Improvement In Ejection Fraction Research Articles

Clinical use of [15O]H2O/[18F]FDG viability positron emission tomography does not reliably predict left ventricular ejection fraction improvement or survival after revascularization.

Previous observational studies suggest that preoperative imaging in patients with chronic ischemic heart failure (iHF) may identify non-contractile, hypoperfused, yet metabolically viable (hibernating) myocardial segments that can regain function after coronary revascularization. Various imaging techniques, including positron emission tomography (PET) with retention tracers like 82Rb, have shown equivocal results. However, recent randomized studies have found limited value in these methods for predicting postoperative recovery and survival. This study, therefore, aims to assess whether PET viability imaging using the optimal perfusion tracer [15O]H2O, combined with [18F]FDG, provides better predictive accuracy. Seventy-three patients with chronic iHF and reduced LVEF (mean baseline LVEF 31±9%) underwent [15O]H2O/[18F]FDG PET viability imaging before potential revascularization. The primary endpoint was a ≥5% absolute increase in LVEF from baseline to follow-up, assessed by echocardiography. In total, 31 of 73 (42%) patients were revascularized, with 16 of 31 (52%) experiencing a ≥5% LVEF improvement postoperatively. Baseline characteristics and revascularization type did not significantly differ between improvers and non-improvers. ROC analysis of PET metrics to predict LVEF improvement yielded AUC values ≤0.60, and no baseline characteristics or PET measures predicted survival in revascularized patients. No [15O]H2O/[18F]FDG PET parameters predicted post-revascularization LVEF improvement or survival in patients with suspected chronic iHF. Thus, clinical use of PET viability imaging still warrants reconsideration, particularly if non-ischemic HF is present.

Convergent procedure for long-standing persistent atrial fibrillation in heart failure with reduced ejection fraction.

Catheter ablation for atrial fibrillation in patients with heart failure with reduced ejection fraction is associated with a significant reduction in morbimortality. The convergent procedure is a valid ablation option for the treatment of long-standing persistent atrial fibrillation. To describe the outcomes of patients with heart failure with reduced ejection fraction and long-standing persistent atrial fibrillation who underwent the convergent procedure. We studied consecutive patients included in two French centres between 2009 and 2020. Primary endpoint was freedom from any atrial arrhythmia assessed on 24-hour Holter electrocardiogram at 3, 6 and 12 months after the procedure. Left ventricular ejection fraction was assessed on transthoracic echocardiography before and 1 year after the procedure. All patients had at least 12 months of follow-up. Forty-three patients were included (86% were men). Baseline left ventricular ejection fraction was 38±10.5% and indexed left atrial volume was 50±27mL/m2. Among the study population, 34 patients (79%) were free from atrial fibrillation/tachycardia at the end of follow-up. No periprocedural death occurred. We observed two groin haematomas and four mild pericardial effusions. At 12-month follow-up, 21 patients (49%) were still on antiarrhythmic drug therapy, and a reduction in antiarrhythmic drug dosage was achieved in 10 patients (23%). The absolute median improvement in left ventricular ejection fraction was 8% at 12 months (P=0.003). The convergent procedure has been shown to be effective and safe for patients with patients with heart failure with reduced ejection fraction and long-standing persistent atrial fibrillation, with significant left ventricular function improvement.

Autoimmunity in Cardiomyopathy-Induced Heart Failure and Cardiac Autoantibody Removal by Immunoadsorption

There is increasing evidence that β1-adrenoreceptor autoantibody (β1AR-AAb) elimination can break the vicious circle induced by certain pathological conditions associated with alteration of the physiological self-tolerance, followed by generation of such AAbs and activation of cell-mediated immune processes directed against the myocardium. Concerning this, the present narrative review article provides an updated overview of the state of knowledge about the role of auto-immunity in the etiopathogenesis of cardiomyopathies, with a particular focus on immunoadsorption (IA) therapy for β1AR-AAb-positive adult patients with a dilated cardiomyopathy (DCM)-associated refractory heart failure (HF). Among many relevant findings, the increasing prevalence (up to 97%) of β1AR-AAb-positive patients related to the aggravation of HF, the high prevalence (between 84% and 91%) of HF patients in which IA can reduce to a minimum any increased β1AR-AAb level, as well as the high prevalence (about 80%) of responders to the IA-induced normalization of β1AR-AAb levels by long-term improvement in LV ejection fraction with increase in LV stroke volume and cardiac output, are of particular relevance. Given that after the elimination of β1AR-AAbs in potential candidates for heart transplantation (HTx), the post-IA 3- and 5-year HTx-/mechanical support-free survival probability reached 80% and 63-69%, respectively, the good tolerability of IA and the possibility to repeat that therapy also in elderly persons strongly suggest that in appropriately selected patients, this therapy deserves much more attention in the future.

