scholarly journals The Changes of Gene Expression and Protein Level of Stretch-Activated Chloride Channel in Atrial Myocardium of Dogs with Atrial Fibrillation

2021 ◽  
Vol 24 (5) ◽  
pp. E877-E881
Author(s):  
Hongwei Shi ◽  
Zhenming Jiang ◽  
Teng Wang ◽  
Yuting Chen ◽  
Desheng Hu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Heart Failure ◽  
Atrial Fibrillation ◽  
Right Ventricular ◽  
Protein Level ◽  
Left Atrial ◽  
Left Ventricular ◽  
Control Group ◽  
Atrial Myocardium ◽  
Failure Group

Introduction: ICl,stretch have been reported to be involved in the development of atrial fibrillation, so we observed the changes of transcription and translation levels of ICl,stretch in isolated atrial myocardium of heart failure canine models. Material and methods: In the control group (N = 10), five dogs were untreated and the other five received sham operation, while dogs in the heart failure group (N = 10) were implanted with cardiac pacemakers and underwent right ventricular pacing to induce heart failure. Cardiac structure and function were evaluated. The gene expression and protein level of ICl,stretch in the left atrial appendage were detected. Results: The left atrial diameter, right atrial dimension, left ventricular diastolic dimension, and right ventricular diastolic dimension were significantly larger in the heart failure group (P < 0.05). In contrast, the ejection fraction and the left ventricular shorten fraction were higher in the control group (P < 0.05). Both the mRNA and protein expression levels of ICl,stretch in atrial myocardium of the heart failure group were significantly higher compared with the control group. Conclusion: ICl,stretch might play an important role in the vulnerability to atrial fibrillation in dilated atria with heart failure and could be a potential therapeutic target for atrial fibrillation.

scholarly journals Analysis of Genes Involved in Persistent Atrial Fibrillation: Comparisons of ‘Trigger’ and ‘Substrate’ Differences

2018 ◽  
Vol 47 (3) ◽  
pp. 1299-1309 ◽  
Author(s):  
Rongjun Zou ◽  
Minglei Yang ◽  
Wanting Shi ◽  
Chengxi Zheng ◽  
Hui Zeng ◽  
...  
Keyword(s):  
Gene Expression ◽  
Atrial Fibrillation ◽  
Signaling Pathways ◽  
Differential Expression ◽  
Microarray Data ◽  
Left Atrial ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Genetic Traits ◽  
Receptor Interactions

Background/Aims: Recent research has improved our understanding of the pulmonary vein and surrounding left atrial (LA-PV) junction and the left atrial appendage (LAA), which are considered the ‘trigger’ and ‘substrate’ in the development of atrial fibrillation (AF), respectively. Herein, with the aim of identifying the underlying potential genetic mechanisms, we compared differences in gene expression between LA-PV junction and LAA specimens via bioinformatic analysis. Methods: Microarray data of AF (GSE41177) were downloaded from the Gene Expression Omnibus database. In addition, linear models for microarray data limma powers differential expression analyses and weighted correlation network analysis (WGCNA) were applied. Results: From the differential expression analyses, 152 differentially expressed genes and hub genes, including LEP, FOS, EDN1, NMU, CALB2, TAC1, and PPBP, were identified. Our analysis revealed that the maps of extracellular matrix (ECM)-receptor interactions, PI3K-Akt and Wnt signaling pathways, and ventricular cardiac muscle tissue morphogenesis were significantly enriched. In addition, the WGCNA results showed high correlations between genes and related genetic clusters to external clinical characteristics. Maps of the ECM-receptor interactions, chemokine signaling pathways, and the cell cycle were significantly enriched in the genes of corresponding modules and closely associated with AF duration, left atrial diameter, and left ventricular ejection function, respectively. Similarly, mapping of the TNF signaling pathway indicated significant association with genetic traits of ischemic heart disease, hypertension, and diabetes comorbidity. Conclusions: The ECM-receptor interaction as a possible central node of comparison between LA-PV and LAA samples reflected the special functional roles of ‘triggers’ and ‘substrates’ and may be closely associated with AF duration. Furthermore, LEP, FOS, EDN1, NMU, CALB2, TAC1, and PPBP genes may be implicated in the occurrence and maintenance of AF through their interactions with each other.

