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Trpm4 gene invalidation leads to cardiac hypertrophy and electrophysiological alterations.
PLoS One
August 2015
INSERM U1046, Université Montpellier1, Université Montpellier2, Montpellier, France.
Article Synopsis
- TRPM4 is a protein in the heart that helps control electrical signals and can cause problems if mutated, linked to conditions like Brugada syndrome.
- Researchers studied mice without the TRPM4 gene and found they had enlarged hearts but no signs of damage or disease, showing differences in heart cells compared to normal mice.
- The TRPM4-less mice also experienced issues with heart electrical signals, suggesting that this protein is important for healthy heart function.
Paroxysmal atrioventricular block has been reported in patients without acute coronary syndrome and without significant coronary artery stenosis, in patients with acute coronary syndrome and without significant coronary artery stenosis, in patients without acute coronary syndrome and with significant coronary artery stenosis and in patients with acute coronary syndrome and significant coronary artery stenosis. Conflicting roles for alternating periods of second degree atrioventricular block (also known as Mobitz I or Luciani-Wenckebach periodicity) have been reported. Both hypotheses have been reported, that paroxysmal Wenckebach periods are compatible with a benign prognosis and that paroxysmal Wenckebach periods are associated with hemodynamic deterioration.
View Article and Find Full Text PDFFetal Doppler echocardiographic diagnosis and successful steroid therapy of Luciani-Wenckebach phenomenon and endocardial fibroelastosis related to maternal anti-Ro and anti-La antibodies.
J Am Soc Echocardiogr
April 2005
Department of Pediatrics, St-Justine Hospital, Montreal, Quebec, Canada.
Background: Complete fetal heart block (HB) and endocardial fibroelastosis (EFE) are known to be associated with maternal anti-Ro and anti-La antibodies. Complete fetal HB is irreversible.
Objectives: We sought to (1) assess the value of the superior vena cava/ascending aorta Doppler approach in the early detection of abnormal delay in the fetal atrioventricular (AV) time of conduction, before appearance of complete fetal HB; and (2) report the effect of prenatal steroid therapy on EFE, HB, or both.
Fetal arrhythmias: the Saint-Justine hospital experience.
Prenat Diagn
December 2004
Foetal Cardiology Unit, Pediatric Cardiology Service, Department of Pediatrics, Saint-Justine Hospital, University of Montreal Quebec, Canada.
We intend to review our experience with the investigation and management of foetal arrhythmia on the basis of superior vena cava/ascending aorta (SVC/AA) Doppler flow velocity recordings. Irregular rhythms n = 307. Premature atrial and ventricular contractions were easily identified and generally self-limited in time.
View Article and Find Full Text PDF[Nodal conduction].
Arch Mal Coeur Vaiss
April 2002
Service de cardiologie, centre hospitalier Princesse-Grace, avenue Pasteur, 98000 Monaco.
The existence of a single atrio-ventricular fascicle had been suggested in the 19th century by Wilhelm His junior. In 1906, Sunao Tawara described in details the existence of a specific muscular fascicle in charge of the atrio-ventricular conduction. Since, it has remained famous under the name of atrio-ventricular node.
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