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Cellular mechanisms of depressed atrial contractility in patients with chronic atrial fibrillation.
| Content Provider | Semantic Scholar |
|---|---|
| Author | Schotten, Ulrich Ausma, Jannie Stellbrink, Christoph Sabatschus, I. Vogel, Michael Frechen, Dirk A. Schoendube, Friedrich Hanrath, Peter |
| Copyright Year | 2001 |
| Abstract | BACKGROUND After cardioversion of atrial fibrillation (AF), the contractile function of the atria is temporarily impaired. Although this has significant clinical implications, the underlying cellular mechanisms are poorly understood. METHODS AND RESULTS Forty-nine consecutive patients submitted for mitral valve surgery were investigated. Twenty-three were in persistent AF (>/=3 months); the others were in sinus rhythm. Before extracorporal circulation, the right atrial appendage was excised. ss-Adrenoceptors were quantified by radioligand binding, and G proteins were quantified by Western blot analysis. The isometric contractile response to Ca(2+), isoproterenol, Bay K8644, and the postrest potentiation of contractile force were investigated in thin atrial trabeculae, which were also examined histologically. The contractile force of the atrial preparations obtained from AF patients was 75% less than that in preparations from patients in sinus rhythm. Also, the positive inotropic effect of isoproterenol was impaired, and Bay K8644 failed to increase atrial contractile force. In contrast, the response to extracellular Ca(2+) was maintained, and the postrest potentiation was preserved. Beta-adrenoceptor density and G-protein expression were unchanged. Histological examination revealed 14% more myolysis in the atria of AF patients. CONCLUSIONS After prolonged AF, atrial contractility was reduced by 75%. The impairment of beta-adrenergic modulation of contractile force cannot be explained by downregulation of ss-adrenoceptors or changes in G proteins. Dysfunction of the sarcoplasmic reticulum does not occur after prolonged AF. Failure of Bay K8644 to restore contractility suggests that the L-type Ca(2+) channel is responsible for the contractile dysfunction. The restoration of contractile force by high extracellular Ca(2+) shows that the contractile apparatus itself is nearly completely preserved after prolonged AF. |
| File Format | PDF HTM / HTML |
| Alternate Webpage(s) | http://circ.ahajournals.org/content/circulationaha/103/5/691.full.pdf?download=true |
| Alternate Webpage(s) | http://circ.ahajournals.org/content/circulationaha/103/5/691.full.pdf |
| Alternate Webpage(s) | http://circ.ahajournals.org/content/103/5/691.full.pdf |
| PubMed reference number | 11156881v1 |
| Volume Number | 103 |
| Issue Number | 5 |
| Journal | Circulation |
| Language | English |
| Access Restriction | Open |
| Subject Keyword | Adrenergic Receptor Atrial Septal Defects Biologic Preservation Calcium Chronic atrial fibrillation Depressive disorder Down-Regulation Heart Atrium Hippocampus (Brain) Isoproterenol Mitral Valve Nasal sinus Patients Sarcoplasmic Reticulum Schisandra glabra Sinus - general anatomical term Structure of auricular appendage Ventricular Fibrillation Western Blot chemosensitization/potentiation |
| Content Type | Text |
| Resource Type | Article |
