BACKGROUND:Atrial high-rate episodes (AHRE) detected by cardiac implantable electronic devices (CIEDs) represent subclinical atrial tachyarrhythmias that are strongly associated with an increased risk of progression to clinical atrial fibrillation (AF) and thromboembolic events. The underlying bi-atrial electrical and mechanical remodeling that precedes AHRE remains incompletely understood, particularly the role of right atrial (RA) function. OBJECTIVES:This study aimed to identify combined electrocardiographic (ECG) and echocardiographic predictors of device-detected AHRE in patients with dual-chamber pacemakers, with a specific focus on the incremental predictive value of RA strain assessed by two-dimensional speckle-tracking echocardiography (2D-STE). METHODS:A single-center, case-control study was conducted on a cohort of prospectively followed patients involving 60 adult patients with dual-chamber (DDD) pacemakers, divided into two groups: 30 patients with device-detected AHRE (AHRE⁺) and 30 age- and sex-matched controls without AHRE (AHRE⁻). All participants underwent detailed clinical evaluation, 12-lead ECG analysis (including P-wave duration and dispersion), and comprehensive transthoracic echocardiography, including 2D-STE for assessment of RA reservoir strain (RASr) and contractile strain (RASct). AHRE was defined as an atrial tachyarrhythmia ≥180 bpm lasting ≥6 min, verified by intracardiac electrograms. RESULTS:AHRE⁺ patients exhibited significantly prolonged P-wave duration (118 ± 14 ms vs 108 ± 12 ms; p = 0.04) and greater P-wave dispersion (42 ± 8 ms vs 36 ± 7 ms; p = 0.03). They also Echocardiographically, they demonstrated significantly higher left atrial volume index (LAVI) (34.2 ± 6.8 vs 28.5 ± 5.2 mL/m²; p = 0.012) and right atrial volume index (RAVI) (26.4 ± 5.1 vs 22.7 ± 4.3 mL/m²; p = 0.028), RA function was markedly impaired in the AHRE⁺ group, with reduced right atrial reservoir and contractile strain (RASr 15.8 % vs 25.9 %, p = 0.041; RASct -2.0 % vs -11.6 %, p = 0.012). Multivariate analysis identified four independent predictors of AHRE: RASr < 20 % (OR 3.8; 95 % CI 1.7-8.4; p < 0.001), LAVI ≥ 34 mL/m² (OR 3.1; 95 % CI 1.5-6.2; p = 0.003), P-wave dispersion ≥ 40 ms (OR 2.6; 95 % CI 1.2-5.8; p = 0.008), Ventricular pacing > 90 % (OR 2.1; 95 % CI 1.0-4.4; p = 0.032). The model achieved strong discrimination (AUC = 0.84; 95 % CI 0.76-0.92) and good calibration (Hosmer-Lemeshow p = 0.47). CONCLUSIONS:The occurrence of AHRE in DDD pacemaker patients is independently associated with a combination of electrical and mechanical bi-atrial remodeling. Impaired right atrial strain (RASr < 20%) provides significant incremental predictive value beyond conventional metrics like P-wave dispersion and left atrial enlargement. Integrating RA strain into routine echocardiographic assessment may serve as a powerful, early marker for risk stratification of atrial arrhythmogenic remodeling in this high-risk population.
