HCM

Mano, Toshiaki

doi:10.1536/ihj.18-103

Cited by 4 publications

(4 citation statements)

References 11 publications

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“…ypertrophic cardiomyopathy (HCM), which is a genetic disease caused by mutations in sarcomeric proteins, is the most common cause of sudden cardiac death (SCD) in the young. 1,2) Hypertrophy and fibrosis are the major determinants of mortality, morbidity, and SCD in HCM. 3) Myocardial fibrosis has been implicated in the pathogenesis of SCD and is thought to play a key role in arrhythmia and the development of systolic dysfunction.…”

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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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Predictive Values of Apelin for Myocardial Fibrosis in Hypertrophic Cardiomyopathy

et al. 2019

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“…HCM characterized by sarcomeric protein mutation causes sudden death in young. Hypertrophy and fibrosis are the two causes of all adverse events in HCM [ 35 , 36 ]. Plasma apelin levels correlate with the degree of late gadolinium increase (LGE) in HCM patients.…”

Section: Apelin In Hypertrophic Cardiomyopathy (Hcm)mentioning

confidence: 99%

Serum Apelin Levels and Cardiovascular Diseases

Aşkın¹

2021

North Clin Istanbul

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Apelin is a G protein-linked receptor endogenous ligand, synthesized as a 77-amino acid pre-propeptide. Increased expression of apelin is present in many cardiovascular (CV) tissues, including cardiomyocytes. It is a peripheral vasodilator and one of the most potent stimulants of ventricular contraction. Apelin may be a valuable therapeutic for both blood pressure regulation and myocardial performance. More information is needed for the CV pathophysiology of apelin. We will discuss the importance of apelin level in CV diseases in this review.

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“…HCM is an important cause of sudden cardiac death (SCD), especially in young individuals 4‐6 . The European Society of Cardiology (ESC) 2014 guideline on HCM has suggested an easily applicable risk prediction model for estimating the 5‐year risk of SCD in HCM patients 7 .…”

Section: Introductionmentioning

confidence: 99%

Correlations between cardiac troponin I and nonsustained ventricular tachycardia in hypertrophic obstructive cardiomyopathy

Liu

Shen

et al. 2020

Clinical Cardiology

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Background: Nonsustained ventricular tachycardia (NSVT) is an independent risk factor for sudden cardiac death (SCD) in patients with hypertrophic obstructive cardiomyopathy (HOCM). However, data concerning the correlations of cardiac biomarkers and NSVT in HOCM are rather limited. Hypothesis: Our study aimed to investigate the associations between the occurrence of NSVT and circulating biomarkers representing myocardial injury (cardiac troponin I, cTnI), cardiac function (N-terminal pro-brain natriuretic peptide, NT-pro BNP), and inflammation (high-sensitivity C-reactive protein) in a large Chinese HOCM cohort. Methods: A total of 755 consecutive HOCM patients were recruited. Systematic cardiac evaluations and circulating biomarkers were examined routinely in all subjects under the clinically stable status. According to the results of 24-hour Holter monitoring, patients were divided into the NSVT group (n = 138) and the nonventricular tachycardia (non-VT) group (n = 617). Results: Compared with the non-VT group, circulating levels of both cTnI and NT-pro BNP elevated significantly in patients with positive NSVT episodes (P < .001). Multivariable analyses demonstrated that cTnI was independently associated with the presence of NSVT (OR = 1.675, 95% CI: 1.406-1.994, P < .001). Concentrations of cTnI increased progressively not only with the aggravation of ventricular arrhythmic events (P < .001), but also with the growing risk of SCD in HOCM patients (P < .001). Serum cTnI ≥ 0.0265 ng/mL indicated predictive value for the occurrence of NSVT in the HOCM cohort (area under the curve = 0.707, 95% CI: 0.660-0.754, P < .001). Conclusions: Elevated cTnI was an independent determinant of NSVT, and it seemed to be valuable for assessing the clinical status of ventricular arrhythmias and the risk of SCD in patients with HOCM.

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HCM

Cited by 4 publications

References 11 publications

Predictive Values of Apelin for Myocardial Fibrosis in Hypertrophic Cardiomyopathy

Predictive Values of Apelin for Myocardial Fibrosis in Hypertrophic Cardiomyopathy

Serum Apelin Levels and Cardiovascular Diseases

Correlations between cardiac troponin I and nonsustained ventricular tachycardia in hypertrophic obstructive cardiomyopathy

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