Significant Improvement In Ejection Fraction Research Articles

Angiographic Outcomes in STEMI Patients: Evaluating Pre-dilatation and Thrombus Aspiration Effects

Introduction ST-elevation myocardial infarction (STEMI) poses significant challenges in cardiovascular care, necessitating rapid and effective reperfusion strategies. The present study assesses the angiographic outcomes of pre-dilatation and thrombus aspiration (PD+TA) versus conventional treatment without thrombus aspiration (NOTA) in patients undergoing PPCI for STEMI. Methods This prospective cohort study included a total of 155 patients, with 78 assigned to the PD+TA group and 77 to the NOTA group. Baseline demographics, cardiovascular risk factors, and angiographic assessments including TIMI flow, TMPG flow, corrected TIMI frame count (CTFC), ST segment changes, and ejection fraction were compared between the groups. Results The PD+TA group exhibited significantly lower systolic (p-value: 0.021) and diastolic blood pressures (p-value: 0.046), better glucose control (p-value: 0.015), and a more pronounced reduction in ST segment elevation (p-value: 0.027) compared to the NOTA group. Although ejection fraction at presentation was similar between groups, the PD+TA group (52.29±8.80%) demonstrated a statistically significant improvement at one-month follow-up from NOTA (49.14±8.20%). TIMI 3 and TMPG 3 flow rates were comparable between groups before and after drug administration, with significant improvements in CTFC observed in the PD+TA group. Conclusion Pre-dilatation and TA during PPCI for STEMI patients may lead to improved acute angiographic outcomes, including enhanced myocardial reperfusion and reduced ischemic burden. The significant improvement in ejection fraction at one-month follow-up further supports the potential benefits of PD+TA in cardiac function recovery. Larger studies with longer-term follow-up are needed to validate these findings and determine the broader clinical implications of TA in STEMI management. Clinical trial registration: CTRI/2019/02/017520, 7th February 2019, https://ctri.nic.in/Clinicaltrials/pmaindet2.php?EncHid=Mjk5Mjc=&Enc=&userName=CTRI/2019/02/017520

The Management Outcome of Heart Failure Reduced Ejection Fraction with or without Angiotensin Receptor Neprilysin Inhibitor

INTRODUCTION: Heart failure is associated with recurrent admission, higher mortality and low quality of life. Angiotensin receptor neprilysin inhibitor (ARNI) is a novel agent that has been used for treating heart failure reduced ejection fraction (HFrEF) patients. Thus, it is interesting to evaluate the effect of ARNI on the reverse cardiac remodelling, rehospitalization, cardiac biomarker and quality of life in HFrEF patients. MATERIALS AND METHODS: A case controlled study was conducted to assess the treatment outcome of HFrEF with or without ARNI. During the study, the patients’ basic demography, co-morbidities, baseline echocardiography (ECHO) findings, NYHA classification, NT-pro BNP levels and KCCQ score were evaluated. The patients’ admission history within 90 days from initiation of ARNI or non ARNI were obtained retrospectively. A follow up ECHO was obtained after at least 3 months of intervention. RESULTS: A total of 81 patients were recruited in which 54 patients were on ARNI and 27 were on non ARNI treatment. There was a statistically significant improvement of ejection fraction, left ventricular internal diameter end diastole and systole, and left ventricular end-systolic volume in ARNI group. The NYHA class was also noted to improve after ARNI treatment. The NT-proBNP value was lower whereas the KCCQ score was higher in ARNI group compared to non ARNI group. CONCLUSION: HFrEF patients with ARNI treatment had better reverse cardiac remodelling effect, cardiac biomarker and quality of life compared to non ARNI treatment. Furthermore, patient received ARNI demonstrated improved heart failure classification after treatment

Efficiency and Safety of Intracoronary Epinephrine Administration in Patients With ST-Elevation Myocardial Infarction With Refractory Coronary No-Reflow

Studies assessing the treatment of refractory no-reflow in ST-elevation myocardial infarction (STEMI) patients are limited to clinical cases and pilot studies. This study aimed to evaluate the efficacy and safety of intracoronary epinephrine administration in such patients. Ninety consecutive patients with refractory coronary no-reflow during percutaneous coronary intervention (PCI) were prospectively included after initial failure of conventional treatment. They were randomized into 2 groups: 45 patients in group 1 received epinephrine, and 45 patients in group 2 (control) received conventional treatments alone. Following intracoronary drug administration, the epinephrine group demonstrated significantly higher rates of coronary flow restoration in the infarct-related artery to the level of thrombolysis in myocardial infarction (TIMI) grade 3 (56% versus 29% (p=0.01)) and resolution of ST-segment elevation >50% post PCI (78% versus 36% (p<0.001)). Additionally, the epinephrine group showed a lower indexed microvascular obstruction (MVO) volume compared to the control group (0.9 (0.3; 3.1)% versus 1.9 (0.6; 7.9)% (p=0.048)). A significant improvement in ejection fraction (EF) was observed in the epinephrine group (p=0.025). Intracoronary epinephrine administration during PCI in STEMI patients with refractory no-reflow is more effective compared to conventional treatments. This approach improves coronary flow in the infarct-related artery, facilitates a faster resolution of ST segment elevation, enhances EF, and reduces MVO volume. Intracoronary epinephrine administration demonstrates a comparable safety profile to conventional treatment strategies in terms of life-threatening arrhythmias occurrence. The study suggests that intracoronary epinephrine administration during PCI could be an effective treatment strategy for STEMI patients with refractory no-reflow.

