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Ventricular remodeling (VR) after acute ST-elevation myocardial infarction (STEMI) is an important predictor for medium- and long-term prognosis. This study focuses on the relevant indexes of VR in patients with AMI, in which, the intervention effects of sacubitril/valsartan and enalapril were compared, guiding the clinical treatment. 58 patients with acute STEMI treated with PCI were divided into research group and control group. UCG was performed at 1 week, 1 month and 3 months after MI, and the patients' indexes were collected to compare VR and adverse reactions in the two groups. The test results showed that there was no statistical difference in the baseline data of patients in the two groups, which were comparable. In the blood biochemical index examination, no statistical difference was found in cTnI and NT-proBNP between the two groups. At 1 week after operation, the levels of cTnI and NT-proBNP in research group were lower than those in the control group. In ECG examination, there was no statistical significance in the levels of LVEF, LVEDD and LVESD at admission between the two groups. After 1 week, the results of LVEF, LVEDD, LVESD in the research group were higher than those in the control group. The results of this study show that sacubitril/valsartan can be used in patients with AMI instead of enalapril. Sacubitril/valsartan improves cardiac function in patients with emergency percutaneous coronary intervention (PCI) for AMI, inhibits ventricular remodeling, and has a low incidence of adverse cardiac events and adverse drug reactions. [ABSTRACT FROM AUTHOR]

The Chinese visceral adipose index (CVAI) is more significantly associated with cardiometabolic risk factors than other obesity indices. This study investigated the relationship between CVAI and left ventricular (LV) remodeling. This study included 75,132 Koreans who underwent echocardiography during a health checkup. They were grouped according to quartile levels of the CVAI, body mass index (BMI), waist circumference (WC), and visceral adiposity index (VAI). LV remodeling was defined as the presence of abnormal relative wall thickness (ARWT) and left ventricular hypertrophy (LVH). Multivariate adjusted logistic regression analysis (adjusted OR [95% confidence interval]) was used to analyze the association between ARWT and LVH according to the quartile levels of each index. Receiver operating characteristic (ROC) graphs and areas under the curve (AUC) were calculated to identify the predictive ability of the indices for ARWT and LVH. ARWT was associated proportionally with CVAI quartiles in both men (second quartile: 1.42 [1.29–1.56], third quartile: 1.61 [1.46–1.77], fourth quartile: 2.01 [1.84–2.21]), and women (second quartile: 1.06 [0.78–1.45], third quartile: 1.15 [0.86–1.55], and fourth quartile: 2.09 [1.56–2.80]). LVH was significantly associated with third (1.74 [1.07–2.83]) and fourth quartile (1.94 [1.18–3.20]) groups of CVAI in women. ROC and AUC analyses indicated that CVAI was superior to other indices in predicting ARWT in men and LVH and ARWT in women. The CVAI is an effective surrogate marker of LV remodeling, particularly in women. • CVAI predicted the likelihood of LVH and ARWT better than BMI, waist circumference, and VAI in women. • Our study suggests that the VAI has poor predictive power for LV remodeling, whereas the CVAI is significantly better in the Asian population. [ABSTRACT FROM AUTHOR]

Background: In heart failure with reduced ejection fraction (HFrEF), sodium–glucose co-transporter inhibitors (SGLT-2i) have persistently shown cardiovascular benefits through different trials. However, their impact on ventricular remodeling and cardiac hemodynamics has not been sufficiently studied. This study aimed to study how SGLT-2i initiation affects invasive hemodynamics and cardiac magnetic resonance imaging (CMR)-derived ventricular volumes, function, and fraction of the extracellular volume (ECV) in HFrEF patients with non-ischemic dilated cardiomyopathy (NIDCM). Results: In this study, 23 patients with HFrEF and a mean age of 42, including 82.6% males, all have NIDCM and underwent right heart catheterization and CMR at the initiation of dapagliflozin and at 6-month follow-up. The addition of dapagliflozin resulted in significant reductions in the following invasive hemodynamic parameters compared to baseline: left ventricular end-diastolic pressure (23.4 vs 19.7 mmHg, p = 0.003), mean pulmonary artery pressure (31.3 vs 27.7 mmHg, p = 0.03), and systemic vascular resistance (18 vs 15 Wood units, p = 0.047). Among the studied CMR-derived measurements, only the percentage of extracellular volume fraction was significantly less at follow-up (33.7 vs 32.16%, p = 0.001). Additionally, functional class showed significant improvement with a notable reduction of the NT-proBNP level and a considerable decrease in diuretic dose (median: 40 vs 80 mg, p = 0.01). Conclusion: Adding dapagliflozin to patients with HFrEF due to NIDCM improved invasively measured hemodynamics and significantly reduced left ventricular extracellular volume fraction measured by CMR, with no significant change in ventricular volumes or ejection fraction. [ABSTRACT FROM AUTHOR]

BACKGROUND: Recent studies have shown that remnant cholesterol (RC) is associated with incident heart failure; however, its association with left ventricular (LV) structure and function is unclear. We aimed to evaluate the association between RC levels in young adulthood and LV structure and function in middle age. METHODS: We included 3321 participants from the CARDIA study (Coronary Artery Risk Development in Young Adults) at baseline. RC was calculated as total cholesterol minus high-density lipoprotein cholesterol minus calculated low-density lipoprotein cholesterol, and the RC trajectories that followed a similar pattern of change over time were identified using the latent class growth mixture model. LV structure and function were assessed using echocardiography at CARDIA study year 25. Multivariable linear regression models were performed to assess the associations of both baseline and trajectories of RC levels with LV structure and function. RESULTS: Among 3321 participants, the mean age was 24.99±3.62 years: 1450 (43.90%) were male, and 1561 (47.00%) were Black. After multivariate adjustment, higher baseline RC (per SD in log-transformed) was associated with higher LV mass index (β=1.29; P=0.004), worse global longitudinal strain (β=0.19; P<0.001), worse global circumferential strain (β=0.16; P=0.014), lower septal e' (β=-0.26; P<0.001), lower lateral e' (β=-0.18; P=0.003), and higher E/e' (β=0.15; P=0.003). Three RC trajectories were identified during follow-up: low increasing (42.4%), moderate increasing (45.5%), and high increasing (12.1%). Similarly, compared with the low-increasing group, the high-increasing RC trajectory group was related to higher LV mass index, worse global longitudinal strain, lower septal e', lower lateral e', and higher E/e'. CONCLUSIONS: Elevated RC levels in young adulthood were related to adverse LV structural and functional alterations in midlife. Long-term trajectories of RC levels during young adulthood help identify individuals at a higher risk for adverse LV remodeling and dysfunction. [ABSTRACT FROM AUTHOR]

