Common Cause Of Heart Failure Research Articles

Research Progress on the Combination of Traditional Chinese Medicine and Western Medicine for the Treatment of Ischemic Cardiomyopathy

Ischemic cardiomyopathy (ICM) refers to contractile left ventricular dysfunction in the case of severe coronary stenosis, which is the most common cause of heart failure. In recent years, the incidence of ICM has shown a significant upward trend, and the quality of life and life safety of patients have been seriously affected. At present, the treatment of ICM mainly focuses on dilating blood vessels, diuresis, improving myocardial metabolism and enhancing myocardial function. Research shows that traditional Chinese medicine has unique advantages in improving the prognosis and quality of life of ICM patients. There are a variety of treatment methods, including decoction, injections, proprietary Chinese medicine, etc. This article summarizes the research progress of ICM's traditional Chinese medicine, western medicine and integrated traditional Chinese and western medicine, with a view to providing reference for clinical treatment.

Comparing outcomes in cardiogenic shock patients with ischemic versus nonischemic cardiomyopathy: A nationwide retrospective observational study

Abstract Introduction Ischemic and non-ischemic cardiomyopathy are common causes of heart failure. In our study, we compare the in-hospital outcomes between these two groups of patients with cardiogenic shock. Methods Data was obtained from the Nationwide Inpatient Sample database between January 2016 to December 2020. The study included all adult patients who were in cardiogenic shock and either ischemic cardiomyopathy (ICM) or non-ischemic cardiomyopathy (NICM). The primary outcome was inpatient mortality. Secondary outcomes were cardiac arrest, arrhythmias, acute respiratory failure, and acute renal failure, as well as the need for ventilators, dialysis, and ECMO. Results Among 168,591 adult patients who had cardiogenic shock during their hospitalization, 72,538 patients had either ischemic cardiomyopathy or nonischemic cardiomyopathy. Among them, 31,854 (43.9%) had ischemic cardiomyopathy (ICM) vs 40,684 (56.1%) who had nonischemic cardiomyopathy (NICM). Patients with NICM had higher in-patient mortality (24.6% vs 26.1, aOR: 1.12; 95% CI: 1.08-1.16, p<0.001); when adjusted for age, sex, race, and Charlson comorbidity index. Furthermore, patients with NICM also had a higher risk of respiratory failure (54.1% vs 53.8%, aOR:1.11, 95% CI: 1.07-1.14, p<0.001) and required more life-saving treatments like pressors (1.6% vs 0.7%, aOR: 1.14; 95% CI: 1.10-1.20, p< 0.001) and dialysis (12.7.1% vs 11.3%, aOR:1.20, 95% CI: 1.14-1.26, p<0.001). However, these patients with NICM had a lower risk of cardiac arrest (7.2% vs 7.8%, aOR: 0.88; 95% CI: 0.84-0.94, p< 0.001) and ventricular arrhythmias (29.5% vs 32.2%, aOR: 0.82; 95% CI: 0.80-0.86, p<0.001) as well as lower ECMO utilization (2.5 vs 2.1, aOR:0.82; 95% CI: 0.73-0.92, p <0.001) and blood transfusions (9.8% vs 11.7%, aOR:0.839; 95% CI: 0.80-0.88, p< 0.001). There was no significant difference in the ventilator use between the 2 groups (40.3% vs 39.7%, aOR:1.01, 95% CI: 0.97-1.04, p=0.714). Conclusion The findings of this study underscore the higher in-patient mortality among patients with non-ischemic cardiomyopathy (NICM) presenting with cardiogenic shock. These results emphasize the need for tailored treatment approaches targeting NICM-CS, warranting dedicated diagnostic and therapeutic strategies to improve prognosis in this vulnerable patient subset.Odd's ratios for NICM-CS vs ICM-CS

