Search Results (161)

Background: Arteriovenous fistulas (AVFs) may contribute to cardiac remodeling and consequently to an increased risk of heart failure and cardiovascular mortality in patients with end-stage kidney disease (ESKD). We aimed to assess cardiac changes following AVF creation and identify potential parameters associated with cardiac remodeling. Methods: In our prospective, single-center study, ESKD patients without significant pre-existing cardiac disease underwent 2D and 3D echocardiographic evaluation before and after AVF creation, along with AVF flow measurement. Cardiac remodeling was assessed using 3D indexed left and right ventricular end-diastolic volumes (LVEDVi, RVEDVi), while systolic function was assessed using longitudinal strain and 3D ejection fraction. Results: We included 20 patients (18 men; median age 73.5 years [IQR: 67–77]) with a mean AVF flow of 1140 ± 345 mL/min. At a median of 8.2 months (IQR: 7.3–9.3) following AVF creation, significant biventricular dilatation was observed: LVEDVi increased from 89 ± 14 to 97 ± 21 mL/m² (p < 0.05) and RVEDVi from 80 ± 15 to 91 ± 18 mL/m² (p < 0.05), while the systolic function of both ventricles did not change significantly. The right ventricle showed the most pronounced remodeling and it was independently associated with volume overload (p = 0.003) and elevated left ventricular filling pressure (p = 0.030), but not with AVF flow. Conclusions: Moderate AVF flow was associated with cardiac remodeling, primarily affecting the right ventricle. Fluid overload and left ventricular filling pressure were key factors associated with right ventricular remodeling, underscoring the need for careful fluid management and vascular access planning in ESKD patients. Full article

Background/Objectives: Nelumbo nucifera Gaertn. (lotus) seeds have traditionally been used to treat hypertension, though their mechanisms remain unclear. This study investigated the antihypertensive effects of lotus seed extract (LSE) and its mechanisms in rats with N^ω-nitro-L-arginine methyl ester (L-NAME)-induced hypertension. Methods: Male Sprague Dawley rats received L-NAME (40 mg/kg/day) in drinking water and were treated orally with LSE (5, 10, or 100 mg/kg/day), captopril (5 mg/kg/day), or a combination of LSE and captopril (2.5 mg/kg/day each) for 5 weeks. Hemodynamic parameters and histological changes in the left ventricle and aorta were assessed. Mechanistic studies included measurements of plasma nitric oxide (NO) metabolites, malondialdehyde (MDA), superoxide dismutase (SOD) activity, angiotensin II (Ang II), angiotensin-converting enzyme (ACE) activity, and protein expression via western blot. Results: L-NAME elevated systolic blood pressure and induced cardiovascular remodeling, oxidative stress, and renin-angiotensin system activation. LSE treatment reduced blood pressure, improved antioxidant status, increased NO bioavailability, and downregulated gp91^phox and AT₁R expression. The combination of low-dose LSE and captopril produced stronger effects than LSE alone, with efficacy comparable to captopril. Conclusions: These findings suggest that LSE exerts antihypertensive effects via antioxidant activity and inhibition of the renin-angiotensin system, supporting its potential as an adjunct therapy for hypertension. Full article

Cardiac remodeling in feline hypertrophic cardiomyopathy (HCM) is poorly understood. To investigate underlying molecular mechanisms, we determined microRNA–mRNA interactions, regulatory networks, and upstream regulators using left ventricle (LV) and left atrium (LA) mRNA and microRNA sequencing datasets from cats with HCM and controls. Upstream regulators, molecules, and pathways associated with ischemia, inflammation, fibrosis, and cellular changes were observed in the HCM heart. In both the HCM LV and LA, TNFα, IL1β, and TGFβ were identified as upstream regulators, along with FGF23, THBS4, and FAMB177 as the top increased molecules. Relevant microRNAs included upstream regulator miR-132, enriched miR-124-3p, miR-122b-3p, miR-146-5p (HCM LV and LA), miR-370, miR-1185-5p, miR-12194-3p (HCM LV), miR-153-3p, miR-185-5p, and miR-185-3p (HCM LA). Macrophage pathways were activated, and granulocyte and agranulocyte adhesion and diapedesis were the most connected pathways. The HIF1α signaling pathway in the HCM LV, upstream regulators miR-1-3p and miR-204, and reduced miR-29 and miR-122-5p suggest cardioprotective mechanisms. Observed in the healthy heart and suspected to be involved in cardiac homeostasis were upstream regulators miR-96, inhibited WNT3A and miR-145, as well as miR-140-5p, miR-141-3p, miR-208b-3p, and miR-885-3p. This study provides further insights into the pathogenesis of HCM, and identifies the factors involved in the maintenance of a healthy LV and LA. Full article

