Second Hits in Dilated Cardiomyopathy

Marstrand, Peter; Picard, Kermshlise; Lakdawala, Neal K.

doi:10.1007/s11886-020-1260-3

Cited by 16 publications

(5 citation statements)

References 58 publications

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“…Furthermore, an MVP-related cardiomyopathy could be induced only in patients with a genetic substrate and an additional environmental risk factor that acts as a second hit. This mechanism has been described in dilated cardiomyopathy secondary to pregnancy, alcohol and anthracyclines ( 47 ). Most commonly, the culprit mutations that serve as a first hit are related to known cardiomyopathy genes, again the TTN gene in particular ( 48 – 50 ).…”

Section: Mechanisms Of Global Left Ventricular Remodeling In Mitral V...mentioning

confidence: 89%

Left Ventricular Remodeling in Non-syndromic Mitral Valve Prolapse: Volume Overload or Concomitant Cardiomyopathy?

Pype

Bertrand

Paelinck

et al. 2022

Front. Cardiovasc. Med.

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Mitral valve prolapse (MVP) is a common valvular disorder that can be associated with mitral regurgitation (MR), heart failure, ventricular arrhythmias and sudden cardiac death. Given the prognostic impact of these conditions, it is important to evaluate not only mitral valve morphology and regurgitation, but also the presence of left ventricular (LV) function and remodeling. To date, several possible hypotheses have been proposed regarding the underlying mechanisms of LV remodeling in the context of non-syndromic MVP, but the exact pathophysiological explanation remains elusive. Overall, volume overload related to severe MR is considered the main cause of LV dilatation in MVP. However, significant LV remodeling has been observed in patients with MVP and no/mild MR, particularly in patients with bileaflet MVP or Barlow’s disease, generating several new hypotheses. Recently, the concept of “prolapse volume” was introduced, adding a significant volume load to the LV on top of the transvalvular MR volume. Another possible hypothesis is the existence of a concomitant cardiomyopathy, supported by the link between MVP and myocardial fibrosis. The origin of this cardiomyopathy could be either genetic, a second hit (e.g., on top of genetic predisposition) and/or frequent ventricular ectopic beats. This review provides an overview of the different mechanisms and remaining questions regarding LV remodeling in non-syndromic MVP. Since technical specifications of imaging modalities impact the evaluation of MR severity and LV remodeling, and therefore might influence clinical decision making in these patients, this review will also discuss assessment of MVP using different imaging modalities.

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Section: Mechanisms Of Global Left Ventricular Remodeling In Mitral V...mentioning

confidence: 89%

Left Ventricular Remodeling in Non-syndromic Mitral Valve Prolapse: Volume Overload or Concomitant Cardiomyopathy?

Pype

Bertrand

Paelinck

et al. 2022

Front. Cardiovasc. Med.

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“…We therefore speculated that the R453H variant might affect the disease phenotype more severely than the R453C variant. However, genetic variants, social factors, and one's lifestyle reportedly affect the clinical phenotypes of cardiomyopathy ( 18 , 19 ). Therefore, we also speculated that the genetic background or environmental factors might have affected the clinical course of Patient 3.…”

Section: Discussionmentioning

confidence: 99%

End-stage Hypertrophic Cardiomyopathy with Advanced Heart Failure in Patients Carrying <i>MYH7</i> R453 Variants: A Case Series

et al. 2023

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The MYH7 R453 variant has been identified in inherited hypertrophic cardiomyopathy (HCM) and is associated with sudden death and a poor prognosis. The detailed clinical course of HCM with the MYH7 R453 variant, from a preserved to a reduced left ventricular ejection fraction, has not been reported. We identified the MYH7 R453C and R453H variants in three patients who progressively developed advanced heart failure requiring circulatory support and summarized the clinical course and echocardiographic parameters of these patients over the years. Because of the rapid disease progression, we consider genetic screening for patients with HCM imperative for future prognosis stratification.

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“…DCM is a heterogeneous type of cardiomyopathy, and the etiology of DCM is divided into primary and secondary groups based on genetics [ 51 ]. Primary DCM is mainly related to genetic factors, while secondary DCM refers to systemic disease involving the myocardium, of which cardiomyopathy is only a part of the systemic disease [ 52 ]. Currently, the causes of DCM are known to include viral infection, noninfectious inflammatory reactions, endocrine and metabolic disorders, poisoning, autoimmune dysfunction, gene mutation, and genetic factors, which lead to damage to heart morphology and function, resulting in unilateral or bilateral ventricular enlargement, accompanied by ventricular systolic dysfunction, arrhythmia, varying degrees of myocardial hypertrophy, myocardial fibrosis, heart failure, and other symptoms, sudden death or embolism, and other complications [ 53 , 54 ].…”

Section: Discussionmentioning

confidence: 99%

Immune Mechanism, Gene Module, and Molecular Subtype Identification of Astragalus Membranaceus in the Treatment of Dilated Cardiomyopathy: An Integrated Bioinformatics Study

Chen

Han

et al. 2021

Evidence-Based Complementary and Alternative Medicine

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Astragalus membranaceus has complex components as a natural drug and has multilevel, multitarget, and multichannel effects on dilated cardiomyopathy (DCM). However, the immune mechanism, gene module, and molecular subtype of astragalus membranaceus in the treatment of DCM are still not revealed. Microarray information of GSE84796 was downloaded from the GEO database, including RNA sequencing data of seven normal cardiac tissues and ten DCM cardiac tissues. A total of 4029 DCM differentially expressed genes were obtained, including 1855 upregulated genes and 2174 downregulated genes. GO/KEGG/GSEA analysis suggested that the activation of T cells and B cells was the primary cause of DCM. WGCNA was used to obtain blue module genes. The blue module genes are primarily ADCY7, BANK1, CD1E, CD19, CD38, CD300LF, CLEC4E, FLT3, GPR18, HCAR3, IRF4, LAMP3, MRC1, SYK, and TLR8, which successfully divided DCM into three molecular subtypes. Based on the CIBERSORT algorithm, the immune infiltration profile of DCM was analyzed. Many immune cell subtypes, including the abovementioned immune cells, showed different levels of increased infiltration in the myocardial tissue of DCM. However, this infiltration pattern was not obviously correlated with clinical characteristics, such as age, EF, and sex. Based on network pharmacology and ClueGO, 20 active components of Astragalus membranaceus and 40 components of DMCTGS were obtained from TCMSP. Through analysis of the immune regulatory network, we found that Astragalus membranaceus effectively regulates the activation of immune cells, such as B cells and T cells, cytokine secretion, and other processes and can intervene in DCM at multiple components, targets, and levels. The above mechanisms were verified by molecular docking results, which confirmed that AKT1, VEGFA, MMP9, and RELA are promising potential targets of DCM.

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Second Hits in Dilated Cardiomyopathy

Cited by 16 publications

References 58 publications

Left Ventricular Remodeling in Non-syndromic Mitral Valve Prolapse: Volume Overload or Concomitant Cardiomyopathy?

Left Ventricular Remodeling in Non-syndromic Mitral Valve Prolapse: Volume Overload or Concomitant Cardiomyopathy?

End-stage Hypertrophic Cardiomyopathy with Advanced Heart Failure in Patients Carrying <i>MYH7</i> R453 Variants: A Case Series

Immune Mechanism, Gene Module, and Molecular Subtype Identification of Astragalus Membranaceus in the Treatment of Dilated Cardiomyopathy: An Integrated Bioinformatics Study

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