Direct Apical Cannulation With Protek Duo Rapid Deployment Cannula via Mini Thoracotomy for Ambulatory Venoarterial-Extracorporeal Membrane Oxygenation.

National trends show rapid increases in the use of mechanical circulatory support devices (MCSD) over the last 20 years. While current literature has not proven a mortality benefit in cardiogenic shock as a complication of acute myocardial infarction (AMI-CS) with percutaneous MCSD, these devices are vital to maximizing cardiopulmonary parameters for definitive therapy. To minimize complications, many different techniques have been described including a novel off-pump direct apical cannulation for venoarterial-extracorporeal membrane oxygenation (VA-ECMO). This technique allows early ambulation and avoids peripheral artery access complications but has only been described in small case series. Our case series represents the largest summary of patients (50) using this technique and contains the only comparison data to date. Fifty-four percentage of our patients were Society for Cardiovascular Angiography and Interventions (SCAI) stage D and 22% were arrested before cannulation. We achieved flows on average >5 L/min and most patients required biventricular drainage (86%) and an oxygenator (92%). Thirty day survival was 56% and most survivors were bridged to heart transplant (30%). Our most common complication was bleeding (16%). This technique showed significant improvement in ejection fraction (EF), cardiac output/index (CO/CI), and pulmonary artery pressures. This case series demonstrates the safety and efficacy of this novel technique for central cannulation in cardiogenic shock at large scale within a single institution.

The Safety and Efficacy of Human Umbilical Cord-Derived Mesenchymal Stem Cells in Patients With Heart Failure and Myocardial Infarction: A Meta-Analysis of Clinical Trials.

Evidence from preclinical and clinical studies suggests that human umbilical cord-derived mesenchymal stromal cells (HUC-MSCs) may be useful in treating heart failure and acute myocardial infarction (MI). However, the effects of stem cell therapy on patients with heart failure remain the subject of ongoing controversy, and the safety and effectiveness of HUC-MSCs therapy have not yet been proven. To date, there has been no systematic overview and meta-analysis of clinical studies using HUC-MSCs therapy for heart failure and MI. The purpose of this study is to assess the safety and efficacy of HUC-MSC therapy versus a placebo in patients with heart failure and MI. While preparing this systematic review and meta-analysis, we adhered to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. A computer literature search of PubMed was performed. We considered randomized controlled trials (RCTs) that reported data on the safety and efficacy of HUC-MSC transplantation in patients with heart failure and MI. Two investigators independently searched the literature, extracted data, and rated the quality of the included research. Pooled data were analyzed using the fixed-effect model or the random-effect model in Review Manager 5.3. The Cochrane risk of bias tool was used to assess the bias of included studies. The primary outcome was ejection fraction (EF), whereas the secondary outcomes were readmission and mortality rates. Three RCTs (201 patients) were included in this meta-analysis. The overall effect did not favor either of the two groups in terms of risk of readmission (risk ratio = 0.5, 95% confidence interval (CI) = 0.22-1.15, p = 0.10) as well as mortality rate (risk ratio = 0.44, 95% CI = 0.14-1.44, p = 0.18). However, there was an improvement in EF in patients who received HUC-MSCs compared to placebo after 12 months of transplantation (mean difference (MD) = 3.21, 95% CI = 2.91-3.51, p < 0.00001). At the six-month follow-up period, there was no significant improvement in EF (MD = 1.30, 95% CI = -1.94-4.54), p = 0.43), indicating that the duration of follow-up can shape the response to therapy. Our findings indicate that HUC-MSC transplantation can improve EF but has no meaningful effect on readmission or mortality rates. Existing evidence is insufficient to confirm the efficacy of HUC-MSCs for broader therapeutic applications. Therefore, additional double-blind RCTs with larger sample sizes are required.

Treatment of ischemic heart failure through ultrasound-targeted microbubble destruction and it's mechanism

