[Molecular basis of remodelling in atrial fibrillation].
Dobrev
D
D
Institut für Pharmakologie und Toxikologie, Medizinische Fakultät der Technischen Universität Dresden. dobrev@rcs.urz.tu-dresden.de
D000200:Action Potentials / Q000502:physiology; D000368:Aged; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000627:therapeutic use; D001281:Atrial Fibrillation / Q000209:etiology / Q000235:genetics* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology* / Q000628:therapy; D016275:Atrial Function; D015220:Calcium Channels / Q000235:genetics / Q000378:metabolism / Q000502:physiology; D004554:Electric Countershock; D004562:Electrocardiography; D006325:Heart Atria / Q000473:pathology*; D006801:Humans; D007473:Ion Channels / Q000235:genetics / Q000378:metabolism / Q000502:physiology; D015221:Potassium Channels / Q000235:genetics / Q000502:physiology; D012008:Recurrence; D012084:Renin-Angiotensin System / Q000502:physiology; D012307:Risk Factors; D013997:Time Factors
D000806:Angiotensin-Converting Enzyme Inhibitors; D000889:Anti-Arrhythmia Agents; D015220:Calcium Channels; D007473:Ion Channels; D015221:Potassium Channels