BACKGROUND:The heterogeneous nature of coronary artery disease (CAD) progression significantly contributes to cardiovascular morbidity and mortality. Accurately identifying patients at high risk for progression is paramount for effective secondary prevention. This study aimed to develop and internally validate a novel clinical nomogram to precisely predict the probability of angiographic progression in patients with established CAD. METHODS:This retrospective case-referent study enrolled 333 patients with established CAD who underwent at least two coronary angiograms at Beijing Friendship Hospital between January 2018 and December 2023. The cohort comprised 222 patients with angiographic progression and 111 referents without progression, matched at a 2:1 ratio to minimize potential bias. A comprehensive set of 146 pre-selected potential predictors was systematically collected. The Least Absolute Shrinkage and Selection Operator (LASSO) regression was employed for robust initial variable selection, followed by univariable and multivariable logistic regression to identify independent risk factors, which were subsequently integrated into the nomogram. Model performance was rigorously evaluated through assessment of discrimination (area under the receiver operating characteristic curve, AUC), calibration (calibration curve and Hosmer-Lemeshow test), and clinical utility (decision curve analysis, DCA). Internal validation was conducted using a non-parametric bootstrap resampling technique to mitigate optimism and provide robust performance estimates. RESULTS:Seven independent predictors of angiographic progression were identified: a shorter interval between angiograms (odds ratio OR 0.99, 95% CI 0.99-1.00, p=0.015), a higher preoperative Gensini score (OR 1.08, 95% CI 1.05-1.10, p<0.001), male gender (vs. female, OR 3.31, 95% CI 1.69-6.45, p<0.001), the absence of a prior history of stroke (vs. presence of stroke, OR 0.16, 95% CI 0.03-0.79, p=0.025), elevated low density lipoprotein cholesterol (LDL C) levels (OR 2.32, 95% CI 1.46-3.71, p<0.001), higher glycated hemoglobin (HbA1c) levels (OR 1.52, 95% CI 1.12-2.05, p=0.006), and increased antithrombin III levels (OR 1.04, 95% CI 1.01-1.07, p=0.008). The developed nomogram demonstrated promising discrimination (apparent AUC 0.88, 95% confidence interval CI 0.84-0.92) and superior calibration (Hosmer-Lemeshow test p=0.990) within the internal validation cohort. Decision curve analysis indicated that the nomogram offered a statistically and clinically significant net benefit across a range of threshold probabilities (5-80%). CONCLUSION:We successfully developed and internally validated a novel nomogram integrating seven readily available clinical and laboratory variables to accurately predict angiographic progression in CAD. This tool provides an individualized, quantitative risk assessment with promising predictive performance for risk stratification. Nonetheless, its ultimate clinical utility and broader generalizability mandate rigorous external validation in diverse patient cohorts.
PURPOSE:To evaluate the feasibility of telemetry-guided optimization of guideline-directed medical therapy (GDMT) and continuous arrhythmic surveillance in ambulatory patients with heart failure with reduced ejection fraction (HFrEF). METHODS:TELEMETRIC-HF was a single-center, randomized, open-label pilot study including 30 patients with HFrEF assigned to telemetry-guided management (n=15) or standard outpatient care (n=15). Patients in the telemetry group underwent 8 weeks of continuous ambulatory monitoring using the CPC12 CE MDR Class IIb wearable system, providing continuous electrocardiographic and physiological monitoring with clinician oversight. The primary endpoint was the between-group difference in beta-blocker (BB) target-dose achievement at 8 weeks. Secondary endpoints included optimization of other GDMT classes, ventricular arrhythmia detection, clinical status, quality of life, safety, and healthcare utilization. RESULTS:Telemetry-guided management was associated with significantly greater BB target-dose achievement at 8 weeks than standard care (60.0% vs. 39.2% of the guideline-recommended target dose; absolute difference 20.8 percentage points, 95% CI 2.7-39.2; p=0.028). Target-dose achievement for angiotensin receptor-neprilysin inhibitors, mineralocorticoid receptor antagonists, and sodium-glucose cotransporter-2 inhibitors did not differ significantly between groups. Recurrent non-sustained ventricular tachycardia was detected only in the telemetry group, prompting additional clinical evaluation, antiarrhythmic therapy, and primary prevention implantable cardioverter-defibrillator implantation in one patient. Hemodynamic, laboratory, and echocardiographic parameters remained stable throughout follow-up, and telemetry was well tolerated. No heart failure hospitalizations or deaths occurred during the 8-week study period. CONCLUSION:In this pilot randomized study, telemetry-guided remote monitoring was feasible and was associated with earlier BB optimization and improved detection of clinically relevant ventricular arrhythmias without compromising safety. These exploratory findings support further evaluation of telemetry-guided outpatient heart failure management in larger, adequately powered multicenter randomized trials.