Characterization of ferroptosis-triggered pyroptotic signaling in heart failure

Pressure overload–induced cardiac hypertrophy is a common cause of heart failure (HF), and emerging evidence suggests that excessive oxidized lipids have a detrimental effect on cardiomyocytes. However, the key regulator of lipid toxicity in cardiomyocytes during this pathological process remains unknown. Here, we used lipidomics profiling and RNA-seq analysis and found that phosphatidylethanolamines (PEs) and Acsl4 expression are significantly increased in mice with transverse aortic constriction (TAC)–induced HF compared to sham-operated mice. In addition, we found that overexpressing Acsl4 in cardiomyocytes exacerbates pressure overload‒induced cardiac dysfunction via ferroptosis. Notably, both pharmacological inhibition and genetic deletion of Acsl4 significantly reduced left ventricular chamber size and improved cardiac function in mice with TAC-induced HF. Moreover, silencing Acsl4 expression in cultured neonatal rat ventricular myocytes was sufficient to inhibit hypertrophic stimulus‒induced cell growth. Mechanistically, we found that Acsl4-dependent ferroptosis activates the pyroptotic signaling pathway, which leads to increased production of the proinflammatory cytokine IL-1β, and neutralizing IL-1β improved cardiac function in Acsl4 transgenic mice following TAC. These results indicate that ACSL4 plays an essential role in the heart during pressure overload‒induced cardiac remodeling via ferroptosis-induced pyroptotic signaling. Together, these findings provide compelling evidence that targeting the ACSL4-ferroptosis-pyroptotic signaling cascade may provide a promising therapeutic strategy for preventing heart failure.

In silico evaluation of cell therapy in acute versus chronic infarction: role of automaticity, heterogeneity and Purkinje in human

Human-based modelling and simulation offer an ideal testbed for novel medical therapies to guide experimental and clinical studies. Myocardial infarction (MI) is a common cause of heart failure and mortality, for which novel therapies are urgently needed. Although cell therapy offers promise, electrophysiological heterogeneity raises pro-arrhythmic safety concerns, where underlying complex spatio-temporal dynamics cannot be investigated experimentally. Here, after demonstrating credibility of the modelling and simulation framework, we investigate cell therapy in acute versus chronic MI and the role of cell heterogeneity, scar size and the Purkinje system. Simulations agreed with experimental and clinical recordings from ionic to ECG dynamics in acute and chronic infarction. Following cell delivery, spontaneous beats were facilitated by heterogeneity in cell populations, chronic MI due to tissue depolarisation and slow sinus rhythm. Subsequent re-entrant arrhythmias occurred, in some instances with Purkinje involvement and their susceptibility was enhanced by impaired Purkinje-myocardium coupling, large scars and acute infarction. We conclude that homogeneity in injected ventricular-like cell populations minimises their spontaneous beating, which is enhanced by chronic MI, whereas a healthy Purkinje-myocardium coupling is key to prevent subsequent re-entrant arrhythmias, particularly for large scars.

Integrated analysis of single-cell RNA sequencing and bulk RNA data reveals gene regulatory networks and targets in dilated cardiomyopathy

Dilated cardiomyopathy (DCM) is a common cause of heart failure, thromboembolism, arrhythmias, and sudden cardiac death. The quality of life and long-term survival rates of patients with dilated DCM have greatly improved in recent decades. Nevertheless, the clinical prognosis for DCM patients remains unfavorable. The primary driving factors underlying the pathogenesis of DCM remain incompletely understood. The present study aimed to identify driving factors underlying the pathogenesis of DCM from the perspective of gene regulatory networks. Single-cell RNA sequencing data and bulk RNA data were obtained from the Gene Expression Omnibus (GEO) database. Differential gene analysis, single-cell genomics analysis, and functional enrichment analysis were conducted using R software. The construction of Gene Regulatory Networks was performed using Python. We used the pySCENIC method to analyze the single-cell data and identified 401 regulons. Through variance decomposition, we selected 19 regulons that showed significant responsiveness to DCM. Next, we employed the ssGSEA method to assess regulons in two bulk RNA datasets. Significant statistical differences were observed in 9 and 13 regulons in each dataset. By intersecting these differentiated regulons and identifying shared targets that appeared at least twice, we successfully pinpointed three differentially expressed targets across both datasets. In this study, we assessed and identified 19 gene regulatory networks that were responsive to the disease. Furthermore, we validated these networks using two bulk RNA datasets of DCM. The elucidation of dysregulated regulons and targets (CDKN1A, SAT1, ZFP36) enhances the molecular understanding of DCM, aiding in the development of tailored therapies for patients.