Diastolic dysfunction is regarded as an important predictor of outcome after liver transplantation (LT). We investigated the influence of liver disease severity on left ventricular diastolic properties using end-diastolic pressure-volume relationship (EDPVR) analysis in patients with end-stage liver disease (ESLD). Association between alterations of the EDPVR and mortality after LT was evaluated. In this observational retrospective cohort study, 3,211 patients who underwent LT for ESLD were included in analysis. Variables derived from single-beat EDPVR (diastolic stiffness-coefficient [β] and end-diastolic volume at an end-diastolic pressure of 20 mmHg [EDVI 20 ] indicating ventricular capacitance) were estimated using preoperative echocardiographic data. Alterations in EDPVR with increased stiffness (β > 6.16) were categorized into 3 groups; leftward-shifted (EDVI 20 <51 mL/m2), rightward-shifted (EDVI 20 > 69.7 mL/m2), and intermediate (EDVI 20 51-69.7 mL/m2). As the model for ESLD score increases, both EDVI 20 and β gradually increased, which indicated ventricular remodeling with larger capacitance and higher diastolic stiffness. Among patients with increased stiffness (β > 6.16, n = 1,090), survival rates after LT were lower in leftward-shifted EDPVR than in rightward-shifted EDPVR (73.7% vs 82.9%; log-rank P = 0.002). In the adjusted Cox proportional hazard model, risk of cumulative all-cause mortality at 11 years was the highest in leftward-shifted EDPVR (hazard ratio [HR]: 1.93; 95% confidence interval [CI]: 1.27-2.92), followed by intermediate EDPVR (HR: 1.55; 95% CI: 1.12-2.26), compared with rightward-shifted EDPVR. The SHapley Additive exPlanation model revealed that the variables associated with leftward-shifted EDPVR were diabetes, female sex, old age, and hypertension. As ESLD advances, diastolic ventricular properties are characterized by increased EDVI 20 and β on rightward-shifted EDPVR, indicating larger capacitance and higher stiffness. However, leftward-shifted EDPVR with left ventricle remodeling failure is associated with poor post-LT survival. [Display omitted] [ABSTRACT FROM AUTHOR]

BACKGROUND: Concentric remodeling (cRM) can precede heart failure with preserved ejection fraction (HFpEF), a condition prevalent in women. METHODS: Patients (n=60 593, 54.2% women) visiting outpatient clinics of Cardiology Centers of the Netherlands were analyzed for cRM, HFpEF development, and mortality risk. We studied risk factors for relative wall thickness both sex- stratified and in women and men combined. Biomarker profiling was performed (4534 plasma proteins) in a substudy involving 557 patients (65.4% women) to identify pathways involved in cRM. RESULTS: cRM was present in 23.5% of women and 27.6% of men and associated with developing HFpEF (HR, 2.15 [95% CI, 1.51–2.99]) and mortality risk (HR, 1.09 [95% CI, 1.00–1.19]) in both sexes. Age, heart rate, and hypertension were statistically significantly stronger risk factors for relative wall thickness in women than men. Higher circulating levels of IFNA5 (interferon alpha-5) were associated with higher relative wall thickness in women only. Pathway analysis revealed differential pathway activation by sex and increased expression of inflammatory pathways in women. CONCLUSIONS: cRM is prevalent in approximately 1 in 4 women and men visiting outpatient cardiology clinics and associated with HFpEF development and mortality risk in both sexes. Known risk factors for cRM were more strongly associated in women than men. Proteomic analysis revealed inflammatory pathway activation in women, with a central role for IFNA5. Differential biologic pathway activation by sex in cRM may contribute to the female predominance of HFpEF and holds promise for identification of new therapeutic avenues for prevention and treatment of HFpEF. [ABSTRACT FROM AUTHOR]

Patients who survive a myocardial infarction have progressive cardiac dysfunction and ventricular remodeling. Mitral regurgitation is often diagnosed in these patients, and is a risk factor that portends poor prognosis. Whether such postinfarction mitral regurgitation magnifies adverse left ventricular remodeling is unclear, which was studied in an animal model. Forty-one adult rats were induced with myocardial infarction using left coronary artery ligation and assigned to 3 groups: group 1, myocardial infarction only; group 2, myocardial infarction with severe mitral regurgitation introduced after 4 weeks; and group 3, myocardial infarction with severe mitral regurgitation introduced after 10 weeks. Valve regurgitation was introduced by advancing a transapical ultrasound-guided needle into the mitral valve anterior leaflet. Animals were survived to 20 weeks from the index procedure, with biweekly cardiac ultrasound, and invasive hemodynamics and histology at termination. At 20 weeks, end diastolic volume was largest in the groups with mitral regurgitation, compared with the group without the valve lesion (group 1, 760.9 ± 124.6 μL; group 2, 958.0 ± 115.1 μL; group 3, 968.3 ± 214.9 μL). Similarly, end systolic volume was larger in groups with regurgitation (group 1, 431.2 ± 152.6 μL; group 2, 533.2 ± 130.8 μL; group 3, 533.1 ± 177.5 μL). In the infarction-only group, left ventricular remodeling was maximal until 6 weeks and plateaued thereafter. In groups with mitral regurgitation, left ventricular remodeling was significantly elevated at the onset of regurgitation and persisted. Mitral regurgitation is a potent driver of adverse cardiac remodeling after a myocardial infarction, irrespective of the timing of its onset. [Display omitted] [ABSTRACT FROM AUTHOR]

The relationship between left ventricular (LV) remodeling and clinical outcomes after treatment of severe mitral regurgitation (MR) in heart failure (HF) has not been examined. The aim of this study was to evaluate the association between LV reverse remodeling and subsequent outcomes and assess whether transcatheter edge-to-edge repair (TEER) and residual MR are associated with LV remodeling in the COAPT (Cardiovascular Outcomes Assessment of the MitraClip Percutaneous Therapy for Heart Failure Patients With Functional Mitral Regurgitation) trial. Patients with HF and severe MR who remained symptomatic on guideline-directed medical therapy (GDMT) were randomized to TEER plus GDMT or GDMT alone. Baseline and 6-month core laboratory measurements of LV end-diastolic volume index and LV end-systolic volume index were examined. Change in LV volumes from baseline to 6 months and clinical outcomes from 6 months to 2 years were evaluated using multivariable regression. The analytical cohort comprised 348 patients (190 treated with TEER, 158 treated with GDMT alone). A decrease in LV end-diastolic volume index at 6 months was associated with reduced cardiovascular death between 6 months and 2 years (adjusted HR: 0.90 per 10 mL/m2 decrease; 95% CI: 0.81-1.00; P = 0.04), with consistent results in both treatment groups (P interaction = 0.26). Directionally similar but nonsignificant relationships were present for all-cause death and HF hospitalization and between reduced LV end-systolic volume index and all outcomes. Neither treatment group nor MR severity at 30 days was associated with LV remodeling at 6 or 12 months. The treatment benefits of TEER were not significant regardless of the degree of LV remodeling at 6 months. In patients with HF and severe MR, LV reverse remodeling at 6 months was associated with subsequently improved 2-year outcomes but was not affected by TEER or the extent of residual MR. (Cardiovascular Outcomes Assessment of the MitraClip Percutaneous Therapy for Heart Failure Patients With Functional Mitral Regurgitation [The COAPT Trial] and COAPT CAS [COAPT]; NCT01626079) [Display omitted] [ABSTRACT FROM AUTHOR]