Background and Clinical Significance: The incidence of persistent ductus arteriosus (PDA) in preterm infants is the highest and depends on their birth weight (BW) and respiratory condition after birth. Previously, after the unsuccessful drug treatment, surgical ligation was the primary treatment option. However, according to clinical studies, the Amplatzer Piccolo Occluder was approved for PDA closure for patients ≥700 g. In our country, percutaneous PDA embolization has not been performed yet. Case Presentation: We present three premature infants with hemodynamically significant patent ductus arteriosus (hsPDA) in whom percutaneous occlusion was performed using the Amplatzer Piccolo Occluder (APO). The average gestational week (GW) was 27 ± 1, while body weight was 1030 ± 60 g. All patients had respiratory deterioration, with dilatation of the left heart chambers, and renal failure. The second developed a severe form of broncho-pulmonary dysplasia. Transthoracic echocardiography (TTE) examinations revealed a hemodynamically significant PDA (LA/Ao 1.8–2.2) and medical closure was unsuccessfully carried out. Due to the hemodynamically significant PDA maintenance in all neonates, transvenous PDA closure was performed using the APO (APO 9-PDAP-04-02-L, 9-PDAP-04-04-L, 9-PDAP-05-054L, respectively). The entire devices, with both retention discs, are implanted within the duct. TTE pointed out adequate device position without descending aorta, left pulmonary artery obstruction, residual shunt, and reverse remodelling of the left ventricle and left atrium. The first newborn was weaned from mechanical ventilation three days after the procedure and discharged three weeks after. The second patient was extubated 2 weeks after the procedure, and even the severe BPD, X-ray showed improvement. The third patient’s renal failure completely resolved, weaned from inotropic drug support and mechanical ventilation. Conclusions: Due to a significantly lower complication rate than surgical ligation, we will strive to make percutaneous PDA occlusion a new standard for treatment in newborns, especially preterm newborns, in our country. Full article

Background: Aging and the female sex are considered risk factors for the development of heart failure with preserved ejection fraction (HFpEF). Unlike other risk factors, such as hypertension, obesity, or diabetes, they do not represent therapeutic targets. Methods: In a recently developed two-hit murine HFpEF model (angiotensin II + high-fat diet; MHS), we studied the relative contributions of the biological sex, aging, and gonadal hormones to cardiac remodeling and function. We aimed to reproduce a frequent HFpEF phenotype in mice characterized by aging, hypertension, the female sex, menopause, and metabolic alterations. Using the MHS mouse model, we studied cardiac remodeling and function in C57Bl6/J mice of both sexes, young (12 weeks) and old (20 months), that were gonadectomized (Gx) or not. Results: We observed that in mice, aging was associated with body weight gain, cardiac hypertrophy (CH), left ventricle (LV) concentric remodeling, and left atrial (LA) enlargement. Diastolic parameters such as E and A wave velocities were modulated by aging but only in females. Submitting young and old mice to MHS for 28 days induced the expected HFpEF phenotype consisting of CH, LV wall thickening, LA enlargement, and diastolic dysfunction with a preserved EF except for old males, in which it was significantly reduced. Young mice were Gx at five weeks, and old mice at six months (over a year before MHS). Gx increased myocardial fibrosis in MHS females and helped preserve the EF in males. Conclusions: Our results suggest that MHS has sex-specific effects on old mice, and the loss of gonadal hormones significantly impacts the observed heart failure phenotype. Full article

