Postsystolic motion (PSM) is a delayed ejection motion of the myocardium occurring after the aortic valve closure, during a generally prolonged isovolumic relaxation time (IVRT). In this review we analyze the physiopathologic mechanisms underlying PSM and the contribution of tissue Doppler for its understanding. By using various techniques, this phenomenon has been described in experimental observations and related to myocardial ischemia produced by gradual or abrupt coronary occlusion. In clinical studies, it is associated with recovery of regional myocardial function. Tissue Doppler, providing a velocity map of myocardial motion, allows an easy, noninvasive detection of PSM in the clinical setting. PSM, as identified by tissue Doppler, appears a hallmark of myocardial ischemia and viability but it may occur also in nonischemic conditions as left ventricular (LV) hypertrophy and volume overload, left bundle branch block and even in normal individuals. Strain and strain rate (SR), obtainable by off-line color tissue Doppler, may be useful to identify the mechanisms underlying PSM since these measurements reflect, respectively, the intrinsic rate and the percentage of deformation of a given myocardial segment, and are relatively independent of both overall cardiac movement and tethering of the neighboring LV segments. By using SR imaging, the ratio of PSM to regional systolic longitudinal strain can be used to separate ischemic from nonischemic PSM and appears the best quantitative parameter to identify ischemia during dobutamine stress. A method to detect LV wall asynchrony and immediate benefit of cardiac resynchronization therapy has been developed combining the assessment of tissue-tracking (TT) derived delayed longitudinal contraction and of SR-derived PSM.
Myocardial postsystolic motion in ischemic and not ischemic myocardium: the clinical value of tissue Doppler
Citro R;
2005-01-01
Abstract
Postsystolic motion (PSM) is a delayed ejection motion of the myocardium occurring after the aortic valve closure, during a generally prolonged isovolumic relaxation time (IVRT). In this review we analyze the physiopathologic mechanisms underlying PSM and the contribution of tissue Doppler for its understanding. By using various techniques, this phenomenon has been described in experimental observations and related to myocardial ischemia produced by gradual or abrupt coronary occlusion. In clinical studies, it is associated with recovery of regional myocardial function. Tissue Doppler, providing a velocity map of myocardial motion, allows an easy, noninvasive detection of PSM in the clinical setting. PSM, as identified by tissue Doppler, appears a hallmark of myocardial ischemia and viability but it may occur also in nonischemic conditions as left ventricular (LV) hypertrophy and volume overload, left bundle branch block and even in normal individuals. Strain and strain rate (SR), obtainable by off-line color tissue Doppler, may be useful to identify the mechanisms underlying PSM since these measurements reflect, respectively, the intrinsic rate and the percentage of deformation of a given myocardial segment, and are relatively independent of both overall cardiac movement and tethering of the neighboring LV segments. By using SR imaging, the ratio of PSM to regional systolic longitudinal strain can be used to separate ischemic from nonischemic PSM and appears the best quantitative parameter to identify ischemia during dobutamine stress. A method to detect LV wall asynchrony and immediate benefit of cardiac resynchronization therapy has been developed combining the assessment of tissue-tracking (TT) derived delayed longitudinal contraction and of SR-derived PSM.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
