Summary

Recent description of a clinical syndrome of post-infarction “papillary muscle dysfunction”, which is occasionally associated with severe mitral regurgitation, prompted this experimental study. Extensive research was devoted to studies of the spread of electrical activation in the myocardium in animal experiments, but its spread in the papillary muscles in normal and abnormal conditions was not studied in detail. We undertook a study of activation in the anterolateral papillary muscle of anesthetized, open-chest dogs. Recordings were obtained simultaneously from four intramural  multi-electrode needles inserted into the myocardium at the base of the papillary muscle and directed towards its apex. Baseline studies of the normal spread of activation were performed in 30 dogs. Normal recordings were compared with those obtained in spontaneously occurring premature ventricular contractions.  In 23 dogs, they were followed by induction of localized ischemia by ligation of the small epicardial coronary branches supplying the base of the papillary muscle. Progress of ischemia was followed in 10 acute experiments for 4 to 5 hours. Ischemia of long duration with resulting scarring was produced in 6 dogs and its results studied after 4 to 7 weeks. In 7 experiments, severe local damage was induced by intramyocardial injecting of formaline solution mixed with staining dye for later study of its extent and correlation with local electrocardiographic changes. Serial electrocardiograms and vectorcardiograms were recorded in all animals. Serial phonocardiograms were obtained in dogs with induced localized myocardial ischemia.

The endocardial wave of activation was found to approach the papillary muscle from its septal side and spread in the direction toward the free left vetricular wall and toward the apex of the papillary muscle. The anterolateral papillary muscle of the left ventricle was activated simultaneously by the penetration of wave fronts: (1) from the endocardium into deeper portions of the papillary muscle; and (2) from the central portions of the papillary muscle and from the area of its attachment to the left ventricular wall.

The shorter time needed for the excitation wave to arrive at the epicardium in areas overlying the papillary muscle and the higher calculated velocity of spread in these areas indicate more abundant penetration of Punkinje tissue than in the adjacent portions of the free left ventricular wall.

The pathologic influence on the spread of activation in the papillary muscle was limited to the time interval between 6 and 36 msec. of the cardiac electric cycle, with no significant delays in the time of arrival of the process of activation at the points of earliest activation within the papillary muscle or at its endocardial surface. Ischemia and injection of formaline produced local decrease or disappearance of electric activity and local reversals of the direction of spread of activation in limited portions of the papillary muscle or in the overlying wall of the left ventricle.

Three types of aberrant spread of activation in the papillary muscle during premature ventricular contractions were described.

Publication:

1. Spread of activation in the anterolateral papillary muscle of the left ventricle of the dog under normal and pathologic conditions. Burch GE, Wajszczuk WJ, Cronvich JA. Am Heart J. 1970 Jun;79(6):769-88.