Skeletal muscle changes occur in heart failure (HF). Despite the cardioprotective effects of sodium–glucose co-transporter 2 (SGLT2) inhibitors in HF, their impact on skeletal muscle remains poorly understood. We investigated the effects of the SGLT2 inhibitor empagliflozin (EMPA) on cardiac remodeling and the soleus muscle of rats with myocardial infarction (MI)-induced HF. Methods: One week after MI induction, rats were assigned to Sham, Sham + EMPA, MI, and MI + EMPA groups. EMPA was administered (5 mg/kg/day) for 12 weeks. Results: MI + EMPA and MI had dilated left cardiac chambers; the left atrium diameter and left ventricle end-diastolic area were smaller in MI + EMPA than MI. The ejection fraction did not differ between infarcted groups. MI + EMPA had a larger soleus cross-sectional area and higher Type II myosin heavy chain expression than MI. Carbonylated protein and malondialdehyde levels were lower and superoxide dismutase activity higher in MI + EMPA than MI. Respiratory Complex I expression was higher in MI + EMPA than MI. Metabolic enzyme activities, altered in MI, were normalized in MI + EMPA. EMPA up-regulated anabolic proteins and down-regulated catabolic proteins. Conclusion: Empagliflozin attenuates infarction-induced cardiac remodeling in rats. In soleus muscle, empagliflozin preserves cell trophism, reduces oxidative stress, normalizes muscle and mitochondrial metabolism, and positively modulates proteins involved in synthesis and degradation-related pathways. Full article

Background/Objectives: Cardiac resynchronization therapy (CRT) and angiotensin receptor–neprilysin inhibitors (ARNIs) are cornerstone therapies for patients with heart failure with reduced ejection fraction (HFrEF). However, nearly 30% of patients show no significant response to CRT alone. The potential of ARNI to enhance CRT outcomes—especially in non-responders—is an emerging field of interest. The objective of this review is to systematically evaluate and synthesize the available evidence on the clinical outcomes of combining CRT with ARNI therapy in patients with HFrEF. Methods: We conducted a comprehensive search of PubMed, Scopus, and Google Scholar up to September 2024, using the keywords “CRT and ARNI” and “cardiac resynchronization therapy and sacubitril/valsartan”. We included retrospective and prospective clinical studies, observational studies, and review articles reporting on patients with HFrEF treated with both CRT and ARNI. Studies not in English, animal studies, and those without full-text availability were excluded. Study selection and data extraction were performed in duplicate by independent reviewers, using PRISMA guidelines for transparency. The final selection included 8 studies published in the last four years, summarized by design, population, outcomes, and statistical significance. Results: The reviewed studies suggest that ARNI therapy, when combined with CRT, may contribute to improvements in left ventricle ejection fraction (LVEF), NYHA functional class, and ventricular remodeling, particularly in CRT non-responders. Some studies also report a potential reduction in ventricular arrhythmias and implantable cardioverter-defibrillator (ICD) interventions. However, outcomes varied across subgroups, and the influence of ARNI timing relative to CRT implantation remains inconclusive. Limitations: Heterogeneity in study designs and small sample sizes in some included studies limited the ability to conduct a meta-analysis. This review is not registered. Conclusions: ARNI therapy shows promise in enhancing CRT response in patients with HFrEF, particularly in non-responders. Further large-scale, prospective studies are needed to clarify optimal patient selection and treatment sequencing. Full article

