Left ventricular (LV) fiber orientation changes from a right-handed helix in the subendocardium to a left-handed helix in the subepicardium (A). During isovolumic contraction (IVC), circumferential components of force (arrows) are generated by endocardial fiber shortening, which rotates the LV about the long axis clockwise as viewed from the apex (B). During ejection, shortening of subepicardial fibers wrapped in an opposite, left-handed helix rotates the LV counterclockwise (C). Twisting force by epicardial shortening overcomes the forces of subendocardial shortening because the torque of the epicardial force is larger due to a greater radius of the epicardial fibers from the central LV long axis.

Examples of left ventricular (LV) twist assessed with speckle tracking echocardiography in acute myocardial infarction (MI), and chronic ischemic versus nonischemic heart failure (HF). Of note, LV twist is markedly reduced in the patients with HF as compared with the patient with acute MI. In HF patients, LV twist impairment likely results from a long-standing process, with a rearrangement of LV myofibers and a consequent loss of the specific LV architecture that is responsible for the wringing motion. Conversely, in the setting of acute MI, the reduction in LV twist may result from an acute impairment in rotation of the LV region that is involved in the infarction.

Example of left ventricular (LV) twist during sinus rhythm (baseline) and during right ventricular (RV) pacing in a patient without structural heart disease. A standard diagnostic catheter was positioned in the RV apex as illustrated in the posteroanterior (PA) view at fluoroscopy (upper left) and the 4-chamber apical view at standard 2-dimensional echocardiography (upper right). The curves of LV rotational parameters at baseline (lower left panel) and during RV pacing (lower right panel) are shown. RV pacing induced a severe impairment in LV twist by decreasing both LV apical and basal rotation.

Example of left ventricular (LV) twist in 2 patients with dilated cardiomyopathy and severe LV dysfunction (LV ejection fraction <30%). Example of patients with synchronous (A) and with dyssynchronous LV contraction (B). In both the synchronous (A) and the dyssynchronous LV (B), the curves of the LV rotational parameters reveal reduced LV twist. Of note, the peaks of apical and basal rotation occur almost at the same time interval in the synchronous LV (A), whereas they occur at different time intervals in the dyssynchronous LV (B). In particular, in the dyssynchronous LV (B), apical rotation is markedly earlier as compared with the basal rotation, which may result in further worsening of LV twist.

A significant and progressive improvement of left ventricular (LV) twist was observed immediately after cardiac resynchronization therapy (CRT) and at 6 months' follow-up (22). ANOVA = analysis of variance.

(A) Example of responder to CRT. Peak LV twist increases progressively from baseline to 6-month follow-up. Immediately after CRT, LV twist increases secondary to an improved electromechanical activation of the LV. Further improvement is observed at 6-month follow-up when LV reverse remodeling has also occurred. The lower panels show the improvement in left ventricular ejection fraction (LVEF) and reduction in left ventricular end-systolic volume (LVESV) after 6-month follow-up. (B) Example of nonresponder to CRT. Peak LV twist declines progressively from baseline to 6 months' follow-up. The direction of LV apical rotation is reversed (negative pink dashed curve) immediately after CRT and at 6 months follow-up. At 6 months' follow-up, a reduction in LV basal rotation is also observed, which contributes to a further deterioration of LV twist. The lower panels show the parallel worsening in LVEF and LVESV after 6 months follow-up. Abbreviations as in Figure 5.

(A) Example of responder to cardiac resynchronization therapy (CRT) with the LV lead placed in a (postero)lateral vein with an apical position. Biplane fluoroscopy (left) displays the LV lead position. Particularly, the left anterior oblique (LAO) view shows the LV lead in the (postero)lateral vein whereas the PA view shows the LV lead in an apical position. Peak LV twist increased from 3.8° at baseline to 10.6° at 6-month follow-up. Left ventricular ejection fraction (LVEF) improved from 24% at baseline to 38% at 6-month follow-up. In this patient, pacing close to the LV apical region may produce a more physiological pattern of electromechanical activation, resulting in a significant improvement in LV twist. (B) Example of nonresponder with the LV lead placed in a lateral vein (LAO view) with a basal position (PA view). Peak LV twist decreased from 9.4° at baseline to 4.7° at 6-month follow-up. LVEF decreased from 30% at baseline to 26% at 6-month follow-up. In this patient, pacing close to the LV basal region may induce a further worsening of the electromechanical activation with a significant worsening of LV twist. Abbreviations as in Figure 3.