P1766Clinical impact of atrial fibrillation and heart failure in a cohort of patients with hypertrophic cardiomyopathy

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
I Esteve Ruiz ◽  
H Llamas Gomez ◽  
I M Esteve Ruiz ◽  
M J Romero Reyes ◽  
R Pavon Jimenez ◽  
...  
Keyword(s):  
Risk Factors ◽  
Heart Failure ◽  
Atrial Fibrillation ◽  
Hypertrophic Cardiomyopathy ◽  
Left Atrial ◽  
Left Ventricular ◽  
Left Atrial Diameter ◽  
Myocardial Thickness ◽  
Worse Prognosis ◽  
Echocardiographic Findings

Abstract Background Atrial fibrillation (AF) and heart failure (HF) are common complications in Hypertrophic Cardiomyopathy (HCM) patients, leading to a worsening of their quality of life, need of hospitalization and prognosis. Purpose To analyze clinical variables associated with the presence of AF and HF in HCM patients. Methods HCM patients followed-up in cardiological visits from 2005 to 2017 were included and a descriptive analysis of those with AF and HF was performed. Results Out of 168 patients, 28% had reported AF. They were older than those without arrhythmia (68±15 years (yrs) vs 56±20 yrs, p<0.001) and had more comorbidities such as diabetes (27.7% vs 12.4%, p=0.02) and chronic renal disease (21.3% vs 6.6%, p=0.006). Echocardiographic findings are summarized in Table 1. In our cohort, 27.4% of the patients had HF with a functional class according to the New York Heart Association criteria ≥2. They were older than those without HF (69.3±11.6 yrs vs 55.9±20.6 yrs, p<0.001) and had higher rate of cardiovascular (CV) risk factors such as hypertension (65.2% vs 44.3%, p=0.015). The presence of HF was directly associated with the presence of AF: 52.2% of the patients with HF and 18.9% of the patients without HF developed this arrhythmia (p<0.001). HF patients associated larger left atrial diameter (48±8.1 vs 41.6±7.2mm, p<0.001), myocardial thickness (21.7±3.9 vs 19.2±5.8mm, p=0.002) and higher left ventricular outflow obstruction (LVOO) (55±32 vs 34.3±31.3mmHg, p=0.021), without any differences in the left ventricular ejection fraction. HF patients had a worse prognosis (Picture 1). Multivariate analysis showed that the presence of AF (OR 2.6, CI 95% 1.1–6.3) and LVOO (OR 4.8, CI 95% 1.5–14.8) were independent risk factors of developing HF. Table 1. Echocardiographic findings AF (n=47) Non AF (n=121) p LVOO 27.7 19 0.22 Aortic regurgitation 12.8 3.3 0.02 Mitral regurgitation 27.7 12.4 0.02 Left atrial diameter (mm) 48.8±7.2 40.7±7 <0.001 Myocardial thickness (mm) 20±5.4 19±5.2 0.02 Qualitative variables are expressed as percentages (%) and quantitative variables as mean and standard deviation (M ± SD). Picture 1. Main outcomes of HF patients Conclusions AF and HF were directly associated in our cohort, especially in elderly patients with higher comorbidities, leading to a worse prognosis with a higher hospitalization rate and CV death. This emphasizes the importance of a thorough search of both complications in order to initiate early treatment and improve the prognosis of HCM patients.

scholarly journals Game changer? A sporting indication to implant a left atrial appendage closure device in a rugby player with atrial fibrillation: a case report

2020 ◽  
Vol 4 (1) ◽  
pp. 1-5
Author(s):  
Andre Briosa e Gala ◽  
Andrew Cox ◽  
Michael Pope ◽  
Timothy Betts
Keyword(s):  
Heart Failure ◽  
Atrial Fibrillation ◽  
Left Atrial ◽  
Left Atrial Appendage ◽  
Left Ventricular ◽  
Atrial Appendage ◽  
Rugby Player ◽  
Management Options ◽  
Left Atrial Appendage Occlusion ◽  
Occlusion Device