Background: Cell-specific epigenetic editing provides a new approach to the therapy of cardiovascular disease (CVD) by rewriting pathological chromatin and RNA marks in exactly those cell populations responsible for causing disease. CVD is caused by interactions of genetics and environment on cell-type-specific epigenomic programs. Interventions that alter DNA methylation, histone marks, or RNA modifications can therefore correct maladaptive gene expression without altering DNA sequence. Summary: Recently developed technologies such as dCas9 fused to writers/erasers allow programmable, locus-directed modulation of promoters, enhancers, and transcripts. Proof-of-principle in vivo work has shown durable target silencing, illustrating both the potency and persistence of epigenetic edits. To achieve therapeutic benefit, cell-targeting strategies and rigorous single-cell/multi-omic validation of on-target activity and off-target safety will be required. Major translational challenges include scalable, cardiac-selective delivery, immune responses to vectors/editors, long-term monitoring for unintended chromatin changes, and regulatory pathways for nongenotoxic but durable interventions. Key Messages: Altogether, cell-specific epigenetic editing holds very high therapeutic value for atherosclerosis, cardiomyopathy, and fibrosis, provided that delivery, specificity, and safety challenges are also addressed.
Introduction Comparative long-term outcomes of transcatheter aortic valve replacement (TAVR) versus surgical aortic valve replacement (SAVR) in younger patients remain incompletely defined, particularly beyond early follow-up. This study evaluated short-, mid-, and long-term outcomes between TAVR and SAVR in patients aged 50 to 65 years using a multicenter retrospective cohort. Methods Patients with aortic stenosis aged 50–65 years undergoing TAVR or SAVR were identified using the TriNetX database. Patients were matched 1:1 using propensity score matching (PSM). Outcomes were assessed at 30 days, 1 year, and 5 years. The primary endpoint was a composite of all-cause mortality or stroke; secondary endpoints included hospitalization, major bleeding, acute kidney injury (AKI), cardiogenic shock, and valve dysfunction. Hazard ratios (HRs) with 95% confidence intervals (CIs) were used to estimate the overall effect size. Results PSM yielded 1,041 well-balanced pairs. At 30 days, TAVR was associated with a lower risk of the primary composite endpoint (3.0% vs. 5.6%; HR 0.53; 95% CI 0.34–0.82; p=0.004), all-cause mortality (HR 0.50; p=0.03), major bleeding (HR 0.29; p<0.001), AKI (HR 0.39; p<0.001), and cardiogenic shock (HR 0.28; p<0.001). At 1 year, the composite endpoint, mortality, and stroke did not differ significantly between groups; major bleeding remained lower with TAVR (HR 0.50; p<0.001). At 5 years, TAVR was associated with higher risks of the primary composite endpoint (18.6% vs. 15.5%; HR 1.27; 95% CI 1.03–1.57; p=0.02) and all-cause mortality (13.7% vs. 8.3%; HR 1.81; 95% CI 1.39–2.37; p<0.001), while major bleeding remained lower (HR 0.65; p<0.001). Conclusion TAVR demonstrated early safety but a higher long-term risk of mortality and composite adverse outcomes at 5 years compared with SAVR.
