A proposed alternative mechanism of action for transmyocardial revascularization prefaced by a review of the accepted explanations.

Laser transmyocardial revascularization, a procedure originally intended to simulate the perfusion mechanism of the reptilian heart, has evolved into an effective but poorly understood treatment for angina when traditional revascularization is not an option. Herein, we review the explanations that have been proposed over the years and suggest a new one. We hypothesize that the long-term mechanism of action of transmyocardial revascularization is the redistribution of stresses on the ventricular wall through the creation of fibrous transmyocardial scars, which penetrate the various layers of muscle that surround the left ventricular cavity. The stress redistribution of a load in an otherwise unchanged ventricular wall reduces the wall stress per unit of wall volume, which in turn decreases the workload for the hyperkinetic compensating areas. This reduces both oxygen demand and local metabolite production, lowering the level of angina.