TY - JOUR
T1 - Vascular delay of the Latissimus dorsi provides an early hemodynamic benefit in dynamic cardiomyoplasty
AU - Ali, Ahsan T.
AU - Santamore, William P.
AU - Chiang, Ben Y.
AU - Dowling, Robert D.
AU - Tobin, Gordon R.
AU - Slater, A. David
N1 - Funding Information:
We thank Medtronic Inc (Minneapolis, MN) for providing technical support and ITREL pulse generators; Dr Sam Haydar for his technical expertise with computer software and data acquisition; and Drs James B. Sharp, Nancy I. Hughes, Edwin Ford, Dorothy Wilson, and rest of the RRC staff at the University of Louisville, Kentucky for providing dedicated animal care in the pre- and postoperative period. This study was supported in part by a grant by The Jewish Hospital Heart and Lung Foundation.
PY - 1999/5/1
Y1 - 1999/5/1
N2 - Objectives. Dynamic cardiomyoplasty (CMP) as a surgical treatment for chronic heart failure improves functional class status for most patients. However, significant hemodynamic improvement with latissimus dorsi muscle (LDM) stimulation has not been consistent. The current protocols do not allow early LDM stimulation after CMP surgery. We hypothesized that vascular delay of LDM would increase myocardial assistance after CMP and allow early (48-h) LDM stimulation after CMP. Methods. Mongrel dogs (n = 24) were divided in four groups: 1) controls (n = 6), single-stage CMP; 2) Group ES (n = 6), single-stage CMP with early LDM stimulation beginning 48 h, postoperatively; 3) Group VD (n = 6), vascular delay of the LDM followed by CMP without early LDM stimulation, and 4) Group VDES (n = 6), vascular delay of LDM (14-18 days), followed by CMP with early stimulation (48 h postoperatively). Two weeks after CMP, global Cardiac dysfunction was induced by injecting microspheres into the left coronary artery. LDM-assisted (S) beats were compared with nonstimulated beats (NS) by measuring aortic pressure (AoP), LV pressure, aortic flow, and by calculating first derivative of LV contraction (±dP/dt), stroke volume (SV), and stroke work (SW). Results. In ES, LDM stimulation had no effect on the hemodynamic parameters. In the other groups, LDM stimulation significantly (p < 0.05) increased AoP, LVP, dP/dt, SV, and SW. However, these increases were much larger in VD and VDES. In VD, LDM stimulation increased peak AoP by 21.5 ± 3.8 mm Hg, LVP by 22.1 ± 4.1 mm Hg, dP/dt by 512 ± 163 mm Hg/sec, SV by 10.4 ± 2.3 mL, and SW by 22.1 ± 5.4 g/m-1. Similarly, in VDES, LDM stimulation increased peak AoP by 24.1 ± 4.7 mm Hg, LVP by 26.2 ± 4.3 mm Hg, dP/dt by 619 ± 47 mm Hg/sec, SV by 6.5 ± 0.7 mL, and SW by 16.7 ± 4.1 g/m-1. Conclusions. In dogs with global LV dysfunction, CMP after vascular delay resulted in a significant improvement in hemodynamic function measured 2 weeks after surgery. This improvement was not provided by single-stage CMP with or without early stimulation. Vascular delay of the LDM before surgery may play an important role for early benefit after CMP, shorten the overall muscle training period, as well as increase hemodynamic response to LDM stimulation.
AB - Objectives. Dynamic cardiomyoplasty (CMP) as a surgical treatment for chronic heart failure improves functional class status for most patients. However, significant hemodynamic improvement with latissimus dorsi muscle (LDM) stimulation has not been consistent. The current protocols do not allow early LDM stimulation after CMP surgery. We hypothesized that vascular delay of LDM would increase myocardial assistance after CMP and allow early (48-h) LDM stimulation after CMP. Methods. Mongrel dogs (n = 24) were divided in four groups: 1) controls (n = 6), single-stage CMP; 2) Group ES (n = 6), single-stage CMP with early LDM stimulation beginning 48 h, postoperatively; 3) Group VD (n = 6), vascular delay of the LDM followed by CMP without early LDM stimulation, and 4) Group VDES (n = 6), vascular delay of LDM (14-18 days), followed by CMP with early stimulation (48 h postoperatively). Two weeks after CMP, global Cardiac dysfunction was induced by injecting microspheres into the left coronary artery. LDM-assisted (S) beats were compared with nonstimulated beats (NS) by measuring aortic pressure (AoP), LV pressure, aortic flow, and by calculating first derivative of LV contraction (±dP/dt), stroke volume (SV), and stroke work (SW). Results. In ES, LDM stimulation had no effect on the hemodynamic parameters. In the other groups, LDM stimulation significantly (p < 0.05) increased AoP, LVP, dP/dt, SV, and SW. However, these increases were much larger in VD and VDES. In VD, LDM stimulation increased peak AoP by 21.5 ± 3.8 mm Hg, LVP by 22.1 ± 4.1 mm Hg, dP/dt by 512 ± 163 mm Hg/sec, SV by 10.4 ± 2.3 mL, and SW by 22.1 ± 5.4 g/m-1. Similarly, in VDES, LDM stimulation increased peak AoP by 24.1 ± 4.7 mm Hg, LVP by 26.2 ± 4.3 mm Hg, dP/dt by 619 ± 47 mm Hg/sec, SV by 6.5 ± 0.7 mL, and SW by 16.7 ± 4.1 g/m-1. Conclusions. In dogs with global LV dysfunction, CMP after vascular delay resulted in a significant improvement in hemodynamic function measured 2 weeks after surgery. This improvement was not provided by single-stage CMP with or without early stimulation. Vascular delay of the LDM before surgery may play an important role for early benefit after CMP, shorten the overall muscle training period, as well as increase hemodynamic response to LDM stimulation.
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U2 - 10.1016/S0003-4975(99)00186-1
DO - 10.1016/S0003-4975(99)00186-1
M3 - Article
C2 - 10355402
AN - SCOPUS:0032989697
SN - 0003-4975
VL - 67
SP - 1304
EP - 1311
JO - Annals of Thoracic Surgery
JF - Annals of Thoracic Surgery
IS - 5
ER -