• A lower serum vitamin D 3 concentration has been associated with an increased risk of cardiovascular disease. However, the associations between serum vitamin D 3 levels and heart failure with preserved ejection fraction (HFpEF) have not been well-characterized. • Lower serum vitamin D 3 levels were associated with left ventricular concentric remodeling and incident HF, mainly HFpEF in Black Americans. • Further investigation is required to examine whether supplementation of vitamin D 3 can prevent left ventricular concentric remodeling and incident HFpEF in Black Americans. In observational studies, a lower serum vitamin D 3 concentration has been associated with an increased risk of cardiovascular disease. However, the associations between serum vitamin D 3 levels and left ventricular (LV) structure and heart failure with preserved ejection fraction (HFpEF) have not been well-characterized among Black Americans. The prevalence of vitamin D 3 deficiency is higher among Black Americans than in other race/ethnicity groups. We hypothesized that serum vitamin D 3 levels are associated with LV concentric remodeling and incident HFpEF in Black Americans. Among 5306 Black Americans in the Jackson Heart Study cohort, we investigated the relationships between serum vitamin D 3 levels and LV structure and function, evaluated with echocardiography, and incident HF hospitalization, categorized as either HF with reduced EF (HFrEF; an EF of <50%) or HFpEF (an EF of ≥50%). After adjustment for possible confounding factors, lower vitamin D 3 levels were associated with greater relative wall thickness (β for 1 standard deviation [SD] increase –0.003, 95% confidence interval –0.005 to –0.000). Over a median follow-up period of 11 years (range 10.2–11.0 years), 340 participants developed incident HF (7.88 cases per 1000 person-years), including 146 (43%) HFrEF and 194 (57%) HFpEF cases. After adjustment, higher serum vitamin D 3 levels were associated with decreased hazard for HF overall (hazard ratio for 1 SD increase 0.88, 95% confidence interval 0.78–0.99) driven by a significant association with HFpEF (hazard ratio for 1 SD increase 0.84, 95% confidence interval 0.71–0.99). In this community-based Black American cohort, lower serum vitamin D 3 levels were associated with LV concentric remodeling and an increased hazard for HF, mainly HFpEF. Further investigation is required to examine whether supplementation with vitamin D 3 can prevent LV concentric remodeling and incident HFpEF in Black Americans. [Display omitted] [ABSTRACT FROM AUTHOR]

Pulmonary arterial hypertension (PAH) and the consequent right heart dysfunction persist with high morbidity and mortality, and the mechanisms and pharmacologic interventions for chronic right-sided heart failure (RHF) have not been adequately investigated. Research has shown that prolonged inflammation is critical in precipitating the progression of PAH-associated right heart pathology. Some research demonstrated that Lingguizhugan decoction (LGZGD), as a classical Chinese medicine formula, had beneficial effects in alleviating PAH and RHF, while its underlying mechanisms involved are not fully elucidated. Based on that, this study aims to investigate the effects and underlying mechanisms of LGZGD on PAH-induced RHF. In this study, we identified the serum constituents and deciphered the potential anti-inflammatory mechanism and crucial components of LGZGD using combined approaches of UPLC-HRMS, transcriptomic analysis, and molecular docking techniques. Finally, we used in vivo experiments to verify the expression of key targets in the monocrotaline (MCT)-induced RHF model and the intervene effect of LGZGD. Integrated strategies based on UPLC-HRMS and systems biology approach combined with in vivo experimental validation showed that LGZGD could improve right heart fibrosis and dysfunction via regulating diverse inflammatory signaling pathways and the activity of immune cells, including chemokine family CCL2, CXCR4, leukocyte integrins family ITGAL, ITGB2, and M2 macrophage infiltration, as well as lipid peroxidation-associated HMOX1, NOX4, and 4-HNE. The present research demonstrated for the first time that LGZGD might improve PAH-induced RHF through multiple anti-inflammatory signaling and inhibition of ferroptosis, which could provide certain directions for future research in related fields. [Display omitted] [ABSTRACT FROM AUTHOR]

Despite tremendous progress in cell-based therapies for heart repair, many challenges still exist. To enhance the therapeutic potential of cell therapy one approach is the combination of cells with biomaterial delivery vehicles. Here, we developed a biomimetic and biodegradable micro-platform based on polymeric microparticles (MPs) capable of maximizing the therapeutic potential of cardiac progenitor cells (CPCs) and explored its efficacy in a rat model of chronic myocardial infarction. The transplantation of CPCs adhered to MPs within the infarcted myocardial microenvironment improved the long-term engraftment of transplanted cells for up to one month. Furthermore, the enhancement of cardiac cellular retention correlated with an increase in functional recovery. In consonance, better tissue remodeling and vasculogenesis were observed in the animals treated with cells attached to MPs, which presented smaller infarct size, thicker right ventricular free wall, fewer deposition of periostin and greater density of vessels than animals treated with CPCs alone. Finally, we were able to show that part of this beneficial effect was mediated by CPC-derived extracellular vesicles (EVs). Taken together, these findings indicate that the biomimetic microcarriers support stem cell survival and increase cardiac function in chronic myocardial infarction through modulation of cardiac remodeling, vasculogenesis and CPCs-EVs mediated therapeutic effects. The biomimetic microcarriers provide a solution for biomaterial-assisted CPC delivery to the heart. In this study, we evaluate the possibility of using a biomimetic and biodegradable micro-platform to improve cardiovascular progenitor therapy. The strategy reported herein serves as an injectable scaffold for adherent cells due to their excellent injectability through cardiac catheters, capacity for biomimetic three-dimensional stem cell support and controllable biodegradability. In a rat model of chronic myocardial infarction, the biomimetic microcarriers improved cardiac function, reduced chronic cardiac remodeling and increased vasculogenesis through the paracrine signaling of CPCs. We have also shown that extracellular vesicles derived from CPCs cultured on biomimetic substrates display antifibrotic effects, playing an important role in the therapeutic effects of our tissue-engineered approach. Therefore, biomimetic microcarriers represent a promising and effective strategy for biomaterial-assisted CPC delivery to the heart. [Display omitted] [ABSTRACT FROM AUTHOR]

Some patients with hypertrophic cardiomyopathy (HCM) present with reduced left ventricular (LV) stroke volume and elongated systolic cavity obliteration due to symmetric LV hypertrophy. In this report, we detail our experience with transapical septal myectomy to enlarge the LV volume and to relieve cavity obliteration in this unique subgroup of patients with HCM. We analyzed 38 patients with HCM who had extended symmetric LV hypertrophy and underwent transapical septal myectomy to enlarge the LV cavity from February 2001 to May 2021. At the time of evaluation for operation, 84.2% (n = 32) of the patients were in New York Heart Association class III/IV. The peak oxygen consumption was 51.5% (44.0%-58.0%) of the normal predicted values on the preoperative exercise stress test (n = 16). Preoperative left atrial sizes in this cohort were enlarged (left atrial volume index, 39.0 [33.5-51.5] mL/m2), despite only 4 patients with moderate or greater mitral valve regurgitation. All patients underwent transapical septal myectomy to enlarge the LV cavity size. There was no postoperative (within 30 days) death. During a median (interquartile range) follow-up of 3.4 (0.7-6.9) years, the estimated survival rates were 100%, 92%, and 87% at 1, 3, and 5 years, respectively. Follow-up surveys suggested that 16 of the 17 contacted patients experienced improvement in their heart function after the procedure. Transapical myectomy to enlarge LV cavity volume can be performed safely with good early survival and functional results. This procedure is an important alternative to cardiac transplantation for HCM patients with systolic cavity obliteration and progressive heart failure. [ABSTRACT FROM AUTHOR]

Left ventricular remodeling is an adaptive process initially developed in response to acute myocardial infarction (AMI), but it ends up with negative adverse outcomes such as infarcted wall thinning, ventricular dilation, and cardiac dysfunction. A prolonged excessive inflammatory reaction to cardiomyocytes death and necrosis plays the crucial role in the pathophysiological mechanisms. The pharmacological treatment includes nitroglycerine, β-blockers, ACEi/ARBs, SGLT2i, mineralocorticoid receptor antagonists, and some miscellaneous aspects. Stem cells therapy, CD34+ cells transplantation and gene therapy constitute the promissing therapeutic approaches for post AMI cardiac remodeling, thereby enhancing angiogenesis, cardiomyocytes differenciation and left ventricular function on top of inhibiting apoptosis, inflammation, and collagen deposition. All these lead to reduce infarct size, scar formation and myocardial fibrosis. [ABSTRACT FROM AUTHOR]