Abstract Background Caring for athletes with cardiac disease requires an approach that caters to the specific needs of the athlete. Case summary A 27-year-old professional rugby player was admitted with decompensated heart failure and atrial fibrillation (AF). Transthoracic echocardiogram showed features in keeping with a dilated cardiomyopathy with severe left ventricular (LV) systolic impairment. He made good progress on evidence-based heart failure medication and his LV systolic function returned to normal. He failed to maintain sinus rhythm with cardioversion and remained in persistent AF. He then suffered a transient ischaemic attack despite appropriate anticoagulation. At 1-year follow-up, he was asymptomatic and against medical advice continued to play competitive rugby whilst taking rivaroxaban. He subsequently underwent implantation with a percutaneous left atrial appendage occlusion device, allowing him to discontinue anticoagulation, reduce his bleeding risk and resume his career, whilst simultaneously lowering the thromboembolic risk. Discussion Counselling should include different management options aimed at minimizing the risks to athletes if they to return to competitive sports. Left atrial appendage occlusion devices are a suitable AF-related stroke prevention strategy in athletes competing in full-contact sports.

scholarly journals Elevated Swelling-Activated Chloride Current Densities in Hypertrophied Ventricular Myocytes in a Rabbit Heart Failure Model

2019 ◽  
Vol 22 (2) ◽  
pp. E107-E111
Author(s):  
Hongwei Shi ◽  
Zhenming Jiang ◽  
Teng Wang ◽  
Yongting Chen ◽  
Feng Cao
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Protein Expression ◽  
Diastolic Pressure ◽  
Rabbit Model ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Control Group ◽  
Sham Operation ◽  
Failure Group

Background: The status of the swelling-activated chloride channel (ICl, swell) during heart failure remains unclear. This study aimed to investigate whether the ICl, swell activity is altered during heart failure and to determine how the ICl, swell influences atrial arrhythmias of the failing heart. Methods: We established a heart failure rabbit model and analyzed the hemodynamic indicators 8 weeks after myocardial infarction, which include left ventricular systolic pressure (LVSP) and left ventricular end-diastolic pressure (LVDEP). Five untreated rabbits and 5 receiving a sham operation served as the control group. Left auricular appendage tissues were obtained and CLCN3 mRNA/CLCN3 protein expression levels were examined by using reverse transcription–polymerase chain reaction and Western blot, respectively. Results: Compared to the control group, the heart failure group showed a significantly decreased LVSP (14.2 ± 0.27 versus 16.9 ± 0.86 kPa, P <.05)and elevated LVDEP (2.49 ± 0.30 versus 0.15 ± 0.03 kPa, P <.05), indicating that myocardial infarction leads to progressive heart failure of rabbits in the heart failure group. CLCN3 mRNA and CLCN3 protein expression were both significantly elevated in the heart failure group compared to the control group (P <.05). Conclusion: In sum, we propose that the dynamic nature of ICl, swell upregulation may contribute to the elevated expression of CLCN3 mRNA and CLCN3 protein, resulting in myocardial cell remodeling induced by heart failure. However, further study is needed to investigate the potential functions of ICl, swell, especially the relation between ICl, swell augmentation and arrhythmia after heart failure.

scholarly journals Risk Factors Contributing to the Progression of Paroxysmal and Persistent Atrial Fibrillation in Heart Failure Patients with Mid-Range Ejection Fraction

2021 ◽  
Author(s):  
Lusine Hazarapetyan ◽  
Lyudmila Budaghyan ◽  
Alina Maloyan ◽  
Svetlana Grigoryan
Keyword(s):  
Risk Factors ◽  
Heart Failure ◽  
Atrial Fibrillation ◽  
Ejection Fraction ◽  
Transforming Growth Factor ◽  
Ventricular Remodeling ◽  
Hypertensive Crisis ◽  
Left Ventricular ◽  
Control Group ◽  
Increased Risk

