Literature DB >> 16036032

The molecular basis of cardiac arrhythmias in patients with cardiomyopathy.

Sen Ji1, David Cesario, Miguel Valderrabano, Kalyanam Shivkumar.   

Abstract

Cardiac arrhythmias are a leading cause of mortality and morbidity in Western society. In some specific instances, these arrhythmias are caused by abnormalities of cardiac ion channels, such as sodium, calcium, and potassium channels, which carry ionic currents and are fundamental determinants of cardiac excitability. Abnormalities of these ion channels are attributed to mutations in the genes encoding the channel protein and cause altered function of channels, which can predispose to arrhythmias. During heart failure, many channels also malfunction because of altered expression, resulting in lethal arrhythmias.

Entities:  

Mesh:

Substances:

Year:  2004        PMID: 16036032     DOI: 10.1007/s11897-004-0018-3

Source DB:  PubMed          Journal:  Curr Heart Fail Rep        ISSN: 1546-9530


  41 in total

Review 1.  Electrophysiological remodeling in hypertrophy and heart failure.

Authors:  G F Tomaselli; E Marbán
Journal:  Cardiovasc Res       Date:  1999-05       Impact factor: 10.787

Review 2.  Molecular and cellular mechanisms of cardiac arrhythmias.

Authors:  M T Keating; M C Sanguinetti
Journal:  Cell       Date:  2001-02-23       Impact factor: 41.582

3.  Actin mutations in dilated cardiomyopathy, a heritable form of heart failure.

Authors:  T M Olson; V V Michels; S N Thibodeau; Y S Tai; M T Keating
Journal:  Science       Date:  1998-05-01       Impact factor: 47.728

4.  Identification of a gene responsible for familial Wolff-Parkinson-White syndrome.

Authors:  M H Gollob; M S Green; A S Tang; T Gollob; A Karibe; A S Ali Hassan ; F Ahmad; R Lozado; G Shah; L Fananapazir; L L Bachinski; R Roberts; A S Hassan
Journal:  N Engl J Med       Date:  2001-06-14       Impact factor: 91.245

5.  Arrhythmogenesis and contractile dysfunction in heart failure: Roles of sodium-calcium exchange, inward rectifier potassium current, and residual beta-adrenergic responsiveness.

Authors:  S M Pogwizd; K Schlotthauer; L Li; W Yuan; D M Bers
Journal:  Circ Res       Date:  2001-06-08       Impact factor: 17.367

Review 6.  Abnormalities of calcium cycling in the hypertrophied and failing heart.

Authors:  S R Houser; V Piacentino; J Weisser
Journal:  J Mol Cell Cardiol       Date:  2000-09       Impact factor: 5.000

Review 7.  Molecular biology and the prolonged QT syndromes.

Authors:  J A Towbin; M Vatta
Journal:  Am J Med       Date:  2001-04-01       Impact factor: 4.965

Review 8.  Electrophysiological changes in heart failure and their relationship to arrhythmogenesis.

Authors:  Michiel J Janse
Journal:  Cardiovasc Res       Date:  2004-02-01       Impact factor: 10.787

9.  Sudden death associated with short-QT syndrome linked to mutations in HERG.

Authors:  Ramon Brugada; Kui Hong; Robert Dumaine; Jonathan Cordeiro; Fiorenzo Gaita; Martin Borggrefe; Teresa M Menendez; Josep Brugada; Guido D Pollevick; Christian Wolpert; Elena Burashnikov; Kiyotaka Matsuo; Yue Sheng Wu; Alejandra Guerchicoff; Francesca Bianchi; Carla Giustetto; Rainer Schimpf; Pedro Brugada; Charles Antzelevitch
Journal:  Circulation       Date:  2003-12-15       Impact factor: 29.690

10.  The relationships among ventricular arrhythmias, left ventricular dysfunction, and mortality in the 2 years after myocardial infarction.

Authors:  J T Bigger; J L Fleiss; R Kleiger; J P Miller; L M Rolnitzky
Journal:  Circulation       Date:  1984-02       Impact factor: 29.690

View more
  1 in total

1.  The ShcA phosphotyrosine docking protein uses distinct mechanisms to regulate myocyte and global heart function.

Authors:  Rachel D Vanderlaan; W Rod Hardy; M Golam Kabir; Adrian Pasculescu; Nina Jones; Pieter P deTombe; Peter H Backx; Tony Pawson
Journal:  Circ Res       Date:  2010-12-09       Impact factor: 17.367

  1 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.