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Graphical abstract Abstract Heart disease remains a leading killer in western society and irreversibly impacts the lives of millions of patients annually. While adult mammals do not possess the ability to regenerate functional cardiac tissue, neonatal mammals are capable of robust cardiomyocyte proliferation and regeneration within a week of birth. Given this change in regenerative function through development, the extracellular matrix (ECM) from adult tissues may not be conducive to promoting cardiac regeneration, although conventional ECM therapies rely exclusively on adult-derived tissues. Therefore the potential of ECM derived from neonatal mouse hearts (nmECM) to prevent adverse ventricular remodeling in adults was investigated using an in vivo model of acute myocardial infarction (MI). Following a single administration of nmECM, we observed a significant improvement in heart function while adult heart-derived ECM (amECM) did not improve these parameters. Treatment with nmECM limits scar expansion in the left ventricle and promotes revascularization of the injured region. Furthermore, nmECM induced expression of the ErbB2 receptor, simulating a neonatal-like environment and promoting neuregulin-1 associated cardiac function. Inhibition of the ErbB2 receptor effectively prevents these actions, suggesting its role in the context of nmECM as a therapy. This study shows the potential of a neonatal-derived biological material in vivo , diverting from the conventional use of adult-derived ECM therapies in research and the clinic. Statement of significance The of use extracellular matrix biomaterials to aid tissue repair has been previously reported in many forms of injury. The majority of ECM studies to date utilized ECM derived from adult tissues that are not able to fully regenerate functional tissue. In contrast, this study tests the ability of ECM derived from a regenerative organ, the neonatal heart, to stimulate functional cardiac repair after MI. This study is the first to test its potential in vivo. Our results indicate that extracellular factors present in the neonatal environment can be used to alter the healing response in adults, and we have identified the role of ErbB2 in neonatal ECM-based cardiac repair. [ABSTRACT FROM AUTHOR]

The typical ECG changes in tetralogy of Fallot are right axis deviation, large R waves in the anterior precordial leads and large S waves in the lateral precordial leads. We present a patient with extreme deviation of the frontal QRS axis between −90° and ± 180°. The child underwent open heart surgery twice before one year of age and a third time at nine years of age. The axis change persisted into adulthood. • In tetralogy of Fallot the ECG findings reflect right ventricular remodeling. • A frontal QRS axis between −90° and ±180 (northwest axis) is a rare ECG finding. • QRS duration ≥150 ms and northwest axis associate with an enlarged right ventricle in tetralogy of Fallot. [ABSTRACT FROM AUTHOR]

Surgical ventricular remodeling (SVR) is an invasive method of treating patients with heart failure who also have ischemic cardiomyopathy and reduced ejection fraction (EF). Introduced in the mid-1980s, this technique was met with varying success and relatively high morbidity and mortality despite its theoretical benefits. The development of the BioVentrix Revivent TC System (BioVentrix, Inc., San Ramon, CA) as a less-invasive method of surgical ventricular remodeling has created a novel, multidisciplinary approach to heart failure management, which necessitates multiple subspecialties. Currently in the trial phase in the United States and widely used in Europe, the positive results to date appear promising for the rapid adoption of this procedure. For the cardiac anesthesiologist, a thorough understanding of the patient population, procedural goals, and intraoperative management is essential. This overview discusses the advancement in surgical ventricular remodeling, the pertinent surgical steps of the BioVentrix Revivent TC System placement, and specific anesthetic considerations for this novel procedure. [ABSTRACT FROM AUTHOR]

Angiotensin receptor neprilysin inhibitors (ARNI), a new therapeutic class of agents acting on the renin angiotensin aldosterone system (RAAS) and neutral endopeptidase system has been developed in treatment of ventricular remodeling and has attracted considerable attention. The first in class is LCZ696, which is a molecule that combines Valsartan (ARB) and Sacubitril (neprilysin inhibitor) within a single substance. Sacubitril-Valsartan is the first angiotensin receptor enkephalin inhibitors (ARNI), which can block angiotensin II type 1 receptor (AT1R) while inhibiting enkephalin (NEP) and effectively reverse ventricular remodeling in heart failure patients. It has been recommended by the European and American authoritative guidelines on heart failure as Class I for the treatment of chronic heart failure particularly as intensive care medicine. Sacubitril-Valsartan demonstrated significant effects in improving left ventricular performance and remodeling in patients with heart failure with reduced ejection fraction. Sacubitril acts on increased levels of circulating natriuretic peptides by preventing their enzymatic breakdown and Valsartan, which acts to lessen the effects of the RAAS. However, not more research has been done on its effects on the right ventricle remodeling. This review aimed to assess the impact of angiotensin receptor neprilysin inhibitors on left and right ventricular remodeling in heart failure patients. [ABSTRACT FROM AUTHOR]

Background: Ventricular septal defect (VSD) is the most common congenital heart disease. In patients with large VSD, left side chambers are subjected to volume overload with subsequent chambers dilatation and eccentric left ventricular hypertrophy. Percutaneous closure of VSD has been shown to be an effective method with equal safety and efficacy when compared to surgery. The effect of VSD closure on LV remodeling has been mainly assessed in patients treated with surgery and to date published data remain scarce. Therefore, we aim to evaluate the effect of percutaneous VSD closure on different LV parameters. Results: Seventeen patients (median age 6 years (IQR 4.75–8 years), 70.6% females) who underwent percutaneous VSD closure were enrolled in the study. Sixteen patients (94%) had perimembranous VSD, and one patient had muscular VSD. The procedure was successful in all patients with no major complications. Nit Occlud® Lê coil device was implanted in 16 patients (94%), and one patient received Amplatzer PDA duct occlude device. At 6-months follow-up, there was a significant reduction in indexed LV dimensions [LVEDD/BSA (median 46.5 mm/m2 vs. 42.9 mm/m2, p = 0.03), LVESD/BSA (median 31.7 mm/m2 vs. 26.7 mm/m2, p = 0.02)], indexed LV volumes [LVEDV/BSA (median 52.6 ml/m2 vs. 37.3 ml/m2, p = 0.02), LVESV/BSA (median 31.7 ml/m2 vs. 23.3 ml/m2, p = 0.02)] and indexed LV mass (median 62.4 gm/m2 vs. 57.9 ml/m2, p = 0.01). There was a significant reduction in LVEDD Z-score (p = 0.01) and LVESD Z-score (p = 0.04). There was no significant change in LV EF. Conclusions: Percutaneous VSD closure is associated with improvement of various LV parameters with consequential favorable LV remodeling and function. [ABSTRACT FROM AUTHOR]

To investigate the effects of hydralazine combined with nitrate on serum levels of Adropin and brain natriuretic peptide (BNP), left ventricular remodeling and prognosis in patients with chronic heart failure (CHF). 126 CHF patients were divided into control group (n=13, sodium nitroprusside) and combined treatment group (n=63, sodium nitroprusside + hydralazine). Serum Adropin and BNP levels and left ventricular mass index (LVMI) of patients before treatment and 10 days after treatment were recorded, so did patient's end-point events. It was found that compared with those before treatment, the serum levels of Adropin, BNP, and LVMI in combined group and control group after 10 days of treatment were lower (P<0.05). The end-point event rate in the combined group was 19.05% (12/63). The serum levels of Adropin, BNP, and LVMI in the combined group with end-point events were higher than those of patients without end-point events (P<0.05). Spearman correlation analysis showed that serum levels of Adropin and BNP were positively correlated with LVMI and the end-point events rate (P<0.05). To sum up, hydralazine combined with sodium nitroprusside treatment can effectively reduce serum Adropin and BNP levels, and the risk of left ventricular remodeling and poor prognosis in patients with CHF. [ABSTRACT FROM AUTHOR]