Abstract Background The cavitation effect mediated by ultrasonic-targeted microbubble destruction (UTMD) can regulate the microenvironment and circulation of ischemic myocardium. The UTMD cavitation effect can rapidly enhance blood perfusion and improve cardiac function in patients with ischemic heart failure. However, the internal mechanism of this treatment has yet to be reported. Objective The objective of this study was to explore the underlying mechanism of UTMD-mediated cavitation effect to rapidly improve cardiac function in rats with ischemic heart failure. Methods In the first part of the study, the ischemic heart failure model was induced by ligation of the left anterior descending branch coronary in Sprague-Dawley rats, the rats were randomly divided into 7 groups: sham group, HF group, HF+MB(microbubble) group, HF+US(ultrasound) group, HF+UTMD group, HF+UTMD+LY294002(PI3K inhibitor) group, and HF+LY294002 group. Serum BNP level and echocardiographic parameters were measured to evaluate cardiac function. Thereafter, SD rats were treated with UTMD by specific ultrasonic parameters and microbubble concentration, cardiac function should be reassessed after treatment. Finally, the myocardial tissues were extracted for Western Blot and immunohistochemical analysis to detect the protein expression of the PI3K/Akt/eNOS signaling pathway, and the contents of serum nitric oxide(NO) and myocardial ATP were detected by Elisa. Results The application of UTMD resulted in significant improvements in ejection fraction (EF) and fractional shortening (FS) in rats with ischemic heart failure, as compared to the HF group (EF: 37.16 ± 1.21% vs. HF+UTMD: 46.31 ± 3.00%, P=0.0057; FS: 18.53 ± 0.58% vs. HF+UTMD: 24.05 ± 1.84%, P=0.0089). Additionally, UTMD treatment led to the activation of the PI3K/Akt/eNOS signaling pathway (HF vs. HF+UTMD, P &amp;lt; 0.01), and promoted the production of NO and ATP (HF vs. HF+UTMD, both, P&amp;lt; 0.05). However, when a PI3K inhibitor was used, the cardiac protective effects of UTMD treatment were largely eliminated. EF and FS deteriorated significantly (EF: HF+UTMD+LY294002: 42.84±2.88% vs. HF+LY294002: 32.73±3.05%, P&amp;lt;0.0001; FS: HF+UTMD+LY294002: 21.94±1.69% vs. HF+LY294002: 16.36±1.76%, P&amp;lt;0.0001), and the production of NO and ATP decreased significantly (HF+UTMD+LY294002 vs. HF+LY294002, both, P&amp;lt; 0.05). Conclusion The UTMD-mediated cavitation effect can rapidly improve the cardiac function of ischemic heart failure rats by activating PI3K/Akt/eNOS signaling pathway and promoting the release of NO and ATP.

Abstract P3071: Targeting Neutrophil Sting And Type I Interferon Activation In Myocardial Ischemia-Reperfusion Injury

Introduction: Inflammation following myocardial ischemia/reperfusion (MI/R) plays a significant role in damaging cardiomyocytes and influencing infarct size, with neutrophils being the most rapid and numerous cells in the post-MI/R heart at 24 hours post reperfusion. Preliminary single-cell RNA sequencing data shows type I interferon (IFN) responding neutrophils are present in the hearts of mice 24 hours post-MI/R. The following study aims to address how the type I IFN responding neutrophil phenotype identified in single-cell RNA sequencing data affects cardiac inflammation in MI/R. We hypothesize that STING and type I IFN activation in neutrophils in the early stages of inflammation can exacerbate inflammation, causing further damage to the heart in MI/R. Methods: Male C57BL/6J mice (10-11 weeks old) underwent 60 minutes of ischemia followed by reperfusion, and were dosed with either vehicle, a STING inhibitor (H151), or an IFNAR1 antibody (ab) at reperfusion and at 24 hours following reperfusion. Cardiac function was assessed two weeks post-reperfusion via echocardiography and tissue samples were collected for histological analysis. Results: Mice treated with IFNAR1 ab showed significant improvement in ejection fraction (44.9% ± 6.8) compared to mice treated with vehicle (31.9% ± 6.2; One-way ANOVA, N=5-6, p&lt;0.05). Additionally, mice treated with IFNAR1 ab showed significant improvements in left ventricular end systolic volume (LVESD) (3.16mm ± 0.52) compared to vehicle treated mice (3.89mm ± 0.40; One-way ANOVA, N=5-6, p&lt;0.05). Mice treated with H151 showed significant improvement in ejection fraction (43.8% ± 7.1) compared to mice treated with vehicle (31.9% ± 6.2; One-way ANOVA, N=5-6, p&lt;0.05). Treatment with H151 or IFNAR1 ab reduced scar size (7.22% ± 3.6; 7.88% ± 3.1%) compared to mice treated with vehicle (9.74% ± 3.7; N=5-6). Conclusion: These data show that targeting the early IFN response in MI/R can improve cardiac function, and provide a basis for studies identifying the effects of the neutrophil specific STING and type I IFN activation following MI/R. If correct, this pathway could be a powerful and clinically feasible point of intervention to improve cardiac recovery after MI/R.

Iron Deficiency Might Impair the Recovery of Left Ventricular Function after Surgical Revascularization in Diabetic Patients: A Retrospective Study.

Iron deficiency (ID) is one of the most common micronutrient deficiencies affecting public health. Studies show that ID affects the prognosis of patients with heart disease, including heart failure, coronary artery disease and myocardial infarction. However, there is limited information regarding the impact of ID on patients undergoing cardiac surgery. This study aimed to evaluate the influence of preoperative ID on the prognosis of type 2 diabetes mellitus (T2DM) patients undergoing coronary artery bypass grafting (CABG). In the Glycemic control using mobile-based intervention in patients with diabetes undergoing coronary artery bypass to promote self-management (GUIDEME) study, patients with T2DM undergoing CABG were prospectively recruited. In this study, only those patients with preoperative iron metabolism results were enrolled. Patients were grouped based on the presence of preoperative ID. The primary endpoint was defined as the significant improvement of follow-up ejection fraction (EF) compared to postoperative levels (classified according to the 75th percentile of the change, and defined as an improvement of greater than or equal to 5%). Univariable logistic regression was performed to explore the potential confounders, followed by multiple adjustment. A total of 302 patients were enrolled. No deaths were observed during the study period. A higher incidence of the primary endpoint was observed in the ID group (25.4% vs 12.9%, p = 0.015). The postoperative and follow-up EF were similar beween the two groups. In the regression analysis, ID was noticed to be a strong predictor against the significant improvement of EF in both univariable (odds ratio [OR]: 0.44, 95% confidence interval [CI]: 0.22-0.86, p = 0.017) and multivariable (OR: 0.43, 95% CI: 0.24-0.98, p = 0.043) logistic regression. In the subgroup analysis, ID was a predictor of significant improvement of EF in age 60 years, male, EF 60%, and on-pump CABG patients. In T2DM patients undergoing CABG, ID might negatively affect the early recovery of left ventricular systolic function in terms of recovery of EF 3-6 months after surgery, especially in patients age 60 years, males, EF 60% and in those undergoing on-pump CABG.