Clinical Characteristics and Segmental Qualities of Young Patients with Heart Failure in a Tertiary Care Centre

Background: The prevalence and hospitalizations of patients with heart failure aged <55 years have increased. The study aims to evaluate the clinical traits and segmental qualities of young patients experiencing heart failure at a tertiary care center. Methods: This cross-sectional study design enrolled 83 individuals who had recently developed heart failure at a young age. The study encompassed individuals aged 18 to 55 years, from whom clinical indicators and potential risk elements were obtained followed by 2D transthoracic echocardiography performed as part of the routine assessment. Results: The study comprised of 83. The participants with a mean age of 51.5 ± 4.0 years. A significant proportion of the individuals were noted to have diabetes (65%), while 74.7% were identified with hypertension. A statistically significant association was noted between patients who had a prior history of Ischemic heart disease (IHD) and their probability of developing Heart failure (HF) (p-value = 0.02). The primary and the most prevalent cause of heart failure among these study participants was dilated cardiomyopathy. Patients with reduced Ejection fraction (EF) had a notably higher occurrence (68%) compared to mid-range EF (14%) and preserved EF (23%). Conclusion: The study comprised of involved individuals those belonging to the age group between 45-55 years, exhibited higher rates of hypertension and diabetes. Heart Failure with reduced Ejection Fraction (HFrEF) was dominant, wherein dilated cardiomyopathy invariably being the most common cause of heart failure in younger patients. Notably, a significant portion of these individuals had a past history of IHD, which contributed a substantial role in the development of HF

In vivo rescue of genetic dilated cardiomyopathy by systemic delivery of nexilin

BackgroundDilated cardiomyopathy (DCM) is one of the most common causes of heart failure. Multiple identified mutations in nexilin (NEXN) have been suggested to be linked with severe DCM. However, the exact association between multiple mutations of Nexn and DCM remains unclear. Moreover, it is critical for the development of precise and effective therapeutics in treatments of DCM.ResultsIn our study, Nexn global knockout mice and mice carrying human equivalent G645del mutation are studied using functional gene rescue assays. AAV-mediated gene delivery is conducted through systemic intravenous injections at the neonatal stage. Heart tissues are analyzed by immunoblots, and functions are assessed by echocardiography. Here, we identify functional components of Nexilin and demonstrate that exogenous introduction could rescue the cardiac function and extend the lifespan of Nexn knockout mouse models. Similar therapeutic effects are also obtained in G645del mice, providing a promising intervention for future clinical therapeutics.ConclusionsIn summary, we demonstrated that a single injection of AAV-Nexn was capable to restore the functions of cardiomyocytes and extended the lifespan of Nexn knockout and G645del mice. Our study represented a long-term gene replacement therapy for DCM that potentially covers all forms of loss-of-function mutations in NEXN.

#2033 Patient characteristics and outcomes of an inter- and multidisciplinary nephrology and cardiology clinic

Abstract Background and Aims The prevalence of cardiorenal syndrome is increasing due to the growing number of patients with chronic kidney disease (CKD) and heart failure (HF). To further improve outcomes in this high risk population, an interdisciplinary, evidence-based and patient-centered approach is advocated. Hence, it was the aim of this study to identify and describe the patient population which might profit from an inter- and multidisciplinary nephrology and cardiology clinic at a tertiary university hospital. Method We screened 552 patients who from 01.01.2015 and 30.06.2022 had been in the nephrology and in the cardiology outpatient clinics of the University Hospital of Zurich. Patients with kidney or heart transplantation or on dialysis were excluded. Out of the remaining patients, we identified 223 patients having CKD 2-5 and HF. Characteristics with respect to entity and cause of kidney and heart disease, cardiovascular risk factors, therapy, incidence of acute kidney injury (AKI), hospitalisations and patient survival were recorded. Results The most common cause of CKD was a cardiorenal syndrome type 2 (42%, 95/223). 59/223 (26%) had at least moderate albuminuria. At the beginning of follow-up, 61/223 (26%) were in CKD2, 95/223 (42%) in CKD3a, 47/223 (21%) in CKD3b, 6/223 (7%) in CKD4 1, 2/223 (1%) in CKD5. Ischemic cardiomyopathy was the most common cause of heart failure, (36%, 80/223 patients). 119/223 patients (53%) had HFrEF, 41/223 (19%) HFmrEF and 63/223 (28%) HFpE. 64/223 (28%) of the patients were treated with SGLT2i,159/223 (71%) with RASi of which 37 (17%) were on an ARNI. Patients under combined RASi and SGLT2i were younger (66 vs 73 years, p = 0.005), were more likely to have diabetes (44% vs 30%), HFrEF rather than HFpEF (70% vs 7% p = 0.002) and had a better kidney function at the beginning of follow-up (eGFR 65 vs 55 ml/min/1.73 m2, p < 0.001). Hospitalization-rate due to HF and incidence of AKI were high with 0.6/patient/year and 4.8/patient/year respectively. 72/223 (32%) patients died during the mean follow-up of 3.1 years. Conclusion We identified a high-risk patient population with cardiorenal disease that might particularly benefit from evidence-based and patient-centered interdisciplinary care. A cardiorenal outpatient clinic may have the potential to improve a personalized approach in more vulnerable patients.

