K. Fujita et al., THE EFFECTS OF LEFT-HEART ASSIST ON RIGHT-VENTRICULAR MUSCLE MECHANICS AND VENTRICULAR COUPLING IN THE INJURED HEART, Journal of thoracic and cardiovascular surgery, 108(3), 1994, pp. 477-486
So that we could better characterize the effects of left heart assist
on right ventricular myocardial muscle mechanics and ventricular mecha
nical coupling in the injured heart, nine dogs underwent 30 minutes of
global cardiac ischemia supported by cardiopulmonary bypass followed
by randomly varied levels of left heart assist at 0, 1.0, and 2.0 L/mi
n (0, 37 +/- 4, and 74 +/- 7 ml/kg per minute). A centrifugal pump wit
h left ventricle-to-aorta bypass was used with the intent to cause lef
t ventricular volume unloading but without complete left ventricular p
ressure unloading. Right ventricular regional free wall and septal-fre
e wall dimensions were measured by a sonomicrometer and right ventricu
lar pressure by a micromanometer. Pressure and dimension data were acq
uired over a range of preloads produced by transient vena caval occlus
ion and at steady state at an initial control point and after ischemia
at each level of left heart assist. Right ventricular regional early
diastolic function was assessed by percent segmental relaxation during
the first third of diastole, end-diastolic compliance by the end-dias
tolic pressure-dimension relationship, systolic contractile performanc
e by the slope (M(w)) and dimension axis intercept (L(w)) of the linea
r preload recruitable stroke work relationship, and right ventricular
isovolumic relaxation by the pressure decay time constant. Ischemia re
duced M(w) of both the free wall (38.3 +/- 16.1 to 16.4 +/- 4.2 erg cm
(-3) 10(3), p < 0.01) and septal free wall (30.2 +/- 12.7 to 13.4 +/-
4.9 erg.cm(-3).10(3), p < 0.01) and shifted L(w) rightward (1.3 +/- 0.
3 to 1.4 +/- 0.3 mm, p < 0.01, and 2.8 +/- 0.8 to 3.0 +/- 0.9 mm, p <
0.01), which confirmed myocardial ischemic injury. There were no effec
ts of left heart assist on free wall or septal-free wall systolic cont
ractile performance assessed by M(w) and L(w) or on early diastolic re
laxation assessed by percent segmental relaxation during the first thi
rd of diastole in either right ventricular region (all p = not signifi
cant). There were also no observed characteristic alterations of free
wall or septal-free wall end-diastolic pressure-dimension relationship
s with left heart assist. The pressure decay time constant decreased w
ith increasing levels of left heart assist (51 +/- 14, 49 +/- 16, and
43 +/- 11 msec, p < 0.05), which indicated an improvement in right ven
tricular isovolumic relaxation attributable to left heart assist. Thes
e data demonstrate that mechanical ventricular interactive effects dur
ing left heart assist are beneficial, but limited to isovolumic relaxa
tion in the injured heart. The likely optimal method of left heart ass
ist for postcardiotomy support should sufficiently augment cardiac out
put and arterial pressure but maintain left ventricular systolic press
ure generation to preserve beneficial ventricular mechanical coupling.