Identification of Safe and Effective Intravenous Dose of AAVrh.10hFXN to Treat the Cardiac Manifestations of Friedreich's Ataxia.

Friedreich's ataxia (FA) is a life-threatening autosomal recessive disorder characterized by neurological and cardiac dysfunction. Arrhythmias and heart failure are the main cause of premature death. From prior studies in murine models of FA, adeno-associated virus encoding the normal human frataxin gene (AAVrh.10hFXN) effectively treated the cardiac manifestations of the disease. However, the therapeutic dose window is limited by high level of human frataxin (hFXN) gene expression associated with toxicity. As a therapeutic goal, since FA heterozygotes have no clinical manifestations of FA, we estimated the level of frataxin (FXN) necessary to convert the heart of a homozygote to that of a heterozygote. In noncardiac cells, FA heterozygotes have 30-80% of normal FXN levels (17.7-47.2 ng/mg, average 32.5 ng/mg) and FA homozygotes 2-30% normal levels (1.2-17.7 ng/mg, average 9.4 ng/mg). Therefore, an AAV vector would need to augment endogenous in an FA homozygote by >8.3 ng/mg. To determine the required dose of AAVrh.10hFXN, we administered 1.8 × 1011, 5.7 × 1011, or 1.8 × 1012 gc/kg of AAVrh.10hFXN intravenously (IV) to muscle creatine kinase (mck)-Cre conditional knockout Fxn mice, a cardiac and skeletal FXN knockout model. The minimally effective dose was 5.7 × 1011 gc/kg, resulting in cardiac hFXN levels of 6.1 ± 4.2 ng/mg and a mild (p < 0.01 compared with phosphate-buffered saline controls) improvement in mortality. A dose of 1.8 × 1012 gc/kg resulted in cardiac hFXN levels of 33.7 ± 6.4 ng/mg, a significant improvement in ejection fraction and fractional shortening (p < 0.05, both comparisons) and a 21.5% improvement in mortality (p < 0.001). To determine if the significantly effective dose of 1.8 × 1012 gc/kg could achieve human FA heterozygote levels in a large animal, this dose was administered IV to nonhuman primates. After 12 weeks, the vector-expressed FXN in the heart was 17.8 ± 4.9 ng/mg, comparable to the target human levels. These data identify both minimally and significantly effective therapeutic doses that are clinically relevant for the treatment of the cardiac manifestations of FA.

P176 GLOBAL LONGITUDINAL STRAIN AS A PREDICTOR OF RESPONSE TO CARDIAC CONTRACTILITY MODULATION IN PATIENTS WITH HEART FAILURE: A CASE SERIES

Abstract Background Cardiac contractility modulation (CCM) in heart failure (HF) patients with reduced ejection fraction (HFrEF) is an innovative therapy which may contribute to increased exercise capacity and quality of life and reduced hospitalizations. With speckle–tracking echocardiography and global longitudinal strain (GLS), changes in myocardial function can be detected with greater sensitivity than conventional approaches for measuring diastolic and systolic function, including left ventricular ejection fraction. We aim to analyze the usefulness of GLS in detecting improvement in systolic function and response to CCM treatment. Methods We studied 5 patients with CCM referred to our outpatient cardiology clinic. All patients underwent complete echocardiography with evaluation of GLS and ejection fraction. Follow–ups were performed at 1, 3, and 6 months. Results All patients were men (mean age 65.3±15.7 yrs). Mean baseline ejection fraction was 37.1±9.3%, mean GLS was 7.7±3.1%, and patients had mild–to–moderate left ventricular enlargement (mean indexed telediastolic volumes 101.4±8.7 ml/m2). Follow–up performed at the first month showed values similar to baseline values. Between the third and sixth months, a non–significant improvement in ejection fraction and GLS was recorded (EF 40.75±9.6% p=0.51; GLS 8.9±4.2 p=0.62). Indexed telediastolic volumes were reduced (101.4±9.3 ml/m2 vs 89.5±7.4 ml/m2 p=0.05). Conclusions CCM therapy seems to be useful in achieving volumetric remodeling in patients with HFrEF. GLS assessment may be useful in detecting improvement in systolic function. Further studies with larger samples and longer follow–up are needed to confirm these results.