The concentration of maternal sacubitril/valsartan transferred into human milk is negligible.

Peripartum cardiomyopathy (PPCM) is a common cause of heart failure (HF) in the peripartum. Some medications are considered safe while breastfeeding. However, sacubitril/valsartan (Entresto), while efficacious, is not recommended in breastfeeding women due to concerns about adverse infant development, and no published data suggest otherwise. This study aimed to assess the transfer of sacubitril/valsartan into human milk and evaluate the infant's risk of drug exposure. The InfantRisk Human Milk Biorepository released samples and corresponding health information from five breastfeeding maternal-infant dyads exposed to sacubitril/valsartan. Sacubitril, valsartan, and LBQ657 (sacubitril active metabolite) concentrations were determined using liquid chromatography-mass spectrometry (LC/MS/MS) from timed samples 0, 1, 2, 4, 6, 8, 10, and 12 h following medication administration at steady state conditions. Valsartan levels were below the detection limit of 0.19 ng/mL in all milk samples. Sacubitril was measurable in all milk samples of the five participants, peaking 1 h after drug administration at a mean concentration of 1.52 ng/mL for a total infant dose of 0.00049 mg/kg/12 h and a relative infant dose (RID) calculated at 0.01%. The maximum concentration of its active metabolite LBQ657 in the milk samples was observed 4 h after medication administration and declined over the remaining 12-h dosing interval, for an average concentration of 9.5 ng/mL. The total infant dose was 0.00071 mg/kg/12 h, and the RID was 0.22%. Two mothers reported continuing to breastfeed while taking sacubitril/valsartan; both mothers stated observing no negative effects in their breastfed infants. The transfer of sacubitril/valsartan into human milk is minimal. These concentrations are unlikely to pose a significant risk to breastfeeding infants, with a combined calculated RID of <0.25%, which is far lower than the industry safety standards (RID <10%).

Percutaneous Coronary Intervention Versus Optimal Medical Therapy for Severe Ischemic Left Ventricular Systolic Dysfunction

Coronary artery disease is the most common cause of heart failure, which is the leading cause of cardiovascular-related death worldwide. There are insufficient data to make strong recommendations for percutaneous coronary intervention (PCI) in patients with severe ischemic left ventricular systolic dysfunction (LVSD). In that context, we performed a meta-analysis to compare the outcomes of PCI with those of optimal medical therapy alone in patients with severe ischemic LVSD. A systematic search was conducted in PubMed, EMBASE, and ClinicalTrials.gov from inception to December 2023. Our outcome of interest was all-cause mortality in patients undergoing PCI vs medical therapy. We used random effects models to aggregate data and to calculate pooled incidence and relative risk with 95% CIs. Four studies including 2 randomized controlled trials with 2080 patients (PCI, 1082; optimal medical therapy, 998) were included. All-cause mortality did not differ significantly between the groups: 168 patients (15.5%) in the PCI group vs 200 patients (20.0%) in the optimal medical therapy group (relative risk, 0.88; 95% CI, 0.75-1.09; P=.25). In conclusion, the available evidence indicates that PCI does not improve all-cause mortality in patients with severe LVSD without lifestyle-limiting anginal symptoms. Further data are needed to identify subgroups of patients better served by each modality.

Comprehensive bioinformatics analytics and in vivo validation reveal SLC31A1 as an emerging diagnostic biomarker for acute myocardial infarction.

Globally, Acute Myocardial Infarction (AMI) is a common cause of heart failure (HF), which has been a leading cause of mortality resulting from non-communicable diseases. On the other hand, increasing evidence suggests that the role of energy production within the mitochondria strongly links to the development and progression of heart diseases, while Cuproptosis, a newly identified cell death mechanism, has not yet been comprehensively analyzed from the aspect of cardiovascular medicine. 8 transcriptome profiles curated from the GEO database were integrated, from which a diagnostic model based on the Stacking algorithm was established. The efficacy of the model was evaluated in a multifaced manner (i.e., by Precision-Recall curve, Receiver Operative Characteristic curve, etc.). We also sequenced our animal models at the bulk RNA level and conducted qPCR and immunohistochemical staining, with which we further validated the expression of the key contributor gene to the model. Finally, we explored the immune implications of the key contributor gene. A merged machine learning model containing 4 Cuproptosis-related genes (i.e., PDHB, CDKN2A, GLS, and SLC31A1) for robust AMI diagnosis was developed, in which SLC31A1 served as the key contributor. Through in vivo modeling, we validated the aberrant overexpression of SLC31A1 in AMI. Besides, further transcriptome analysis revealed that its high expression was correlated with significant potential immunological implications in the infiltration of many immune cell types, especially monocyte. We constructed an AMI diagnostic model based on Cuproptosis-related genes and validated the key contributor gene in animal modeling. We also analyzed the effects on the immune system for its overexpression in AMI.

