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225 results for “Dilated Cardiomyopathy”
Clinical Considerations for a Family with Dilated Cardiomyopathy, Sudden Cardiac Death, and a Novel TTN Frameshift Mutation.
<p>Figures from Micaglio E, Monasky MM, Bernardini A, Mecarocci V, Borrelli V, Ciconte G, Locati ET, Piccoli M, Ghiroldi A, Anastasia L, Pappone C. Clinical Considerations for a Family with Dilated Cardiomyopathy, Sudden Cardiac Death, and a Novel <em>TTN</em> Frameshift Mutation. Int J Mol Sci. 2021 Jan 12;22(2):670. doi: 10.3390/ijms22020670. PMID: 33445410; PMCID: PMC7826882.</p> <p>Abstract</p> <p>Dilated cardiomyopathy (DCM) is the leading indication for heart transplantation. <em>TTN</em> gene truncating mutations account for about 25% of familial DCM cases and for 18% of sporadic DCM cases. The clinical relevance of specific variants in <em>TTN</em> has been difficult to determine because of the sheer size of the protein for which <em>TTN</em> encodes, as well as existing extensive genetic variation. Clinicians should communicate novel clinically-relevant variants and genotype-phenotype associations, so that animal studies evaluating the molecular mechanisms are always conducted with a focus on clinical significance. In the present study, we report for the first time the novel truncating heterozygous variant NM_001256850.1:c.72777_72783del (p.Phe24259Leufs*51) in the <em>TTN</em> gene and its association with DCM in a family with sudden death. This variant occurs in the A-band region of the sarcomere, in a known mutational hotspot of the gene. Truncating titin variants that occur in this region are the most common cause of DCM and have been rarely reported in asymptomatic individuals, differently from other pathogenic <em>TTN</em> gene variants. Further studies are warranted to better understand this particular clinically-relevant variant.</p>
The dilated cardiomyopathy-associated RNA Binding Motif Protein 20 regulates long pre-mRNAs in neurons [seCLIP-Seq]
GEO Series GSE250098. Mus musculus. 10 samples. Type: Other.
LncRNA DCRT protects against dilated cardiomyopathy via binding to PTBP1 (Iso-seq)
GEO Series GSE243738. Homo sapiens. 2 samples. Type: Expression profiling by high throughput sequencing.
Dilated Cardiomyopathy
GEO Series GSE241120. Mesocricetus auratus; Homo sapiens; Mus musculus. 17 samples. Type: Expression profiling by high throughput sequencing.
Data set from the article Petrini M, Alì M, Cannaò PM, Zambelli D, Cozzi A, Codari M, Malavazos AE, Secchi F, Sardanelli F. Epicardial adipose tissue volume in patients with coronary artery disease or non-ischaemic dilated cardiomyopathy: evaluation with cardiac magnetic resonance imaging. Clin Radiol. 2019 Jan;74(1):81.e1-81.e7. doi: 10.1016/j.crad.2018.09.006. Epub 2018 Oct 15. PMID: 30336943.
<p>Data set from the article Petrini M, Alì M, Cannaò PM, Zambelli D, Cozzi A, Codari M, Malavazos AE, Secchi F, Sardanelli F. Epicardial adipose tissue volume in patients with coronary artery disease or non-ischaemic dilated cardiomyopathy: evaluation with cardiac magnetic resonance imaging. Clin Radiol. 2019 Jan;74(1):81.e1-81.e7. doi: 10.1016/j.crad.2018.09.006. Epub 2018 Oct 15. PMID: 30336943.</p> <p> </p> <p>This is the abstract:</p> <p><strong>Aim: </strong> To compare the amount of epicardial adipose tissue (EAT) in patients with coronary artery disease (CAD) or non-ischaemic dilated cardiomyopathy (NIDCM) with that in patients with negative cardiac magnetic resonance imaging (CMR).</p> <p><strong>Materials and methods: </strong> One hundred and fifty patients (median age 57 years, interquartile range [IQR] 46-66 years) who underwent CMR were evaluated retrospectively: 50 with CAD, 50 with NIDCM, and 50 with negative CMR. For each patient, the EAT mass index (EATMI) to body surface area, end-diastolic volume index (EDVI), end-systolic volume index (ESVI), stroke volume (SV), ejection fraction (EF) for both ventricles, and left ventricle (LV) mass index were estimated. Intra and inter-reader reproducibility was tested in a random subset of 30 patients, 10 for each group. Mann-Whitney U test, Kruskal-Wallis test, Spearman's correlation, and Bland-Altman statistics were used.</p> <p><strong>Results: </strong> The EATMI in CAD patients (median 15.7 g/m<sup>2</sup>, IQR 8.3-25.7) or in NIDCM patients (15.9 g/m<sup>2</sup>, 11.5-18.1) was significantly higher than that in negative CMR patients (9.1 g/m<sup>2</sup>, 6-12; p<0.001 both). No significant difference was found between CAD and NIDCM patients (p=1.000). A correlation between EATMI and LV mass index was found in NIDCM patients (r=0.455, p=0.002). Intra- and inter-reader reproducibility were up to 80% and 72%, respectively.</p> <p><strong>Conclusion: </strong> Patients with NIDCM or CAD exhibited an increased EATMI in comparison to negative CMR patients. CMR can be used to estimate EAT with good reproducibility.</p>
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International Brain Laboratory public data
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OpenNeuro
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