The natural history of atrial fibrillation (AF) is characterized by a gradual worsening with time. The recent finding that AF itself produces changes in atrial function and structure has provided a possible explanation for the progressive nature of this arrhythmia. Electrical remodeling (shortening of atrial refractoriness) develops within the first days of AF and contributes to an increase in stability of AF. However, 'domestication of AF' must also depend on a 'second factor' since the persistence of AF continues to increase after electrical remodeling has been completed. Atrial contractile remodeling (loss of contractility) leads to a reduced atrial transport function after cardioversion of AF. An important clinical consequence is that during several days after restoration of sinus rhythm, the risk of atrial thrombus formation is still high. In addition, the reduction of atrial contractility during AF may enhance atrial dilatation which may add to the persistence of AF. Tachycardia-induced structural remodeling takes place in a different time domain (weeks to months). Myolysis probably contributes to the loss of atrial contractile force. Although it might explain the loss of efficacy of pharmacological cardioversion and the development of permanent AF, the role of structural remodeling in the progression of AF is still unclear. Atrial structural remodeling also occurs as a result of heart failure and other underlying cardiovascular diseases. The associated atrial fibrosis might explain intra-atrial conduction disturbances and the susceptibility for AF. Thus, both AF itself and the underlying heart disease are responsible for the development of the arrhythmogenic substrate. New strategies for prevention and termination of AF should be build on our knowledge of the mechanisms and time course of AF-induced atrial remodeling.

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Electrical, contractile and structural remodeling during atrial fibrillation

Background After cardioversion of sustained atrial fibrillation (AF), the electrical and contractile functions of the atria are impaired, and recurrences of AF frequently occur. Whether remodeling of the structure of atrial myocardium is the basis for this problem is not known. Methods and Results Sustained AF was induced by electrical pacing in 13 goats instrumented long-term. The goats were killed after 9 to 23 weeks, and the atrial myocardium was examined by light and electron microscopy. The changes were quantified in left and right atrial free walls, appendages, trabeculae, the interatrial septum, and the bundle of Bachmann. A substantial proportion of the atrial myocytes (up to 92%) revealed marked changes in their cellular substructures, such as loss of myofibrils, accumulation of glycogen, changes in mitochondrial shape and size, fragmentation of sarcoplasmic reticulum, and dispersion of nuclear chromatin. These changes were accompanied by an increase in size of the myocytes (up to 195%). There we...

Structural Changes of Atrial Myocardium due to Sustained Atrial Fibrillation in the Goat

Devices and methods for treating heart valves include members that assist the valve in closing during at least a portion of the cardiac cycle. Such devices include members configured to alter the shape of a valve annulus, reposition at least one papillary muscle, and/or plug an orifice of the valve so as to provide a coaptation surface for the valve leaflets.

Devices and methods for heart valve treatment

An apparatus for treatment of a failing heart by reducing the wall tension therein. In one embodiment, the apparatus includes a tension member for drawing at least two walls of a heart chamber toward each other. Methods for placing the apparatus on the heart are also provided.

Heart wall tension reduction apparatus and method

A device for heart valve repair including at least one tension member having a first end and second end. A basal anchor is disposed at the first end of the tension member and a secondary anchor at the second end. The method includes the steps of anchoring the basal anchor proximate a heart valve and anchoring the secondary anchor at a location spaced from the valve such that the chamber geometry is altered to reduce heart wall tension and/or stress on the valve leaflets.

Valve to myocardium tension members device and method

Surgical repair of single ventricle.

Bypass grafts for recurrent or complex coarctations of the aorta

Intraoperative unidirectional intra-aortic balloon pumping in the management of left ventricular power failure.

MECHANICAL circulatory support with the intra-aortic balloon has permitted preoperative evaluation of patients in low-output cardiac failure.1 2 3 Such studies show surgically correctable problems in many cases, and temporary assistance with the intra-aortic balloon is maintained until these problems are corrected at operation. In occasional patients, however, studies show that the cardiac disease cannot be corrected by the usual types of cardiac operations, and such patients die when mechanical circulatory support is stopped. In two patients with prior coronary-artery operations and no correctable lesions, we have maintained the circulation with the intra-aortic balloon pump for six days in each while an . . .

Richard N. Edie

Papers

Surgical repair of single ventricle.

Bypass grafts for recurrent or complex coarctations of the aorta

Intraoperative unidirectional intra-aortic balloon pumping in the management of left ventricular power failure.

Cardiac transplantation for patients requiring mechanical circulatory support.

A Pulsatile Assist Device (PAD) for Use During Cardiopulmonary Bypass