Single-Cell RNA Sequencing Reveals Cardiac Fibroblast-Specific Transcriptomic Changes in Dilated Cardiomyopathy.

Dilated cardiomyopathy (DCM) is the most common cause of heart failure, with a complex aetiology involving multiple cell types. We aimed to detect cell-specific transcriptomic alterations in DCM through analysis that leveraged recent advancements in single-cell analytical tools. Single-cell RNA sequencing (scRNA-seq) data from human DCM cardiac tissue were subjected to an updated bioinformatic workflow in which unsupervised clustering was paired with reference label transfer to more comprehensively annotate the dataset. Differential gene expression was detected primarily in the cardiac fibroblast population. Bulk RNA sequencing was performed on an independent cohort of human cardiac tissue and compared with scRNA-seq gene alterations to generate a stratified list of higher-confidence, fibroblast-specific expression candidates for further validation. Concordant gene dysregulation was confirmed in TGFβ-induced fibroblasts. Functional assessment of gene candidates showed that AEBP1 may play a significant role in fibroblast activation. This unbiased approach enabled improved resolution of cardiac cell-type-specific transcriptomic alterations in DCM.

Characterization of Non-Ischemic Dilated Cardiomyopathy in a Native Tanzanian Cohort: MOYO Study.

Non-ischemic dilated cardiomyopathy (NIDCM) is a common cause of heart failure with progressive tendency. The disease occurs in one in every 2,500 individuals in the developed world, with high morbidity and mortality. However, detailed data on the role of NIDCM in heart failure in Tanzania is lacking. To characterize NIDCM in a Tanzanian cohort with respect to demographics, clinical profile, imaging findings and management. Characterization of non-ischemic dilated cardioMyOpathY in a native Tanzanian cOhort (MOYO) is a prospective cohort study of NIDCM patients seen at the Jakaya Kikwete Cardiac Institute. Patients aged ≥18 years with a clinical diagnosis of heart failure, an ejection fraction of ≤45% on echocardiography and no evidence of ischemia were enrolled. Clinical data, echocardiography, electrocardiography (ECG), coronary angiography and stress ECG information were collected from February 2020 to March 2022. Of 402 patients, n = 220 (54.7%) were males with a median (IQR) age of 55.0 (41.0, 66.0) years. Causes of NIDCM were presumably hypertensive n = 218 (54.2%), idiopathic n = 116 (28.9%), PPCM n = 45 (11.2%), alcoholic n = 10 (2.5%) and other causes n = 13 (3.2%). The most common presenting symptoms were dyspnea n = 342 (85.1%), with the majority of patients presenting with New York Heart Association (NYHA) Class III n = 195 (48.5%). The mean (SD) left ventricular ejection fraction (LVEF) was 29.4% (±7.7), and severe systolic dysfunction (LVEF <30%) was common n = 208 (51.7%). Compared with other forms of DCM, idiopathic DCM patients were significantly younger, had more advanced NYHA class (p < 0.001) and presented more often with left bundle branch block on ECG (p = 0.0042). There was suboptimal use of novel guidelines recommended medications ARNI n = 10 (2.5%) and SGLT2 2-inhibitors n = 2 (0.5%). In our Tanzanian cohort, the majority of patients with NIDCM have an identified underlying cause, and they present at late stages of the disease. Patients with idiopathic DCM are younger with more severe disease compared to other forms of NIDCM.

Epidemiology of heart failure in rural Chhattisgarh, India.