Predictors of Improvement in Left Ventricular Systolic Dysfunction in Patients with Atrial Fibrillation Undergoing Catheter Ablation: Systematic Review

Background: Left ventricular systolic dysfunction (LVSD) can improve after catheter ablation (CA) in many patients with AF. However, prospective prediction of response can be challenging. The aim of this study was, therefore, to perform a systematic literature review of features associated with improvement in left ventricular ejection fraction (LVEF) in patients with AF and LVSD undergoing first CA. Method: Systematic search of Ovid MEDLINE, Embase and Cochrane Library databases up to 24 January 2024, for studies involving adult patients with LVSD receiving treatment for AF. The focus was on research articles and clinical trials reporting features associated with changes in LVEF following CA. The review followed PRISMA guidelines. Results: A total of 789 unique articles were reviewed and 20 were included in the systematic review. Sixty-nine per cent (range, 54–79%) of included patients met the criteria for responder status, which were based on LVEF improvement (usually an increase in LVEF >10% or to >50% at follow-up). Baseline surrogates of myocardial fibrosis on MRI (R2=−0.67), electroanatomical mapping (R2=−0.93) and biochemical surrogates have shown the strongest association with LVEF change. Left atrium and LV chamber size, diastolic dysfunction ECG-based parameters and a known heart failure aetiology have shown prognostic value independently and in combination. Discussion: Imaging, clinical and ECG-based surrogates of LV fibrosis may be pre-CA markers of LVEF improvement in patients with AF and LVSD. However, the confounding effect of procedural outcomes should be considered. A composite risk stratification tool would have clinical utility in risk stratification and patient selection; however, prospective studies are needed.

Imaging features of non-dilated left ventricular cardiomyopathy: differences and similarities with dilated cardiomyopathy

Abstract Background and Aim The spectrum of dilated cardiomyopathy (DCM) includes both patients with ventricular dilation and those with systolic dysfunction and no dilation. This latter entity has been called hypokinetic non-dilated cardiomyopathy (H-NDLVC). Our aim was to describe the epidemiological, clinical and imaging features of patients with DCM, comparing those cases of H-NDLVC with patients with classic dilated cardiomyopathy. Methods From January 2014 to December 2022, all patients with a new diagnosis of DCM studied at our tertiary hospital were prospectively included in a multipurpose registry. Transthoracic echocardiogram and cardiac magnetic resonance (CMR) imaging were performed as part of the study. During follow-up, hospitalizations for heart failure (HF), arrhythmic events and mortality were recorded. Results The median age of the patients (n = 227) was 63.8 (53-74) years, and 31.7% were women. Median follow-up was 34.3 (20-56) months. 176 patients (77.5%) had DCM, and 51 patients (22.5%) had H-NDLVC. Epidemiological, clinical, and cardiac imaging characteristics of both groups are shown in the Table. The proportion of men was higher in patients with H-NDLVC, and the presence of left bundle branch block was also more frequent in this group (Figure 1). No differences were found in the distribution of cardiovascular risk factors or comorbidities. Patients with DCM had greater left atrial dilation and more significant mitral regurgitation, as well as worse diastolic function. In relation to the CMR findings, the presence of late enhancement and late enhancement with a high-risk pattern was similar between both groups (Figure 2). Both groups experienced significant improvement in LV systolic volumes (77ml/m2 vs 45 mL/m2 in DCM and 38 ml/m2 vs 28 mL/m2 in H-NDLVC; p<001) and LV ejection fraction (29% vs 43% in DCM and 36% vs 51% in H-NDLVC; p<001) during follow-up. Interestingly, in the subset of patients who had genetic information available (n=78), we found a trend towards higher frequency of positive genetic testing in the group of patients with H-NDLVC (31.2 vs 17.7%; p=0.107). There was a non-significant trend towards lower incidence of events (hospitalization for HF, ventricular arrhythmias, mortality) in patients with H-NDLVC. Conclusions H-NDLVC represent one in 5 patients in our DCM cohort. These patients have less reduction in systolic function, less alteration in diastolic function and less frequency of significant mitral regurgitation. However, the percentage of patients with late gadolinium enhancement and a high-risk pattern is similar to those with true ventricular dilation, and genetic testing was positive in one out of three patients tested. Thus, these patients benefit from an integrated approach with using advance imaging and genetics. Clinical characteristics Imaging findings

Dapagliflozin improves ejection fraction, radial/longitudinal strain and reduces systemic H-FABP and pro-inflammatory cytokines in models of dororubicin/trastuzumab induced cardiotoxicity

