Vascular delay and intermittent stimulation: keys to successful latissimus dorsi muscle stimulation.
BACKGROUND
The goal of this study was to obtain physiologically significant increases in peak left ventricular (LV) systolic pressure and stroke volume with latissimus dorsi muscle (LDM) stimulation in cardiomyoplasty (CMP). We hypothesized that preserving LDM integrity by vascular delay and intermittent stimulation would significantly increase LDM cardiac assistance.


METHODS
In 4 control dogs and 12 dogs that had undergone a vascular delay (VD) procedure, LV dysfunction was induced by intracoronary microsphere injections. Cardiomyoplasty surgery was performed 14 days later, followed by progressive LDM conditioning. In the control dogs and in 6 of the VD dogs, the LDM was stimulated 24 hours per day (VD plus constant stimulation [CS]). In the other 6 VD dogs, LDMs were stimulated on a daily schedule of 10 hours on and 14 hours off (VD plus interrupted stimulation [IS]). Latissimus dorsi muscle stimulated beats were compared with nonstimulated beats 9 weeks later.


RESULTS
In the control dogs, LDM stimulation had minimal effects. In VD + CS and VD + IS, LDM stimulation increased peak LV pressure, stroke volume, stroke work, and stroke power (p < 0.05). However, these changes were greater in the VD + IS group, in which LDM stimulation increased peak aortic pressure by 17.6 +/- 1.7 mm Hg, peak LV pressure by 19.7 +/- 1.1 mm Hg, peak positive LV dp/dt by 398 +/- 144 mm Hg per second, stroke volume by 5.1 +/- 0.7 mL, stroke work by 10.9 +/- 0.9 gm.m, and stroke power by 122.7 +/- 11.6 gm.m per second (p < 0.05 compared with VD + CS). Quantitative morphometric analysis showed minimal LDM degeneration in the VD + IS group (7.5% +/- 1.1%), and VD + CS group (10.5% +/- 4.5%) compared with the control group (29.5% +/- 4.5%, p < 0.05).


CONCLUSIONS
VD and IS considerably increased the LV assistance with LDM stimulation. Further studies of this combined approach to CMP should be planned.
Kashem
A
A
Division of Cardiovascular Research, Temple University, Philadelphia, Pennsylvania 19140, USA. mkashem@temple.edu
Santamore
W P
WP
Chiang
B
B
Unger
L
L
Ali
A T
AT
Slater
A D
AD
D000818:Animals; D018421:Cardiomyoplasty / Q000379:methods*; D003971:Diastole / Q000502:physiology; D004285:Dogs; D004558:Electric Stimulation / Q000379:methods; D019157:Ischemic Preconditioning, Myocardial; D009200:Myocardial Contraction / Q000502:physiology*; D013318:Stroke Volume / Q000502:physiology*; D013599:Systole / Q000502:physiology; D018487:Ventricular Dysfunction, Left / Q000503:physiopathology / Q000601:surgery*; D016277:Ventricular Function, Left / Q000502:physiology*