Myocardial interstitial fibrosis is part of the advanced disease stage of most cardiovascular pathologies. It has been characterized histologically in various disease settings from hypertensive heart disease and diabetic cardiomyopathy to severe aortic stenosis. It is also involved in the process of aging. In cardiovascular medicine, myocardial interstitial fibrosis is associated with several adverse outcomes, especially heart failure (HF) and sudden cardiac death. Until recently, clinical measures of interstitial fibrosis could only be made by invasive myocardial biopsy. The availability of cardiac magnetic resonance (CMR) T1 mapping techniques allows for the indirect measurement of interstitial space characteristics and extracellular volume size, which is closely correlated with collagen content and interstitial infiltration by amyloid and other molecules. There has been significant improvement in the accuracy and reproducibility of T1 acquisition sequences in the last decade; however, the correct use of this technique requires a solid CMR expertise in daily imaging practice. CMR has become the gold standard to assess left ventricular (LV) remodeling and functional features associated with interstitial fibrosis. These features can be detected in the early stages of HF. The main objective of this paper is to review the relevant results of preclinical and clinical observational studies that demonstrate the prognostic impact of interstitial fibrosis assessed by T1 mapping, as well as adverse left ventricular remodeling, as determinants of HF. Therefore, this review focuses on the pathological mechanisms underlying LV remodeling and interstitial fibrosis, in addition to the technical considerations involved in the assessment of interstitial LV fibrosis by CMR. It provides a thorough review of clinical evidence that demonstrates the association of interstitial fibrosis and other-CMR derived LV phenotypes with Stages A and B HF. [Display omitted] • The myocardium undergoes important tissue composition (hypertrophy, interstitial and replacement fibrosis, and so on) and remodeling changes in Stage A and B HF. • CMR offers a comprehensive and reproducible assessment of LV tissue and anatomy modifications, with the potential to monitor different phenotypes in Stage A and B HF. • T1 mapping and ECV assessment by CMR requires careful acquisition protocol and solid expertise for routine practice. • Clinical use of these CMR measurements for therapeutic management still requires randomized controlled clinical trials. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To investigate the role of SIRT1 in ventricular remodeling after myocardial infarction using ultrasound three-dimensional speckle tracking (3D-STI). PATIENTS AND METHODS: Fifty-eight patients with acute myocardial infarction diagnosed in the Second Affiliated Hospital of Qiqihar Medical College from June 2015 to July 2017 were enrolled in the study. They were divided into ventricular remodeling group and ventricular non-remodeling group. Fifty-eight healthy people underwent physical examination were controls. 3D-STI was used to detect end-diastolic ventricular septal thickness (LVST), end-diastolic left ventricular posterior wall thickness (LVPWT), left ventricular end-diastolic volume (LVEDV), left ventricular end-systolic volume (LVESV), left ventricular ejection fraction (LVEF), systolic peak radial strain (PRS). SIRT1 expression levels in peripheral blood samples of the 3 groups were measured. Rats with acute myocardial infarction were treated with SIRT1 agonist. After 4 weeks, LVEDV, LVESV, LVEF, stroke volume (SV) were recorded by three-dimensional ultrasound; rat myocardial tissue protein was extracted, and SIRT1 and TGF-β, α-SMA, Vimentin and other fibrosis indicators were detected to explore the effects of SIRT1 on ventricular remodeling and myocardial fibrosis. RESULTS: At the time of initial diagnosis, SIRT1 level in healthy group > non-ventricular remodeling group > remodeling group (p<0.05); at the return visit, SIRT1 levels in the remodeling group and non-ventricular remodeling group were significantly elevated (p<0.05), but that in the remodeling group was significantly lower than that in the non-ventricular group (p<0.05). The expression level of SIRT1 in H9c2 hypoxia-reperfusion cell model control group > SIRT agonist treatment model group > model group. CONCLUSIONS: In summary, SIRT1 in the peripheral blood is negatively correlated with the degree of ventricular remodeling. The expression of SIRT1 in myocardial tissue is related to the cardiac morphology expansion and relief of reduced function in vivo after acute myocardial infarction. Up-regulation of SIRT1 expression in cell models can reduce cardiomyocyte apoptosis and inhibit cardiomyocyte fibrosis. SIRT1 has a good application prospect in predicting and treating myocardial infarction and delaying ventricular remodeling. [ABSTRACT FROM AUTHOR]

This study aimed to identify a subset of patients based on echocardiographic parameters who might have benefited from transcatheter correction using the MitraClip system in the MITRA-FR (Percutaneous Repair with the MitraClip Device for Severe Functional/Secondary Mitral Regurgitation) trial. It has been suggested that differences in the degree of mitral regurgitation (MR) and left ventricular (LV) remodeling may explain the conflicting results between the MITRA-FR and the COAPT (Cardiovascular Outcomes Assessment of the MitraClip Percutaneous Therapy for Heart Failure Patients with Functional Mitral Regurgitation) trials. In a post hoc analysis, we evaluated the interaction between the intervention and subsets of patients defined based on MR severity (effective regurgitant orifice [ERO], regurgitant volume [RVOL] and regurgitant fraction [RF]), LV remodeling (end-diastolic and end-systolic diameters and volumes) and combination of these parameters with respect to the composite of death from any cause or unplanned hospitalization for heart failure at 24 months. We observed a neutral impact of the intervention in subsets with the highest MR degree (ERO ≥30 mm2, RVOL ≥45 ml or RF ≥50%) as in patients with milder MR degree. The same was seen in subsets with the milder LV remodeling using either diastolic or systolic diameters or volumes. When parameters of MR severity and LV remodeling were combined, there was still no benefit of the intervention including in the subset of patients with an ERO/end-diastolic volume ratio ≥ 0.15 despite similar ERO and LV end-diastolic volume compared with COAPT patients. In the MITRA-FR trial, we could not identify a subset of patients defined based on the degree of the regurgitation, LV remodeling or on their combination, including those deemed as having disproportionate MR, that might have benefited from transcatheter correction using the MitraClip system. (Multicentre Study of Percutaneous Mitral Valve Repair MitraClip Device in Patients With Severe Secondary Mitral Regurgitation [MITRA-FR]; NCT01920698) [Display omitted] [ABSTRACT FROM AUTHOR]

BACKGROUND: Right ventricular (RV) dysfunction is a significant prognostic determinant of morbidity and mortality in pulmonary arterial hypertension (PAH). Despite the importance of RV function in PAH, the underlying molecular mechanisms of RV dysfunction secondary to PAH remain unclear. We aim to identify and compare molecular determinants of RV failure using RNA sequencing of RV tissue from 2 clinically relevant animal models of PAH. METHODS: We performed RNA sequencing on RV from rats treated with monocrotaline or Sugen with hypoxia/normoxia. PAH and RV failure were confirmed by catheterization and echocardiography. We validated the RV transcriptome results using quantitative real-time polymerase chain reaction, immunofluorescence, and Western blot. Immunohistochemistry and immunofluorescence were performed on human RV tissue from control (n=3) and PAH-induced RV failure patients (n=5). RESULTS: We identified similar transcriptomic profiles of RV from monocrotaline- and Sugen with hypoxia-induced RV failure. Pathway analysis showed genes enriched in epithelial-to-mesenchymal transition, inflammation, and metabolism. Histological staining of human RV tissue from patients with RV failure secondary to PAH revealed significant RV fibrosis and endothelialto-mesenchymal transition, as well as elevated cellular communication network factor 2 (top gene implicated in epithelial-tomesenchymal transition/endothelial-to-mesenchymal transition) expression in perivascular areas compared with normal RV. CONCLUSIONS: Transcriptomic signature of RV failure in monocrotaline and Sugen with hypoxia models showed similar gene expressions and biological pathways. We provide translational relevance of this transcriptomic signature using RV from patients with PAH to demonstrate evidence of epithelial-to-mesenchymal transition/endothelial-to-mesenchymal transition and protein expression of cellular communication network factor 2 (CTGF [connective tissue growth factor]). Targeting specific molecular mechanisms responsible for RV failure in monocrotaline and Sugen with hypoxia models may identify novel therapeutic strategies for PAH-associated RV failure. [ABSTRACT FROM AUTHOR]

