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Ann Thorac Surg 2002;74:514-521
© 2002 The Society of Thoracic Surgeons
a Department of Cardiac Surgery, Bundes Krankenhaus, Koblenz, Germany
b Department of Cardiac Surgery, Civic Hospital, Brescia, Italy
c Department of Cardiothoracic Surgery, Tel Aviv Medical Center, Tel Aviv, Israel
d Department of Cardiac Surgery, St Raphael Hospital, Milan, Italy
e Department of Cardiothoracic Surgery, Academic Hospital, Cardiovascular Research Institute Maastricht, Maastricht, The Netherlands
Accepted for publication April 21, 2002.
* Address reprint requests to Dr van der Veen, Department of Cardio-thoracic Surgery, Academic Hospital Maastricht, P. de Bijelaan 25, 6229 HX Maastricht, The Netherlands
e-mail: fvv{at}scpc.azm.nl
Background. Reduction of ventricular dilatation, rather than direct improvement of pump function, has been suggested to be the main working mechanism of dynamic cardiomyoplasty (CMP). This working mechanism was examined in the goat using a chronic cardiac dilatation model induced by the creation of a cervical arteriovenous shunt and submitted to passive and active CMP.
Methods. Fourteen female goats underwent surgical creation of a shunt between the left carotid artery and the jugular vein. Seven goats had no additional operation (control group). The other 7 goats (CMP group) underwent CMP approximately 8 weeks after the creation of the shunt. The wrapped left latissimus dorsi muscle was left unstimulated for 2 weeks, and subsequently stimulated electrically for a 3-month period, using a 1:4 muscle-to-heart contraction ratio. Hemodynamic measurements included heart catheterization and determination of left ventricular (LV) pressure-volume relations by means of the conductance catheter method at baseline, after 8 weeks (only in the CMP group), and after 5 months. Transthoracic echocardiography was performed just before opening the AV shunt and every 2 weeks thereafter.
Results. Significant ventricular enlargement, as well as persistent increase in filling pressures, were observed after 8 weeks. Animals in the control group dilated further beyond 2 months (LV end-diastolic diameter from 39 ± 2 to 67 ± 6 mm). In contrast, the ongoing LV dilatation process was stopped by passive CMP, and LV end-diastolic diameter significantly decreased after electrical activation of the wrapped skeletal muscle (from 63 ± 7 to 42 ± 6 mm). Cardiomyoplasty also significantly increased the slope of the end-systolic pressure-volume relation (elastance) when compared with pre-CMP values (from 0.9 ± 0.2 to 1.7 ± 0.5 mm Hg/mL), which indicated an improvement of the LV contractile state. No significant hemodynamic effects could be observed at the tuned stimulation settings on a beat-to-beat basis during electrical muscle stimulation.
Conclusions. The contribution of CMP to LV dimension and contractility appeared to be either passive or active, and this study suggests the importance of stimulating the latissimus dorsi muscle to enhance the girdling effects of the wrapped latissimus dorsi muscle and to improve LV contractility.
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