RC-related TVF risk was more pronounced in patients with low-density lipoprotein cholesterol (LDL-C) <1.8 mmol/L (2.75 for each one standard deviation (SD) increase, 95% CI: 1.66–4.55; p for interaction < 0.001). In the discordance analysis, individuals with discordantly high RC levels rather than high LDL-C levels had an increased risk of TVF (HR = 2.02, 95% CI: 1.33–3.07; p < 0.001).
An increased RC level was associated with an elevated risk of TVF in patients with ISR who underwent PCI. Further, the RC-related risk was more pronounced in patients with LDL-C levels <1.8 mmol/L.
Ventricular tachycardia (VT) can originate from diseased myocardium resulting from ischemic or nonischemic cardiomyopathy. Scar-related VT is predominantly sustained by reentrant circuits within areas of myocardial scar. The therapeutic target within these circuits is the isthmus—an electrically insulated pathway bounded by electrical barriers. To elucidate the mechanisms of isthmus formation and the structural characteristics of VT circuits, electrophysiological mapping during VT has advanced in parallel with technological innovations, including intraoperative mapping, electroanatomical mapping, and, more recently, high-density mapping using multipolar catheters. We have recently characterized VT circuits involving the intramural component and proposed a hyperboloid model to conceptualize three-dimensional VT propagation. Furthermore, we demonstrated that the majority of isthmus boundaries are formed by anatomically fixed lines of conduction block, as identified by substrate mapping. Novel technologies, such as a frequency analysis of intracardiac electrograms and micro-mapping catheters for the coronary vessels, have also been developed to investigate intramural VT circuits.
Post-traumatic stress disorder (PTSD), which develops in susceptible individuals after life-threatening or traumatizing events, manifests as a heightened anxiety and startle reflex, disordered sleep, nightmares, flashbacks, and avoidance of triggers. Moreover, PTSD is a predictor and independent risk factor of numerous cardiovascular comorbidities, including stroke, myocardial infarction, coronary atherosclerosis, and atrial fibrillation. Compounding the direct detrimental effects of PTSD on the cardiovascular system, this condition provokes classical cardiovascular risk factors, including high cholesterol and triglycerides, platelet hyperaggregation, endothelial dysfunction, hypertension, and sympathetic hyperactivation. Although most people who have experienced traumatic events do not develop PTSD and are considered PTSD resilient, a substantial minority experience persistent cardiovascular comorbidities. Experimental and clinical studies have revealed a myriad of biomarkers and/or mediators of PTSD susceptibility and resilience, including pro- and anti-inflammatory cytokines, oxidized proteins and lipids, antioxidants, troponin, catecholamines and their metabolites, glucocorticoids, and pro-coagulation factors. The use of biomarkers to predict cardiovascular susceptibility or resilience to PTSD may stratify the risk of a patient developing cardiovascular complications following severe stress. Indeed, since many PTSD biomarkers either inflict or attenuate cardiovascular damage, these biomarkers can be applied to monitor the efficacy of exercise, dietary modifications, and other interventions to enhance cardiovascular resilience and, thereby, restrict the detrimental effects of PTSD on the cardiovascular system. Biomarker-informed therapy is a promising strategy to minimize the risk and impact of cardiovascular diseases in individuals with PTSD.
Tuberculosis (TB) is a contagious disease caused by Mycobacterium tuberculosis (M. tuberculosis) and is transmitted through airborne particles. Although TB usually damages the lungs, this disease can also cause complications in various organs, including the cardiovascular system. Indeed, pericarditis represents the most frequently reported cardiac manifestation of TB, and may present alongside fever, dyspnea, cough, or increased central venous pressure, hepatomegaly, and peripheral edema. Tuberculous-related pericarditis treatment is challenging due to the poor penetration of anti-tuberculous drugs into the pericardium. Myocarditis is another form of cardiac manifestation and is often associated with arrhythmias. Tuberculous aortitis typically causes dilatation leading to pseudoaneurysm formation and is usually asymptomatic; however, this manifestation can result in sepsis, aortic rupture, or even death, although rarely. Cardiac tuberculomas may present with general symptoms and can impair heart function by obstructing the outflow tracts, leading to ventricular dysfunction. Additionally, the primary treatment of TB carries cardiotoxicity risks, such as various arrhythmias. Moreover, TB significantly increases the risk of cardiovascular conditions, including myocardial infarction and coronary artery obstruction. Therefore, early recognition and a multidisciplinary approach are crucial to prevent severe outcomes such as sudden cardiac death, sepsis, or aortic rupture. Thus, this review highlights the spectrum of TB-related cardiac complications and underscores the importance of greater awareness and timely multidisciplinary care.