PO-02-009 LEAD REVISION AND OPTIMIZATION OF CRT NONRESPONDERS USING ELECTRICAL DYSSYNCHRONY MAPPING

Identification and treatment of CRT nonresponders who have poor LV lead position is a significant clinical problem. To describe how a new technology for measuring electrical dyssynchrony can be used to identify CRT patients with poor LV lead position and optimize their device programming with or without LV lead revision. An ECG system of 9 anterior/9 posterior leads was used to quantify a novel measure of electrical dyssynchrony called cardiac resynchronization index (CRI), defined as % change in area under the curve between all combinations of anterior and posterior electrodes as compared to native (CRT off). An electrical dyssynchrony map (EDM) was used to graphically display CRI values at multiple different atrial-ventricular delays (AVD) and ventricular-ventricular delays (VVD). Poor LV lead position was defined as optimal CRI (CRIopt) < 90% or need for VVD > -80 ms (LV ahead) to achieve CRIopt. We studied 19 CRT nonresponder patients with poor LV lead position based on EDM criteria. Mean CRI was 31.8±21.5%. LV lead location was anterior (n=8), apical (n=6) and posterior/lateral (n=5). Figure 1 shows an EDM of a patient before and after lead revision. Initial lead was an anterior epicardial lead. CRIopt was at VVD of -90 ms (LV-paced ahead) and EF did not improve with optimization. After placement of a lateral LV lead, VVD optimization of -30 ms resulted in an improvement in EF from 25% to 33%. Fifteen patients were programmed to CRIopt. Four patients were optimized to LV-only pacing at the optimal AVD and 11 were programmed biventricular with mean VVD -61±25 ms (LV-paced ahead). Five of these patients had minimal or no improvement with optimization. and underwent lead revision. Four patients did not have a device setting with a substantially improved CRI and 2 of 4 underwent LV lead revision. All 7 patients with LV lead revision had repeat optimization after lead revision. LV ejection fraction (EF) measured 4-6 months post-optimization improved significantly (p ≤ 0.05) from 29.1 ± 7.1% to 33.5 ± 5.8% in the 17 patients optimized by reprogramming and/or lead revision. EDM is a noninvasive, practical methodology that can be used to identify CRT nonresponder patients with poor LV lead position, determine whether lead revision may be of benefit, and optimize device programming before and/or after lead revision. This clinical approach results in a significant improvement in EF of 4.4%.

Heart Failure and Myocarditis in a 27-Year-Old Male with Human Immunodeficiency Virus

HIV-associated cardiomyopathy is a complication of HIV infection that affects the structure and function of the heart. Early detection and diagnosis is crucial and routine cardiac workup is recommended with people living with HIV. In this report, we have a 27-year-old, Male, who identifies as gay, with a history of AIDS and has been living with HIV since 5 years from admission with a recent undetectable viral load. He presented with undocumented fever, cough and dyspnea over 7 days nonresponsive to Azithromycin. Multimodality imaging stands in the forefront of diagnosis of HIV-associated Cardiomyopathy and cardiomyopathies in general. Transthoracic 2D echocardiography or Cardiac MRI is recommended on initial evaluation among patients suspected to have the disease in order to identify its specific phenotype. Echocardiography is further recommended in monitoring the progression of the disease and response to therapy. Patient’s initial echocardiogram fulfilled the criteria for DCM with an LVEDD of 59mm and a reduced ejection fraction of 40%. Due to scheduling issues, Cardiac MRI was done 77 days after guideline-directed medical therapy for heart failure with reduced ejection fraction ARNI, beta-blockers, SGLT-2 inhibitors, and diuretics as needed. Results showed significant improvement in ejection fraction to 60%, with resolution of previously seen hypokinesia, but persistence of the LV dilatation with an LV volume index of 121 mL/m2. More importantly, post-contrast imaging on the short axis show that there are linear mid-wall enhancement indicative of non-ischemic patterns of enhancement involving the basal to mid anterior septum, basal to mid inferior septum, basal to mid inferolateral, and basal lateral segments characteristic of a post-myocarditis cause of dilated cardiomyopathy.

Effects of angiotensin receptor-neprilysin inhibitors (ARNIs) on the glucose and fat metabolism biomarkers leptin and fructosamin

Abstract Background Heart Failure with reduced ejection fraction (HFrEF) has a life time risk about 20% among adults aged 40 years or older and a 5-year mortality rate about 60% [1,2]. However novel therapies have shown to improve this outcome. One novel agent are angiotensin receptor-neprilysin inhibitors (ARNIs) that increase the BNP levels via inhibiting neprilsyin [3]. This has beneficial effects on heart failure by reducing preload, inflammation and fibrosis. Neprilysin also interacts with leptin and is known to correlate with the incidence and progression of heart failure if chronically elevated [4]. Furthermore beneficial affects of ARNI therapy on glucose metabolism were reported in a post-hoc analysis of the PARADIGM-HF trial [5]. In this study we aim to investigate the effect of ARNI therapy on the fat metabolism markers leptin and on the glucose metabolism marker fructosamin. Methods In total, we included 74 patients with HFrEF with ischemic (N=37) and non-ischemic (n=37) origin in the present study. The mean NYHA class was II–III, the mean BMI 28 (SD 6.3). Patients had well established heart failure therapy before starting ARNI therapy with sacubitril/valsartan. 88% of patients were on ACE-inhibitors, 86% on beta blockers and 68% on mineralocorticoid receptor antagonists. Serum samples were obtained and analyzed for leptin, fructosamin and pBNP before and 3–6 month after ARNI therapy. The clinical parameters LVEF and NYHA class were assessed before and 3–6 month after ARNI therapy. Results Baseline leptin level was 15.0 (SD 17.2), baseline fructosamin level was 370.1 (SD 167.7) and baseline pBNP level was 1494.9 (SD 1281.4). Under therapy a significant improvement of ejection fraction from 29,8% to 37,5% (7,7 SD 8,5 P≤0.001), an improvement of NYHA stadium from 2.46 (SD 0.62) to 1.96 (SD 0.63, p=0.005) and a significant decrease of pBNP (562.1 SD 1256.4, p=0.018) was found. Along with that, a significant increase in leptin levels (3.6 SD 8.85, p=0.012) and a significant increase in fructosamine levels (93.5 SD 160.6, p=0.013) was shown. Conclusion Under therapy with ARNI we showed a sufficient therapy response with improvement of ejection fraction and decrease of pBNP in line with literature. Surprisingly metabolism biomarkers did significantly worsen under the first three to six month after new ARNI therapy. To distinguish between a side effect of ARNI therapy or consequence of heart failure itself further investigations are needed. Funding Acknowledgement Type of funding sources: None.