Acute myocardial necrosis activates the immune response and inflammatory processes. Although the initial response is helpful in restoring tissue injury, dysregulated and exacerbated inflammation contributes to the progression of cardiac remodeling. Inflammasomes play important roles in post-infarction inflammation. NALP1/NLRP1, NLRP 3, and NLRC4 are the best-known inflammasomes. NLRP3, which has received the most study in cardiovascular disease, has been linked to increased IL-1β (IL1B) production and caspase-1 activity, as well as impaired cardiac function. The role of NLRP1 and NLRC4 inflammasomes after acute myocardial infarction (MI) is poorly understood. We evaluated the expression of myocardial inflammasomes and inflammatory markers 72 h after MI in rats. Male Wistar rats were divided into Sham (n = 15) and MI (n = 16) groups. MI was induced by ligating the left anterior descending coronary artery. Infarct size was assessed by histology. Myocardial protein and gene expression was analyzed by Western blot and RT-qPCR, respectively. IL-1β (Il1b) concentrations in serum and heart macerate supernatant were evaluated by ELISA. Statistical analysis was performed using Student’s t test. Rats with an MI size less than 30% of the total left ventricle (LV) area were excluded; infarct size was 46 ± 11% of the total LV area in MI. The interstitial collagen fraction was higher in MI. Nlrc4, caspase-1 (Casp1), and IL-1β (Il1b) protein expressions were higher in MI. Nlrp3, Nlrp1, ASC (Pycard), pro-caspase-1, and pro-IL-1β (Il1b) expressions did not differ between groups. Expression of the Nlrp3 and ASC (Pycard) genes, as well as myocardial and serum IL-1β (Il1b) concentrations, was higher in MI. Acute post-myocardial infarction inflammation is characterized by increased protein expression of Nlrc4, caspase-1, and interleukin-1β; increased gene expression of Nlrp3 and ASC (Pycard); and elevated serum and myocardial concentrations of interleukin-1β in combination with an increased myocardial collagen interstitial fraction. Full article

Objective: To investigate whether the regular administration of blueberry extract and low-intensity resistance exercise training (RT), either alone or in combination, during the development of monocrotaline (MCT)-induced severe pulmonary arterial hypertension (PAH) in rats protect the left ventricle (LV) from redox dysregulation and pathological remodeling. Methods: Groups of seven male Wistar rats were formed for the experiment: sedentary control; sedentary hypertensive; sedentary hypertensive blueberry; exercise hypertensive; and exercise hypertensive blueberry. PAH was experimentally induced through a single intraperitoneal administration of MCT at a dose of 60 mg/kg. One day after injection, the blueberry groups started receiving a daily dose of blueberry extract (100 mg/kg) by gavage, while the exercise groups initiated a three-week program of RT (ladder climbing; 15 climbs carrying 60% of maximum load; one session/day; 5 times/week). Echocardiographic evaluations were conducted 23 days after injection, and the rats were euthanized the next day to harvest LV tissue. Results: Separately, blueberry extract and RT mitigated augments in pulmonary artery resistance, LV tissue redox dysregulation (i.e., increased PC levels) and detrimental remodeling (i.e., reduced inflammation), and reductions in ejection fraction (EF) and fractional shortening (FS) caused by PAH. The combination of treatments prevented reductions in EF and FS, along with the development of a D-shaped LV. Conclusions: blueberry extract and moderate-intensity resistance training administered during the development of MCT-induced severe PAH in rats prevented LV redox dysregulation and pathological remodeling, thereby preserving its function. Full article

Hypertrophic cardiomyopathy (HCM) is the most frequent type of cardiac disease in cats. Due to its high prevalence and risk of sudden and severe signs, the disease is an important topic of various research. Despite the focus on the clinical course of the disease, studies presenting the pathological and histopathological patterns are rare. The study was conducted as a retrospective analysis of feline patients subjected to postmortem examination in the Cardiopathology Unit due to a clinical diagnosis of hypertrophic cardiomyopathy based on echocardiographic examination and ACVIM guidelines. Thirty-four cats clinically diagnosed with HCM were enrolled in the study. During the postmortem examination, hearts were subjected to gross morphometric and histopathological evaluation. Our results show that the histopathological pattern in cats with clinically stated HCM is very diverse, affecting both ventricles and atria. The histopathological picture is more complex in animals diagnosed earlier and treated for a longer period. Moreover, it is generally unrelated to wall thickness, with only left ventricular fibrosis affecting the thickness of the left ventricular wall. In conclusion, further research combining clinical and pathological results is required to unambiguously determine the histopathological remodelling that takes place in the myocardium of cats with hypertrophic cardiomyopathy. Full article