This review aims to summarize the status and future directions of pediatric heart failure (HF) pharmacotherapy. Notably, managing HF in children presents unique challenges due to heterogeneous etiologies and a longstanding paucity of pediatric-specific data. While historically reliant on adult-derived evidence, current treatment strategies are evolving through an integration of novel and pediatric-focused therapies. Indeed, present pediatric HF algorithms, adapted from adult guidelines, now include four pharmacologic pillars: angiotensin-converting enzyme (ACE) inhibitors/angiotensin receptor blockers/angiotensin receptor–neprilysin inhibitors (ARNIs), β-blockers, mineralocorticoid receptor antagonists, and sodium–glucose cotransporter-2 (SGLT2) inhibitors. Multicenter registries, such as the Pediatric HF Registry, the Pediatric Cardiomyopathy Registry (PCMR), and the Advanced Cardiac Therapies Improving Outcomes Network (ACTION) HF medication titration projects, are further shaping a more evidence-informed and personalized approach. A comprehensive literature search was conducted using PubMed, Scopus, and Google Scholar to identify recent review articles, clinical trials, and guideline documents relevant to pediatric HF pharmacotherapy. The search focused on articles published in the English language from the past decade, with particular attention to transformative therapeutic insights. Data from adult HF studies were also included to provide context and bridge gaps in pediatric evidence. Where available, pediatric-specific data were prioritized to inform applicability. Relevant findings were critically appraised, synthesized, and integrated to develop a cohesive narrative reflecting current trends and emerging directions in pharmacological management of pediatric HF. This review examined the evolving landscape of medical therapies for chronic pediatric HF, underscoring the limitations of a one-size-fits-all approach. The heterogeneity of underlying etiologies complicates the development of guideline-directed treatments tailored to children, particularly when attempting to stratify care by phenotypes such as heart failure with reduced ejection fraction (HFrEF) and preserved ejection fraction (HFpEF), as is commonly practiced in adult populations. There is an urgent need to individualize treatment strategies based on the hemodynamic profile of each pediatric patient, advocating for the integration of precision-based care into guideline-directed medical therapy. Such an approach not only enhances clinical outcomes in a population marked by etiologic diversity and developmental variability but also informs scalable care models and future guideline frameworks that reflect the unique needs of children with HF.
Electrocardiographic imaging (ECGi) is an innovative noninvasive mapping technique. Indeed, ECGi enables the identification of the earliest points of cardiac activation in both atrial and ventricular focal arrhythmias, as well as rotors and high-frequency domains that could act as potential drivers of atrial fibrillation. Currently, ECGi is most widely used in the management of ventricular tachycardia (VT). Meanwhile, in cases of macro-reentrant arrhythmias, ECGi assists in outlining the re-entry circuit and identifying the myocardial exit site. Additionally, current research is focusing on detecting myocardial scars and critical isthmuses. This information is particularly valuable for planning stereotactic arrhythmia radioablation procedures for VT in patients where invasive electroanatomic maps are unavailable, and a fully noninvasive approach is preferred. The present review aims to examine commercially available options for noninvasive ECG mapping (Amycard, CardioInsight, VIVO, Acorys, and vMAP), highlighting key features and limitations.