Aims: Heart failure (HF) is frequently accompanied by atrial fibrillation (AF), a combination that worsens the outcomes of both diseases. Despite advances in the treatment of AF, it remains a serious and unsolved problem for clinicians and researchers. The aim of this study was to examine risk factors for incidents of paroxysmal and persistent AF in patients having heart failure with mid-range ejection fraction (HFmrEF). Methods. Overall, 71 patients with HFmrEF and non-valvular AF, including paroxysmal and persistent types, were enrolled in this study. As a control group, 42 HFmrEF patients without AF were also enrolled. All patients underwent detailed physical examination, including resting electrocardiography, echocardiography, and 24-hour ambulatory Holter monitoring. Levels of the inflammation markers high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), and tumor necrosis factor α (TNF-α) and the fibrotic marker transforming growth factor-β1 (TGF-β1) were measured by ELISA and expressed as odds ratios. Results: We show that paroxysmal AF was associated with higher diastolic blood pressure, whereas both paroxysmal and persistent forms of AF were associated with more frequent occurrence of hypertensive crisis episodes and greater body mass index. Progression from paroxysmal to persistent AF was associated with significant ventricular remodeling. Persistent and paroxysmal AF were associated with higher levels of inflammatory markers when compared to HFmrEF patients having no AF. In addition, TGF-1 was significantly increased in HFmrEF patients having persistent but not paroxysmal AF. Conclusions: Occurrence of AF, first paroxysmal and then persistent, in HFmrEF patients is associated with left ventricular remodeling and the appearance of systemic inflammatory and fibrotic markers. Changes in those parameters may be indicators by which to identify patients at increased risk of atrial fibrillation. Further studies are needed to determine the prognostic validity of these markers.

scholarly journals Transitioning from Preclinical to Clinical Heart Failure with Preserved Ejection Fraction: A Mechanistic Approach

2020 ◽  
Vol 9 (4) ◽  
pp. 1110 ◽  
Author(s):  
Antoni Bayes-Genis ◽  
Felipe Bisbal ◽  
Julio Núñez ◽  
Enrique Santas ◽  
Josep Lupón ◽  
...  
Keyword(s):  
Heart Failure ◽  
Pulmonary Hypertension ◽  
Ejection Fraction ◽  
Right Ventricular ◽  
Left Atrial ◽  
Interstitial Fibrosis ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Preserved Ejection Fraction ◽  
Ventricular Ejection Fraction

To better understand heart failure with preserved ejection fraction (HFpEF), we need to better characterize the transition from asymptomatic pre-HFpEF to symptomatic HFpEF. The current emphasis on left ventricular diastolic dysfunction must be redirected to microvascular inflammation and endothelial dysfunction that leads to cardiomyocyte remodeling and enhanced interstitial collagen deposition. A pre-HFpEF patient lacks signs or symptoms of heart failure (HF), has preserved left ventricular ejection fraction (LVEF) with incipient structural changes similar to HFpEF, and possesses elevated biomarkers of cardiac dysfunction. The transition from pre-HFpEF to symptomatic HFpEF also involves left atrial failure, pulmonary hypertension and right ventricular dysfunction, and renal failure. This review focuses on the non-left ventricular mechanisms in this transition, involving the atria, right heart cavities, kidneys, and ultimately the currently accepted driver—systemic inflammation. Impaired atrial function may decrease ventricular hemodynamics and significantly increase left atrial and pulmonary pressure, leading to HF symptoms, irrespective of left ventricle (LV) systolic function. Pulmonary hypertension and low right-ventricular function are associated with the incidence of HF. Interstitial fibrosis in the heart, large arteries, and kidneys is key to the pathophysiology of the cardiorenal syndrome continuum. By understanding each of these processes, we may be able to halt disease progression and eventually extend the time a patient remains in the asymptomatic pre-HFpEF stage.

Abstract 2439: Invasive Right Ventricular Hemodynamics and Tricuspid Annular Plane Systolic Excursion to Predict Right Ventricular Dysfunction After Left Ventricular Assist Device Implantation

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Elizabeth A Ketner ◽  
Paul R Forfia ◽  
Stuart R Russell ◽  
Ilan S Wittstein ◽  
John V Conte ◽  
...  
Keyword(s):  
Heart Failure ◽  
Right Ventricular ◽  
Left Ventricular ◽  
Ventricular Assist ◽  
Failure Group ◽  
Group I ◽  
Left Ventricular Assist ◽  
Patients With Heart Failure ◽  
Pulmonary Arterial ◽  
Rv Function

