Get access

Ventricular Torsion and Untwisting: Further Insights into Mechanics and Timing Interdependence: A Viewpoint


Disclosure: Dr. Buckberg consults with Helical Heart Company LLC (, which makes a spatial heart model of helical ventricular myocardial band anatomic configuration. The other authors report no conflicts.

Address for correspondence and reprint requests: Gerald D. Buckberg, M.D., Department of Cardiothoracic Surgery, David Geffen School of Medicine at UCLA, 10833 Le Conte Avenue, 62–258 CHS, Los Angeles, California 90095. Fax: 210-825-5895; E-mail:


Ventricular torsion and untwisting are essential for normal ventricular function and their mechanisms are related to the temporal responses of the helical and circular muscle fibers that comprise cardiac architecture. Explanation of the presystolic isovolumic contraction (IVC) period is essential for analysis of these interactions. Structural and imaging studies by magnetic resonance, speckle tracking, velocity vector encoding, and sonomicrometer crystals are described to define why and how different muscular components contract asynchronously. Mechanical and functional relationships are described for pre-systolic IVC, torsion, postejection isovolumic interval, and rapid and slow filling. Circular fibers dominate to cause pre- and posttwisting global counterclockwise and clockwise movement, and helical fibers govern torsion whereby the base rotates clockwise and apex counterclockwise; untwisting cannot begin until torsion is completed. Prolonged torsion extends into the postejection isovolumic interval and delays untwisting, and is caused by prolonged contraction of the right-handed helical arm or descending segment of the helical ventricular myocardial band that narrows the ∼80 ms “timing hiatus” between end of shortening of the descending and the ascending segment or left-handed arm of the helical muscle. Longer torsion duration by this mechanism becomes the common theme for unbalanced torsion and untwisting in diastolic dysfunction, physiological, structural, and electrical disease processes, whose management may be guided by changing the interconnected reasons for these adverse mechanical and timing factors. (Echocardiography 2011;28:782-804)

Get access to the full text of this article