The aim of this study was to describe the anatomic and functional changes in left-sided chambers using computed tomographic angiography (CTA) from baseline to 1 month after transcatheter mitral valve replacement (TMVR) with the Tendyne prosthesis. Data on changes in left atrial and left ventricular (LV) volumes after TMVR implantation are very limited. Patients who underwent TMVR with the Tendyne prosthesis between 2015 and 2018 were analyzed. Changes in LV end-diastolic volume, ejection fraction, LV mass, left atrial volume, and global longitudinal strain were assessed at baseline and 1 month after TMVR using CTA. Specific Tendyne implant characteristics were identified and correlated with remodeling changes. A total of 36 patients (median age 74 years; interquartile range [IQR]: 69 to 78 years; 78% men; 86% with secondary mitral regurgitation) were included in this study. There were significant decreases in LV end-diastolic volume (281 ml [IQR: 210 to 317 ml] vs. 239 ml [IQR: 195 to 291 ml]; p < 0.001), LV ejection fraction (37% [IQR: 31% to 48%] vs. 30% [IQR: 23% to 40%]; p < 0.001), LV mass (126 g [IQR: 96 to 155 g] vs. 116 g [IQR: 92 to 140 g]; p < 0.001), left atrial volume (171 ml [IQR: 133 to 216 ml] vs. 159 ml [IQR: 125 to 201 ml]; p = 0.027), and global longitudinal strain (−11% [IQR: −17% to −8%] vs. −9% [IQR: −12% to −6%]; p < 0.001) from baseline to 1-month follow-up. Favorable LV end-diastolic volume reverse remodeling occurred in the majority (30 of 36 patients [83%]). Closer proximity of the Tendyne apical pad to the true apex (24 mm [IQR: 21 to 29 mm] vs. 35 mm [IQR: 26 to 40 mm]) was predictive of favorable remodeling (p = 0.037). TMVR with Tendyne results in favorable left-sided chamber remodeling in the majority of patients treated, as detected on CTA at 1 month after implantation. CTA identifies favorable post-TMVR changes, which could be related to specific characteristics of the device implantation. [ABSTRACT FROM AUTHOR]

The purpose of this retrospective cohort study was to compare remodeling of left ventricular (LV) structure and function after transcatheter stent therapy with remodeling of LV structure and function after surgical therapy for COA. Transcatheter stent therapy is as effective as surgery in producing acute hemodynamic improvement in patients with coarctation of aorta (COA). However, LV remodeling after transcatheter COA intervention has not been systematically investigated. LV remodeling was assessed at 1, 3, and 5 years post-intervention by using LV mass index (LVMI), LV end-diastolic dimension, LV ejection fraction, LV global longitudinal strain (LVGLS), LV mitral annular tissue Doppler early velocity (LVe′), and ratio of mitral inflow pulsed wave Doppler early velocity and e′ (E/e′) ratio. There were 44 patients in the transcatheter group and 128 patients in the surgical group. Compared to the surgical group, the transcatheter group had less regression of LVMI (−4.6; 95% confidence interval [CI]: −5.5 to −3.7 vs. −7.3; 95% CI: −8.4 to −6.6 g/m2; p < 0.001), less improvement in LVGLS (2.1; 95% CI: 1.8 to 2.4 vs. 2.9; 95% CI: 2.6 to 3.2%; p = 0.024), and in e′ (1.0 ; 95% CI: 0.7 to 1.2 vs. 1.5 ; 95% CI: 1.3 to 1.7 cm/s; p = 0.009) at 5 years post-intervention. Exploratory analysis showed a correlation between change in LVMI and LVGLS, and between change in LVMI and mitral annular tissue Doppler early velocity (e′), and this correlations were independent of the type of intervention received. Transcatheter stent therapy was associated with less remodeling of LV structure and function during mid-term follow-up. As transcatheter stent therapy becomes more widely used in the adult COA population, there is a need for ongoing clinical monitoring to determine if these observed differences in LV remodeling translate to differences in clinical outcomes. [ABSTRACT FROM AUTHOR]

Adipocytokine dysfunction is considered as causative factor of target organ damage in metabolic disease. The aim of the study was to investigate whether altered adipocytokine profile predicts left ventricular (LV) remodeling in hypertensive patients with type 2 diabetes mellitus (T2DM). A total of 186 patients (125 hypertensive and 61 non-hypertensive individuals) with established T2DM and 20 healthy volunteers were enrolled in the study. LV remodeling was determined at baseline. Concentrations of adipocytokines were measured with ELISA at baseline. The most important predictors of LV hypertrophy in T2DM patients were serum levels of omentin-1 (B-coefficient = −0.64, p = 0.001), Zinc-α2-glycoprotein [ZA2G] (B-coefficient = −0.57, p = 0.002), visfatin (B-coefficient = 0.26, p = 0.034), hs-CRP (B-coefficient = 0.38, p = 0.002), HOMA-IR (B-coefficient = 0.34, p = 0.001), age (B-coefficient = 0.31, p = 0.022), glypican-4 (B-coefficient = −0.23, p = 0.042), and male sex (B-coefficient = 0.11, p = 0.048). After entering combined depending variable (LV hypertrophy and LV diastolic dysfunction) to the model the significant predictors remained serum levels of omentin-1 (B-coefficient = −0.82, p = 0.001), ZA2G (B-coefficient = −0.54, p = 0.001) and HOMA-IR (B-coefficient = 0.44, p = 0.001). Regression analyses showed that the most influential determinants of depending variable (LV hypertrophy + LV diastolic dysfunction) in T2DM patients were omentin-1 (B-coefficient = −1.6, p = 0.001) and ZA2G (B-coefficient = −0.78, p = 0.044). We found that serum levels of omentin-1 and ZA2G were the most important predictors for LV hypertrophy + LV diastolic dysfunction in T2DM patients. Large clinical trials are required to confirm this assumption and get clear explanation of issues unveiled. • Pro- and contra inflammatory adipose-derived cytokines related to the presence of cardiovascular events in diabetics. • Omentin-1 and zinc-α2-glycoprotein have yielded pro-inflammatory and fibrotic response. • Visfatin and glypican-4 were associated with adaptive mechanisms preventing from diabetes-induced tissue injury. • Altered adipocytokine profile in diabetics was independent predictor for early adverse cardiac remodeling. [ABSTRACT FROM AUTHOR]