Background Cardiovascular diseases, including heart failure (HF), are leading causes of death and disability in India. However, most studies in India only include urban populations or rural regions with improved access and may not represent the poorest patients or regions. We studied the epidemiology of HF patients admitted to a secondary care hospital in rural Chhattisgarh, India. Methods We did a retrospective chart review of patients hospitalized with HF in 2018 to obtain their demographic data and risk factors for developing HF. We reviewed echocardio-grams to assign patients to their most probable HF category. Results We studied 88 HF patients with a mean age of 42 years including 55 (62.5%) women. The most common categories of HF were cardiomyopathy (36.8%), rheumatic heart disease (RHD; 25.3%) and right heart failure (RHF; 18.4%). Prior tuberculosis was more prevalent in patients with RHF compared with other types of HF (43.8% v. 13.9%). Conclusions HF patients in this study from rural central India were young and predominantly women. Cardiomyopathy, RHD and RHF due to past tuberculosis were common causes of HF in this population. Further studies are needed to expand upon these single centre findings to better understand the risk factors and outcomes of HF among the rural poor.

Waitlist Outcomes in Candidates With Rare Causes of Heart Failure After Implementation of the 2018 French Heart Allocation Scheme.

In 2018, an algorithm-based allocation system for heart transplantation (HT) was implemented in France. Its effect on access to HT of patients with rare causes of heart failure (HF) has not been assessed. In this national study, including adults listed for HT between 2018 and 2020, we analyzed waitlist and posttransplant outcomes of candidates with rare causes of HF (restrictive cardiomyopathy [RCM], hypertrophic cardiomyopathy, and congenital heart disease). The primary end point was death on the waitlist or delisting for clinical deterioration. Secondary end points included access to HT and posttransplant mortality. The cumulative incidence of waitlist mortality estimated with competing risk analysis and incidence of transplantation were compared between diagnosis groups. The association of HF cause with outcomes was determined by Fine-Gray or Cox models. Overall, 1604 candidates were listed for HT. At 1 year postlisting, 175 patients met the primary end point and 1040 underwent HT. Candidates listed for rare causes of HF significantly differed in baseline characteristics and had more frequent score exceptions compared with other cardiomyopathies (31.3%, 32.0%, 36.4%, and 16.7% for patients with hypertrophic cardiomyopathy, RCM, congenital heart disease, and other cardiomyopathies). The cumulative incidence of death on the waitlist and probability of HT were similar between diagnosis groups (P=0.17 and 0.40, respectively). The adjusted risk of death or delisting for clinical deterioration did not significantly differ between candidates with rare and common causes of HF (subdistribution hazard ratio (HR): hypertrophic cardiomyopathy, 0.51 [95% CI, 0.19-1.38]; P=0.18; RCM, 1.04 [95% CI, 0.42-2.58]; P=0.94; congenital heart disease, 1.82 [95% CI, 0.78-4.26]; P=0.17). Similarly, the access to HT did not significantly differ between causes of HF (hypertrophic cardiomyopathy: HR, 1.18 [95% CI, 0.92-1.51]; P=0.19; RCM: HR, 1.19 [95% CI, 0.90-1.58]; P=0.23; congenital heart disease: HR, 0.76 [95% CI, 0.53-1.09]; P=0.14). RCM was an independent risk factor for 1-year posttransplant mortality (HR, 2.12 [95% CI, 1.06-4.24]; P=0.03). Our study shows equitable waitlist outcomes among HT candidates whatever the indication for transplantation with the new French allocation scheme.

Optimisation of conservative treatment of patients with severe heart failure by using hemosorption

Background. Heart failure (HF) is a complex cardiac pathology that is the main cause of hospitalisation among adults and is characterised by a high mortality. Dilated cardiomyopathy (DCM) is the most common cause of HF, and it can be fatal within a few years after the first symptoms appear. Many patients with HF remain refractory to medical therapy, despite its constant development and improvement. The study aims to compare the effectiveness of conservative treatment of patients with severe HF that occurred on the background of DCM using drug therapy and its combination with a course of hemosorption (HS). Materials and methods. We analysed treatment outcomes in 30 patients with severe HF against DCM (New York Heart Association class III–V, left ventricular ejection fraction (LV EF) &lt; 30 %). Patients in group 1 (n = 13; N-terminal fragment of brain natriuretic peptide precursor (NT-pro BNP) 4,546.23 ± ± 3,265.01 pg/ml; LV EF 16.77 ± 2.92 %; LV end-diastolic volume (EDV) 261.31 ± 60.60 ml, LV end-systolic volume (ESV) 214.85 ± 49.44 ml) received drug therapy according to local protocols. In group 2 (n = 17; NT-pro BNP 3,974.49 ± 3,550.17 pg/ml; LV EF 18.18 ± 4.36 %; LV EDV 261.12 ± 79.96 ml, LV ESV 212.06 ± 71.67 ml), medical treatment was supplemented with a course of 3 HS procedures using granular deligandizing hemosorbent. Results. Patients in both study groups noted an improvement in well-being and a decrease in the severity of symptoms. The level of NT-pro BNP decreased to 2,609.92 ± 1,465.14 pg/ml (p &lt; 0.01) in group 1 and to 975.35 ± 511.55 pg/ml (p &lt; 0.05) in group 2. LV EF increased to 22.77 ± 4.69 % and 26.76 ± 5.02 %, respectively, in the groups (p &lt; 0.01). In patients of group 1, LV EDV and LV ESV changed to 262.22 ± 40.92 ml and 211.33 ± 35.22 ml, respectively. In group 2, there was a significant decrease in LV EDV to 228.94 ± 73.16 ml and LV ESV to 170.88 ± 60.28 ml (p &lt; 0.01). Conclusions. The use of HS in combination with drug therapy for severe HF on the background of DCM improves the clinical status of patients and LV systolic function.