INTRODUCTION:Assessment of pulmonary vascular disease in children with congenital heart disease (CHD) relies primarily on invasive hemodynamic measurements, including pulmonary vascular resistance index (PVRi). However, these parameters may not fully reflect the underlying structural changes associated with pulmonary vascular remodeling. This study aimed to evaluate the utility of optical coherence tomography (OCT) for in vivo assessment of pulmonary arterial remodeling and examined the relationship between OCT-derived parameters and pulmonary hypertension (PH) severity. METHODS:Eleven patients with CHD (mean age 10 years, range 2-23 years; 7 females) undergoing clinically indicated cardiac catheterization were prospectively enrolled. OCT imaging was successfully performed in 63 pulmonary artery (PA) segments. Hemodynamic parameters, including mean pulmonary arterial pressure (mPAP), mPAP/systemic arterial pressure ratio (MAP), and PVRi, were compared between the PH and control groups. Correlations between OCT-derived measurements and hemodynamic indices were analyzed. RESULTS:Patients with PH had significantly higher mPAP (39±16 vs. controls, p=0.002), mPAP/MAP ratio (0.58±0.24, p=0.017), and PVRi (median 6.05 [IQR 2.27-6.60] WU·m², p=0.008). OCT demonstrated significantly greater %PA wall thickness in the PH group compared with controls (19.4±1.1% vs. 13.5±0.9%, p<0.0001). Percentage wall thickness showed significant positive correlations with mPAP (r=0.58), mPAP/MAP ratio (r=0.62), transpulmonary gradient (r=0.60), PVRi (r=0.55), and Rp/Rs ratio (r=0.45) (all p<0.001). Notably, marked wall thickening (21.8%) was identified in a patient with only mildly elevated PVRi (2.2 WU·m²). CONCLUSIONS:OCT provides structural insights into pulmonary vascular remodeling and complements to conventional hemodynamic assessment in PH related to CHD in children. Pulmonary artery wall thickness percentage correlates closely with PH severity and may serve as a sensitive marker of pulmonary vascular disease in children with CHD.
Background: In this two-sample, two-step Mendelian randomization (MR) study, we aimed to elucidate the causal associations between sarcopenia-related characteristics and heart failure (HF) risk, and to identify the factors mediating these associations, with a particular focus on the mediating roles of obesity and sedentary habits. Methods: Genetic instruments for appendicular lean mass (ALM), hand grip strength (HGS), walking pace (WP) and potential mediators were extracted from genome-wide association studies (GWASs). Inverse‐variance weighting (IVW) was used as the primary analytical method, supplemented by MR‐Egger regression, weighted median, and weighted mode analyses. Sensitivity analyses including Cochran’s Q test and MR-Egger intercept method were performed to assess heterogeneity and pleiotropy. Bidirectional MR was conducted to exclude reverse causation. Results: IVW revealed that a faster genetically predicted walking pace (WP) was associated with lower HF risk (odds ratio [OR] 0.44, 95% confidence interval [CI] 0.33-0.60, P = 5.806 × 10−7). The mediation analysis indicated that body mass index accounted for 32% of this effect, while time spent watching television accounted for 14%. Elevated appendicular lean mass showed a slight but significant positive association with HF risk (OR 1.06, 95% CI 1.03-1.09, P = 5.437 × 10−4). However, multivariable MR adjusting for BMI completely attenuated this association (P = 0.693), suggesting ALM reflects overall body composition rather than isolated muscle mass. No significant associations were found between HGS and HF. Bidirectional MR showed no robust reverse effects. Conclusions: These findings suggest that genetically predicted increased WP exerts beneficial effects against HF, partially mediated by obesity and sedentary habits. Targeting weight management and anti-sedentary interventions may mitigate HF risk in individuals with sarcopenia-related characteristics.
