Left Ventricular Twist Mechanics in Heart Failure: Evolving Role in the Assessment of Cardiac Dyssynchrony

M Bertini, PP Sengupta, G Nucifora, V Delgado, ACT Ng, N Ajmone Marsan, M Shanks, RJ van Bommel, MJ Schalij, J Narula, JJ Bax

JACC Cardiovascular Imaging 2009

Disclosures

• Jeroen Bax received grants from Medtronic, Boston Scientific, Biotronik, St. Jude Medical, BMS medical imaging, Edwards Lifesciences & GE Healthcare

• Martin Schalij received grants from Biotronik, Medtronic & Boston Scientific

Introduction

The opposite rotation of LV apex and base leads to a LV systolic

wringing motion during systole referred to as twist. LV twist contributes significantly

to LV systolic function LV twist is an important aspect of cardiac mechanics that may be useful to characterize HF patients and effects of CRT on HF

Objects of the Review:

1. Overview of physiology of LV rotational mechanics;

2. Discussion on different LV twist patterns in systolic HF;

3. The evolving role of LV twist as a marker of LV dyssynchrony

for understanding response to CRT.

Normal LV Twist Mechanics

LV Twist is affected by:

1. Preload (directly related to LV end-diastolic volume)

2. Afterload (inversely related to LV end-systolic volume)

3. Contractility (directly related to positive inotropic interventions)

4. Increase gradually from infancy to adulthood

LV Twist in the Dyssynchronous, Failing Ventricle

Ischemic vs. Non-ischemic Failing Ventricle:

LV twist is more reduced in HF as compared to acute myocardial infarction

Different mechanisms underlying the reduction in LV twist:

1. In HF patients, LV twist impairment results from a long-standing process,

with a rearrangement of LV myofibers and loss of the specific LV architecture.

2. In acute myocardial infarction, the LV twist reduction may result from

an acute impairment in rotation of the LV region that is involved in the infarction.

LV Twist in the Dyssynchronous, Failing Ventricle

Relation LV Twist-Dyssynchrony:

Deleterious effects of asynchronous ventricular activation on LV performance

and the relation between the LV activation pattern and LV twist

RV pacing may determine

a dyssynchronous mechanical activation

and a deterioration of LV twist

LV Twist in CRT

Zhang et al. (Heart 2008): 39 HF pts• LV twist reduced in HF as compared to

normal• Improvement of LVEF 3 months after

CRT• No improvement of LV twist 3 months

after CRT

Sade et al. (Am J Cardiol 2008): 33 HF pts• LV twist reduced in HF as compared to

normal• Improvement of LVEF immediately after

CRT• Improvement of LV twist immediately after

CRT

Bertini et al. (J Am Coll Cardiol 2009): 80 HF pts• LV twist reduced in HF as compared to

normal• Improvement of LVEF immediately after and

6 months after CRT• Improvement of LV twist immediately after

and 6 months after CRT

LV Twist in CRT

LV twist progressively

improved in responders

Gradual deterioration

of LV twist in non-responders

Responders vs. Non-responders

LV Twist in CRT

Postero-lateral LV leads positioned in mid-ventricular and apical as compared to basal regions had a larger increase in systolic function with a significant increase in LV twist

LV Twist and LV Lead Position

Conclusions

LV twist mechanics is a promising tool for characterizing the pathophysiology of HF.

In advanced systolic HF, the rotational parameters are severely deteriorated and may be improved by restoring electro-mechanical activation through CRT.

LV lead position is important for modifying the extent of LV twist after CRT; in particular pacing sites which provide the greatest improvement of LV twist likely determine the largest reversal of LV remodeling after CRT