Abstract Background The use of anthracyclines as a standard cancer therapy is limited by the potential for the development of cardiac dysfunction, arrhythmias, and clinical heart failure. The incidence of cardiac dysfunction or heart failure post-trastuzumab plus anthracycline therapy is higher compared to monotherapy regimen, exposing cancer patients to cardiotoxic risk. Dapagliflozin exerts several cardiometabolic benefits in patients with and wthout T2DM through SGLT2-NLRP3 mediated pathways. In this study, we highlighted on new beneficial properties of Dapagliflozin in preclinical models of doxorubicin-HER-2 blocking agent induced cardiotoxicity. Methods Female C57Bl/6 mice were untreated (Sham, n=6) or treated for 10 days with doxorubicin i.p at 2.17 mg/kg associated to HER-2 blocking agent i.p at 2,25 mg/kg (DOXO/TRA, n=6), DAPA at 12 mg/kg (DAPA, n=6) or doxorubicin-HER-2 blocking agent combined to DAPA (DOXO/TRA–DAPA, n=6). Cardiac function studies, including EF, FS and radial/longitudinal strain were analysed through transthoracic echocardiography (Vevo 2100) . Systemic levels of ferroptosis-related biomarkers, galectin-3, high-sensitivity C-reactive protein (hs-CRP), and pro-inflammatory chemokines (IL-1α, IL-1β, IL-2, IL-4, IL-6, IL-10, IL-12, IL17-α, IL-18, IFN-γ, TNF-α, G-CSF, and GM-CSF) were quantified. Results Dapagliflozin increased EF and FS compared to DOXO groups (p < 0.01), prevented the reduction of radial and longitudinal strain after 10 days of treatment with DOXO-TRA (RS) 40.2% in EMPA-DOXO vs 14.9% in DOXO-TRA mice; LS – 26,8 % in DOXO/TRA-DAPA vs – 9,7.3% in DOXO/TRA mice (p < 0.001 for both). Dapagliflozin associated to Doxorubicin reduces of 53,8 % plasma levels of H-FABP compared to DOXO group (p<0.001). Myocardial expression of H-FABP were also reduced, indicating cardioprotective properties of SGLT2i. Significant reductions in ferroptosis, xanthine oxidase expression, cardiac fibrosis and apoptosis in DAPA associated to DOXO/TRA were also seen. A reduced expression of systemic pro-inflammatory cytokines and NLRP3 was also seen in in DOXO/TRA-DAPA group compared to DOXO/TRA (p < 0.001). Conclusion For the first time, Dapagliflozin demonstrated significant improvements in cardiac functions and reductions of systemic H-FABP and troponin levels during doxorubicin associated to HER- blocking agent therapy, indicating new potential pathways of cardioprotection in cancer patients.

Predictive model for ejection fraction improvement at one year in patients with acute ST-segment elevation myocardial infarction complicated with heart failure with reduced ejection fraction

Objective: To develop a predictive model for improvement of ejection fraction 1 year after heart failure with reduced ejection fraction (HFrEF) following acute ST-segment elevation myocardial infarction (STEMI). Methods: This nested case-control study included STEMI patients diagnosed with HFrEF from a prospective multicenter multimodality imaging cohort between August 2014 and March 2021. Based on the improvement of left ventricular ejection fraction (LVEF) at baseline and 1-year follow-up, the patients were classified into the heart failure with improved ejection fraction (HFimpEF) group and the persistent HFrEF group. The clinical data were collected, and cardiac histological changes were assessed using cardiac magnetic resonance imaging. Multivariate logistic regression analysis was performed to identify factors associated with ejection fraction improvement at one year, and a predictive model was developed and internally validated. The performance and clinical applicability of the model were evaluated using receiver operating characteristic (ROC) curves, calibration curves, and decision curve analysis. Results: A total of 117 STEMI patients (102 males and 15 females) aged (61.6±11.6) years were included in the study. At the 1-year follow-up, there were 61 patients (52.1%)in the HFimpEF group,and 56 patients (47.9%) in the HFrEF group . Compared with persistent HFrEF group, patients in HFimpEF group had smaller baseline left ventricular end-systolic diameter (LVESD) [33.0 (30.0, 36.0) mm vs 35.5 (32.0, 39.0) mm], smaller infarct size [26.1% (20.3%, 36.0)% vs 40.6% (33.0%, 45.4)%], lower peak B-type natriuretic peptide (BNP) level [340.0 (190.5, 692.5) ng/L vs 636.0 (318.5, 1 188.8) ng/L], lower peak level of soluble suppression of tumorigenicity 2 (sST2) [36.7 (25.8, 60.5) μg/L vs 62.4 (30.6, 120.7) μg/L], and higher hematocrit [(43.5%±3.5%) vs (40.8%±5.6%)] (all P<0.05). Multivariate logistic regression analysis revealed that smaller baseline LVESD (OR=0.825, 95%CI: 0.745-0.914), smaller infarct size (OR=0.967, 95%CI: 0.939-0.995), peak BNP level≤400 ng/L (OR=3.062, 95%CI: 1.283-7.306), peak sST2 level≤35 μg/L (OR=2.600, 95%CI: 1.040-6.501), and higher hematocrit (OR=1.109, 95%CI: 1.030-1.193) were predictors of LVEF improvement in STEMI patients with HFrEF. The predictive model formula: logit (P)=2.619-0.034×infarcted myocardium percentage (%)+1.119×(peak BNP level≤400 ng/L)+0.956×(peak sST2 level≤35 μg/L)+0.103×hematocrit (%)-0.192×LVESC (mm) (where peak BNP level≤400 ng/L and peak sST2 level≤35 μg/L are binary variables: Yes=1, No=0). The area under the ROC curve (AUC) was 0.805 (95%CI: 0.723-0.887), indicating good predictive ability. Calibration curves and decision curve analysis indicated good model consistency and clinical utility. Conclusions: Smaller LVESD, smaller infarct size, peak BNP level≤400 ng/L, peak sST2 level≤35 μg/L and higher hematocrit are predictive factors for LVEF improvement after STEMI. The predictive model has good performance for predicting HFimpEF.

