The Dor procedure is a medical technique used as part of heart surgery and originally introduced by the French cardiac surgeon Vincent Dor (b.1932). It is also known as endoventricular circular patch plasty (EVCPP).
In 1985, Dor introduced EVCPP as a viable method for restoring a dilated left ventricle (LV) to its normal, elliptical geometry. The Dor procedure uses a circular suture and a Dacron patch to correct LV aneurysms and exclude scarred parts of the septum and ventricular wall and would prove to be the best option amongst the other methods of ventricular remodeling, i.e. Cooley’s linear suturing and Jatene’s circular external suturing. EVCPP is a relatively easy procedure that covers all aspects of successful heart restoration—restores ventricular shape, increases ejection fraction, decreases the left ventricular end systolic volume index (LVESVI), and allows for complete coronary revascularization.
The myocardium consists of a single, continuous tissue that wraps around itself, spiraling up from the apex of the heart, to form a helix with elliptically shaped ventricles. This spiral produces an oblique muscle fiber orientation, meaning that the fibers form a more ventricle ‘x’ shape, so that when fibers shorten 15%, it produces a 60% ejection fraction. Because of its elliptical shape and defined apex, the ventricle is subjected to a relatively low level of lateral stress.
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 contraction. 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.