This study aimed to investigate the impact of a Western diet and resistance training on cardiac remodeling in a rat model of chemically induced mammary cancer. Fifty-six female Wistar rats were randomly assigned to one of eight experimental groups, evaluating the impact of Western and standard diets, exercise and sedentarism, and the induction of mammary cancer. Mammary cancer was induced via the intraperitoneal administration of N-methyl-N-nitrosourea (MNU) (50 mg/kg) at seven weeks of age. The resistance training protocol consisted of ladder climbing three times per week for an 18-week period, with a gradual increase in load over time. At the end of the 20-week experimental period, the animals were anesthetized and underwent echocardiography. Subsequently, the animals were euthanized, and organs and visceral adipose tissue (VAT) were collected and analyzed. A histopathological examination was performed on the mammary tumors. The Western diet increased relative VAT and contributed to cardiovascular and tumor-related changes, including an increase in interventricular septum thickness (IVS) and left ventricle posterior wall thickness (LVPW) at end-systole. Exercise reduced fat accumulation, improved cardiac performance, and helped regulate cardiovascular function, as indicated by a higher eccentricity index (EI) in the WD+EX group compared to the WD group. The WD was associated with increased VAT accumulation and initially delayed tumor initiation; however, over time, it contributed to bigger tumor aggressiveness. This diet also delayed tumor initiation but increased LVPW. Exercise, when combined with a WD, accelerated tumorigenesis, malignant transformation and invasiveness, resulted in the higher prevalence of invasive tumors. These findings underscore the complex and potentially compounding effects of diet and exercise on cancer progression. Full article

Left ventricular hypertrabeculation (LVHT) used to be a rare phenotypic trait. With advances in diagnostic imaging techniques, LVHT is being recognised in an increasing number of people. The scientific data show the possibility of the overdiagnosis of this cardiomyopathy in a population of people who have very high levels of physical activity. We describe the case of a young athlete with no medical history, who presented with syncope during a marathon running race. Initial evaluation showed elevated troponin I; transthoracic echocardiography showed a trabeculated ventricle and subsequent cardiac magnetic resonance (CMR) revealed left ventricular hypertrabeculation (LVHT). During subsequent evaluation by tilt table testing, vasovagal syncope was identified as the likely aetiology of the syncope. The patient was advised to cease sports and stimulants like caffeine use. At the 29-month follow-up, CMR showed the normalisation of the non-compacted to compacted myocardial ratio and an improvement in left ventricular function, with no further syncopal episodes reported. This is an example of the physiological hypertrabeculation of the LV apex in a recreational endurance athlete, with the normalisation of the non-compacted to compacted myocardial layer ratio after detraining. Physiological hypertrabeculation, a benign component of exercise-induced cardiac remodelling, must be differentiated from non-compaction cardiomyopathy and other pathologies causing syncope. This case underscores the importance of distinguishing physiological hypertrabeculation from pathological LVHT in athletes, highlighting that exercise-induced cardiac remodelling can normalise with detraining. Full article

Background: Secondary mitral regurgitation (SMR) is characterized by a pathological process impacting the left ventricle (LV) as opposed to the mitral valve (MV). In the absence of structural alterations to the MV, the expansion of the LV or impairment of the papillary muscles (PMs) may ensue. A number of technical procedures are accessible for the purpose of determining the optimal resolution for MR. Nevertheless, there is a dearth of rigorous data to facilitate a comparative analysis of MV replacement, MV repair (including subvalvular repair), and transcatheter mitral valve interventions (TMV-Is). The objective of this investigation is to evaluate and compare the efficacy and clinical outcomes of transcatheter mitral valve repair (TMV-r) utilizing the edge-to-edge mitral valve repair (TEER) procedure in comparison to conventional surgical mitral valve interventions (S-SMVis) in patients with secondary mitral regurgitation. Methods and analysis: A consortium of five cardiac surgery institutions from four European states and Japan have joined forces to establish a multicenter observational registry, designated TEERMISO. Patients who underwent technical procedures for SMR between January 2007 and December 2023 will be enrolled consecutively into the TEERMISO registry. The investigation team evaluated the comparative efficacy of replacement and repair techniques, utilizing both the standard surgical methodology and the transcatheter intervention. The primary clinical outcome will be the degree of left ventricular remodeling, as assessed by the left ventricular end-diastolic volume index, at 10 years. The forthcoming research will assess a variety of secondary endpoints, among which all-cause mortality will be the primary endpoint. Subsequent assessments will be made in the following order: functional status, hospitalization, neurocognition, physiological measures (echocardiographic assessment), occurrence of adverse clinical incidents, and reoperation. Ethics and dissemination: The multicenter design of the database is anticipated to reduce the potential for bias associated with institutional caseload and surgical experience. All participating centers possess an established mitral valve protocol that facilitates comprehensive follow-up and management of any delayed mitral complications following replacement surgery or surgical repair of the secondary mitral regurgitation. The data collected will provide insights into the impact of diverse surgical approaches on standard mitral valve surgery and TEER. This will facilitate the evaluation of LV remodeling over the course of long-term post-procedural follow-up. Trial Registration: ClinicalTrials.gov ID: NCT05090540; IRB ID: 202201143 Full article