Comprehensive nursing interventions enhance sleep quality in patients with arrhythmia following AMI.

This study aims to assess the impact of comprehensive nursing care on sleep quality and rehabilitation duration in patients experiencing arrhythmia after acute myocardial infarction (AMI). Eighty-four patients with post-AMI arrhythmia treated at our hospital from February 2018 to February 2019 were selected and divided based on the nursing care received. The observation group (n = 44) underwent comprehensive nursing interventions, while the control group (n = 40) received standard nursing care. Evaluations of cardiac function indices and sleep quality were conducted before and after the nursing interventions. In addition, comparisons were made between the 2 groups regarding arrhythmia occurrence, patient compliance during care, visual analog scale scores for pain, self-rating anxiety scale scores, self-rating depression scale scores, and overall nursing satisfaction. Following the nursing interventions, the observation group exhibited a significant increase in cardiac output, unlike the control group, which showed no notable change. Both groups demonstrated significant improvements in left ventricular end-diastolic dimension and left ventricular ejection fraction; however, these enhancements were more pronounced in the observation group. Post-intervention, the Pittsburgh Sleep Quality Index scores were significantly lower in the observation group compared with the control group, indicating better sleep quality. The observation group also experienced a significant reduction in the incidence, frequency, and duration of arrhythmia episodes. Furthermore, this group showed a lower incidence of complications during the intervention period and reported lower visual analog scale, self-rating anxiety scale, and self-rating depression scale scores after nursing care. Nursing satisfaction rates were notably higher in the observation group than in the control group. Comprehensive nursing care significantly enhances sleep quality, speeds up rehabilitation, and increases patient satisfaction in individuals with arrhythmia after AMI. These findings support the clinical adoption of comprehensive nursing interventions for this patient population.

Heart failure treatment and serum carnitines in HFpEF and HFrEF with or without hypertension - a pilot study.

The ratio of serum acylcarnitines to free carnitines (AC/FC) reflects impaired cardiomyocyte β-oxidization. The effect of heart failure (HF) treatment on AC/FC remained unclear. This pilot study retrospectively examined treatment-induced AC/FC changes in patients with HF with preserved ejection fraction (HFpEF) and HF with reduced ejection fraction (HFrEF) in 148 consecutive inpatients undergoing echocardiography and carnitine measurement at admission and discharge. Symptomatic ACCF/AHA HF stage C/D patients (HFpEF, n = 40; HErEF, n = 24) received standard medical therapy and comprehensive cardiac rehabilitation. At admission, AC/FC levels in HFpEF and HFrEF were significantly higher than in asymptomatic stage A/B (n = 84), decreasing to comparable levels at discharge. AC/FC reduction was associated with improvement of left ventricular ejection fraction through HF treatment in HFpEF, particularly in HFpEF with hypertension, but not in HFrEF. Large-scale, multicenter prospective studies with precise cardiac function assessments are essential to validate the preliminary findings and to clarify the underlying pathophysiological mechanisms.

Passive Heat Therapy for Cardiovascular Disease: Current Evidence and Future Directions.

Passive heat therapy is gaining popularity as an intervention to promote cardiovascular, physiological, and to a lesser degree, thermoregulatory, adaptations in patients with cardiovascular disease. Despite this, the efficacy of heat therapy to elicit these adaptations remains unknown. We searched 5 databases for original research, screening 2,913 studies and identifying 18 eligible studies. Heat therapies included Waon therapy, balneotherapy, water perfused trousers, Finnish sauna, and foot immersion. Interventions were administered across various time frames (20- to 90-min) and performed 3 to 7 times per week, for durations of 2- to 8-weeks. The studies collectively involved a diverse population (mean age: 67 (10) years) with cardiovascular diseases. Heat therapy was consistently shown to improve ejection fraction, flow-mediated dilation, brain natriuretic peptide levels, New York Heart Association classification, and six-minute walk distance. However, positive effects on resting heart rate and blood pressure were infrequently observed, and thermoregulatory responses scarcely reported. Heat therapy may increase sweat rate during heat exposure and reduce resting core temperature, but adaptive skin blood flow responses were not observed. Passive heat therapy shows promising utility in patients with cardiovascular disease, while secondary benefits such as markers of thermoregulatory adaptation may also be observed, these require further investigation.