The role of a multidisciplinary heart failure clinic in optimization of guideline-directed medical therapy: HF-optimize

BackgroundGuideline-directed medical therapy (GDMT) reduces mortality and hospitalizations in adults with heart failure with reduced ejection fraction (HFrEF); however, few are receiving GDMT. National registries show as few as 1% of patients are receiving appropriate GDMT. Development of heart failure clinics achieving optimal GDMT are crucial to improve outcomes for HFrEF patients. ObjectiveWe developed a multidisciplinary HF-Optimize clinic aimed at improving GDMT use along with providing education, resources, and comorbidity screening for adults with HFrEF. MethodsWe targeted patients with newly diagnosed HFrEF and/or recent or multiple admissions for 6 visits over 12 weeks. We measured medication use, ejection fraction, 6-minute walk test distance, and health-related quality of life (EuroQol Visual Analog Scale) at visits 1 and 6. ResultsOne-hundred ten patients completed all visits. Patients were a mean age of 58 (±14) years, 37% were female, and 42% were of non-White race. From visit 1 to visit 6, utilization of GDMT increased from 35.5% to 85.5% (p < 0.001) and significant improvements in ejection fraction (25.9% to 35.5%, p < 0.001), 6-minute walk distance (1032 feet to 1121.7 feet, p = 0.001), and quality of life (63.8/100 vs 70.8/100, p = 0.002). Only 2 patients (1.8%) that completed HF-Optimize had a 30-day heart failure readmission. ConclusionOur multidisciplinary HF-Optimize clinic improved medication usage and clinical outcomes. Further studies are needed to validate outcomes of multidisciplinary GDMT clinics.

Midterm Outcome of Hybrid Transcatheter and Minimally Invasive Left Ventricular Reconstruction for the Treatment of Ischemic Heart Failure

BackgroundLeft ventricular (LV) remodeling after anterior myocardial infarction (AMI) can cause a pathological increase in LV volume, reduction in LV ejection fraction (EF), and symptomatic heart failure (HF). This study evaluates the midterm results of a hybrid transcatheter and minimally invasive surgical technique to reconstruct the negatively remodeled LV by myocardial scar plication and exclusion with microanchoring technology. MethodsRetrospective single-center analysis of patients who underwent hybrid LV reconstruction (LVR) with the Revivent TransCatheter System. Patients were accepted for the procedure when they presented with symptomatic HF (New York Heart Association class ≥ II, EF < 40%) after AMI, in the presence of a dilated LV with either akinetic or dyskinetic scar in the anteroseptal wall and/or apex of ≥50% transmurality. ResultsBetween October 2016 and November 2021, 30 consecutive patients were operated. Procedural success was 100%. Comparing echocardiographic data preoperatively and directly postoperatively, LVEF increased from 33 ± 8% to 44 ± 10% (p < 0.0001). LV end-systolic volume index decreased from 58 ± 24 mL/m2 to 34 ± 19 mL/m2 (p < 0.0001) and LV end-diastolic volume index decreased from 84 ± 32 mL/m2 to 58 ± 25 mL/m2 (p < 0.0001). Hospital mortality was 0%. After a mean follow-up of 3.4 ± 1.3 years, there was a significant improvement of New York Heart Association class (p = 0.001) with 76% of surviving patients in class I-II. ConclusionsHybrid LVR for symptomatic HF after AMI is safe and results in significant improvement in EF, reduction in LV volumes, and sustained improvement in symptoms.

Cardiac resynchronization therapy response in cardiac sarcoidosis.