Tricuspid regurgitation (TR), a condition that was once thought to be of little clinical importance, is now recognized as a progressive disease associated with increased morbidity and mortality. Despite the prevalence of TR, this condition remains undertreated due to the absence of effective medical therapy and high surgical risk. However, tricuspid transcatheter edge-to-edge repair (T-TEER) using the TriClip system has emerged as a new approach, offering a minimally invasive alternative for patients with symptomatic severe TR and prohibitive surgical risk. Thus, this comprehensive review outlines a step-by-step approach to TriClip implantation, encompassing anatomical and pathophysiological foundations, patient selection criteria, imaging protocols, and procedural techniques. Emphasis is placed on the critical role of transesophageal echocardiography for device guidance, leaflet grasping, and confirmation of procedural success. Moreover, key intra-procedural challenges and troubleshooting strategies are discussed in detail, along with post-procedural management, including antithrombotic therapy, imaging surveillance, and functional assessment. Comparative insights between TriClip and the PASCAL system are provided, highlighting technical and clinical differences, as well as implications for device selection. The emerging role of combined mitral and tricuspid TEER using a single steerable guide catheter is also explored, supported by early data suggesting the safety and efficacy of this combination. Evidence from randomized trials and real-world registries supports the safety, feasibility, and durability of TriClip-based T-TEER. Notably, as experience and technology continue to evolve, T-TEER is positioned to become a cornerstone in the management of functional TR in high-risk populations.
Pulmonary embolism (PE) is one of the leading causes of cardiovascular mortality, with a high 30-day mortality rate. Despite clear treatment guidelines based on patient risk profiles, evidence suggests a discrepancy between clinical practice worldwide and the recommendations outlined in these guidelines. This deviation is often due to the comorbidities present in patients with PE, which complicate management decisions. As a result, alongside traditional standard-of-care treatments, novel emerging therapies are being explored to address these challenges. This review aims to provide an overview of the current epidemiology, initial assessment strategies, conventional treatment options, and emerging therapeutic approaches for PE.
Current guidelines recommend the use of either fractional flow reserve (FFR) or instantaneous wave-free ratio (iFR) for assessing intermediate coronary stenoses. However, FFR/iFR discordance occurs in approximately 20% of cases. This systematic review and meta-analysis aimed to investigate whether deferring lesions with discordant FFR/iFR classification is associated with worse prognosis compared to those with negative concordant results (FFR–/iFR–).
A systematic search was conducted in literature repositories to identify all studies that compared the clinical prognosis of deferred lesions with discordant and concordant FFR/iFR results. The primary endpoint was a composite clinical outcome of the individual secondary endpoints (death, myocardial infarction, and revascularization).
Three eligible observational studies (1735 deferred vessels) were included in the meta-analysis. Overall, deferred lesions with FFR/iFR discordance presented numerically higher event rates for all primary and secondary endpoints compared to deferred lesions with negative concordance; however, none reached statistical significance. Deferred lesions with FFR–/iFR+ discordance were significantly associated with an increased risk of death (odds ratio [OR]: 3.19; p = 0.049), while deferred lesions with FFR+/iFR– discordance were associated with a greater risk of revascularization compared to deferred lesions with negative concordance (OR: 3.24; p = 0.01).
Compared to deferred lesions with negative concordant results, deferred lesions with discordant FFR/iFR results were overall not significantly associated with worse clinical outcomes; however, there was a significantly greater risk of death for deferred lesions specifically with FFR–/iFR+ discordance, and an increased risk of revascularization for deferred lesions with FFR+/iFR– discordance. Further dedicated trials are needed to improve guidance in clinical decision-making.
CRD420251135424, https://www.crd.york.ac.uk/PROSPERO/view/CRD420251135424.
To accumulate and evaluate current evidence on bleeding complications associated with antiplatelet therapy and the specific contributions of pharmacists and nurses to bleeding-risk mitigation. Antiplatelet agents prevent arterial thrombosis by inhibiting platelet aggregation through blocking cyclooxygenase-1, P2Y12 receptors, glycoprotein (GP) IIb/IIIa receptors, or phosphodiesterase pathways. These mechanisms simultaneously impair primary hemostasis, increasing the risk of intracranial, gastrointestinal, or other clinically significant bleeding. Bleeding risk is dose-, duration-, and drug-dependent; meanwhile, dual antiplatelet therapy (DAPT) and concurrent use of anticoagulants, non-steroidal anti-inflammatory drugs (NSAIDs), corticosteroids, or proton pump inhibitors all amplify the risk. Patient-specific factors, likely older ages, anemia, renal or hepatic impairment, prior bleeding, cancer, diabetes, and frailty further increase the hazard. Shortened DAPT or P2Y12 inhibitor monotherapy reduces bleeding without increasing thrombotic events. Pharmacists optimize regimens, screen for interactions, educate patients, and co-develop institutional protocols; nurses monitor early signs of bleeding, ensure adherence, and coordinate multidisciplinary care. Both roles demonstrably decrease the incidence and severity of bleeding. Individualized antiplatelet strategies, guided by refined risk-stratification tools and delivered through pharmacist-nurse integrated care models, can maximize antithrombotic benefit while minimizing bleeding harm. Thus, large prospective trials and cost-effectiveness analyses are warranted to validate these multidisciplinary interventions.