INTRODUCTION:Left bundle branch block (LBBB) complicates electrocardiographic interpretation in acute heart failure (AHF). This study aimed to evaluate the relationship between electrocardiographic parameters, including QRS duration, QRS morphology, and the Selvester QRS score (SQS), and echocardiographic findings in patients with AHF presenting with LBBB across different heart failure phenotypes. METHODS:In this retrospective cohort, 275 patients hospitalized with AHF and LBBB were analyzed. Patients were classified as heart failure with reduced ejection fraction (HFrEF, left ventricular ejection fraction [LVEF] <40%), heart failure with mildly reduced ejection fraction (HFmrEF, LVEF 40-49%), or heart failure with preserved ejection fraction (HFpEF, LVEF ≥50%). Associations between electrocardiographic (ECG) and echocardiographic parameters were evaluated using Spearman correlation and multivariable regression. Discriminatory performance for reduced systolic function was assessed by receiver operating characteristic (ROC) analysis. RESULTS:Mean age was 61.7 ± 13.8 years and 70.5% were male; median LVEF was 40% (IQR: 27-48%). HFrEF was present in 49.8%. Among ECG indices, only SQS correlated significantly with echocardiographic measures: LVEF (r = -0.447), left ventricular end-diastolic diameter (LVEDD, r = 0.346), left ventricular end-systolic diameter (LVESD, r = 0.373), and LV mass index (r = 0.205) (all p < 0.001). In multivariable analysis, SQS (OR = 1.373, 95% CI: 1.255-1.501, p < 0.001) and LV mass index independently predicted HFrEF. The Hosmer-Lemeshow test confirmed adequate calibration (p = 0.49). ROC analysis showed SQS had moderate discriminatory ability (area under the curve [AUC] 0.768, 95% CI: 0.711-0.825), with an optimal cutoff >43 yielding 74.5% sensitivity and 69.6% specificity. QRS duration and morphology demonstrated no meaningful predictive value (AUC ≈ 0.49). CONCLUSION:In AHF patients with LBBB, SQS outperforms conventional QRS metrics in identifying reduced LV systolic function. An SQS >43 provides moderate diagnostic accuracy and may support early risk stratification when echocardiography is not immediately available.
Introduction: Doxorubicin (DOX), a widely used chemotherapeutic agent, induces dose-dependent cardiotoxicity through mechanisms involving oxidative stress and inflammatory cell death. This study investigates the role of the Klotho-nuclear factor erythroid 2-related factor 2 (Nrf2) signaling axis in mitigating DOX-induced pyroptosis in cardiomyocytes. Methods: AC16 cells were treated with DOX to induce pyroptosis. Klotho was overexpressed or knocked down via plasmids and small interfering RNA (siRNA). Cell viability, lactate dehydrogenase release, reactive oxygen species (ROS)/malondialdehyde/glutathione (GSH) levels, and pyroptosis markers were measured. Methylation-specific polymerase chain reaction (PCR) and methylation-sensitive high-resolution melting analyzed Klotho promoter methylation and DNA methyltransferase (DNMT) binding, while quantitative real-time polymerase chain reaction and luciferase assays assessed gene expression and Nrf2 activity. DNA methyltransferase 3a (DNMT3a) and DNMT3b were silenced with specific siRNAs to explore their epigenetic roles. Results: We demonstrate that DOX triggers pyroptosis via caspase-1 activation, gasdermin D N-terminal fragment, and interleukin-1β and interleukin-18 secretion, accompanied by an increase in ROS and depletion of GSH and antioxidant enzymes. Pyroptosis was ROS-dependent, as pretreatment with N-acetyl-L-cysteine restored redox balance and suppressed cell death. Mechanistically, DOX downregulated Klotho expression via promoter cytosine-phosphate-guanine hypermethylation mediated by DNMTs DNMT3a and DNMT3b, with DNMT3b playing a dominant role. Klotho suppression exacerbated pyroptosis, while its overexpression reducing apoptosis-associated speck-like protein containing a CARD speck formation. Furthermore, Klotho activated the Nrf2 pathway, restoring Nrf2 levels and upregulating antioxidant genes heme oxygenase-1 (HO-1) and NAD(P)H quinone oxidoreductase 1 (NQO1). Critically, the Nrf2 inhibitor ML385 reversed Klotho’s protective effects, confirming Nrf2’s necessity. Silencing of DNMT3a/3b attenuated DOX-induced Klotho promoter hypermethylation, restored Klotho expression, and inhibited pyroptosis, with DNMT3b siRNA exerting a more pronounced protective effect. Conclusion: These findings reveal that DOX induces myocardial cytotoxicity by epigenetically silencing Klotho via DNMT3a/3b-mediated promoter hypermethylation, thereby disrupting the Klotho-Nrf2 antioxidant axis and unleashing inflammasome-driven pyroptosis, with DNMT3b serving as the key epigenetic regulator in this process.