The purpose: Evaluation of the short-term and long-term results of a phased correction of the tetralogy of Fallot (ToF) with stenting of the right ventricular outflow tract (RVOT) in comparison with a one-stage total correction (TC) of the defect. Materials and methods: Two groups of patients with classical ToF were formed. Group 1 (n = 25; median age = 72 days) was initially represented by children with ToF with a more severe clinical status (median weight = 3.6 kg, with more pronounced cyanosis and with comorbidities). The children of group 1 underwent the first stage of RVOT stenting and the second stage of TC of ToF. Group 2 (n = 25) was represented by older patients, with a higher body weight and SpO2 level, and they underwent a single-stage TC of the defect. Results: The application of a step-by-step ToF correction approach with RVOT stenting in low-weight newborns with severe hypoxemia demonstrated an equivalent effect on SpO2 dynamics—reverse remodeling of the heart—when compared with a less severe cohort of patients who underwent simultaneous TC of classical ToF. After RVOT stenting in children from group 1, the median SpO2 increased from 80% to 94.5%, the median Z value of the pulmonary artery trunk decreased from −3.46 mm to −2.54 mm, and the median index of end-diastolic volume of the left ventricle decreased from 23.07 mm/m² to 57.6 mL/m². TC of ToF in children from group 1 with a phased strategy of correction of the defect was no less successful than in children who underwent simultaneous TC. In the long-term follow-up period after TC of ToF, children from both groups, who were obviously unequal in their initial status, were practically comparable in clinical characteristics, exhibiting features of cardiac remodeling and achieving endpoints. And there were no significant differences between the two groups in the frequency of reaching the endpoints such as re-operations, cerebrovascular events, and death during the annual, three-year, and five-year follow-up period. Conclusions: The strategy of RVOT stenting followed by TC of ToF in a severe group of children demonstrated comparable results compared with the results of simultaneous TC of ToF in a more stable group of patients during the in-hospital, annual, three-year, and five-year follow-up periods. Full article

Background: Conventional echocardiography used to assess volumes of the left ventricle (LV) and left atrium (LA) along with mitral regurgitation grade is routine in studies before and after transcatheter edge-to-edge mitral valve repair (Mitral TEER). Previous studies focus on LV parameter changes and comparison of the functions before and a few months following Mitral TEER implantation, as well as LA reverse remodeling, by assessing LV volumes. However, less is known regarding LA strain changes in the early phase after the procedure. The objective of the study was to assess the effect of Mitral TEER on LA strain early after TEER procedure. Methods: The retrospective study included 44 patients who underwent Mitral TEER. LA strain and volumes were evaluated by speckle tracking echocardiography at the baseline and 24–48 h following the procedure. Demographic, echocardiographic, and clinical characteristics were obtained and statistically analyzed. Results: LA global longitudinal strain (GLS) reservoir improved significantly (from 12.2 ± 7 to 14.7 ± 6.4, p = 0.0079) after Mitral TEER. Significant improvements were also seen in LA volumes (LA maximal and minimal volume), which reduced by 17% and 22.5% respectively. LV GLS was significantly changed (from −9.8% to −12.8%, p < 0.0001) following Mitral TEER, whereas LV stroke volume was not significantly different between the baseline and post-Mitral TEER (p = 0.7798). Conclusions: After successful Mitral TEER, there was a very early improvement in LA function. Two-dimensional speckle tracking echocardiography may contribute to our understanding of LA functional changes immediately post-procedure. Full article