Aortic Stiffness and Interstitial Myocardial Fibrosis by Native T1 Are Independently Associated With Left Ventricular Remodeling in Patients With Dilated Cardiomyopathy

Hypertension ◽  
2014 ◽  
Vol 64 (4) ◽  
pp. 762-768 ◽  
Author(s):  
Valentina O. Puntmann ◽  
Eduardo Arroyo Ucar ◽  
Rocio Hinojar Baydes ◽  
Ning Binti Ngah ◽  
Yen-Shu Kuo ◽  
...  
Keyword(s):  
Dilated Cardiomyopathy ◽  
Myocardial Fibrosis ◽  
Aortic Stiffness ◽  
Ventricular Remodeling ◽  
Left Ventricular Remodeling ◽  
Left Ventricular ◽  
Native T1 ◽  
Interstitial Myocardial Fibrosis

scholarly journals Myocardial Fibrosis as a Key Determinant of Left Ventricular Remodeling in Idiopathic Dilated Cardiomyopathy

2013 ◽  
Vol 6 (5) ◽  
pp. 790-799 ◽  
Author(s):  
Pier Giorgio Masci ◽  
Robert Schuurman ◽  
Barison Andrea ◽  
Andrea Ripoli ◽  
Michele Coceani ◽  
...  
Keyword(s):  
Dilated Cardiomyopathy ◽  
Myocardial Fibrosis ◽  
Ventricular Remodeling ◽  
Left Ventricular Remodeling ◽  
Left Ventricular ◽  
Idiopathic Dilated Cardiomyopathy

scholarly journals Cardiac Sodium Channel Dysfunction and Dilated Cardiomyopathy: A Contemporary Reappraisal of Pathophysiological Concepts

2019 ◽  
Vol 8 (7) ◽  
pp. 1029 ◽  
Author(s):  
Asatryan
Keyword(s):  
Dilated Cardiomyopathy ◽  
Sodium Channel ◽  
Ventricular Remodeling ◽  
Left Ventricular Remodeling ◽  
Left Ventricular ◽  
Conduction Disturbances ◽  
Pathogenic Variants ◽  
Cardiac Sodium Channel ◽  
Precision Therapy ◽  
Bona Fide

A key emerging theme in translational cardiovascular medicine is the need to identify specific causes of arrhythmias and heart failure, defined by phenotype and/or genotype that will respond to a particular intervention. Unlike other genes implicated in hereditary arrhythmias and cardiomyopathies, pathogenic/likely pathogenic variants in the cardiac sodium channel alpha subunit gene (SCN5A) produce a remarkably diverse set of electrical and structural phenotypes, one of them being dilated cardiomyopathy. There has been debate about whether left ventricular remodeling is a bona fide phenotypic feature of cardiac sodium channel dysfunction, or a consequence of tachyarrhythmias or conduction disturbances. In light of recent findings, a critical digest of the available experimental and medical literature is necessary. This paper provides a critical appraisal of the evidence linking a dysfunctional cardiac sodium channel to ventricular dysfunction, and discusses the potential mechanisms involved in shaping this phenotype along with implications for precision therapy.

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