Cardiac Binding in Experimental Heart Failure

Background. Cardiomyoplasty is a potential therapy for heart failure. Its benefits are attributed to systolic augmentation (dynamic cardiomyoplasty) and prevention of cardiac dilatation (static cardiomyoplasty). To evaluate the static component, we used an artificial membrane for cardiac binding in...

Full description

Saved in:
Bibliographic Details
Published in:The Annals of thoracic surgery Vol. 64; no. 1; pp. 81 - 85
Main Authors: Vaynblat, Mikhail, Chiavarelli, Mario, Shah, Himansu R, Ramdev, Geeta, Aron, Michelle, Zisbrod, Zvi, Cunningham, Joseph N
Format: Journal Article
Language:English
Published: Netherlands Elsevier Inc 01-07-1997
Subjects:
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Background. Cardiomyoplasty is a potential therapy for heart failure. Its benefits are attributed to systolic augmentation (dynamic cardiomyoplasty) and prevention of cardiac dilatation (static cardiomyoplasty). To evaluate the static component, we used an artificial membrane for cardiac binding in a canine model of heart failure. Methods. Intracoronary doxorubicin was administered weekly for 4 weeks to induce heart failure in 10 dogs, each of which was assigned to one of two treatment groups: (1) no treatment, or (2) cardiac binding. Hemodynamic data were obtained at operation and at 7 weeks after operation. Echocardiography was performed weekly. Results. Left ventricular end-diastolic pressure and diameter, and right ventricular end-diastolic diameter increased in group 1 (from 9.6 ± 6.1 to 19.6 ± 2.3 mm Hg, p = 0.009; from 3.9 ± 0.4 to 5 ± 0.3 cm, p = 0.0013; and from 1.6 ± 0.2 to 1.9 ± 0.3 cm, p = 0.0036, respectively). Ejection fraction fell in group 1 from 0.60 ± 0.10 to 0.40 ± 0.04 ( p = 0.0009) and in group 2 from 0.56 ± 0.02 to 0.40 ± 0.04 ( p = 0.0001), but the difference between groups was not significant. Conclusion. Cardiac binding reduces the ventricular dilatation associated with heart failure without exacerbating left ventricular dysfunction.
ISSN:0003-4975
1552-6259
DOI:10.1016/S0003-4975(97)00349-4