Introduction: Chronic pulmonary regurgitation (PR) is a common late sequela after repair of Tetralogy of Fallot (TOF) and contributes to progressive right ventricular (RV) dilation, dysfunction, and adverse clinical outcomes. Multimodality imaging plays a central role in longitudinal assessment and in informing the timing of pulmonary valve replacement (PVR). Methods: We report a single-center, retrospective case series of seven adults with surgically repaired TOF followed at a tertiary care center. Each patient underwent serial transthoracic echocardiography (TTE) and at least two cardiac magnetic resonance (CMR) examinations over follow-up periods ranging from 5 to more than 15 years. PR severity was classified using CMR-derived regurgitant fraction according to established thresholds. RV size, systolic function, right ventricular outflow tract (RVOT) morphology, and clinical outcomes including PVR were recorded. Analyses were descriptive given the small sample size and heterogeneous nature of the cohort. Results: All seven patients (4 female, 3 male) survived to the most recent follow-up in 2025. PR was present in every patient, with CMR regurgitant fractions ranging from 21% to 57% at latest follow-up. Greater PR severity was associated with larger RV end-diastolic volume index (RVEDVi) and lower RV ejection fraction (RVEF) on serial imaging. RVEDVi ranged from 77 to 163 mL/m2 and RVEF from 37% to 61%. Qualitative concordance between TTE and CMR for RV remodeling was observed in 6 of 7 patients (86%). Several RVOT morphologic patterns were observed: patch-augmented RVOT with dilation, subpulmonic narrowing with turbulent flow acceleration, asymmetric branch pulmonary artery anatomy, and prosthetic pulmonary valve degeneration. Three patients underwent PVR during follow-up for severe PR, RVEDVi ≥150 mL/m2, declining RVEF, or symptomatic deterioration, and demonstrated post-procedural stabilization of RV size and improved functional status. Conclusions: In this single-center case series, integrated TTE and CMR provided complementary structural and functional information across a heterogeneous spectrum of post-repair RVOT anatomy, with CMR offering superior quantitative resolution of RV volumes and regurgitant fraction. The observed phenotypic variability illustrates the importance of multimodality, individualized surveillance in adults with repaired TOF, and reinforces the role of imaging integrated with clinical assessment in PVR decision-making.
INTRODUCTION:Shortness of breath while bending and its more objective version, bending oxygen saturation index (BOSI), are the latest additions to pulmonary arterial hypertension (PAH) symptom and signs armamentarium. In this study, we aimed to evaluate the association between BOSI and clinical outcomes in patients with PAH and to explore its potential to complement current risk estimation schemes. METHODS:In this single-center, prospective, observational study, we enrolled patients with PAH who are under stable treatment. Baseline mortality risk was estimated using established risk schemes. Primary endpoint was defined as the combination of all-cause hospitalization and all-cause mortality at 1 year. The discriminative performance of BOSI was evaluated using ROC curve analysis. RESULTS:A total of 102 patients were enrolled into the study. BOSI was equal to or more than 3 in 33 patients (32.4%). Primary endpoint occurred in 20 (60.6%) in BOSI ≥3 group and 16 (23.2%) in BOSI <3 group (p < 0.001). ROC analysis showed that BOSI had a significant discriminative ability (AUC 0.687, p = 0.002). Cox regression analysis showed that a BOSI ≥3 was significantly associated with adverse events, even after adjustment for baseline risk estimated by the four most used risk schemes (REVEAL, REVEAL Lite, COMPERA, and European Society of Cardiology/European Respiratory Society risk scores). CONCLUSION:BOSI is independently associated with adverse events in patients with PAH and its addition to current risk scores may improve baseline risk estimation.
