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J Thorac Cardiovasc Surg 2002;124:43-49
© 2002 The American Association for Thoracic Surgery

Cardiopulmonary Support and Physiology (CSP)

Alterations in left ventricular torsion in tachycardia-induced dilated cardiomyopathy

From the Department of Cardiovascular and Thoracic Surgery,^a Division of Cardiovascular Medicine,^b Stanford University School of Medicine, Stanford, Calif, and the Laboratory of Cardiovascular Physiology and Biophysics,^c Research Institute of the Palo Alto Medical Foundation, Palo Alto, Calif.

Supported by grants HL-29589 and HL-67025 from the National Heart, Lung, and Blood Institute. Drs Tibayan, Lai, Timek, and Dagum are Carl and Leah McConnell Cardiovascular Surgical Research Fellows. Dr Timek is a recipient of the Thoracic Surgery Foundation Research Fellowship. Drs. Timek, Dagum, and Tibayan were supported by NHLBI Individual Research Service Awards HL-10452, HL-09569, and HL-67563, respectively. Dr Lai was supported by a fellowship from the American Heart Association, Western States Affiliate.

Received for publication Aug 8, 2001. Revisions requested Sept 17, 2001; revisions received Oct 12, 2001. Accepted for publication Oct 24, 2001. Address for reprints: D. Craig Miller, MD, Department of Cardiovascular Surgery, Falk Cardiovascular Research Center, Stanford University School of Medicine, Stanford, CA 94305-5247 (E-mail: dcm{at}leland.stanford.edu).

Objective: Left ventricular torsion reduces transmural systolic gradients of fiber strain, and torsional recoil in early diastole is thought to enhance left ventricular filling. Left ventricular remodeling in dilated cardiomyopathy may result in changes in torsion dynamics, but these effects are not yet characterized. Tachycardia-induced cardiomyopathy is accompanied by systolic and diastolic heart failure and left ventricular remodeling. We hypothesized that cardiomyopathy would alter systolic and diastolic left ventricular torsion mechanics, and this hypothesis was tested by studying sheep before and after the development of tachycardia-induced cardiomyopathy.
Methods: Implanted miniature radiopaque markers were used in 8 sheep to measure left ventricular geometry and function, maximal torsional deformation, and early diastolic recoil before and after rapid ventricular pacing was used to create tachycardia-induced cardiomyopathy.
Results: All animals had significant heart failure with ventricular dilatation and remodeling. With tachycardia-induced cardiomyopathy, maximum torsion relative to control conditions decreased (1.69° ± 0.61° vs 4.25° ± 2.33°), and early diastolic recoil was completely abolished (0.53° ± 1.19° vs -1.17° ± 0.94°).
Conclusions: Cardiomyopathy is accompanied by decreased and delayed systolic left ventricular torsional deformation and loss of early diastolic recoil, which may contribute to left ventricular dysfunction by increasing systolic transmural strain gradients and impairing diastolic filling. Analysis of left ventricular torsion with radiofrequency-tagging magnetic resonance imaging should be explored to elucidate the role of torsion in patients with cardiomyopathy.

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