BACKGROUND: Valvular heart disease has become an important public health concern. The increased wall stress and underlying disease entity associated with mitral valve disease provide unfavorable circumstances for atrial cardiomyocytes. The expression of the alpha-smooth muscle actin isoform is considered characteristic of cardiomyocyte dedifferentiation (embryonic cardiomyocyte), and cardiomyocyte dedifferentiation may indicate an adaptive state, enabling cardiomyocytes to survive despite unfavorable circumstances. METHODS: This study comprised 20 adult patients with symptomatic severe mitral valve disease and moderate to severe tricuspid valve disease and without coronary artery disease undergoing valve operations for congestive heart failure. Ten patients had persistent atrial fibrillation and 10 patients had never been in atrial fibrillation by history and electrocardiograms before surgery. Atrial tissues of the right atrial appendage were obtained during surgery. RESULTS: Immunohistochemical study demonstrated that alpha-smooth muscle actin protein expression was not altered by atrial fibrillation, and alpha-smooth muscle actin protein expression in atrial tissues was higher in patients with sinus rhythm than in those with atrial fibrillation (the percentage of cells that were alpha-smooth muscle actin-positive was 51.5+/-34.9% for right atria from patients in sinus rhythm vs. 16.2+/-15.0% for right atria from patients with atrial fibrillation) (P<.03). Semiquantitation of alpha-smooth muscle actin by immunoblotting of extracts from atrial tissues showed similar findings as in the immunohistochemical observations: that is, atrial fibrillation did not influence the expression of alpha-smooth muscle actin protein. Interstitial fibrosis represented 43.2+/-13.9% of the right atrial tissue in the sinus group, whereas interstitial fibrosis comprised 49.8+/-8.2% of the right atrial tissue in the atrial fibrillation group (P=.320). CONCLUSIONS: Dedifferentiation of atrial cardiomyocytes occurs in patients with cardiac valve disease, even without atrial fibrillation.
BACKGROUND:Valvular heart disease has become an important public health concern. The increased wall stress and underlying disease entity associated with mitral valve disease provide unfavorable circumstances for atrial cardiomyocytes. The expression of the alpha-smooth muscle actin isoform is considered characteristic of cardiomyocyte dedifferentiation (embryonic cardiomyocyte), and cardiomyocyte dedifferentiation may indicate an adaptive state, enabling cardiomyocytes to survive despite unfavorable circumstances. METHODS: This study comprised 20 adult patients with symptomatic severe mitral valve disease and moderate to severe tricuspid valve disease and without coronary artery disease undergoing valve operations for congestive heart failure. Ten patients had persistent atrial fibrillation and 10 patients had never been in atrial fibrillation by history and electrocardiograms before surgery. Atrial tissues of the right atrial appendage were obtained during surgery. RESULTS: Immunohistochemical study demonstrated that alpha-smooth muscle actin protein expression was not altered by atrial fibrillation, and alpha-smooth muscle actin protein expression in atrial tissues was higher in patients with sinus rhythm than in those with atrial fibrillation (the percentage of cells that were alpha-smooth muscle actin-positive was 51.5+/-34.9% for right atria from patients in sinus rhythm vs. 16.2+/-15.0% for right atria from patients with atrial fibrillation) (P<.03). Semiquantitation of alpha-smooth muscle actin by immunoblotting of extracts from atrial tissues showed similar findings as in the immunohistochemical observations: that is, atrial fibrillation did not influence the expression of alpha-smooth muscle actin protein. Interstitial fibrosis represented 43.2+/-13.9% of the right atrial tissue in the sinus group, whereas interstitial fibrosis comprised 49.8+/-8.2% of the right atrial tissue in the atrial fibrillation group (P=.320). CONCLUSIONS: Dedifferentiation of atrial cardiomyocytes occurs in patients with cardiac valve disease, even without atrial fibrillation.
Authors: Thomas J van Brakel; Thomas van der Krieken; Sjoerd W Westra; Jeroen A van der Laak; Joep L Smeets; Henry A van Swieten Journal: J Interv Card Electrophysiol Date: 2013-09-12 Impact factor: 1.900
Authors: Andreas Goette; Jonathan M Kalman; Luis Aguinaga; Joseph Akar; Jose Angel Cabrera; Shih Ann Chen; Sumeet S Chugh; Domenico Corradi; Andre D'Avila; Dobromir Dobrev; Guilherme Fenelon; Mario Gonzalez; Stephane N Hatem; Robert Helm; Gerhard Hindricks; Siew Yen Ho; Brian Hoit; Jose Jalife; Young-Hoon Kim; Gregory Y H Lip; Chang-Sheng Ma; Gregory M Marcus; Katherine Murray; Akihiko Nogami; Prashanthan Sanders; William Uribe; David R Van Wagoner; Stanley Nattel Journal: Heart Rhythm Date: 2016-06-10 Impact factor: 6.343
Authors: Andreas Goette; Jonathan M Kalman; Luis Aguinaga; Joseph Akar; Jose Angel Cabrera; Shih Ann Chen; Sumeet S Chugh; Domenico Corradi; Andre D'Avila; Dobromir Dobrev; Guilherme Fenelon; Mario Gonzalez; Stephane N Hatem; Robert Helm; Gerhard Hindricks; Siew Yen Ho; Brian Hoit; Jose Jalife; Young-Hoon Kim; Gregory Y H Lip; Chang-Sheng Ma; Gregory M Marcus; Katherine Murray; Akihiko Nogami; Prashanthan Sanders; William Uribe; David R Van Wagoner; Stanley Nattel Journal: J Arrhythm Date: 2016-07-11