Downregulation of Immunodetectable Atrial Connexin4O in a Canine Model of Chronic Left Ventricular Myocardial Infarction: Implications to Atrial Fibrillation
| Autor: | Moon Hyoung Lee, Toshihiko Ohara, Yasushi Miyauchi, Hrayr S. Karagueuzian, Shengmei Zhou, Keiko Oahara, Peng Sheng Chen, Michael C. Fishbein, William J. Mandel |
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| Rok vydání: | 2002 |
| Předmět: |
Pharmacology
medicine.medical_specialty business.industry P wave Electrocardiography in myocardial infarction Atrial fibrillation 030204 cardiovascular system & hematology Anterior Descending Coronary Artery medicine.disease 03 medical and health sciences 0302 clinical medicine medicine.anatomical_structure Ventricle Internal medicine Occlusion cardiovascular system medicine Cardiology Myocyte Pharmacology (medical) cardiovascular diseases 030212 general & internal medicine Myocardial infarction Cardiology and Cardiovascular Medicine business |
| Zdroj: | Journal of Cardiovascular Pharmacology and Therapeutics. 7:89-94 |
| ISSN: | 1940-4034 1074-2484 |
| DOI: | 10.1177/107424840200700205 |
| Popis: | Background: The substrate(s) for atrial fibrillation associated with chronic left ventricular myocardial infarction remain poorly defined. Since atrial connexin40 has a rapid turnover rate and may cause atrial fibrillation, we hypothesized that chronic left ventricular myocardial infarction downregulates atrial Connexin40 and increases atrial fibrillation vulnerability. Methods and Results: The left anterior descending coronary artery was occluded distal to the first diagonal branch in five dogs and studied 7 weeks later. Five dogs with no left anterior descending coronary artery occlusion served as control. Vulnerability to atrial fibrillation was tested by burst atrial stimulation (50 milliseconds for 3 seconds). Atrial fibrillation was induced in all myocardial infarction dogs, lasting from 20 seconds to several minutes. In contrast, only rapid repetitive activity and short-lasting atrial fibrillation (< 5 seconds) could be induced in control dogs. The mean refractory periods of epicardial RA and LA appendages were not significantly different in the two groups. Mean left ventricular myocardial infarction size was 17 ± 4% of the left ventricle. Histologic analyses showed no signs of atrial ischemic injury or interstitial fibrosis in either group. Atrial myocyte diameter measured at the level of the nuclei of longitudinally sectioned myocytes was not significantly different in the two groups (10.1 ± 1.2 pm vs. 10.2 ± 1.2 pm; P = 0.3). Atrial Connexin40 (both left and right atria) in the left ventricular myocardial infarction group was highly heterogeneous and had significantly smaller total area stained than in the control (0.48 ± 0.09% vs. 0.82 ± 0.13%; P < 0.01). Conclusions: Chronic left ventricular myocardial infarction downregulates immunodetectable atrial Connexin40, a property that might contribute to the increased atrial fibrillation vulnerability in this model. |
| Databáze: | OpenAIRE |
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