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PubMed1994

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

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) degrees, posterior 9.9(1.0) degrees] was less than that of the endocardium [anterior 8.1(2.6) degrees, posterior 14.9(2.0) degrees, 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) degrees, posterior 12.6(1.7) degrees, p < 0.05 for both] and the endocardium [anterior 24.6(2.3) degrees, posterior 16.5(2.1) degrees, p < 0.05 for both]. Atrial pacing at 160% baseline rate increased torsion of both the anterior wall [epicardium 6.6(1.0) degrees, endocardium 11.3(1.2) degrees, p < 0.05] and the posterior wall [epicardium 13.0(1.3) degrees, endocardium 19.4(1.9) degrees, p < 0.05]. Anterior wall ischaemia reduced torsion of the anterior wall only [epicardium -2.0(1.0) degrees, endocardium 6.7(2.3) degrees, both p < 0.05]. Posterior wall ischaemia reduced torsion of the posterior wall of the epicardium only [7.1(1.2) degrees, p < 0.05] but also reduced torsion of the anterior wall [epicardium 0.7(1.0) degrees, endocardium 2.4(1.6) degrees, 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) degrees, p < 0.05] and of the anterior [3.6(1.9) degrees, p < 0.05] and posterior [7.1(1.6) degrees, 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.

Animals↗
PubMed1984

Purkinje-muscle coupling and endocardial response to hyperkalemia, hypoxia, and acidosis.

Previously we found that combined hyperkalemia, hypoxia, and acidosis depressed the electrical activity of canine epicardium more than that of endocardium or Purkinje fibers. In this study, we determined whether the resistance of endocardium to these components of ischemia was due to electrotonic interactions with Purkinje fibers. The effects of combined hyperkalemia, hypoxia, and acidosis were tested on endocardial cells that were electrically uncoupled from Purkinje cells ("uncoupled" endocardium), due to their location or to prior exposure to elevated [Ca2+]. During control, action potentials in uncoupled endocardium had shorter durations than endocardium coupled to Purkinje ("coupled" endocardium), but had similar amplitudes, upstroke velocities, and resting potentials. During combined hyperkalemia, hypoxia, and acidosis, action potentials in uncoupled endocardium were more depressed than in coupled endocardium and resembled those in depressed epicardium. In addition, the combination of these components of ischemia produced electrical uncoupling at the Purkinje-muscle junction, although each component alone did not. Thus the resistance of endocardial cells to some components of ischemia appears to involve electrotonic interactions with Purkinje cells, which may be prevented by ischemia-induced electrical uncoupling.

Acidosis↗