Cardiac sarcoidosis (CS) is a nonischemic cardiomyopathy (NICM) characterized by infiltration of noncaseating granulomas involving the heart with highly variable clinical manifestations that can include conduction abnormalities and systolic heart failure. Cardiac resynchronization therapy (CRT) has shown significant promise in NICM, though little is known about its efficacy in patients with CS. To determine if CRT improved cardiac remodeling in patients with CS. We retrospectively reviewed all patients with a clinical or histological diagnosis of CS who underwent CRT implantation at the Mayo Clinic enterprise from 2000 to 2021. Baseline characteristics, imaging parameters, heart failure hospitalizations and need for advanced therapies, and major adverse cardiac events (MACE) were assessed. Our cohort was comprised of 55 patients with 61.8% male and a mean age of 58.7 ± 10.9 years. Eighteen (32.7%) patients had definite CS, 21 (38.2%) had probable CS, while 16 (29.1%) had presumed CS, and 26 (47.3%) with extracardiac sarcoidosis. The majority underwent CRT-D implantation (n = 52, 94.5%) and 3 (5.5%) underwent CRT-P implantation with 67.3% of implanted devices being upgrades from prior pacemakers or implantable cardioverter defibrillators. At 6 months postimplantation there was no significant improvement in ejection fraction (34.8 ± 10.9% vs. 37.7 ± 14.2%, p = .331) or left ventricular end-diastolic diameter (58.5 ± 10.2 vs. 57.5 ± 8.1 mm, p = .236), though mild improvement in left ventricular end systolic diameter (49.1 ± 9.9 vs. 45.7± 9.9 mm, p < .0001). Within the first 6 months postimplantation, 5 (9.1%) patients sustained a heart failure hospitalization. At a mean follow-up of 4.1± 3.7 years, 14 (25.5%) patients experienced a heart failure hospitalization, 11 (20.0%) underwent cardiac transplantation, 1 (1.8%) underwent left ventricular assist device implantation and 7 (12.7%) patients died. Our findings suggest variable response to CRT in patients with CS with no overall improvement in ventricular function within 6 months and a substantial proportion of patients progressing to advanced heart failure therapies.

Impact of exercise training on myocardial contractile functions assessed by cardiac magnetic resonance in post-myocardial infarction patients

BackgroundImprovement of functional capacity and mortality reduction in post-MI patients were found to be associated with regular exercise training. The cardiac magnetic resonance (CMR) is considered the most accurate non-invasive modality in quantitative assessment of left ventricular (LV) volumes and systolic functions. Our main objective was to investigate the impact of exercise training on LV systolic functions in patients post anterior MI using CMR. 32 patients on recommended medical treatment 4 week after having a successful primary PCI for an anterior MI were recruited, between May 2018 and May 2019. They were divided into two groups, training group (TG): 16 assigned to a 12 week exercise training program and control group (CG): 16 who received medical treatment without participating in the exercise training program. Treadmill exercise using modified Bruce protocol was done to TG before and after the training program in order to record the resting and maximum HR, metabolic equivalent (MET), and calculate HR reserve. CMR was performed for all patients 4 weeks after PCI and was repeated after completion of the study period to calculate ejection fraction (EF), left ventricular end-systolic volume (LVESV), left ventricular end-diastolic volume (LVEDV), and wall motion score index (WMSI).Results100% were males. 6 patients from CG dropped during follow-up, no statistically significant difference between the two groups regarding age, BMI, smoking status, hypertension, diabetes mellitus and dyslipidemia. Using the CMR, the TG showed significant improvement in EF (36.6 ± 14.2% to 43.1 ± 12.4%; P < 0.001) and WMSI (2.03 ± 0.57 to 1.7 ± 0.49; P < 0.001), without statistically significant change in LV volumes. Regarding CG no significant changes in EF, WMSI, LV volumes were found. There was significant improvement in EF and WMSI change before and after study in TG vs. CG [6.5 (2.3–9.0) vs. − 2.0 (− 6.8 to 1.3), P value < 0.001] and [− 0.3 (− 0.5 to 0.1) vs. 0.1 (− 0.1 to − 0.5), P value 0.001] respectively.Conclusions12 weeks of exercise training program in post-MI patients have a favorable impact on LV global and regional systolic functions without adversely affecting LV remodeling (as assessed by CMR).

Comparing the effect of bone marrow mono-nuclear cells with mesenchymal stem cells after acute myocardial infarction on improvement of left ventricular function: a meta-analysis of clinical trials

BackgroundThe effect of transplantation of bone-marrow mononuclear cells (BM-MNCs) and mesenchymal stem cells (MSCs) on ejection fraction (LVEF) has been studied in patients with acute myocardial infarction (AMI) in clinical trials. This raises the question that which type of cell may help improve LVEF better in AMI patients. No meta-analysis of clinical trials has yet addressed this question.MethodsElectronic databases were searched thoroughly to find eligible trials on the effects of transplantation of BM-MNCs and MSCs in patients with AMI. The primary outcome was improvement in LVEF. Data were synthesized using random-effects meta-analysis. For maximizing the credibility of subgroup analysis, we used the instrument for assessing the Credibility of Effect Modification of Analyses (ICEMAN) for meta-analyses.ResultsA total of 36 trials (26 on BM-MNCs and 10 on MSCs) with 2489 patients (1466 were transplanted [1241 with BM-MNCs and 225 with MSCs] and 1023 as controls) were included. Both types of cells showed significant improvements in ejection fraction in short-term follow-up (BM-MNCs: WMD = 2.13%, 95% CI = 1.23 to 3.04, p < 0.001; MSCs: WMD = 3.71%, 95% CI = 2.32 to 5.09, p < 0.001), and according to ICEMAN criteria, MSCs are more effective. For selected population of patients who received stem cell transplantation in early course after AMI (less than 11 days), this effect was even more pronounced (BM-MNC: WMD = 3.07%, 95% CI = 1.97 to 4.17, p < 0.001, I2 = 40.7%; MSCs: WMD = 5.65%, 95% CI = 3.47 to 7.84, p < 0.001, I2 = 84.6%).ConclusionOur results showed that transplantation of MSCs after AMI might increase LVEF more than BM-MNCs; also, based on ICEMAN, there was likely effect modification between subgroups although uncertainty still remained.

