Non-ion channel blockers as anti-arrhythmic drugs (reversal of structural remodeling)

被引:34
作者
Goette, Andreas
Bukowska, Alicja
Lendeckel, Uwe
机构
[1] Univ Hosp Magdeburg, Div Cardiol, D-39120 Magdeburg, Germany
[2] Univ Hosp Magdeburg, Inst Expt Internal Med, D-39120 Magdeburg, Germany
关键词
D O I
10.1016/j.coph.2006.09.006
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Approximately 90% of patients with atrial fibrillation have concomitant cardiovascular disease, such as hypertension, heart failure or valve disease. These diseases have been found to substantially affect the structure of atria[ tissue, and thereby the occurrence of atrial fibrillation. At the molecular level, angiotensin II, oxidative stress and pro-inflammatory mediators are of particular importance in the induction of pro-arrhthymic atrial dilation, myocardial hypertrophy and interstitial atrial fibrosis. Elucidating the signalling pathways responsible for the process of structural atrial remodeling has helped to define novel non-ion channel drug targets for atrial fibrillation.
引用
收藏
页码:219 / 224
页数:6
相关论文
共 57 条
[1]   Myocardial cell death in fibrillating and dilated human right atria [J].
Aimé-Sempé, C ;
Folliguet, T ;
Rücker-Martin, C ;
Krajewska, M ;
Krajewski, S ;
Heimburger, M ;
Aubier, M ;
Mercadier, JJ ;
Reed, JC ;
Hatem, SN .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 1999, 34 (05) :1577-1586
[2]   Disease mechanisms and emerging therapies: protein kinases and their inhibitors in myocardial disease [J].
Anderson, Mark E. ;
Higgins, Linda S. ;
Schulman, Howard .
NATURE CLINICAL PRACTICE CARDIOVASCULAR MEDICINE, 2006, 3 (08) :437-445
[3]   Matrix metalloproteinases and atrial remodeling in patients with mitral valve disease and atrial fibrillation [J].
Anné, W ;
Willems, R ;
Roskams, T ;
Sergeant, P ;
Herijgers, P ;
Holemans, P ;
Ector, H ;
Heidbüchel, H .
CARDIOVASCULAR RESEARCH, 2005, 67 (04) :655-666
[4]   Structural changes of atrial myocardium due to sustained atrial fibrillation in the goat [J].
Ausma, J ;
Wijffels, M ;
Thone, F ;
Wouters, L ;
Allessie, M ;
Borgers, M .
CIRCULATION, 1997, 96 (09) :3157-3163
[5]   Changes in ultrastructural calcium distribution in goat atria during atrial fibrillation [J].
Ausma, J ;
Dispersyn, GD ;
Duimel, H ;
Thoné, F ;
Donck, LV ;
Allessie, MA ;
Borgers, M .
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 2000, 32 (03) :355-364
[6]  
Azpitarte J, 1997, EUR HEART J, V18, P1649
[7]   ACE-inhibitor treatment attenuates atrial structural remodeling in patients with lone chronic atrial fibrillation [J].
Boldt, A ;
Scholl, A ;
Garbade, J ;
Resetar, ME ;
Mohr, FW ;
Gummert, JF ;
Dhein, S .
BASIC RESEARCH IN CARDIOLOGY, 2006, 101 (03) :261-267
[8]   Fibrosis in left atrial tissue of patients with atrial fibrillation with and without underlying mitral valve disease [J].
Boldt, A ;
Wetzel, U ;
Lauschke, J ;
Weigl, J ;
Gummert, J ;
Hindricks, G ;
Kottkamp, H ;
Dhein, S .
HEART, 2004, 90 (04) :400-405
[9]   CHARACTERISTICS AND PROGNOSIS OF LONE ATRIAL-FIBRILLATION - 30-YEAR FOLLOW-UP IN THE FRAMINGHAM-STUDY [J].
BRAND, FN ;
ABBOTT, RD ;
KANNEL, WB ;
WOLF, PA .
JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION, 1985, 254 (24) :3449-3453
[10]   Activation of the calcineurin signaling pathway induces atrial hypertrophy during atrial fibrillation [J].
Bukowska, A ;
Lendeckel, U ;
Hirte, D ;
Wolke, C ;
Striggow, F ;
Röhnert, P ;
Huth, C ;
Klein, HU ;
Goette, A .
CELLULAR AND MOLECULAR LIFE SCIENCES, 2006, 63 (03) :333-342