This study sought to establish the best definition of left ventricular adverse remodeling (LVAR) to predict outcomes and determine whether its assessment adds prognostic information to that obtained by early cardiac magnetic resonance (CMR). LVAR, usually defined as an increase in left ventricular end-diastolic volume (LVEDV) is the main cause of heart failure after an ST-segment elevated myocardial infarction; however, the role of assessment of LVAR in predicting cardiovascular events remains controversial. Patients with ST-segment elevated myocardial infarction who received percutaneous coronary intervention within 6 h of symptom onset were included (n = 498). CMR was performed during hospitalization (6.2 ± 2.6 days) and after 6 months (6.1 ± 1.8 months). The optimal threshold values of the LVEDV increase and the LV ejection fraction decrease associated with the primary endpoint were ascertained. Primary outcome was a composite of cardiovascular mortality, hospitalization for heart failure, or ventricular arrhythmia. The study was completed by 374 patients. Forty-nine patients presented the primary endpoint during follow-up (72.9 ± 42.8 months). Values that maximized the ability to identify patients with and without outcomes were a relative rise in LVEDV of 15% (hazard ratio [HR]: 2.1; p = 0.007) and a relative fall in LV ejection fraction of 3% (HR: 2.5; p = 0.001). However, the predictive model (using C-statistic analysis) failed to demonstrate that direct observation of LVAR at 6 months adds information to data from early CMR in predicting outcomes (C-statistic: 0.723 vs. 0.795). The definition of LVAR that best predicts adverse cardiovascular events should consider both the increase in LVEDV and the reduction in LV ejection fraction. However, assessment of LVAR does not improve information provided by the early CMR. [ABSTRACT FROM AUTHOR]

OBJECTIVE: The aim of this study was to investigate the effect of microRNA-150 on the regulation of myocardial fibrosis and ventricular remodeling in rats with acute myocardial infarction (AMI). MATERIALS AND METHODS: The AMI rats model was established by the ligation of the left anterior descending coronary artery (LAD) in vivo. After AMI procedures, the rats were injected with microRNA-150 lentivirus overexpression or negative control, respectively. Cardiac function of rats was evaluated by echocardiography. Hematoxylin and eosin (HE) staining and Masson trichrome were performed to evaluate myocardial fibrosis in each rat. Meanwhile, cardiomyocyte apoptosis was detected by terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end labeling (TUNEL) method. The expression levels of microRNA-150, col1a1, col1a2, col3 and a smooth muscle actin (a-SMA) in the border zone of rat infarct myocardium were detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) and Western blot, respectively. RESULTS: MicroRNA-150 expression in the border zone of infarct myocardium decreased significantly at day 28 after AMI (p<0.05). Overexpressing microRNA-150 significantly improved cardiac function, decreased collagen volume fraction (CVF) and attenuated cardiomyocyte apoptosis in rats. Furthermore, the expression levels of col1α1, col1α2, col3 and α-SMA in the border zone of infarct myocardium were remarkably down-regulated in rats overexpressing microRNA-150 compared with those of controls (p<0.001). CONCLUSIONS: MicroRNA-150 expression in the border zone of rat infarct myocardium decreased at day 28 after AMI. In addition, the upregulation of microRNA-150 in myocardial tissue could inhibit myocardial fibrosis and improve ventricular remodeling at post-AMI. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To elucidate the effect of estrogen on right ventricular remodeling of pulmonary arterial hypertension (PAH) induced by monocrotaline (MCT) in rats and its underlying mechanism. MATERIALS AND METHODS: Male Sprague-Dawley (SD) rats were adaptively fed for one week, and then, randomly divided into control group, MCT group, MCT+17-β estradiol (50 mg·kg− 1·d−1) group, and MCT+17-β estradiol (100 mg·kg−1·d−1) group, with 8 rats in each group. PAH rat model was constructed by subcutaneous injection of 60 mg·kg−1 MCT for consecutive 4 weeks. The right external jugular vein was intubated to monitor rat RVSP (right ventricular systolic pressure) and mPAP (mean pulmonary arterial pressure). After animal procedures, RV (right ventricle) and LV+S (left ventricle+ventricular septum) of rat were harvested and weighed. Rat tibia was collected and recorded for its length, followed by calculation of RV/(LV+S) and RV/length of the tibia. HE staining and Masson staining were conducted to observe the pathological change and collagen deposition in RV, respectively. RV was prepared for homogenate, followed by detection of total antioxidant capacity (T-AOC) and malondialdehyde (MDA) activities. Expression levels of collagen I, collagen III, NOX4, and NF-κB in RV of PAH rats were detected by qRT-PCR and Western blot. RESULTS: Lower RVSP, mPAP, RV/(LV+S) and RV/length of the tibia were observed in rats of MCT+17-β estradiol (50 mg·kg−1·d−1) group and MCT+17-β estradiol (100 mg·kg−1·d−1) group compared with those of MCT group. Injection of 17-β estradiol (50 mg·kg−1·d−1 and 100 mg·kg−1·d−1) in PAH rats remarkably alleviated pathological changes and collagen deposition in RV. T-AOC activity increased, whereas MDA activity decreased in PAH rats injected with 17-β estradiol. Expression levels of collagen I, collagen III, NOX4, and NF-κB in RV of PAH rats were all downregulated by 17-β estradiol treatment. CONCLUSIONS: 17-β e stradiol could remarkably alleviate MCT-induced right ventricular remodeling of PAH rats. It is suggested that 17-β estradiol exerts its protective role in PAH by inhibiting NOX4-mediated oxidative stress and NF-κB-mediated collagen deposition. [ABSTRACT FROM AUTHOR]

Abstract Acute myocardial infarction (AMI) remains a leading cause of morbidity and mortality worldwide. LV remodeling is an important factor in the pathophysiology of advancing heart failure (HF). Aim of the work To evaluate the value of speckle tracking imaging as a predictor of left ventricular remodeling 6 months after first anterior STEMI in patients managed by primary PCI. Methodology Eighty-five patients with first acute anterior STEMI underwent primary PCI. Patients were followed up for 6 months. Echocardiography was done within 48 h [1] Standard transthoracic 2D echocardiographic examination: LV internal dimensions and volumes, Left Ventricular EF, and Wall Motion Score Index: [2] LV peak systolic global longitudinal strain and Torsion dynamics were assessed. Echocardiography was repeated at 6 months LV volumes and EF were calculated. LV remodeling was defined as an increase in LV EDV ≥ 20% 6 months after infarction as compared to baseline data. Patients were then classified into Group I : did not develop LV remodeling. Group II : developed LV remodeling. Both groups were studied to determine predictors of LV remodeling. Results At baseline echocardiographic evaluation there was no statistically significant difference between both groups regarding both LVEDD and LVEDV, while there was statistically significant increase in both LV ESD and LV ESV, with statistically significant lower Ejection Fraction, in LV remodeling group. There was also statistically significant higher LV peak systolic GLS values in LV remodeling group, the best cut-off value was >−12.5 (Sensitivity 87%, Specificity 85%) and LV torsion was also statistically significantly lower in the LV remodeling group, with the best cut-off value for LV torsion was <9.5°, [Sensitivity 91%, Specificity 85%]. Independent predictors of LV remodeling after AMI: baseline WMSI > 1.8, baseline LV EF < 40, GLS > −12.5%, LV torsion < 9.5°, CK-MB > 500 U/L, baseline Thrombus grade > 4 and total ischemic time. Conclusion Average peak systolic GLS and LV torsion at echocardiography done early after myocardial infarction are independent predictors of LV remodeling after anterior STEMI and can be used to predict occurrence of LV remodeling after 6 months. [ABSTRACT FROM AUTHOR]

