Gene expression data from left ventricular free wall of male adult Macaca fascicularis with and without chronic atrioventricular block
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PROVIDER: PRJNA822304 | ENA |
REPOSITORIES: ENA
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Project description:We studied time course of pathological remodeling occurring in the hearts of cynomolgus monkey, Macaca fascicularis against atrioventricular block condition. We used microarrays to detail the pathological changes in the hearts which had obtained sensitivity for detecting dl-sotalol-induced TdP by 7th month after the production of atrioventricular block.
2023-01-05 | GSE199943 | GEO
Project description:Goals of this study were to identify new candidates involved in the development of the Atrioventricular cushions in the mouse heart. Experiment Overall Design: The atrioventricular junction and ventricular region were dissected from 80 embryonic day 10.5-11.0, wild type, C57BL/6 mouse hearts. RNA was isolated from the respective regions, amplified using the Arcturus RiboAmp HS RNA amplification kit, and hybridized to Affymetrix MOE430A expression chips in duplicate. Comparison between atrioventricular gene expression and ventricular gene expression will allow for the identification of genes necessary in the development of the AV cushions.
2008-06-13 | E-GEOD-4903 | biostudies-arrayexpress
Project description:Hypereosinophilic syndrome is a progressive disease with extensive eosinophilia that results in organ damage. Patients suffer from frequent cardiac pathologies and a high mortality rate. A better understanding of the mechanisms of eosinophil-mediated tissue damage would benefit the development of new therapies. Here, we describe the cardiac pathologies that develop in a mouse model of hypereosinophilic syndrome. These IL-5 transgenic mice exhibited decreased left ventricular function already at a young age. Cardiac function worsened with age and heart weight increased. Moreover, hypereosinophilic mice developed different pathologies of the cardiac conductive system, including 2nd degree atrioventricular block and atrioventricular reentry. Cardiomyocytes from IL-5 transgenic mice showed reduced contractility. Despite immune infiltrates in the lungs, doppler echocardiography revealed no signs of pulmonary hypertension in these mice. Mechanistically, we demonstrated eosinophil infiltration of the heart tissue that lead to an inflammatory environment. Eosinophils were 100-fold more abundant in the hearts of hypereosinophilic mice than controls. Gene expression signatures showed tissue damage as well as repair and remodeling processes. Our results suggest that hypereosinophilia leads to infiltration of the heart tissue by eosinophils and tissue damage. The ongoing remodeling and repair processes are insufficient or maladapted to maintain heart function resulting in progressive deterioration.
2023-10-25 | GSE185300 | GEO
Project description:Human left ventricular free wall heart tissue was obtained from end-stage heart failure patients at the moment of heart transplantation Left ventricular free wall samples were also obtained from healthy hearts of organ donors, which were not used for transplantation due to size mismatch with available recipients.
2017-09-30 | GSE84796 | GEO
Project description:Tissue-resident macrophages abound in the distal atrioventricular (AV) node of the heart, electrically couple to conducting cardiomyocytes via Connexin (Cx) 43-containing gap junctions and are implicated in normal and aberrant cardiac conduction. Moreover, conditional deletion of Cx43 in macrophages (tamoxifen-inducible Cx3cr1 Cx43-/- mice) delays AV conduction and acute depletion of macrophages in Cd11bDTR mice induces progressive AV block.
2017-04-20 | GSE86306 | GEO
Project description:An 86-year-old man with unremarkable clinical history complaining of asthenia and dyspnea was diagnosed with low-flow low-gradient aortic stenosis [LFLG-AS; left ventricular ejection fraction (LVEF) 40% and transaortic mean gradient 37 mmHg, increasing to 52% and 55 mmHg after dobutamine infusion]. The patient underwent transcatheter aortic valve implantation (TAVI; Edwards CENTERA™ 29, Irvine, CA, USA). The procedure and the following hospital stay were free from complications, with no changes on electrocardiography (ECG). Six months later, few syncopal episodes occurred. No signs of orthostatic hypotension or neurologic disorders were present. Echocardiography showed normal functioning of the prosthetic valve and recovery of LV systolic function (LVEF 55%). Baseline ECG and 24-h Holter monitoring were unremarkable. An implantable loop recorder (ILR) was implanted to verify the occurrence of paroxysmal conduction disturbances. One month later, during a syncopal episode, ILR interrogation showed a complete atrioventricular (AV) block. Therefore, a dual chamber, single lead pacemaker was implanted. We are providing the first report of complete AV block occurring months after TAVI, possibly because of reverse LV remodeling following TAVI, with ensuing relative oversizing of the prosthetic valve. This possibility should be considered in patients with syncope not otherwise explained, and previous TAVI, especially in cases of LFLG-AS. <Learning objective: Complete atrioventricular block can occur even months after transcatheter aortic valve implantation (TAVI), possibly because of left ventricular reverse remodeling following valve replacement, with ensuing relative valve oversizing. This possibility should be considered in patients with syncope not otherwise explained, and previous TAVI, especially in cases of low flow low gradient aortic stenosis. Loop recorder implantation should be considered in this group of patients.>.
