Left atrial enlargement: An electrocardiographic misnomer? An electrocardiographic–echocardiographic study

Dam, I. Van; Roelandt, Jos R.T.C.; Medina, Etienne O. Robles de

doi:10.1093/oxfordjournals.eurheartj.a062032

Cited by 13 publications

(5 citation statements)

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“…Using a combination of ECG LAE criteria is thus highly sensitive for detection of anatomic LAE, with a low false negative rate. This study indicates that commonly used ECG LAE criteria are more sensitive for anatomic LAE than the 6–69% sensitivity previously reported using echocardiographic standards [ 16 , 18 , 22 , 23 , 38 ]. The criteria of P mitrale, P wave axis < 30°, and terminal P wave in V1 > 0.04s·mm were each highly specific although not sensitive for CMR LAE.…”

Section: Discussionmentioning

confidence: 49%

Accuracy of electrocardiographic criteria for atrial enlargement: validation with cardiovascular magnetic resonance

Tsao

Josephson

Hauser

et al. 2008

Journal of Cardiovascular Magnetic Resonance

103

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Background: Anatomic atrial enlargement is associated with significant morbidity and mortality. However, atrial enlargement may not correlate with clinical measures such as electrocardiographic (ECG) criteria. Past studies correlating ECG criteria with anatomic measures mainly used inferior M-mode or two-dimensional echocardiographic data. We sought to determine the accuracy of the ECG to predict anatomic atrial enlargement as determined by volumetric cardiovascular magnetic resonance (CMR).

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Section: Discussionmentioning

confidence: 49%

Accuracy of electrocardiographic criteria for atrial enlargement: validation with cardiovascular magnetic resonance

Tsao

Josephson

Hauser

et al. 2008

Journal of Cardiovascular Magnetic Resonance

103

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show abstract

“…3,4,17 Subsequent studies using echocardiography reported moderate specificity and poor sensitivity of abnormal PTF for detecting left atrial enlargement. [18][19][20] In a recent report using cardiovascular magnetic resonance, abnormal PTF was shown to be a highly specific but insensitive ECG sign of left atrial enlargement. 21 In a pathology study, abnormal PTF was shown to correlate with left atrial hypertrophy but was also observed in 22% subjects without atrial hypertrophy and 12% structurally normal hearts.…”

Section: Substrate Of Variable P-wave Morphology: Structural Electrimentioning

confidence: 99%

Abnormal P‐Wave Morphology Is a Predictor of Atrial Fibrillation Development and Cardiac Death in MADIT II Patients

Holmqvist¹,

Platonov²,

McNitt³

et al. 2010

Noninvasive Electrocardiol

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“…TAZ is part of the WNT signaling pathway, which participates in NSPC regulation at the SVZ and SGZ during development, in the adult and aging brain [ 4 , 16 , 17 , 18 ]. Neurogenesis is attenuated by the downregulation of WNT signaling with aging and in age-related neurodegenerative diseases such Alzheimer’s or Parkinson’s diseases [ 2 , 3 , 5 ].…”

Section: Introductionmentioning

confidence: 99%

TAZ Represses the Neuronal Commitment of Neural Stem Cells

Robledinos-Antón

Escoll

Guan

et al. 2020

Cells

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The mechanisms involved in regulation of quiescence, proliferation, and reprogramming of Neural Stem Progenitor Cells (NSPCs) of the mammalian brain are still poorly defined. Here, we studied the role of the transcriptional co-factor TAZ, regulated by the WNT and Hippo pathways, in the homeostasis of NSPCs. We found that, in the murine neurogenic niches of the striatal subventricular zone and the dentate gyrus granular zone, TAZ is highly expressed in NSPCs and declines with ageing. Moreover, TAZ expression is lost in immature neurons of both neurogenic regions. To characterize mechanistically the role of TAZ in neuronal differentiation, we used the midbrain-derived NSPC line ReNcell VM to replicate in a non-animal model the factors influencing NSPC differentiation to the neuronal lineage. TAZ knock-down and forced expression in NSPCs led to increased and reduced neuronal differentiation, respectively. TEADs-knockdown indicated that these TAZ co-partners are required for the suppression of NSPCs commitment to neuronal differentiation. Genetic manipulation of the TAZ/TEAD system showed its participation in transcriptional repression of SOX2 and the proneuronal genes ASCL1, NEUROG2, and NEUROD1, leading to impediment of neurogenesis. TAZ is usually considered a transcriptional co-activator promoting stem cell proliferation, but our study indicates an additional function as a repressor of neuronal differentiation.

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Left atrial enlargement: An electrocardiographic misnomer? An electrocardiographic–echocardiographic study

Cited by 13 publications

References 0 publications

Accuracy of electrocardiographic criteria for atrial enlargement: validation with cardiovascular magnetic resonance

Accuracy of electrocardiographic criteria for atrial enlargement: validation with cardiovascular magnetic resonance

Abnormal P‐Wave Morphology Is a Predictor of Atrial Fibrillation Development and Cardiac Death in MADIT II Patients

TAZ Represses the Neuronal Commitment of Neural Stem Cells

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