Public Awareness of Heart Failure Among the Population of Makkah City, Saudi Arabia: A Cross-Sectional Study.

Background Heart failure (HF), a major public health problem worldwide, is a complex clinical syndrome caused by structural or functional heart disorders occurring when the heart cannot supply sufficient blood to the body. The most common cause of HF is impairment of the left ventricle. Public awareness of HF is critical for controlling the disease burden, recognizing disease severity, and determining its prognosis. Therefore, this study assesses the awareness and perception of HF among the population in Makkah City, Saudi Arabia. Methods A cross-sectional study was conducted among 1,053 participants over 18 years of age who lived in Makkah City between October 2022 and February 2023. Participants were randomly selected and recruited using a validated online questionnaire. Results Of the participants, 62.4% had heard of HF, and the majority (59.5%) correctly identified it. Regarding the etiology of the disease, about 50.6% indicated that it was related to the aging process, and 82.9% indicated it was related to high blood pressure. Only 24.1% of participants correctly recognized HF symptoms; most defined the symptoms as general heart disease. Moreover, 51.6% of participants agreed that the current HF medications can reduce deaths from HF and improve quality of life. However, most respondents disagreed that HF drugs can prevent the onset of HF. Conclusion The findings emphasize the need for more awareness programs to raise the public awareness about HF and effectively guide the population to more reliable sources that provide evidence-based information about the disease.

Effects of pericyte and smooth muscle specific knock-out of CXCL12 on cardiac function after myocardial ischemia in mice

Abstract Introduction Ischemic cardiomyopathy as a result of myocardial infarction represents one of the most common causes of heart failure (1). The C-X-C motif chemokine ligand 12 (CXCL12) and its receptor CXCR4 facilitate cardiac repair after myocardial ischemia (MI) and play fundamental roles in cardiovascular development (2). However, the cell- and tissue-specific actions of CXCL12 are poorly understood, limiting the introduction of targeted therapies. Here, we aimed to examine the role of pericyte and smooth muscle cell-specific CXCL12 expression on myocardial function after MI. Methods We generated a smooth muscle protein 22-alpha-Cre and a pericyte protein NG2-Cre driven mouse model to ablate CXCL12 specifically in smooth muscle cells (SM22-Cre x CXCL12flox/flox) and in pericytes (NG2-Cre x CXCL12flox/flox). Genotyping was performed using ear hole biopsy by PCR. Hearts were analysed morphologically by histology and immunofluorescence. Cardiac function and dimensions of the wall thicknesses and cardiac cavities were determined by echocardiography. Myocardial infarction was induced in the animals and cardiac function was further investigated 28 days after MI. Results In immunofluorescence, we found that CXCL12 is highly expressed in SM22+ smooth muscle cells and in cells surrounding arterial blood vessels (3). NG2-CXCL12-/- mice did not show increased mortality, they behaved inconspicuously and no obvious developmental defects could be detected. Echocardiographic analysis of cardiac function in NG2-Cre x CXCL12flox/flox mice without infarction showed no significant difference in left ventricular (LV) performance and no evidence of abnormal geometry of the ventricles compared with controls. Assessment of SM22-Cre x CXCL12flox/flox mice after MI revealed reduced ejection fraction (EF) (29.0%±9.7 vs. 40.0%±8.1; n=10; p=0.027) and stroke volume (SV) (19.0µl±3.3 vs. 32.7µl±10.3; n=10; p=0.002) compared to non-transgenic controls. In contrast NG2-Cre x CXCL12flox/flox mice showed no significant changes in EF (34.6%±11.4 vs. 40.0%±8.1; n=10; p=0.368) and SV (27.7µl±7.3 vs. 32.7µl±10.3; n=10; p=0.303). Conclusion Our findings suggest that pericyte specific CXCL12 plays no major role in cardiac development and function after MI. In contrast, KO of CXCL12 in smooth muscle seems to deteriorate cardiac function after ischemia.