Atrial fibrillation (AF) is a major complication of hypertrophic cardiomyopathy (HCM) with significant prognostic implications. Current risk prediction models lack the integration of comprehensive cardiac magnetic resonance (CMR) metrics and subtype-specific analyses.
A retrospective study of 405 HCM patients (86 with AF) was performed from 2019 to 2024. After excluding highly correlated variables (|r| > 0.8), the cohort was split into training and validation sets in a 7:3 ratio. Least Absolute Shrinkage and Selection Operator (LASSO) regression and multivariable logistic regression analyses were used to identify predictors, with model performance assessed via receiver operating characteristic (ROC) curves, calibration plots, and decision curve analysis. Subgroup analyses were conducted for obstructive (HOCM) and non-obstructive (HNCM) subtypes.
Independent predictors of AF in the overall HCM cohort included right atrial diameter anteroposterior (RAD anteroposterior: odds ratio (OR) = 1.819, 95% confidence interval (CI) 1.130–3.007; p = 0.016), left ventricular end-systolic volume (LVESV: OR = 0.978, 95% CI 0.963–0.991; p = 0.002), septal mitral annular plane systolic excursion (MAPSE septal: OR = 0.850, 95% CI 0.736–0.976; p = 0.023), tricuspid annular plane systolic excursion (TAPSE: OR = 0.919, 95% CI 0.852–0.987; p = 0.022), and maximum left atrial volume (MaxLAV: OR = 1.016, 95% CI 1.004–1.029; p = 0.010). The model achieved an area under the curve (AUC) value of 0.850 in the training set and an AUC of 0.861 in the validation set. The HOCM subtype predictors included septal MAPSE and left atrial ejection fraction (LAEF); meanwhile, the HNCM predictors included septal MAPSE, maximal left atrial volume (MaxLAV), and right atrial ejection fraction (RAEF).
A validated multiparametric CMR model can accurately predict AF risk in HCM patients, with subtype-specific predictors enabling personalized monitoring and early intervention.
This review aims to synthesize current evidence on the role of cardiac energy metabolism in the pathogenesis of dilated cardiomyopathy (DCM), with a focus on myocardial blood flow, substrate utilization, genetic and metabolic pathways, and potential energy-targeted therapeutic strategies. DCM involves structural and functional impairments of the myocardium, often linked to genetic mutations (e.g., in titin (TTN) and lamin) or acquired factors, including infection, alcohol, drugs, and endocrine disorders. Moreover, the disruption of cardiac energy homeostasis is central to the pathogenesis of DCM, characterized by compromised energy supply, altered substrate metabolism, and reduced adenosine triphosphate (ATP) production, all of which collectively contribute to contractile dysfunction and disease progression. Emerging evidence indicates that impaired myocardial energetics, including reduced coronary blood flow, shifts in fuel utilization, and dysregulation of energy metabolic pathways, are hallmark features of DCM. Nonetheless, energy deficiency is increasingly being recognized as a key driver of DCM development and heart failure. Cardiac energy metabolic disruption is intimately involved in the pathophysiology of DCM and represents a promising target for novel therapeutic interventions. Current management strategies often overlook metabolic aspects; therefore, this review highlights the need to integrate energy-based approaches into the treatment paradigm for DCM.