Introduction: Acute and critical cardiac illnesses have attracted considerable attention because of their high mortality rates. Various innovative treatment methods including extracorporeal life support have been used to save the lives of patients with critical cardiac illnesses. This study aimed to evaluate the clinical efficacy of venoarterial extracorporeal membrane oxygenation (VA-ECMO) in treating critical cardiac illnesses. Methods: We retrospectively analyzed data from an observational study conducted in China. The study population included adult patients with acute and critical cardiac illnesses admitted to the intensive care unit between January 1, 2021, and December 31, 2023. The primary endpoints were the successful reversal of cardiogenic shock and other related outcomes. Results: A total of 57 patients with acute and critical cardiac illnesses underwent VA-ECMO for refractory cardiogenic shock. These patients included 31 with acute coronary syndrome, 14 with fulminant myocarditis, 4 with stress-induced cardiomyopathy, and 8 with sepsis-induced myocardial depression. The median duration of VA-ECMO support was 120 h. Among the 31 patients with acute coronary syndrome, 17 (54.8%) had successfully reversed cardiogenic shock. In the group of 14 patients with fulminant myocarditis, cardiogenic shock was successfully reversed in 7 patients (50%). All four patients with stress-induced cardiomyopathy achieved successful reversal of cardiogenic shock (100%). Among the eight patients with sepsis-induced myocardial depression, five (62.5%) showed successful recovery of cardiac function. The overall cardiogenic shock reversal, 30-day survival, and 1-year overall survival rates were 54.4% (31/57), 45.6% (26/57), and 43.9% (25/57), respectively. Multivariate logistic regression analysis demonstrated that requiring additional continuous renal replacement therapy following VA-ECMO initiation was independently associated with in-hospital mortality. Conclusions: For refractory cardiogenic shock caused by acute and critical cardiac illnesses, VA-ECMO can effectively improve cardiac function, but it does not significantly increase the survival rate.
Introduction:This study aimed to assess the prognostic value of Aortic valve calcification (AVC) score and CT angiography-derived fractional flow reserve (CT-FFR) for major adverse cardiovascular events (MACE) after transcatheter aortic valve replacement (TAVR). Materials: In this retrospective observational cohort study, we included patients with severe aortic valve diseases undergoing TAVR between February 2016 and April 2022. Patients were followed, and univariable and multivariate Cox regression were applied for outcome analysis using a composite endpoint including all-cause mortality, nonfatal myocardial infarction, unstable angina, heart failure rehospitalization. The incremental prognostic value of CT-FFR was also analyzed. Results: A total of 251 patients were enrolled (mean age, 67 ± 10 years; 176 men). During a mean follow-up period of 36 months, 60 patients (23.9%) experienced MACE. AVC score ≥ 2000 (HR = 1.714, 95%CI: 1.020, 2.882, P = 0.042) and CT-FFR ≤ 0.8 (HR = 3.248, 95% CI: 1.760,5.996, P < 0.001) were independent predictors of MACE. The C statistics revealed that adding CT-FFR to the clinical risk factors alone or combined with AVC score provided incremental prognostic value for MACE after TAVR (C-index: 0.710 vs 0.645 [P = 0.012]; and 0.710 vs 0.672 [P = 0.030]). Conclusion: AVC score and CT-FFR were associated with MACE in patients after TAVR, and CT-FFR presented incremental prognostic value for MACE beyond clinical risk factors alone or combined with AVC score. Therefore, CT-FFR should be incorporated into routine clinical decision-making and risk management for TAVR patients.
