Significance of isolated papillary muscle hypertrophy: A comparison of left ventricular hypertrophy diagnosed using electrocardiography vs echocardiography

Nomura, Namiko; Tani, Tohru; Konda, Toshiko; Kim, Kitae; Kitai, Takeshi; Nomoto, Natsumi; Suganuma, Naoko; Nakamura, Hitomi; Sumida, Toshiaki; Fujii, Yoko; Kawai, Junichi; Kaji, Shuichiro; Furukawa, Yutaka

doi:10.1111/echo.13789

Cited by 3 publications

(2 citation statements)

References 17 publications

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“…Other studies that investigated the prognostic significance of fQRS reported that the presence of fQRS was associated with a significant increase in arrhythmic events in HCM patients (Femenia et al., 2013; Ozyilmaz et al., 2017). Strain pattern is a known ECG sign of HCM and is associated with a higher cardiovascular risk and abnormal left ventricular function (Goldberger, 1979; Nomura et al., 2018; Ogah et al., 2008). It is also known that ECG strain is a marker of myocardial fibrosis in aortic stenosis and in hypertension (Rodrigues et al., 2017; Shah et al., 2014).…”

Section: Discussionmentioning

confidence: 99%

How are ECG parameters related to cardiac magnetic resonance images? Electrocardiographic predictors of left ventricular hypertrophy and myocardial fibrosis in hypertrophic cardiomyopathy

Dohy

Vereckei

Horváth

et al. 2020

Noninvasive Electrocardiol

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Background Structural myocardial changes in hypertrophic cardiomyopathy (HCM) are associated with different abnormalities on electrocardiographs (ECGs). The diagnostic value of the ECG voltage criteria used to screen for left ventricular hypertrophy (LVH) may depend on the presence and degree of myocardial fibrosis. Fibrosis can cause other changes in ECG parameters, such as pathological Q waves, fragmented QRS (fQRS), or repolarization abnormalities. Methods We investigated 146 patients with HCM and 35 healthy individuals who underwent cardiac magnetic resonance imaging (CMR; with late gadolinium enhancement [LGE] in HCM patients) and standard 12‐lead ECGs. On the ECG, depolarization and repolarization abnormalities, the Sokolow–Lyon index, the Cornell index, and the Romhilt–Estes score were evaluated. The left ventricular ejection fraction, volumes, and myocardial mass (LVM) were quantified. Myocardial fibrosis was quantified on LGE images. Results The sensitivity of the Romhilt–Estes score was the highest (75%), and this hypertrophy criterion had the strongest correlation with the LVM index (p < .0001; r = .41). The amount of fibrosis was negatively correlated with the Cornell index (p = .015; r = −.201) and the Sokolow–Lyon index (p = .005; r = −.23), and the Romhilt–Estes score was independent of fibrosis (p = .757; r = 0.026). fQRS and strain pattern predicted more fibrosis, while the Cornell index was a negative predictor of myocardial fibrosis (p < .0001). Among others, the strain pattern was an independent predictor of the LVM (p < .0001). Conclusion The Romhilt–Estes score is the most sensitive ECG criterion for detecting LVH in HCM patients, as myocardial fibrosis does not affect this criterion. The presence of fQRS and strain pattern predicts myocardial fibrosis.

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Section: Discussionmentioning

confidence: 99%

How are ECG parameters related to cardiac magnetic resonance images? Electrocardiographic predictors of left ventricular hypertrophy and myocardial fibrosis in hypertrophic cardiomyopathy

Dohy

Vereckei

Horváth

et al. 2020

Noninvasive Electrocardiol

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“…In the current study, we demonstrate the suppressive function of PRMT7 in the cardiac hypertrophic response. Maladaptive cardiac hypertrophy in disease conditions is accompanied by alterations in the contractile properties with the expression of fetal contractile genes and increased expression of extracellular matrices, such as collagens and bronectins [30][31][32]. PRMT7 KO cardiomyocytes and acute depletion of PRMT7 in NRVMs exhibited enlarged cell size and alteration in the expression of fetal genes, likely contributing to the decreased cardiac contractile function of PRMT7 cKO mice infused with Ang II.…”

Section: Discussionmentioning

confidence: 99%

PRMT7 ablation in cardiomyocytes causes cardiac hypertrophy and fibrosis through β-catenin dysregulation

Ahn

Jeong

Pyun

et al. 2022

Cell. Mol. Life Sci.