Risk and Protective Factors of Poor Clinical Outcomes in Heart Failure with Improved Ejection Fraction Population: A Systematic Review and Meta-Analysis.

Heart failure with improved ejection fraction (HFimpEF) patients could still develop adverse outcomes despite EF improvement. This study evaluates the risk and protective factors of poor clinical outcomes in HFimpEF patients. Systematic searching was done to include studies that evaluate the risks of developing poor outcomes in HFimpEF patients. HFimpEF is defined as improvement of 5-10% EF within 6-12 months or normalization of EF > 40%. Poor clinical outcome is defined as a composite of all-cause mortality, cardiovascular events, HF rehospitalization, and requirement of LVAD/ transplant. Odds ratios of outcome are pooled with random effects model. A subgroup analysis of multivariate analysis-only studies was also conducted. 32 studies comprising 10,740 HFimpEF patients are included. Poor clinical outcomes followed up for approximately 3 years, are seen in 18.9% of HFimpEF patients. Twelve statistically significant factors that increase the risk of outcome are found. Among them, anemia (OR 7.69, CI 3.48-16.99, I2 0%) and baseline NT pro-BNP (OR 3.25) are the two most important predictors. Other significant risk factors are increasing age, ischemic heart disease, NYHA III/IV, diabetes mellitus, atrial fibrillation, dyslipidemia, cerebrovascular disease, hypertension, use of diuretics, and baseline LVEDD. Alternately, protective factors of poor clinical outcome are regression of left atrial diameter (LAD) (OR 0.33, CI: 0.18-0.61, p 0.0003, I2 0%), use beta-blockers, SGLT- 2 inhibitors, and baseline LVEF level (OR 0.60, 0.78, 0.90, respectively). HFimpEF patients are not fully recovered and patient stratification based on risk and protective factors is recommended.

Alström syndrome: A rare cause of dilated cardiomyopathy in five Chinese children.

The ALMS1 gene is predominantly localized to cilia, particularly in the photoreceptor cells of the retina, auditory neurons, kidneys, and other ciliated structures. Pathogenic mutations in this gene cause Alstrom syndrome (AS), which is characterized by dilated cardiomyopathy, retinal degeneration, neurodeafness, and centripetal obesity. However, the genetic mechanism of the ALMS1 gene remains unclear. This study reports five cases of Chinese children with heterozygous variants in the ALMS1 gene, aiming to expand the genetic map of AS and provide insights into its pathogenesis. Whole exome sequencing (WES) was performed on 128 children diagnosed with DCM. ALMS1 variants were identified, and their pathogenicity and conservation were analyzed using bioinformatics tools. A retrospective analysis of genotypephenotype associations was also conducted in conjunction with previously reported cases. A total of eleven variants were identified in the five patients, including seven nonsense variants c.2035C > T(p.R679*), c.10825C > T(p.(R3609*)), c.5230C > T(p.(Q1744*)), c.3008C > A(p.(S1003*)), c.11686delG(p.(V3896*)), c.2090C > A(p.(S697*)), c.12373C > T(p.(Q4125*)), two frameshift variants c.10383delT(p.(I3461fs*48)), c.1685_c.1686insCAG(p.(D563fs*4)), and two missense variants c.12163C > G(p.(R4055G)) and c.7867G > A(p.A2623T). Cardiac ultrasound revealed improvements in left ventricular ejection fraction (LVEF) following treatment, although no significant change in nystagmus was observed. This study expands the genetic spectrum of ALMS1 gene variants and reinforces their pathogenicity through bioinformatics analysis. Additionally, we emphasize the importance of comprehensive cardiac evaluation and genetic testing in patients with DCM presenting with nystagmus.

Early genetic screening and cardiac intervention in patients with cardiomyopathies in a multidisciplinary clinic.