INTRODUCTION:Noninvasive identification of patients with chronic coronary syndrome (CCS) with obstructive coronary artery disease (CAD) remains a clinical challenge. Strain imaging enables detection of subtle myocardial dysfunction at rest and may serve as a sensitive marker of multivessel or left main CAD. This study aimed to assess whether segmental systolic strain at rest can identify patients with obstructive CAD referred for coronary artery bypass grafting (CABG) and to compare diagnostic performance of tissue Doppler imaging strain with two-dimensional speckle-tracking echocardiography in a retrospective analysis of a selected CABG-referred cohort. METHODS:This retrospective study included 61 patients with CCS and obstructive CAD referred for CABG and 61 age- and sex-matched healthy controls from the population-based Nord-Trøndelag Health Study. All participants underwent echocardiography with both tissue Doppler and speckle-tracking strain analysis. The number of hypokinetic segments within one heart was counted, determined at different segmental peak longitudinal strain thresholds of -8% to -16%. The area under curve (AUC) using receiver operating characteristic analysis was used to evaluate diagnostic performance. Late gadolinium enhancement (LGE) cardiac magnetic resonance imaging (MRI) was used to assess myocardial scarring. RESULTS:LGE MRI confirmed that 78% of patients had no visible myocardial scar and that overall scar burden was low (2.8%). At a hypokinetic strain threshold of -8%, tissue Doppler strain demonstrated excellent diagnostic accuracy for identifying myocardial dysfunction in CABG-referred patients (AUC 0.95, 95% confidence interval [CI]: 0.91-1.00), performing at least as well as speckle-tracking strain (AUC: 0.79, 95% CI: 0.70-0.87). Tissue Doppler strain identified obstructive CAD with 95% sensitivity and 86% specificity. Comparable AUCs were found in a subgroup of 20 patients without coronary occlusion or myocardial scarring, indicating that regional hypokinesia was equally detectable in patients with normal EF and no LGE-defined scars. CONCLUSION:Segmental strain imaging at rest - by both tissue Doppler and speckle tracking - can detect subclinical regional dysfunction in CABG-referred patients with obstructive CAD, even in patients with preserved global left ventricular function and no evidence of myocardial scarring. Tissue Doppler strain showed at least as high diagnostic accuracy as speckle-tracking strain. These findings underscore the clinical potential of resting segmental strain analysis as a sensitive, noninvasive tool for identifying obstructive CAD in this selected CABG-referred population.
INTRODUCTION:Whether the mortality impact of ischemic stroke and major bleeding differs across left ventricular ejection fraction (LVEF) categories in patients hospitalized for acute heart failure (AHF) with atrial fibrillation (AF) remains uncertain. METHODS:We retrospectively analyzed 716 patients hospitalized for AHF with prevalent AF (mean age: 79 ± 11 years; 49% female). During up to 3 years of follow-up (median: 1.4 years), 53 patients developed stroke and 89 developed major bleeding. Time-dependent Cox models were used to evaluate associations between poststroke and post-major bleeding states and all-cause and cardiovascular mortality, stratified by LVEF category: heart failure with reduced ejection fraction, mildly reduced ejection fraction, and preserved ejection fraction. RESULTS:There were 160 deaths, including 106 cardiovascular deaths. As first qualifying events, 34 were stroke-first, and 74 were bleeding-first, with the remaining patients experiencing death-first or being censored. In time-dependent Cox models, post-major bleeding status was associated with higher all-cause mortality, whereas the poststroke association was imprecise (hazard ratio [HR] 2.00, 95% confidence interval [CI] 1.22-3.28 vs. HR 1.35 [95% CI 0.67-2.70]). For cardiovascular death, neither exposure reached conventional statistical significance (HR 1.97 [95% CI 0.93-4.17] after stroke and 1.69 [0.88-3.26] after bleeding). LVEF-stratified estimates were imprecise, and interaction tests did not support definitive effect modification. CONCLUSION:In patients hospitalized for AHF with prevalent AF, transition into a post-major bleeding state was associated with higher subsequent all-cause mortality, whereas the poststroke association was imprecise. LVEF-stratified findings were exploratory because interaction tests were not significant and event counts were limited. Bleeding-risk mitigation should accompany continued stroke prevention, not replace it.
