Search Results (34)

Cardiogenic shock (CS) is a complex, life-threatening syndrome characterized by inadequate tissue perfusion due to impaired cardiac function. Acute myocardial infarction (AMI) and acute decompensated heart failure are the leading causes, with mortality remaining high despite advances in revascularization and supportive care. The Society for Cardiovascular Angiography and Interventions (SCAI) classification allows risk stratification and guides clinical decision making by capturing the spectrum of shock severity. Percutaneous mechanical circulatory support (pMCS) devices, such as the intra-aortic balloon pump (IABP) and Impella, aim to stabilize hemodynamics by augmenting cardiac output and unloading the left ventricle. However, randomized trials and meta-analyses have not demonstrated a consistent survival advantage of Impella over IABP, while reporting higher rates of bleeding and vascular complications. Landmark trials, including ECLS-SHOCK and DanGer, have provided conflicting results, likely reflecting differences in baseline severity and timing of device implantation. Veno-arterial extracorporeal membrane oxygenator (VA-ECMO) offers full cardiopulmonary support but increases left ventricular afterload, potentially worsening myocardial injury. Combined strategies such as ECPELLA (Impella + VA-ECMO) or ECMO + IABP may mitigate left ventricle (LV) overload and improve bridging to recovery or advanced therapies, although evidence remains largely observational and complication rates are considerable. In right-sided or biventricular failure, tailored options (e.g., Impella RP, Bi-Pella) guided by invasive hemodynamics may be required. Current evidence suggests that pMCS benefits are limited to carefully selected subgroups, underscoring the importance of early diagnosis, prompt referral, and individualized intervention. Robust randomized data are still needed to define the optimal role of pMCS in AMI-related CS. Full article

The “Movahed sign” refers to the presence of a D-shaped left ventricle on cross-sectional cardiac imaging due to interventricular septal flattening seen during cardiac gated single-photon emission computed tomography (SPECT) This phenomenon arises from significant right ventricular (RV) pressure or volume overload, which pushes the septum toward the left ventricle (LV) and distorts the LV’s normally circular profile into a “D” shape. However, the prevalence and incidence of similar findings during cardiac Magnetic Resonance Imaging (MRI) or computed tomography (CT) are not known. The goal of this study was to perform a literature search focusing on the “Movahed sign” or D-shaped left ventricle in the context of cardiac MRI and CT. Databases searched included PubMed and Google Scholar, and reference lists of relevant articles were reviewed. The echocardiography literature was also consulted for foundational concepts of septal flattening. Key data on pathophysiology, imaging features, clinical correlations, and prognostic significance were extracted. Full article

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 and Objectives: Risk stratification in acute heart failure (AHF) remains challenging, particularly in settings where biomarker availability is limited. Echocardiography offers valuable hemodynamic insights, but no single parameter fully captures the complexity of biventricular dysfunction and pressure overload. This study aimed to evaluate a novel echocardiographic index (ViRTUE Index–VTI-RVRA-TAPSE Unified Evaluation) integrating a peak systolic gradient between the right ventricle and right atrium (RV-RA gradient), tricuspid annular plane systolic excursion (TAPSE), the velocity–time integral in the left ventricular outflow tract (VTI LVOT), NT-proBNP (N-terminal pro–B-type Natriuretic Peptide) levels, and in-hospital mortality among patients with AHF. Materials and Methods: We retrospectively analyzed 123 patients admitted with AHF. Echocardiographic evaluation at admission included TAPSE, VTI LVOT, and the RV-RA gradient. An index was calculated as ${\displaystyle \frac{RV-RA gradient }{TAPSE x VTI LVOT}}$. NT-proBNP levels and in-hospital outcomes were recorded. Statistical analysis included correlation, logistic regression, and ROC curve evaluation. Results: The proposed index showed a significant positive correlation with NT-proBNP values (r = 0.543, p < 0.0001) and good discriminative ability for elevated NT-proBNP (AUC = 0.79). It also correlated with in-hospital mortality (r = 0.193, p = 0.032) and showed moderate prognostic performance (AUC = 0.68). Higher index values were associated with greater mortality risk. Conclusions: This novel index, based on standard echocardiographic measurements, reflects both systolic dysfunction and pressure overload in AHF. Its correlation with NT-proBNP and in-hospital mortality highlights its potential as a practical, accessible bedside tool for early risk stratification, particularly when biomarker testing is unavailable or delayed. Full article