| S-EPMC6149591 | biostudies-literature
Project description:Rationale: The atrioventricular conduction system controls ventricular activation and is delineated by expression of Tbx3. Genome-wide association studies identified genetic variants near TBX3 associated with conduction velocities (PR interval and QRS duration), suggesting minor changes in TBX3 dose affect conduction system function. Objective: To assess whether and how Tbx3 dose reduction affects the integrity of the atrioventricular conduction system. Methods and Results: Electrocardiograms revealed a PR interval shortening and prolonged QT interval and QRS duration in heterozygous Tbx3 mutants compared to wild-types. We observed that the atrioventricular bundle and proximal bundle branches of Tbx3+/- mice after birth became hypoplastic, whereas the size of the atrioventricular node was not affected. The transcriptomes of wild-type and Tbx3+/- atrioventricular nodes were analyzed using BAC-Tbx3-Egfp mice enabling specific isolation of the atrioventricular node by laser capture microdissection followed by RNA-sequencing. Hundreds of genes were slightly but consistently deregulated. Cross-referencing with transcriptome data of isolated cardiomyocytes of the conduction system and chamber myocardium derived from Tbx3+/Venus;BAC-Nppb-Katushka hearts revealed that a set of chamber-enriched genes, including Kcne1 (MinK), Ryr2, and Scn5a, were upregulated in Tbx3+/- atrioventricular nodes, whereas conduction system-enriched genes, including Hcn4 and Cacna2d2, were downregulated. We performed ATAC-sequencing on purified fetal Tbx3+ atrioventricular cardiomyocytes to identify potential atrioventricular-specific regulatory DNA elements on a genome-wide scale, and identified regulatory elements mediating the Tbx3-dependent regulation of Ryr2 and other target genes in the atrioventricular node. Conclusions: Tbx3 dose reduction results in deregulation of a large number of genes affecting the electrical properties of the atrioventricular node and causes failure to maintain the structural integrity of the atrioventricular bundle. These data provide a mechanism underlying differences in PR interval and QRS duration in individuals carrying associated variants in the TBX3 locus.
2019-10-18 | GSE121464 | GEO
Project description:Rationale: The atrioventricular conduction system controls ventricular activation and is delineated by expression of Tbx3. Genome-wide association studies identified genetic variants near TBX3 associated with conduction velocities (PR interval and QRS duration), suggesting minor changes in TBX3 dose affect conduction system function. Objective: To assess whether and how Tbx3 dose reduction affects the integrity of the atrioventricular conduction system. Methods and Results: Electrocardiograms revealed a PR interval shortening and prolonged QT interval and QRS duration in heterozygous Tbx3 mutants compared to wild-types. We observed that the atrioventricular bundle and proximal bundle branches of Tbx3+/- mice after birth became hypoplastic, whereas the size of the atrioventricular node was not affected. The transcriptomes of wild-type and Tbx3+/- atrioventricular nodes were analyzed using BAC-Tbx3-Egfp mice enabling specific isolation of the atrioventricular node by laser capture microdissection followed by RNA-sequencing. Hundreds of genes were slightly but consistently deregulated. Cross-referencing with transcriptome data of isolated cardiomyocytes of the conduction system and chamber myocardium derived from Tbx3+/Venus;BAC-Nppb-Katushka hearts revealed that a set of chamber-enriched genes, including Kcne1 (MinK), Ryr2, and Scn5a, were upregulated in Tbx3+/- atrioventricular nodes, whereas conduction system-enriched genes, including Hcn4 and Cacna2d2, were downregulated. We performed ATAC-sequencing on purified fetal Tbx3+ atrioventricular cardiomyocytes to identify potential atrioventricular-specific regulatory DNA elements on a genome-wide scale, and identified regulatory elements mediating the Tbx3-dependent regulation of Ryr2 and other target genes in the atrioventricular node. Conclusions: Tbx3 dose reduction results in deregulation of a large number of genes affecting the electrical properties of the atrioventricular node and causes failure to maintain the structural integrity of the atrioventricular bundle. These data provide a mechanism underlying differences in PR interval and QRS duration in individuals carrying associated variants in the TBX3 locus.
2019-10-18 | GSE121244 | GEO
Project description:Human left ventricular free wall heart tissue was obtained from end-stage heart failure patients at the moment of heart transplantation
2018-03-08 | GSE111544 | GEO
Project description:Background: Left bundle branch area pacing (LBBAP) is a novel pacing modality with stable pacing parameters and a narrow-paced QRS duration. We compared heart failure (HF) hospitalization events and echocardiographic measures between LBBAP and right ventricular pacing (RVP) in patients with atrioventricular block (AVB). Methods and Results: This multicenter observational study prospectively recruited consecutive AVB patients requiring ventricular pacing in five centers if they received LBBAP or RVP and had left ventricular ejection fraction (LVEF) >50%. Data on electrocardiogram, pacing parameters, echocardiographic measurements, device complications, and clinical outcomes were collected at baseline and during follow-up. The primary outcome was first episode hospitalization for HF or upgrade to biventricular pacing. LBBAP was successful in 235 of 246 patients (95.5%), while 120 patients received RVP. During a mean of 11.4 ± 2.7 months of follow-up, the ventricular pacing burden was comparable (83.9 ± 35.1 vs. 85.7 ± 30.0%), while the mean LVEF differed significantly (62.6 ± 4.6 vs. 57.8 ± 11.4%) between the LBBAP and RVP groups. Patients with LBBAP had significantly lower occurrences of HF hospitalization and upgrading to biventricular pacing than patients with RVP (2.6 vs. 10.8%, P <0.001), and differences in primary outcome between LBBAP and RVP were mainly observed in patients with ventricular pacing >40% or with baseline LVEF <60%. The primary outcome was independently associated with LBBAP (adjusted HR 0.14, 95% CI: 0.04-0.55), previous myocardial infarction (adjusted HR 6.82, 95% CI: 1.23-37.5), and baseline LVEF (adjusted HR 0.91, 95% CI: 0.86-0.96). Conclusion: Permanent LBBAP might reduce the risk of HF hospitalization or upgrade to biventricular pacing compared with RVP in AVB patients requiring a high burden of ventricular pacing. Clinical Trial Registration: URL: https://www.clinicaltrials.gov; Unique identifier: NCT03851315; URL: http://www.chictr.org.cn; Unique Identifier: ChiCTR2100043296.
| S-EPMC8297826 | biostudies-literature