Patients with cardiomyopathies are a heterogeneous group of patients who experience high morbidity and mortality. Early cardiac assessment and intervention with access to genetic counselling in a multidisciplinary Cardiomyopathy Clinic may improve outcomes and prevent progression to advanced heart failure. Our prospective cohort study was conducted at a multidisciplinary Cardiomyopathy Clinic with 421 patients enrolled (42.5% female, median age 58years), including 224 patients with dilated cardiomyopathy (DCM, 42.9% female, median age 57years), 72 with hypertrophic cardiomyopathy (HCM, 43.1% female, median age 60years), 79 with infiltrative cardiomyopathy (65.8% female, median age 70years) and 46 who were stage A/at risk for genetic cardiomyopathy (54.3% female, median age 36years). Patients were seen in follow-up at a median of 18months. A pathogenic/likely pathogenic variant was identified in 28.5% of the total cohort, including 33.3% of the DCM cohort (28% TTN mutations) and 34.1% of the HCM cohort (60% MYBPC3 and 20% MYH7) who underwent genetic testing. The use of angiotensin-converting enzyme inhibitors/angiotensin receptor blockers/angiotensin receptor neprilysin inhibitor (48.3-69.5% of total cohort, P<0.001), β-blockers (58.4-72.4%, P<0.001), mineralocorticoid receptor antagonists (33.9-41.4%, P=0.0014) and sodium/glucose cotransporter-2 inhibitors (5.3-27.9%, P<0.001) all increased at follow-up. Precision-based therapies were also implemented, including tafamidis for transthyretin amyloidosis (n=21), enzyme replacement therapy for Fabry disease (n=14) and mavacamten (n=4) for HCM. Optimization of medications and devices resulted in improvements in left ventricular ejection fraction (LVEF) from 27% to 43% at follow-up for DCM patients with reduced LVEF at baseline (P<0.001) and reduction in left ventricular mass index (LVMI) from 156g/m2 to 128g/m2 at follow-up for HCM patients with abnormal LVMI at baseline (P=0.009). Optimization of therapies was associated with stable plasma biomarkers in stage B patients while lowering levels of BNP (619-517.5pg/mL, P=0.048), NT-proBNP (777.5-356ng/L, P<0.001) and hsTropT (31-22ng/L, P=0.005) at follow-up relative to baseline values for stage C patients. Despite stage B patients having overt cardiomyopathy at baseline, stage A and B patients had a similarly high probability of survival (χ2=0.204, P=0.652). The overall cardiovascular mortality rate was low at 1.7% for the cohort (0.5% for stage B and 3.3% for stage C) over a median of 34-month follow-up. Our study demonstrates that a multidisciplinary cardiomyopathy clinic can improve the clinical profiles of patients with diverse genetic cardiomyopathies.

Catheter ablation in rate-controlled atrial fibrillation with severely reduced ejection fraction: intervention for irregularity-mediated cardiomyopathy.

Recent evidence suggests atrial fibrillation (AF) causes cardiomyopathy due to remodeling driven by both irregular rate and rhythm. Atrial fibrillation (AF) ablation in patients with reduced ejection fraction (EF) ≤ 35% has been shown to improve EF and mortality. It is unknown whether the benefits of AF ablation among patients with reduced EF are affected by the degree of pre-ablation rate control. To evaluate AF ablation echocardiographic outcomes for patients who have EF ≤ 35% with varying degrees of pre-ablation rate control. Single-center, retrospective study of patients with EF ≤ 35% undergoing first-time ablation of persistent AF. Primary analyses evaluated the degree to which pre-ablation rate control impacted echocardiographic outcomes. Rates of EF recovery to > 35% were compared at three different cutoffs: 110bpm, 90bpm, and 70bpm. A linear regression analysis was then performed to evaluate whether baseline heart rate (HR) predicted change in EF. Among 73 patients, the mean pre-ablation resting HR was 90 ± 25bpm, and baseline EF was 27 ± 7%. Patients experienced significant improvements in EF by mean + 14% ± 11% (p < 0.001). Post-ablation EF recovery occurred in 60% of patients. No differences in EF improvement were detected at HR control targets of ≤ 110bpm or ≤ 90bpm, while patients achieving HR ≤ 70bpm had less improvement in EF (+ 9% ± 9%) compared to those with HR above the cutoff (+ 16% ± 11%; p = 0.01). Linear regression analysis did not reveal baseline HR as a significant predictor of change in LVEF (slope = 0.09, r2 = 0.05, p = 0.07). Catheter ablation of persistent AF in patients with reduced EF frequently resulted in recovery in EF > 35%, irrespective of pre-ablation achieved rate control. While patients with HR > 70bpm experienced a greater improvement in EF compared to those ≤ 70bpm, patients with baseline HR below this target still experienced significant EF improvements. Further investigation into irregularity-mediated cardiomyopathy is warranted.

Effects of sodium-glucose cotransporter-2 inhibitors in myocardial infarction patients: A systematic review and meta-analysis.

