Dor Procedure - Indications


A dilated left ventricle is generally due to the effects of a myocardial infarction. An occlusion, or blockage, results in either akinetic (non-beating) or dyskinetic (irregular beating) tissue downstream from the occlusion. This tissue is virtually useless. However, the volume of blood that fills the ventricle prior to contraction, or end-diastolic volume, remains constant, so the tissue that still functions has to do more work to eject the blood, as the Frank-Starling Laws demand.

The tension on the functioning tissue increases as it compensates for the work of the necrotic tissue, so, as per Laplace's law, the radius of the ventricle increases and the thickness of the ventricular wall decreases. The apex of the heart becomes circular, hypertrophy ensues in the viable myocardial tissue, and the valve opening widens. As the ventricle dilates, the muscle fiber orientation, which is critical to a good ejection fraction, becomes transverse, or more horizontal. Subsequently, the ejection fraction decreases; a 15% shortening produces only a 30% ejection fraction. The lateral stress on the ventricle increases. Overall, the dilated left ventricle cannot produce a strong enough Nonviable myocardial muscle mass (NVMMM) implies a distinct, inexpensively reproduced signature (electrocardiography and echocardiography) of several contemporary myocardial performance determinants when compared to viable myocardial muscle mass (VMMM). Ratio between the two in heart failure on a time curve is a determinate of compensatory geometric remodeling of the myocardium. Fick/Frank/Starling describes gas diffusion, fluid and compliance relationships of the myocardium, primarily in systole. Geometric derangement induced by nonviable myocardium (see myocardial infarction)is exponentially impacted and proportional to the weight of the performance determinant measured. Viable/Nonviable myocardial mass fraction is substantially reduced by surgical interventions such as Dor and Batista.

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