Tricuspid regurgitation (TR) represents a significant, often silently progressing, valvular heart disease with historically suboptimal management due to perceived high surgical risks. Transcatheter tricuspid valve interventions (TTVI) offer a promising, less invasive therapeutic avenue. Central to the success of TTVI is Right Ventricular Reverse Remodelling (RVRR), defined as an improvement in RV structure and function, which strongly correlates with enhanced patient survival. The right ventricle (RV) undergoes complex multi-scale biomechanical maladaptations, progressing from adaptive concentric to maladaptive eccentric hypertrophy, coupled with increased stiffness and fibrosis. Molecular drivers of this pathology include early failure of antioxidant defenses, metabolic shifts towards glycolysis, and dysregulation of microRNAs. Accurate RV function assessment necessitates advanced imaging modalities like 3D echocardiography, Cardiac Magnetic Resonance Imaging (CMR), and Computed Tomography (CT), along with strain analysis. Following TTVI, RVRR typically manifests as a biphasic reduction in RV volume overload, improved myocardial strain, and enhanced RV-pulmonary arterial coupling. Emerging molecular biomarkers alongside advanced imaging-derived biomechanical markers like CT-based 3D-TAPSE and RV longitudinal strain, are proving valuable. Artificial intelligence (AI) and machine learning (ML) are transforming prognostication by integrating diverse clinical, laboratory, and multi-modal imaging data, enabling unprecedented precision in risk stratification and optimizing TTVI strategies. Full article

An aorto-right ventricular fistula, a rare condition in humans, is characterized by communication between the ascending aorta and the right ventricle through a defect in the aortic wall. This report describes three cases of dogs with continuous murmurs: a 6-month-old Coton de Tulear, a 5-year-old Maltese, and a 6-month-old Jindo. Notably, all of the dogs presented with no severe clinical signs. Echocardiography revealed a turbulent jet through restrictive perimembranous ventricular septal defects (VSD) during systole and aorto-right ventricular fistulas secondary to ruptured sinuses of Valsalva aneurysm during diastole. In one case, a surgical closure of the VSD simultaneously resolved the aorto-right ventricular fistula. Follow-up echocardiography in the other two cases revealed mild left heart volume overload and a slight increase in the pulmonary-to-systemic blood flow ratio. However, the dogs remained asymptomatic. In conclusion, aorto-right ventricular fistulas with VSDs should be considered in the differential diagnosis of continuous murmurs in dogs. Full article

Pulmonary artery hypertension (PAH) is characterised by increased pulmonary vascular resistance (PVR) resulting in elevated pressure in the pulmonary artery supplying the pulmonary circulation. Disease of the right ventricle (RV) often manifests as a result of PAH placing excessive pressure on the right side of the heart. Although a relatively rare disease in humans, the impact of sustained PAH is severe, with poor outcomes even in treated individuals. As PAH develops, the blood flow is restricted through the pulmonary arteries and the right ventricle hypertrophies due to the increased strain of pumping blood through the pulmonary circulation. With time, RV hypertrophy progresses to right heart failure, impacting the supply of blood to the left ventricle and systemic circulation. Although right heart failure can currently be treated, it cannot be cured. There is therefore a need for more research into the physiological changes that cause the heart to fail under pressure overload. This review aims to evaluate the monocrotaline (MCT) rat model of PAH as a means of studying the cellular mechanisms associated with the development of RV hypertrophy and right heart failure. Full article

Pulmonary arterial hypertension (PAH) is a chronic disorder characterized by excessive pulmonary vascular remodeling, leading to elevated pulmonary vascular resistance and right ventricle (RV) overload and failure. MicroRNA-146a (miR-146a) promotes vascular smooth muscle cell proliferation and vascular neointimal hyperplasia, both hallmarks of PAH. This study aimed to investigate the effects of miR-146a through pharmacological or genetic inhibition on experimental PAH and RV pressure overload animal models. Additionally, we examined the overexpression of miR-146a on human pulmonary artery smooth muscle cells (hPASMCs). Here, we showed that miR-146a genic expression was increased in the lungs of patients with PAH and the plasma of monocrotaline (MCT) rats. Interestingly, genetic ablation of miR-146a improved RV hypertrophy and systolic pressures in Sugen 5415/hypoxia (SuHx) and pulmonary arterial banding (PAB) mice. Pharmacological inhibition of miR-146a improved RV remodeling in PAB-wild type mice and MCT rats, and enhanced exercise capacity in MCT rats. However, overexpression of miR-146a did not affect proliferation, migration, and apoptosis in control-hPASMCs. Our findings show that miR-146a may play a significant role in RV function and remodeling, representing a promising therapeutic target for RV hypertrophy and, consequently, PAH. Full article