Sodium-glucose cotransporter-2 (SGLT2) inhibitors are known to improve cardiovascular outcomes in individuals with heart failure (HF), type 2 diabetes mellitus (T2DM) and chronic kidney disease (CKD). However, their efficacy following myocardial infarction (MI) remains unclear. A systematic search was conducted using PubMed, Embase, Cochrane Library, Web of Science and ClinicalTrials.gov. Primary outcomes included hospitalization for heart failure (HHF), cardiovascular (CV) death, a composite of HHF or CV death, all-cause death, major cardiovascular events (MACE), recurrent MI, severe arrhythmia, renal injury and stroke. Secondary outcomes targeted improvements in left ventricular ejection fraction (LVEF) and left ventricular end-diastolic volume (LVEDV). Thirteen studies comprising 22 370 patients were included. Meta-analysis revealed that SGLT2 inhibitors reduced HHF (RR 0.69, 95% CI 0.61 to 0.78, p < 0.001), combined HHF or CV death (RR 0.87, 95% CI 0.77 to 0.99, p = 0.028), all-cause mortality (RR 0.82, 95% CI 0.73 to 0.93, p = 0.002), MACE (RR 0.68, 95% CI 0.53 to 0.88, p = 0.004), recurrent MI (RR 0.81, 95% CI 0.69 to 0.94, p = 0.007), severe arrhythmia (RR 0.54, 95% CI 0.34 to 0.85, p = 0.009) and renal injury (RR 0.68, 95% CI 0.53 to 0.87, p = 0.002). Improvement in LVEF (MD 3.96%, 95% CI 2.52 to 5.40; p < 0.001) and LVEDV (MD -5.52 mL, 95% CI -10.21 to -0.83; p = 0.021) was notably greater in the SGLT2 inhibitors group. In post-MI patients, we first found that SGLT2 inhibitors significantly lowered the risk of HHF, combined CV death or HHF, all-cause death, MACE, recurrent MI, severe arrhythmias and renal injury. Additionally, SGLT2 inhibitors improved LVEF and LVEDV.

Guideline-directed medical therapy for heart failure in arrhythmia-induced cardiomyopathy with improved left ventricular ejection fraction.

No study has analyzed the impact of guideline-directed medical therapy in preventing heart failure (HF) relapse in patients with arrhythmia-induced cardiomyopathy (AiCM) following left ventricular ejection fraction (LVEF) improvement. We analyzed data from a single-center cohort of 200 patients admitted for HF, LVEF <50% and cardiac arrhythmia considered by cardiologists to be the precipitating cause of the episode. The primary endpoint was time-to-HF relapse, defined as the composite of readmission for HF, Emergency Department (ED) visit for HF, or significant decline in LVEF. Changes in medication were recorded and a time-varying multivariate Cox regression was performed. After a median follow-up period of 6.14 years, diagnostic confirmation was achieved in 188 out of the initial 200 patients with suspected AiCM. A total of 89 patients (47.3%) met the primary endpoint. RAS inhibitors (adjusted hazard ratio (HR) 0.50 [0.31-0.81]; p = 0.005) and beta-blockers (adjusted HR 0.48 [0.28-0.81]; p = 0.006) were associated with a lower incidence of relapse. Mineralocorticoid receptor antagonists were associated with a significantly lower incidence of ED visits for HF (adjusted HR 0.38 [0.15-0.95]; p = 0.038), but did not achieve statistical significance for the combined primary endpoint. Antiarrhythmic drugs did not show a significant impact on the primary endpoint. Maintaining RAS inhibitors and beta-blockers was associated with a significantly lower incidence of relapse in the setting of AiCM with improved LVEF.

Characteristics, outcomes and the necessity of continued guideline-directed medical therapy in patients with heart failure with improved ejection fraction

Background Much remains to be learned about patients with heart failure with improved ejection fraction (HFimpEF). Objective This study sheds light on the characteristics and clinical outcomes of HFimpEF patients, including the consequences of halting guideline-directed medical therapy (GDMT). Methods This retrospective study was conducted on patients diagnosed with heart failure with reduced ejection fraction (HFrEF) who underwent a second echocardiogram at least 6 months apart between January 2009 and February 2023. The primary outcomes were major adverse cardiovascular events (MACEs), including all-cause mortality and heart failure hospitalization. The second outcome was recurrent HFrEF. Results Of 4,560 HFrEF patients were included, 3,289 (72.1%) achieved HFimpEF within a median follow-up period of 3.4 years (IQR: 1.8 − 5.9 years). Among these HFimpEF patients, recurrent HFrEF was observed in 941 (28.6%) patients during a median follow-up period of 2.3 years (IQR: 0.8–4.6 years). The proportion of patients who halted GDMT was 70.4%, 53.2%, 59.8% and 63.8% for MRA, beta-blockers, ACEI/ARB/ARNI and SGLT-2 inhibitors. Multivariable Cox analysis revealed ischemic heart disease, chronic kidney disease, coronary heart disease, lower left ventricular ejection fraction, larger left ventricular diastolic dimension and non-use GDMT are associated with recurrent HFrEF. Individuals without GDMT use exhibited lower chances of persistently recovering ejection fraction and high risks of MACEs compared to those who continue use. Conclusions HFimpEF is a common condition across all clinical follow-ups. Prevalent discontinuation of GDMT medications may contribute significantly to recurrent HFrEF, placing patients at a higher risk for poor prognosis.

Subclinical hypothyroidism: a new predictor of heart failure with improved ejection fraction in HFrEF patients.

