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Cardiovascular Research 1994 28(5):629-635; doi:10.1093/cvr/28.5.629
© 1994 by European Society of Cardiology
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Copyright © 1994, European Society of Cardiology

Rotational deformation of the canine left ventricle measured by magnetic resonance tagging: effects of catecholamines, ischaemia, and pacing

Maurice B Buchalter, Frank E Rademakers, James L Weiss, Walter J Rogers, Myron L Weisfeldt and Edward P Shapiro

Division of Cardiology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA: M B Buchalter, F E Rademakers, J L Weiss, W J Rogers, M L Weisfeldt, E P Shapiro.

Correspondence to Dr Buchalter, at Department of Cardiology, University Hospital of Wales, Heath Park, Cardiff CF4 4XW, United Kingdom.

Objective: The aim was to investigate the generation of rotation of the left ventricular apex with respect to the base by magnetic resonance tagging, a non-invasive method of labelling the myocardium, in a canine model. Methods: 18 dogs were imaged at baseline and during: (1) inotropic stimulation with dobutamine; (2) chronotropic stimulation with atrial pacing; (3) anterior wall ischaemia; (4) posterior wall ischaemia; and (5) varying left ventricular activation site; six dogs underwent each intervention. Apical rotation of the apex (torsion) was quantified. The epicardium and the endocardium were considered separately, as were the anterior and posterior walls. Results: Mean torsion of the epicardium [anterior 3.1(SEM 1.2)°, posterior 9.9(1.0)°] was less than that of the endocardium [anterior 8.1(2.6)°, posterior 14.9(2.0)°, p<0.05 for both]. Anterior torsion was less than posterior torsion for both the epicardium, p<0.05, and the endocardium, p<0.05. Dobutamine increased torsion of both the epicardium [anterior 13.3(2.2)°, posterior 12.6(1.7)°, p<0.05 for both] and the endocardium [anterior 24.6(2.3)°, posterior 16.5(2.1)°, p<0.05 for both]. Atrial pacing at 160% baseline rate increased torsion of both the anterior wall [epicardium 6.6(1.0)°, endocardium 11.3(1.2)°, p<0.05] and the posterior wall [epicardium 13.0(1.3)°, endocardium 19.4(1.9)°, p < 0.05]. Anterior wall ischaemia reduced torsion of the anterior wall only [epicardium –2.0(1.0)°, endocardium 6.7(2.3)°, both p<0.05]. Posterior wall ischaemia reduced torsion of the posterior wall of the epicardium only [7.1(1.2)°, p<0.05] but also reduced torsion of the anterior wall [epicardium 0.7(1.0)°, endocardium 2.4(1.6)°, p<0.05 for both]. Altering the pattern of left ventricular activation by atrioventricular pacing reduced torsion of the posterior wall of the epicardium [6.6(1.2)°, p<0.05] and of the anterior [3.6(1.9)°, p<0.05] and posterior [7.1(1.6)°, p<0.05] walls of the endocardium. Conclusions: Rotational deformation of the left ventricle is dependent on the pattern of left ventricular activation and the contractile state. That a decrease in the contractile state in one area (by ischaemia) can cause a decrease in rotation in another suggests that this rotation depends on the complex fiber arrangement of the whole ventricle.

Cardiovascular Research 1994;28:629-635

KEYWORDS left ventricular torsion; inotropic stimulation; ischaemia; pacing


Supported in part by NHLBI Ischemic Heart Disease SCOR grant HL- 17655-16, RO1-HL-43722 (JLW) and AHA grant 891230 (EPS). MBB performed this study while a research fellow at the Johns Hopkins University, supported by the Dublin University Travelling Scholarship in Medicine. Presented in part at the 62nd American Heart Association Scientific Sessions, November 1989.


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