Non-invasive hemodynamic evaluation following TAVI for severe aortic stenosis

Abstract Funding Acknowledgements Type of funding sources: None. Background Various hemodynamic changes occur following Transcatheter aortic valve implantation (TAVI) that impact treatment decisions. NICaS, a noninvasive whole-body bio-impedance monitoring system to assess hemodynamics and fluid balance, was tested in patients with severe aortic stenosis (AS) before and after TAVI. Methods Between October 2019 and December 2020 all consecutive patients with severe AS undergoing TAVI were assessed by NICaS at several time points – 24 hours before (baseline) and after the procedure, at hospital discharge and at 30 days to 1 year follow-up. Excluded were patients undergoing TAVI due to reasons other than severe AS, patients under general anesthesia and those who died at the catheterization lab or immediately following the procedure. Results We performed hemodynamic analysis on 97 consecutive patients who underwent TAVI using either Medtronic Evolut R (54%), Edwards Sapien 3 (32%) or SYMETIS ACURATE neo (13%). Patients were more often women (54%) and had multiple comorbidities including hypertension (83%), dyslipidemia (79%), coronary artery disease (46%), and diabetes mellitus (37%). Compared to baseline NICaS measurements, we observed increases in systolic blood pressure (BP) and total peripheral resistance (TPR) within 24 hours following TAVI (systolic BP 132.5±22.3 mmHg at baseline versus 148.4±23.9 mmHg after TAVI, P&amp;lt;0.001; TPR 1754±520 versus 2094±752 dynes*s/cm5, respectively, P&amp;lt;0.001) while cardiac output (CO), cardiac index (CI) and stroke volume (SV) decreased (CO 4.2±1.2 versus 3.9±1.2 L/min, respectively, P=0.013; SV 62±15 versus 56±15.8 mL, P=0.002). However, opposite trends were demonstrated exclusively in patients with ejection fraction (EF) under 40%. At follow-up (median 59 days, IQR [39.5-91]) these hemodynamic measurements returned to values that were not statistically different from the baseline, despite a significant improvement in EF from baseline to follow-up (55.6±11.6 to 59.4±9.4%, P&amp;lt;0.001). Conclusion A unique pattern of short and longer term adaptive hemodynamic changes was demonstrated using the NICaS system among patients undergoing TAVI. These findings require validation and further research to their underlying mechanism if NICaS is to be used as a bedside monitoring tool to guide treatment decisions.

Five-Year Outcome of Hybrid Transcatheter and Minimally Invasive Left Ventricular Reconstruction for the Treatment of Ischemic Heart Failure

<h3>Purpose</h3> Remodelling of the left ventricle (LV) after anterior myocardial infarction (AMI) can result in a pathological increase in LV volume, reduction in LV ejection fraction (EF) and symptomatic heart failure (HF). We describe the five-year results of a hybrid transcatheter and minimally invasive surgical technique to reconstruct the remodelled LV by myocardial scar plication and exclusion. <h3>Methods</h3> Patients were eligible for the procedure when they presented with symptomatic HF (NYHA-class ≥II, EF<40%) after AMI. All patients had a dilated LV with a- or dyskinetic scar in the anteroseptal wall and/or apex ≥50% transmurality. Hybrid transcatheter and minimally technique (BioVentrix Revivent TC) that relies on micro-anchoring technology is used to reconstruct the LV by plication of the fibrous scar. A series of internal and external anchors are brought together over a PEEK (poly-ether-ether-ketone) tether to form a longitudinal line of apposition between the LV free wall and the anterior septum from the mid-ventricle to the apex. Internal anchors are deployed by transcatheter technique on the right side of the ventricular septum. External anchors are advanced through a left sided mini-thoracotomy and the anchor-pairs are brought together under measured compression forces. Additional external apical anchor pairs complete the reconstruction. <h3>Results</h3> Between October 2016 and October 2021 29 patients (24 males, 5 females; mean age 62 ± 12 years) were operated in a single Dutch centre. On average 2.3 ± 0.8 anchor-pairs were used for reconstruction. Comparing echocardiographic data pre- and directly postoperatively, LVEF increased from 33 ± 8 to 44 ± 10% (change +35%, P<0.001) and LV-volumes decreased: LVESVI 56 ± 27 to 35 ± 19 ml/m² (change -36%, P<0.001) and LVEDVI 85 ± 33 to 59 ± 25 ml/m² (change -30%, P<0.001). Hospital mortality was 0%. and median length of hospital stay was 7 days (IQR 5-61 days). Survival at 60 months was 86%. At latest follow-up, 85% of surviving patients were in NYHA-class I-II compared to 19% preoperatively. <h3>Conclusion</h3> Hybrid transcatheter and minimally invasive LV reconstruction is a promising treatment option for patients with symptomatic HF after AMI. Five-year results demonstrate that the procedure is safe and results in significant improvement in EF, reduction in LV volumes and sustained improvement in symptoms.