Heart failure (HF) with improved ejection fraction (HFimpEF) has gradually attracted widespread attention in recent years for its better clinical prognosis. In this study, we attempted to investigate the relationship between subclinical hypothyroidism (SCH) and HFimpEF. This study retrospectively collected clinical data on patients with HF with reduced ejection fraction (HFrEF) hospitalized at the First Affiliated Hospital of USTC from March 2015 to September 2023, and divided into two groups as euthyroidism or SCH according to the baseline thyroid function. Then patients were further categorized into HFimpEF (follow-up LVEF > 40% and absolute increase ≥ 10%) and persistent HFrEF based on their LVEF on the echocardiograms during the follow-up period. Afterward, logistic regression was used to estimate the effect of SCH on HFimpEF. A total of 916 patients with HFrEF met the inclusion and exclusion criteria, and 396 patients (43.2%) progressed to HFimpEF status during the follow-up period. Compared with HFrEF patients, the prevalence of SCH is lower in HFimpEF patients (9.3% vs. 14.4%, P = 0.020). Univariate logistic regression analysis indicates that SCH was a potential predictor for HFimpEF (OR: 0.612 [95% CI 0.403-0.928], P = 0.021). After adjusting for multiple factors in logistic regression, the odds ratios of HFrEF patients with SCH progressing to HFimpEF decreased by 37.8% (OR: 0.622 [95% CI 0.397-0.974], P = 0.038) compared with patients with euthyroidism. This study suggests that thyroid function affects the improvement of cardiac function in patients with HFrEF and SCH is an independent predictor for HFimpEF.

SGLT2 inhibition alters substrate utilization and mitochondrial redox in healthy and failing rat hearts.

Previous studies highlight the potential for sodium-glucose cotransporter type 2 (SGLT2) inhibitors (SGLT2i) to exert cardioprotective effects in heart failure by increasing plasma ketones and shifting myocardial fuel utilization toward ketone oxidation. However, SGLT2i have multiple in vivo effects and the differential impact of SGLT2i treatment and ketone supplementation on cardiac metabolism remains unclear. Here, using gas chromatography-mass spectrometry (GC-MS) and liquid chromatography-tandem mass spectrometry (LC-MS/MS) methodology combined with infusions of [13C6]glucose or [13C4]βOHB, we demonstrate that acute SGLT2 inhibition with dapagliflozin shifts relative rates of myocardial mitochondrial metabolism toward ketone oxidation, decreasing pyruvate oxidation with little effect on fatty acid oxidation in awake rats. Shifts in myocardial ketone oxidation persisted when plasma glucose levels were maintained. In contrast, acute βOHB infusion similarly augmented ketone oxidation, but markedly reduced fatty acid oxidation and did not alter glucose uptake or pyruvate oxidation. After inducing heart failure, dapagliflozin increased relative rates of ketone and fatty acid oxidation, but decreased pyruvate oxidation. Dapagliflozin increased mitochondrial redox and reduced myocardial oxidative stress in heart failure, which was associated with improvements in left ventricular ejection fraction after 3 weeks of treatment. Thus, SGLT2i have pleiotropic effects on systemic and heart metabolism, which are distinct from ketone supplementation and may contribute to the long-term cardioprotective benefits of SGLT2i.

Effect of intradialytic exercise training on hemodialysis-induced myocardial stunning: a pilot-controlled trial

Abstract Background Hemodialysis (HD) can lead to left ventricular (LV) transient regional wall motion abnormalities (RWMAs), due to segmental hypoperfusion, well known as myocardial stunning. Repeated episodes of HD-induced ischemia contribute directly to the development of heart failure and increased mortality in patients receiving HD. Intradialytic exercise (IDE) training is capable of exerting favorable effects on the cardiovascular system. However, its impact on HD-induced myocardial stunning remains currently unknown. Methods In this prospective controlled study, 31 patients participating in an intradialytic aerobic and resistance training program (3/week for 16 weeks) were compared to 30 patients receiving usual care. Two-dimensional echocardiography was performed at baseline and follow-up both just before HD onset (T0) and at peak stress of HD (Tpeak). LV longitudinal strain from an 18-segment model were used to assess the presence of RWMAs. Results Training resulted in a significant reduction of RWMAs at Tpeak between groups (-2.22 segments; 95%CI: -0.49/-3.96; p = 0.01). Compared with usual care, trained patients demonstrated also a greater reduction in the decline of global longitudinal strain during HD (-1.45%; 95%CI: -0.24/-2.66; p = 0.01). There were significant reductions in LV mass (-23.3 g; 95%CI: -8.7/-37.9; p = 0.002) and improvements in LV ejection fraction (4%; 95%CI: 1.5/6.6; p = 0.002) between groups favoring IDE. Correlations were found between change in RWMAs with change in LV mass and ejection fraction over the study period. Conclusion IDE training is cardioprotective, improving LV remodeling and reducing HD-induced myocardial stunning.