Myocardial Postsystolic Shortening and Early Systolic Lengthening: Current Status and Future Directions

Abstract

The concept of paradoxical myocardial deformation, commonly referred to as postsystolic shortening and early systolic lengthening, was originally described in the 1970s when assessed by invasive cardiac methods, such as ventriculograms, in patients with ischemia and animal experimental models. Today, novel tissue-based imaging technology has revealed that these phenomena occur far more frequently than first described. This article defines these deformational patterns, summarizes current knowledge about their existence and highlights the clinical potential associated with their understanding.

Keywords: clinical value; deformation; early systolic lengthening; postsystolic shortening; speckle tracking echocardiography.

Figure 1

Longitudinal speckle tracking profile and suggested natural history of postsystolic shortening. Legend: (A): Schematic drawing of longitudinal speckle tracking profile displaying early systolic lengthening and postsystolic shortening as indicated with red dots. (B): Suggested natural history of postsystolic shortening. Relative magnitude of postsystolic shortening throughout different populations as a function of relative magnitude of systolic deformation. ESL: early systolic lengthening.

Figure 2

Invasive and non-invasive methods for assessing deformation patterns. Legend: (A) Ventriculogram depicting the centerline method for assessing wall motion. (B) Circles in the myocardial walls indicate embedded ultrasonic crystals to determine segmental length during the cardiac cycle. (C) Strain rate map during ischemia, where black arrows indicate postsystolic shortening and white arrows indicate delayed systolic shortening. (D) Longitudinal speckle tracking profile showing early systolic lengthening and postsystolic shortening. (E) Tissue Doppler imaging of longitudinal displacement of the mitral valve annulus showing postsystolic shortening. (A–C) are reprinted from Hosokawa et al. [14], Amundsen et al. [15] and Pislaru et al. [16] with permission the American College of Cardiology (Elsevier). (D) is reprinted from Asanuma et al. [6] with permission from the British Medical Journal Publishing Group. (E) is reprinted from Brainin et al. [17] with permission from Springer Nature.

Figure 3

Deformation patterns during myocardial ischemia. Legend: (A) Longitudinal strain profiles in segment with normal wall motion (upper row) and segment with abnormal wall motion (lower row). Obtained before occlusion, 30 to 60 s after occlusion of LAD and 2 min after balloon reperfusion. The normal segment develops ESL and PSS after occlusion. The abnormal segment displays PSS at baseline, and the magnitude increases after occlusion. (B) Radial strain profiles of myocardial area exposed to 15 min (upper row) and 5 min (lower row) of coronary occlusion. Postsystolic thickening continues to appear after reperfusion in the segment exposed to 15 min of ischemia (indicating ‘ischemic memory’), whereas it disappears in the segment exposed to 5 min of ischemia. (A,B) are reprinted from Kukulski et al. [50] and Asanuma et al. [67] with permission from the American College of Cardiology (Elsevier). LAD: left anterior descending artery, AVC: aortic valve closure. PSS: postsystolic shortening, ESL: early systolic lengthening.