Background: Modern treatments for transfusion-dependent β-thalassemia (TDβT) have allowed patients to reach high life expectancy with no iron overload. Despite survival improvement, atrial fibrillation (AF) has emerged as a relevant issue. AF pathophysiology and characteristics in TDβT are different than in the general population. Epicardial adipose tissue (EAT) may play a role but its relationship with AF in patients with TDβT has not been explored. Methods: A monocentric, cross-sectional study, enrolling consecutive patients with TDβT. Epicardial adipose tissue (EAT) was evaluated at magnetic resonance. Characteristics of patients with and without history of AF were investigated. Factors independently associated with AF prevalence were analyzed. Results: A total of 116 patients were enrolled. All patients were treated with regular chelation therapy. The prevalence of AF was 29.3% (34/116). Cardiac T2* and liver iron concentration were no different between patients with and without AF. EAT thickness was significantly higher in patients with AF at left atrium, right atrium and right ventricle (5.0 vs. 4.0 mm, p < 0.01, 4.4 vs. 4.0, p = 0.02 and 5.0 vs. 4.3, p = 0.04). Patients with AF presented with older age, (53 vs. 49 years, p < 0.01), more hypothyroidism (44.1 vs. 20.7%, p = 0.01), pulmonary hypertension (23.5 vs. 2.4% p < 0.01), splenectomy (88.2 vs. 64.6%, p = 0.01), higher right and left atrial volume (61 vs. 40 and 74 vs. 43 mL, both p < 0.01). At multivariable analysis, hypothyroidism, left atrial volume and left atrial EAT were independently associated with AF (odds ratio 9.95, 1.09 and 1.91, respectively). Conclusions: In a contemporary cohort of patients with TDβT, treated with regular chelation therapy, prevalence of AF was unrelated to iron overload. EAT was independently associated with AF. Full article

Cardiac fibrosis is a key aspect of heart failure, leading to reduced ventricular compliance and impaired electrical conduction in the myocardium. Various pathophysiologic conditions can lead to fibrosis in the left ventricle (LV) and/or right ventricle (RV). Despite growing evidence to support the transcriptomic heterogeneity of cardiac fibroblasts (CFs) in healthy and diseased states, there have been no direct comparisons of CFs in the LV and RV. Given the distinct natures of the ventricles, we hypothesized that LV- and RV-derived CFs would display baseline transcriptomic differences that influence their proliferation and differentiation following injury. Bulk RNA sequencing of CFs isolated from healthy murine left and right ventricles indicated that LV-derived CFs may be further along the myofibroblast transdifferentiation trajectory than cells isolated from the RV. Single-cell RNA-sequencing analysis of the two populations confirmed that Postn+ CFs were more enriched in the LV, whereas Igfbp3+ CFs were enriched in the RV at baseline. Notably, following pressure overload injury, the LV developed a larger subpopulation of pro-fibrotic Thbs4+/Cthrc1+ injury-induced CFs, while the RV showed a unique expansion of two less-well-characterized CF subpopulations (Igfbp3+ and Inmt+). These findings demonstrate that LV- and RV-derived CFs display baseline subpopulation differences that may dictate their diverging responses to pressure overload injury. Further study of these subpopulations will elucidate their role in the development of fibrosis and inform on whether LV and RV fibrosis require distinct treatments. Full article

In response to various stressors, cardiac chambers undergo structural remodeling. Long-term exposure of the right ventricle (RV) to pressure or volume overload leads to its maladaptive remodeling, associated with RV failure and increased mortality. While left ventricular adverse remodeling is well understood and therapeutic options are available or emerging, RV remodeling remains underexplored, and no specific therapies are currently available. Accumulating evidence implicates the role of mast cells in RV remodeling. Mast cells produce and release numerous inflammatory mediators, growth factors and proteases that can adversely affect cardiac cells, thus contributing to cardiac remodeling. Recent experimental findings suggest that mast cells might represent a potential therapeutic target. This review examines the role of mast cells in cardiac remodeling, with a specific focus on RV remodeling, and explores the potential efficacy of therapeutic interventions targeting mast cells to mitigate adverse RV remodeling. Full article

Background: Advances in the diagnosis and treatment of congenital heart diseases (CHDs) have resulted in improved survival rates for CHD patients. Up to 90% of individuals with mild CHD and 40% with complex CHD now reach the age of 60. Previous studies have indicated an elevated risk of atherosclerotic cardiovascular disease (ASCVD) and associated risk factors, morbidity, and mortality in adults with congenital heart disease (ACHD). However, there were no comprehensive guidelines for the prevention and management of acquired cardiovascular diseases (CVDs) in ACHD populations until recently. Case presentation: A 55-year-old man with Eisenmenger syndrome and comorbidities (arterial hypertension, heart failure, dyslipidemia, hyperuricemia, and a history of pulmonary embolism (PE)) presented with progressive breathlessness. The electrocardiogram (ECG) revealed signs of right ventricle (RV) hypertrophy and overload, while echocardiography showed reduced RV function, RV overload, and severe pulmonary hypertension (PH) signs, and preserved left ventricle (LV) function. After ruling out a new PE episode, acute coronary syndrome (ACS) was diagnosed, and percutaneous intervention was performed within 24–48 h of admission. Conclusions: This case highlights the importance of increased awareness of acquired heart diseases in patients with pulmonary hypertension due to CHD. Full article