Previous studies on acute myocardial infarction (AMI) complicated by atrial fibrillation (AF) have mainly focused on anatomy or underlying disease state, and its prognostic predictors have not been fully explored. Therefore, there is a need for an effective prognosis model for patients with AMI-AF.
We retrospectively selected 126 patients with acute myocardial infarction complicated with AF hospitalized in Beijing Anzhen Hospital from January 2020 to December 2024 as the case group, and 1719 patients without AF as the control group. The clinical characteristics and laboratory test results of the two groups were compared to determine independent risk factors for AF in patients with acute myocardial infarction. The predictive performance of the model was evaluated by plotting Receiver Operating Characteristic (ROC) for each independent predictor. For the combined model, we used R software to build pattern plots, calibration plots, and Decision Curve Analysis (DCA) based on a multivariate logistic regression model.
Multivariate Logistic regression analysis showed that older age (Odds Ratio (OR) = 1.067, 95% CI: 1.044–1.092), longer hospitalization days (OR = 1.039, 95% CI: 1.013–1.066). The AUCs for age, hospitalization days, history of coronary heart disease, heart rate, International Normalized Ratio (INR), Hemoglobin, and mean platelet volume were 0.721, 0.663, 0.577, 0.614, 0.688, 0.438, and 0.607. The AUC of nomogram model for predicting AF in AMI patients was 0.833 (95% CI: 0.796–0.870, p < 0.001), the sensitivity was 0.817, and the specificity was 0.726. The nomogram model indicated a clinical net benefit when the predicted risk threshold exceeded 0.06.
Multivariable prediction model has good prediction effect. The variables in this nomogram model are easily obtained in clinical practice and can provide reference for individualized prediction of AF in AMI patients.
Current evidence characterizing the association between relative fat mass (RFM) and cardiometabolic disease (CMD) remains limited, with critical gaps persisting in the understanding of age-dependent heterogeneity. Thus, this study aimed to assess the association between RFM and CMD risk across age groups.
This study utilized data from the China Health Evaluation And Risk Reduction Through Nationwide Teamwork (ChinaHEART), and enrolled 93,801 community-dwelling adults. CMD was defined as a composite diagnosis that included diabetes mellitus, myocardial infarction, and stroke. Meanwhile, RFM was derived from height, waist circumference, and sex. Participants were stratified into groups of young and middle-aged adults (35–59 years) and older adults (≥60 years). Multivariable logistic regression models were employed to estimate odds ratios (ORs) and 95% confidence intervals (CIs), and to test for interaction effects. Restricted cubic spline models were applied to examine dose–response relationships.
Among the 93,801 participants, 18,473 (19.69%) had CMD. In the fully adjusted models, each unit increase in RFM was associated with a 9% increase in CMD risk (OR = 1.09, 95% CI: 1.08–1.09). Compared to the lowest RFM quartile (Q1), higher risks were observed in the Q2 (1.68, 1.59–1.77), Q3 (2.56, 2.34–2.80), and Q4 (4.02, 3.68–4.39) groups (p for trend <0.001). A significant RFM–age interaction was identified (p for interaction = 0.001). Restricted cubic splines confirmed significant non-linear dose–response relationships (both p for overall association <0.001; p for non-linear <0.05), with distinct age-specific patterns. Older adults exhibited higher overall CMD risk compared to young and middle-aged adults. The lower RFM inflection point corresponds to an OR of 1 (30 vs. 34), highlighting the greater vulnerability of this age group and informing the future development of age-specific RFM thresholds.
RFM demonstrates a significant positive association with CMD risk, exhibiting age-dependent heterogeneity, and emphasizing age-tailored interventions for CMD prevention strategies.
Transcatheter aortic valve replacement (TAVR) has revolutionized the treatment landscape for severe symptomatic aortic stenosis among all surgical risk groups. Thus, following the expansion of TAVR use and constant improvements in TAVR platforms and implantation techniques, implementation has been extended to special population groups that were previously underrepresented in clinical trials. This review evaluates the role of TAVR in patients with unique clinical considerations, including those with active malignancies, psychiatric disorders, and advanced organ dysfunction. By examining current literature, we provide insights into the safety, efficacy, appropriateness, and specific challenges associated with TAVR in these patient groups.