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Angiotensin II (AngII) has potent cardiac hypertrophic effects mediated through activation of hypertrophic signaling like Wnt/b-Catenin signaling. In the current study, we examined the role of protein arginine methyltransferase 7 (PRMT7) in cardiac function. PRMT7 was greatly decreased in hypertrophic hearts chronically infused with AngII and cardiomyocytes treated with AngII. PRMT7 depletion in rat cardiomyocytes resulted in hypertrophic responses. Consistently, mice lacking PRMT7 exhibited displayed the cardiac hypertrophy and brosis. PRMT7 overexpression abrogated the cellular hypertrophy elicited by AngII, while PRMT7 depletion exacerbated the hypertrophic response caused by AngII. Similar with AngII treatment, the cardiac transcriptome analysis of PRMT7-de cient hearts revealed the alteration in gene expression pro le related to Wnt signaling pathway. Inhibition of PRMT7 by gene deletion or an inhibitor treatment enhanced the activity of b-Catenin. PRMT7 de ciency decreases symmetric dimethylation of b-Catenin. Mechanistic studies reveal that methylation of arginine residue 93 in b-Catenin decreases the activity of b-Catenin. Taken together, our data suggest that PRMT7 is important for normal cardiac function through suppression of b-Catenin activity.

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PRMT7 Ablation in Cardiomyocytes Causes Cardiac Hypertrophy and Fibrosis Through β-Catenin Dysregulation

Ahn¹,

Jeong²,

Pyun³

et al. 2021

Preprint

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Angiotensin II (AngII) has potent cardiac hypertrophic effects mediated through activation of hypertrophic signaling like Wnt/b-Catenin signaling. In the current study, we examined the role of protein arginine methyltransferase 7 (PRMT7) in cardiac function. PRMT7 was greatly decreased in hypertrophic hearts chronically infused with AngII and cardiomyocytes treated with AngII. PRMT7 depletion in rat cardiomyocytes resulted in hypertrophic responses. Consistently, mice lacking PRMT7 exhibited displayed the cardiac hypertrophy and fibrosis. PRMT7 overexpression abrogated the cellular hypertrophy elicited by AngII, while PRMT7 depletion exacerbated the hypertrophic response caused by AngII. Similar with AngII treatment, the cardiac transcriptome analysis of PRMT7-deficient hearts revealed the alteration in gene expression profile related to Wnt signaling pathway. Inhibition of PRMT7 by gene deletion or an inhibitor treatment enhanced the activity of b-Catenin. PRMT7 deficiency decreases symmetric dimethylation of b-Catenin. Mechanistic studies reveal that methylation of arginine residue 93 in b-Catenin decreases the activity of b-Catenin. Taken together, our data suggest that PRMT7 is important for normal cardiac function through suppression of b-Catenin activity.

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Significance of isolated papillary muscle hypertrophy: A comparison of left ventricular hypertrophy diagnosed using electrocardiography vs echocardiography

Abstract: Isolated papillary muscle hypertrophy can cause ECG abnormalities such as LV high voltage and LV strain pattern. Particular attention must be paid to the papillary muscle during echocardiographic examinations.

Cited by 3 publications

References 17 publications

How are ECG parameters related to cardiac magnetic resonance images? Electrocardiographic predictors of left ventricular hypertrophy and myocardial fibrosis in hypertrophic cardiomyopathy

How are ECG parameters related to cardiac magnetic resonance images? Electrocardiographic predictors of left ventricular hypertrophy and myocardial fibrosis in hypertrophic cardiomyopathy

PRMT7 ablation in cardiomyocytes causes cardiac hypertrophy and fibrosis through β-catenin dysregulation

PRMT7 Ablation in Cardiomyocytes Causes Cardiac Hypertrophy and Fibrosis Through β-Catenin Dysregulation

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