Right ventricular failure (RVF) is often caused by increased afterload and disrupted coupling between the right ventricle (RV) and the pulmonary arteries (PAs). After a phase of adaptive hypertrophy, pressure-overloaded RVs evolve towards maladaptive hypertrophy and finally ventricular dilatation, with reduced stroke volume and systemic congestion. In this article, we review the concept of RV-PA coupling, which depicts the interaction between RV contractility and afterload, as well as the invasive and non-invasive techniques for its assessment. The current principles of RVF management based on pathophysiology and underlying etiology are subsequently discussed. Treatment strategies remain a challenge and range from fluid management and afterload reduction in moderate RVF to vasopressor therapy, inotropic support and, occasionally, mechanical circulatory support in severe RVF. Full article

Introduction: Pulmonary valve stenosis determines multiple effects on the right ventricular dimension and function. Percutaneous balloon valvuloplasty is the treatment of choice in severe pulmonary valve stenosis in patients of all ages. However, little is known regarding right ventricular function immediate changes after percutaneous balloon dilation. Pediatric patients with isolated pulmonary valve stenosis represent a pure clinical model of chronic RV pressure overload not affected by other confounders or comorbidities. Aim of the study: This study seeks to explore right ventricle (RV) mechanics in pediatric patients early after percutaneous balloon pulmonary valvuloplasty (BPV) for valvar pulmonary stenosis (PS). Materials and Methods: Forty-three pediatric patients (19 males), mean age 3.2 ± 4.9 years old, with severe pulmonary valve stenosis and indication for percutaneous balloon valvuloplasty were recruited. All patients underwent standard transthoracic echocardiography (TTE), and speckle-tracking echocardiography (STE) with an analysis of right ventricle free-wall longitudinal strain (RVFWLS) one day before and one day after the procedure. For each patient, we collected invasive parameters during the interventional procedure before and after BPV. Results: After the procedure, there was an immediate significant reduction in both peak-to-peak transpulmonary gradient (peak-to-peak PG) and ratio between the right ventricle and aortic systolic pressure (RV/AoP) with a drop of ∆29.3 ± 14.67 mmHg and ∆0.43 ± 0.03, respectively. Post-procedural echocardiography showed peak and mean transvalvar pressure gradient drop (∆50 ± 32.23 and ∆31 ± 17.97, respectively). The degree of pulmonary valve regurgitation was mild in 8% of patients before the procedure, affecting 29% of our patients post-BPV (p = 0.007). The analysis of right ventricular mechanics showed a significant improvement of fractional area change (FAC) immediately after BPV (40.11% vs. 44.42%, p = 0.01). On the other hand, right ventricular longitudinal systolic function parameters, TAPSE and global RVFWLS, did not improve significantly after intervention. The segmental analysis of the RVFWLS showed a significant regional increase in the myocardial deformation of the apical segments. Conclusions: Percutaneous BPV represents an efficient and safe procedure to relieve severe pulmonary valve stenosis. The analysis of the right ventricular function on echocardiography demonstrated an immediate global systolic function improvement, while longitudinal systolic function was persistently impaired 24 h after intervention, possibly due to the necessity of a longer recovery time. Full article

This study analyzed microarray data of right ventricular (RV) tissue from rats exposed to pulmonary embolism to understand the initial dynamic transcriptional response to mechanical stress and compare it with experimental pulmonary hypertension (PH) models. The dataset included samples harvested from 55 rats at 11 different time points or RV locations. We performed principal component analysis (PCA) to explore clusters based on spatiotemporal gene expression. Relevant pathways were identified from fast gene set enrichment analysis using PCA coefficients. The RV transcriptomic signature was measured over several time points, ranging from hours to weeks after an acute increase in mechanical stress, and was found to be highly dependent on the severity of the initial insult. Pathways enriched in the RV outflow tracts of rats at 6 weeks after severe PE share many commonalities with experimental PH models, but the transcriptomic signature at the RV apex resembles control tissue. The severity of the initial pressure overload determines the trajectory of the transcriptomic response independent of the final afterload, but this depends on the location where the tissue is biopsied. Chronic RV pressure overload due to PH appears to progress toward similar transcriptomic endpoints. Full article