Force generation and shortening capabilities of left ventricular myocardium in primary and secondary forms of mitral regurgitation.

Differentiation between primary and secondary forms of mitral regurgitation poses a frequent and important clinical problem. In the primary variety of mitral incompetence, there is distortion of the valve leaflets, rupture or redundancy of the chordae tendineae, or papillary muscle rupture. Heart failure, if present at all in such cases, is assumed to be a consequence of the large regurgitant volume, and surgical correction of the mitral insufficiency, therefore, may result in clinical and haemodynamic improvement. Secondary mitral insufficiency is basically caused by myocardial dysfunction and left ventricular failure: dilatation of the left ventricle produces a malalignment of the papillary muscles, thereby leading to the valvular incompetency. The regurgitant volume is generally small in these instances, however, so that valve replacement is unlikely to be beneficial. This study was undertaken in order to define those physiological features that merely reflect volume overload and those that reflect dominant muscle failure. Since primary mitral insufficiency and primary muscle dysfunction with secondary mitral incompetence both lead to severe disturbances in cardiovascular performance-the ventricular filling pressures may become raised, and the forward cardiac output considerably depressed in each group-it was apparent that some other means of assessing cardiac function should be investigated. One basic mode of characterizing myocardial function is expressed by the inverse relation between the force that a muscle develops and the velocity of shortening (Hill, 1938; Fry, Griggs, and Greenfield, 1964; Sonnenblick, 1962; Levine and Britman, 1964). In this paper, then, we have attempted