Background: Cardiac resynchronization therapy (CRT) response stratified by left ventricular (LV) remodeling revealed differing mortality profiles for distinct patient cohorts. Measuring functional endpoints, as well as mortality, may better assess CRT efficacy and inform patient management. However, the association between LV remodeling and functional outcomes after CRT is not well understood.Objective: To evaluate long-term CRT outcomes by extent of LV remodeling.Methods: REsynchronization reVErses Remodeling in Systolic Left vEntricular Dysfunction (NCT00271154) was a prospective, double-blind, randomized CRT trial. Patients were classified based on LV end-systolic volume (LVESV) change from baseline to 6-months post-CRT: Worsened (increase); Stabilized (0 to ≤15% reduction); Responder (>15 to < 30% reduction); and Super-responder (≥30% reduction). Subjects were evaluated annually for 5 years.Results: The analyses included 353 patients randomized to CRT-ON arm. All-cause mortality was higher in the worsened group compared with the 3 other response groups (29.8% vs 8.0%, p<0.0001), with no difference in survival among those groups (p=0.87). A significant interaction between LVESV group and time was observed for health status and quality of life (both p=0.02). The interaction was not significant for 6-minute hall walk (p=0.79); however, super-responders had increased walk distance compared to the 3 other response groups (p=0.03).Conclusion: Preventing further increase in LVESV with CRT was associated with reduced mortality, whereas functional measure improvement was associated with LV remodeling magnitude. These results support consideration of functional and mortality endpoints to assess CRT efficacy and provide further evidence the dichotomous 'responder and non-responder' classification should be modified. [ABSTRACT FROM AUTHOR]

Traditional Chinese medicine plays an important role in the prevention and treatment of heart failure (HF). Linggui Zhugan decoction has been approved for clinical treatment of chronic HF. However, the mechanism is still unclear. The effect of Linggui Zhugan decoction on the Wnt/β-catenin signaling pathway in rat myocardium was studied to investigate the mechanism by Linggui Zhugan decoction effects ventricular remodeling in rats with heart failure after myocardial infarction. A rat model of HF after myocardial infarction was prepared by ligating the left anterior descending coronary artery. After 6 weeks of intervention with Linggui Zhugan decoction, the effect of Linggui Zhugan decoction on the cardiac function of chronic HF model rats was observed. Myocardial infarct size was measured by triphenyl tetrazolium chloride (TTC) staining. Enzyme linked immunosorbent assays (ELISAs) were used to measure NT-proBNP and sST-2 concentrations in rat serum. Hematoxylin and eosin (H&E) staining, and Masson's trichrome staining were used to observe the morphology of myocardial tissue; immunohistochemistry was used to detect the protein expression of type I collagen and type III collagen in myocardial tissue; and mRNA expression levels of Wnt3a, GSK-3β, β-catenin, and c-Myc in the infarct marginal zone were detected using PCR. Protein expression of Wnt3a, p-GSK-3β, GSK-3β, and β-catenin in the infarct marginal zone was detected using western blot. Compared with the control, Linggui Zhugan decoction reduced the levels of serum ST-2 and NT-proBNP, improved cardiac function, and reduced the deposition of collagen fiber. In addition, Linggui Zhugan decoction inhibited the expression of Wnt3a, p-GSK-3β, and β-catenin in cardiomyocytes. Linggui Zhugan decoction inhibits the expression of several key proteins in the Wnt/β-catenin signaling pathway, delays cardiomyocyte hypertrophy and fibrosis, and improves cardiac function. [ABSTRACT FROM AUTHOR]

OBJECTIVE: This study aims to explore the role and the mechanism of Parkin protein in cardiac function and ventricular remodeling in myocardial infarction (MI) rats, and to provide a new sight for the treatment of myocardial infarction. MATERIALS AND METHODS: Fifty Sprague-Dawley (SD) male rats were randomly divided into 5 groups: sham operation group (Sham group), model group (MI group), low-dose Parkin group (L-Parkin group), middle-dose Parkin group (M-Parkin group) and high-dose Parkin group (H-Parkin group). The rat model of myocardial infarction was established by ligation of the anterior descending branch. Small animal ultrasound was used to measure cardiac function. The myocardial infarct size was observed by triphenyltetrazolium chloride (TTC) staining. The pathological changes of myocardial tissues were observed by hematoxylin-eosin (HE) staining. The myocardial cell apoptosis was detected by TUNEL assay. The mRNA expression of matrix metalloproteinase 2 (MMP2), matrix metalloproteinase 9 (MMP9), tissue inhibitor of matrix metalloproteinase 1 (TIMP1), tissue inhibitor of matrix metalloproteinase 2 (TIMP2) were detected by qRT-PCR. The expression of Parkin protein in myocardial tissue of rats was detected by Western-blot. RESULTS: Compared with MI group, left ventricular end-systolic volume (LVESV) and left ventricular end-diastolic volume (LVEDV) in Parkin overexpressing group were significantly decreased (p<0.05), while the value of left ventricular short axis shortening (FS) and left ventricular ejection fraction (EF %) in Parkin overexpression group were significantly increased (p<0.05). Overexpression of Parkin improved abnormal structure of myocardial tissue, reduced the size of myocardial infarct, made the arrangement of myocardium fibers more neatly and made the stain of myocardial cells more uniformly. Apoptosis index (AI) values were significantly decreased (p<0.05), and MMP2, MMP9, TIMP1 and TIMP2 mRNA levels were significantly decreased (p<0.05), while Parkin protein expression was significantly elevated in a dose-dependent manner (p<0.05). CONCLUSIONS: After treatment with Parkin in myocardial infarction rats, the relevant mRNA levels decreased, the number of apoptotic cells decreased, the myocardial fiber morphology returned to normal, the myocardial infarct size decreased, and the cardiac function of rats improved. Therefore, Parkin therapy plays an active role in cardiac function and ventricular remodeling in myocardial infarction rats. [ABSTRACT FROM AUTHOR]

Background: Left ventricular remodeling (LVR) after ST.elevation myocardial infarction (STEMI) harbingers poor prognosis. Three.dimensional echocardiography (3DE) is more accurate than 2 D echo for the assessment of left ventricle (LV) shape. We assessed LV geometry with 3D ECHO 6 months after STEMI in patients who had primary angioplasty. Materials and Methods: In this prospective study, morphological and functional analysis of LV with 3D ECHO (volumes, LVEF, 3D sphericity index [SI]) was assessed up to 7 days and 6 months in 42 STEMI patients. The LVR was considered for increase >15% of the end diastolic volume of the LV (LVEDV) 6 months after the STEMI, compared to the LVEDV up to 7 days of it. Results: Sixteen (38%) patients had LVR. 3D Echocardiographic measurements up to 7 days after the acute myocardial infarction (AMI) 1.LVEDV in ventricular remodeling group was 99.8 -} 19.1 ml and in no ventricular remodeling group was 87 -} 18.2 mL (P = 0.037); 2.LVEF was 0.48 -} 0.01 and 51 -} 0.02 (P <.001); 3D.SI was 0.41 -} 0.05 and 31 -} 0.05 (P < 0.001) II.after 6 months: 1.LVEDV in remodeling group was 114.2 -} 19.5 mL and no remodeling group was 94.2 -} 18.6 (P = 0.002); 2.LVEF was 0.58 -} 0.01 and 59 -} .01 (P = 0.003); 3D.sphericity was 0.35 -} 0.05 and 28 -} .05 (P < 0.001). Conclusion: LVR was observed in 38% of the patients 6 months after AMI. The 3D SI has been associated with occurrence of LVR and can differentiate patients with and without subsequent development of LVR accurately and early on its basis. [ABSTRACT FROM AUTHOR]