Introduction : Right ventricular (RV) failure is a major cause of morbidity and mortality in heart failure patients undergoing destination left ventricular assist device (LVAD) implantation. Using tricuspid annular plane systolic excursion (TAPSE; an echo based measure of RV function linked to mortality in patients with pulmonary arterial hypertension) and invasive measurement of RV systolic function (dP/dtmax/IP; dP/dt max normalized to instantaneous pressure) we hypothesized that these parameters correlate with the incidence of RV failure post LVAD implantation. Methods : 65 consecutive patients with heart failure and clinical indication for LVAD implantation were prospectively evaluated. All patients underwent transthoracic echocardiography and right heart catheterization within 14 days prior to implantation. TAPSE was measured by M-mode echocardiography as the mean displacement (cm) of the tricuspid annular plane towards the RV apex from end-diastole to end-systole over 3 to 5 cycles. RVFAC was measured as the percent change in RV area from end diastole to end systole as measured in the apical four chamber view. Pressure-dependent measures of RV function were derived from PA catheterization based RV waveforms analyzed using pressure volume loop software (WinPVAN 3.5.8). RV failure post LVAD was defined as IV inotrope therapy requirement >14 days, inhaled NO use >48 hrs, death due to decompensated RV failure, or RVAD implantation. Clinical, hemodynamic and echo data were compared in patients with RV Failure (group I; n=14) vs. those without RV failure (group II; n=51). Results : Groups I and II had similar mean pulmonary arterial pressure, cardiac index, systolic blood pressure, baseline liver function test values, and renal function (P>0.05). Group I had higher right atrial pressure (14±5vs.11±4 mmHg; *p<0.05). TAPSE of less than 1.8 cm and dP/dt max /IP of less than 10 correlated strongly with RV failure post LVAD implantation (P<0.005 and P<0.001, respectively) while RVFAC showed no correlation. Conclusions : TAPSE and the load-independent index dP/dt max/IP correlate strongly with RV failure post-LVAD implantation. These data provide the basis for future study of these endpoints in patients with heart failure and RV dysfunction.

Experimental studies of atrial fibrillation: a comparison of two pacing models

2008 ◽  
Vol 294 (3) ◽  
pp. H1206-H1215 ◽  
Author(s):  
Gabriel Laurent ◽  
Gordon Moe ◽  
Xudong Hu ◽  
Howard Leong-Poi ◽  
Kim A. Connelly ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Left Atrial ◽  
Experimental Studies ◽  
Severe Heart Failure ◽  
Left Ventricular ◽  
Control Group ◽  
Type Iii Collagen ◽  
Atrial Remodeling ◽  
Venous Flow ◽  
Group 2

Rapid ventricular pacing (RVP) is a well-established animal model of atrial fibrillation (AF). However, this model is limited by a high mortality rate and severe heart failure. The purpose of our study was to assess a new canine model of inducible AF. We performed acute, short-term, simultaneous atrioventricular pacing (SAVP) and RVP (in random order) in 14 dogs for 30 s. SAVP produced more echocardiographic pulmonary venous flow reversal, a greater increase in mean pulmonary capillary wedge pressure, and a significantly greater decrease in left atrial emptying function (−84.4 ± 38.6% vs. −23.7 ± 27.1%, P < 0.05) than RVP. Thirty dogs were randomized to three, longer-term, study groups: eight dogs in the control group (no pacing), eight dogs in the RVP group (2 wk at 240 beats/min followed by 3 wk at 220 beats/min), and fourteen dogs in the SAVP group (2 wk at 220 beats/min). SAVP induced less left ventricular dysfunction but more left atrial dysfunction than RVP. SAVP dogs had similar atrial effective refractory periods as RVP dogs but more heterogeneity in conduction and more AF inducibility (83% vs. 40%, P < 0.05) and maintenance (median 1,660 vs. 710 s, P < 0.05) than RVP dogs. SAVP induced more collagen turnover and was associated with a significantly greater increase in type III collagen in the atria compared with RVP dogs (6.9 ± 1.5 vs. 4.8 ± 1.6, respectively, P < 0.05 vs. 1.1 ± 0.7 in unpaced control dogs). In conclusion, the SAVP model induced profound mechanical and substrate atrial remodeling and reproducible sustained AF. This new model is clinically relevant and may be useful for testing AF interventions.

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