Fibrillation pathophysiology

Lashuel, H. A., Petre, B. M., Wall, J., Simon, M., Nowak, R. J., Walz, T., and Lansbury, P. T., Jr. (2002). Alpha-synuclein, especially the Parkinson s disease-associated mutants, forms pore-like annular and tubular protofibrils./. Mol. Biol. 322,1089-1102. LeVine, H. (1993). Thioflavine T interaction with synthetic Alzheimer s disease beta-amyloid peptides Detection of amyloid aggregation in solution. Protein Sci. 2, 404—410. Lin, H., Bhatia, R., and Lai, R. (2001). Amyloid beta protein forms ion channels Implications for Alzheimer s disease pathophysiology. FASEB J. 15, 2433-2444. Lorenzo, A., and Yankner, B. A. (1994). Beta-amyloid neurotoxicity requires fibril formation and is inhibited by Congo red. Proc. Natl. Acad. Sci. USA 91, 12243-12247. Luhrs, T., Ritter, C., Adrian, M., Riek-Loher, D., Bohrmann, B., Dobeli, H., Schubert, D., and Riek, R. (2005). 3D structure of Alzheimer s amyl o id-( be la) (1—12) fibrils. Proc. Natl. Acad. Sci. USA 102, 17342-17347. 

Maisel WH, Stevenson LW. Atrial fibrillation in heart failure epidemiology, pathophysiology, and rationale for therapy. [Review, 48 refs]. Am. J. Cardiol. 2003 91 20. 

Approximately 25% of all patients with hypertrophic cardiomyopathy (HCM) have latent left ventricular outflow obstruction with an intraventricular gradient (I). Pathophysiologic features are asymmetric hypertrophy of the septum and a systolic anterior movement of the anterior leaflet. Medical treatment includes betablockers, and calcium antagonists of the verapamil type. Approximately 5— 10% of the patients with outflow obstruction are refractory to such negative inotropic therapy (2). Positive inotropic drugs such as digitalis or sympathomimetics are strictly contraindicated. In the presence of atrial fibrillation, anticoagulation therapy should be started. Since endocarditis is more common in patients with HCM because of turbulence in the left ventricle, prophylactic antibiotics should be administered for periods of potential bacteraemia. 

Hypercalcemia occurs in horses with chronic renal failure and in a few neoplastic conditions. The clinical signs are usually those of the underlying pathophysiology but soft tissue calcification may occur. In experimental ponies, hypercalcemia induced ventricular fibrillation or cardiac arrest at ionized calcium concentrations of 18.2-40mg/dl (4.55-10.0 mmol/1) (Glazier et al 1979). Treatment for severe hypercalcemia (ionized... 

Rate Versus Rhythm Control 100 Pathophysiology of Atrial Fibrillation 101 Autonomic Effects in Atrial Fibrillation 101 Atrial Remodeling in Atrial Fibrillation 102 History of Catheter Ablation in Atrial Fibrillation 104... 

Cohen M, Naccarelli GV. Pathophysiology and disease progression of atrial fibrillation importance of achieving and... 

Schauerte P, Scherlag BJ, Patterson E, et al. Focal atrial fibrillation experimental evidence for a pathophysiologic role of the autonomic nervous system. J Cardiovasc Electrophysiol 2001 12 592-9. 

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