Left Atrium as an Active Component of the Pathophysiology in HCM

Ko, Toshiyuki

doi:10.1536/ihj.18-441

Cited by 7 publications

(6 citation statements)

References 21 publications

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“…25) For HCM patients with LGE, the atria, which is the main source of plasma apelin, is also affected by fibrosis. 26) This is the possible reason for the decreased level of apelin in LGE-positive patients with HCM. This result is consistent with reduced apelin level in end-stage heart failure patients with cardiac fibrosis.…”

Section: Discussionmentioning

confidence: 99%

Predictive Values of Apelin for Myocardial Fibrosis in Hypertrophic Cardiomyopathy

et al. 2019

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Apelin was proved to attenuate cardiac interstitial fibrosis. However, the association between apelin level and myocardial fibrosis in patients with hypertrophic cardiomyopathy (HCM) is still unclear. This study aims to determine whether apelin is associated with myocardial fibrosis in HCM and investigate the predictive values of apelin for myocardial fibrosis in HCM. One hundred sixteen patients with HCM were enrolled in this study. Plasma apelin-13 and high-sensitivity cardiac troponin I (cTNI) were measured. The cardiac systolic and diastolic functions were evaluated by echocardiography, and the presence and extent of cardiac fibrosis were assessed by cardiac magnetic resonance. All statistical data were analyzed by SPSS version 21.0. The percentage of late gadolinium enhancement (LGE) was negatively correlated with apelin and positively correlated with cTNI, maximum wall thickness (MWT), and left ventricular mass index in the overall patients with HCM and LGE. Apelin, cTNI, MWT, and left ventricular ejection fraction were independent predictors of the presence of LGE. The cutoff values of apelin, cTNI, and MWT were 1.24 pg/mL, 0.031 ng/mL, and 19 mm, respectively, for the prediction of LGE. The combined measurements of MWT "19 mm and/or apelin ! 1.24 pg/mL, as well as the combined measurements of MWT "19 mm and/or cTNI "0.031 ng/mL, obtained higher specificity and higher sensitivity, thus, indicating the presence of LGE. Plasma apelin and cTNI are independent predictors of myocardial fibrosis. The combined measurements of serum apelin and MWT, as well as cTNI and MWT, showed higher predictive values for predicting myocardial fibrosis in patients with HCM.

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Section: Discussionmentioning

confidence: 99%

Predictive Values of Apelin for Myocardial Fibrosis in Hypertrophic Cardiomyopathy

et al. 2019

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Section: Introductionmentioning

confidence: 99%

“…[1,2] However, it has been reported that in HCM, LA dysfunction can occur as a myopathic process itself, irrespective of loading conditions. [4,5] In this regard, genetic contribution to LA structural and functional remodeling has not been well investigated. Tissue Doppler imaging-based late mitral annular velocity (a') and LA phasic function have been validated as good LA functional parameters re ecting active contraction in several studies and are widely used.…”

Section: Introductionmentioning

confidence: 99%

Contribution of Sarcomere Gene Mutations to Left Atrial Function in Patients With Hypertrophic Cardiomyopathy

Chung

Kim

Park

et al. 2020

Preprint

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Background: Left atrial (LA) enlargement and dysfunction are related to clinical course in patients with hypertrophic cardiomyopathy (HCM). We aimed to investigate genetic contribution to LA structural and functional remodeling.Methods: 212 patients were consecutively enrolled, and echocardiography and extensive genetic analysis were performed. Cardiac magnetic resonance (CMR) was performed in 135 patients. Echocardiography was also performed in controls (n=30). Results: Patients with HCM had lower late-diastolic mitral annular velocity (a’) and higher LA volume index (LAVI) than controls. Patients with pathogenic or likely pathogenic sarcomere gene mutations (PSM, n = 67, 32%) had higher LAVI and lower CMR-derived LA total emptying fraction (37.0 ± 18.5 vs. 44.2 ± 12.4%, p=0.025). In patients without AF (n = 187), the PSM had lower a’ (6.9 ± 2.0 vs. 7.8 ± 1.9 cm/s, p = 0.004) than others. The PSM had higher prevalence and amount of late gadolinium enhancement (LGE) in the left ventricle (LV). In multivariate analysis, PSM was significantly related to lower a’ independent of E/e’, LV mass index, and LAVI. However, the relation significantly attenuated after adjustment for the extent of LGE in the LV, suggesting common myopathy in the LV and LA.Conclusions: PSM was related to LA dysfunction independent of LV filling pressure and LAVI, suggesting its contribution to atrial myopathy in HCM.

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“…Although elevated LV filling pressure causes LA dysfunction in HCM, LA dysfunction may occur as a myopathic process irrespective of loading conditions. 4) Additionally, one unique characteristic of HCM is that it is a genetic disorder. Although genetic contribution to LA function has not been well established, we previously reported that LA function (measured by a′ in echocardiography and LA total emptying fraction by cardiovascular magnetic resonance [CMR]) was significantly reduced in HCM patients with pathogenic or likely-pathogenic sarcomere gene mutation.…”

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confidence: 99%

Emerging Indicators of Left Atrial Function Evaluation Considering the Unique Characteristics of Hypertrophic Cardiomyopathy

Chung

2023

J Cardiovasc Imaging

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Left Atrium as an Active Component of the Pathophysiology in HCM

Cited by 7 publications

References 21 publications

Predictive Values of Apelin for Myocardial Fibrosis in Hypertrophic Cardiomyopathy

Predictive Values of Apelin for Myocardial Fibrosis in Hypertrophic Cardiomyopathy

Contribution of Sarcomere Gene Mutations to Left Atrial Function in Patients With Hypertrophic Cardiomyopathy

Emerging Indicators of Left Atrial Function Evaluation Considering the Unique Characteristics of Hypertrophic Cardiomyopathy

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