Echocardiography-based risk score predicts cardiovascular outcomes in ischemic heart failure patients with reduced ejection fraction

Abstract Background Ischemic heart disease (IHD) is the most common cause of heart failure (HF) and serves as an important prognostic factor across the whole HF spectrum. Prognostic assessment is important for optimal patient care, and a number of prediction models or prognostic scores have been developed in the past years for risk stratification of HF patients. Purpose Present study aimed to develop a comprehensive echocardiography-based score algorism for risk assessment of ischemic heart failure (IHF) patients with reduced left ventricular ejection fraction (&amp;lt;50%). Methods This study included 1355 IHF patients with ejection fraction &amp;lt;50%, the median clinical follow-up was 25 months. Multivariable Cox hazard models were used to assess the associations between echocardiography variables [including 13 standard parameters and global longitudinal strain (GLS)] and major adverse outcomes [including all-cause mortality, cardiovascular (CV) death, and CV related hospitalization]. Results Rates of all-cause mortality, CV mortality, and combined CV events including death and hospitalization, were 29.2%, 18.2%, 41.1%, respectively. Right ventricular mid-cavity diameter (RVD)&amp;gt;38mm, mitral annular plane systolic excursion (MAPSE)&amp;lt;8mm, tricuspid annular plane systolic excursion (TAPSE)&amp;lt;12mm, transmitral early flow velocity to mitral annular velocity ratio (E/E´)&amp;gt;14.5, systolic pulmonary artery pressure (sPAP)&amp;gt;38mmHg, and absolute GLS&amp;lt;8% were identified as independent echocardiographic indexes for worse clinical outcome in the multivariable Cox models. An echocardiography-based risk score (Echo Risk Score, ranged from 0 to 6 points) was established based on these markers and patients were classified into 3 risk groups: a score of 0 to 1 as low-risk, 2 to 3 as intermediate-risk, and 4-6 as high-risk. After adjustment for all clinical covariates, high-risk patients faced 2 to 3-fold increased risk of all-cause mortality (HR 2.42, 95% CI 1.81-3.24), CV mortality (HR 2.75, 95% CI 1.88-4.02), and combined CV events (HR 1.84, 95% CI 1.43-2.36) compared with low-risk patients. Incremental predicting efficacy was evidenced after the addition of Echo Risk Score either to the model including clinical risk factors or to the model including clinical risk factors and N-terminal prohormone of brain natriuretic peptide (all P&amp;lt;0.001, Figure 1). Conclusions This new echocardiography-based risk score is significantly and independently associated with all-cause mortality and CV mortality or hospitalization in ischemic heart failure patients with reduced ejection fraction. Future studies are warranted to validate the predicting efficacy of this echocardiography-based risk score in ischemic heart failure patients with reduced ejection fraction.Figure 1

Metabolome Profiling in the Plasma of Dogs with Idiopathic Dilated Cardiomyopathy: A Multiplatform Mass-Spectrometry-Based Approach.

Dilated cardiomyopathy is one of the important diseases in dogs and humans. The second most common cause of heart failure in dogs is idiopathic dilated cardiomyopathy (iDCM), which results in heart failure or sudden cardiac death due to arrhythmia. This study aimed to determine changes in the plasma metabolome of dogs with iDCM compared to healthy dogs. For that purpose, a multiplatform mass-spectrometry-based approach was used. In this study, we included two groups of dogs: 12 dogs with iDCM and 8 healthy dogs. A total of 272 metabolites were detected in the plasma samples of dogs by combining three approaches but four MS-based platforms (GC-MS, LC-MS (untargeted), LC-MS (targeted), and FIA-MS (targeted) methods). Our findings demonstrated changes in the canine plasma metabolome involved in the development of iDCM, including the different concentrations of amino acids, biogenic amines, acylcarnitines, triglycerides and diglycerides, sphingomyelins, and organic acids. The results of this study will enable the detection and monitoring of pathophysiological mechanisms involved in the development of iDCM in the future.