October 1, 1992
View Full PaperLeft ventricular hypertrophy due to volume overload versus pressure overload
Key Result
Chronic severe mitral regurgitation produced significantly less left ventricular hypertrophy (LVBW 5.0 vs 7.5; P<0.05) and more contractile dysfunction than aortic stenosis for similar stroke work.
Structured PICO
Does volume overload from mitral regurgitation produce a different hypertrophic response compared to pressure overload from aortic stenosis in a canine model?
P
Population
16 dogs with chronic severe mitral regurgitation or aortic stenosis, matched by stroke work or degree of hypertrophy.
E
Exposure
Chronic severe mitral regurgitation (volume overload)
C
Comparator
Severe chronic aortic stenosis (pressure overload)
O
Outcome
Adequacy of compensatory hypertrophy (left ventricular weight to body weight ratio, normalized stroke work, and contractile function)surrogate
In a canine model, the hypertrophic response to a similar stroke work demand is less in mitral regurgitation (volume overload) than in aortic stenosis (pressure overload), which is associated with contractile dysfunction in MR.
Main Result
Absolute Event Rate: 5% vs 7.5%
p-value: p=< 0.05
Abstract
Left ventricular hemodynamic overload produces an increase in stroke work (SW), which is compensated by the development of left ventricular hypertrophy. However, recent reports question the adequacy of this compensation in mitral regurgitation (MR). Accordingly, we examined the adequacy of compensatory hypertrophy in chronic experimental MR. Six dogs with chronic severe MR were matched according to SW with six dogs that had severe chronic aortic stenosis (ASSW). SW in the two groups was increased identically (40%) compared with normals. However, the hypertrophic response was much greater in the AS group left ventricular wt (g) to body wt (kg) ratio (LVBW) 4.0 +/- 0.2 normals, 5.0 +/- 0.2 MR, and 7.5 +/- 0.2 ASSW; P < 0.05 MR vs. ASSW. This differing hypertrophic response increased normalized SW, the area within the stress-volume loop, in MR (90 +/- 5 g) vs. 63 +/- 5 g in ASSW (P < 0.05). Thus in MR, each unit of myocardium had to perform more work than in AS. In a separate comparison, four different dogs with AS (ASHy), which had a similar amount of hypertrophy to the MR dogs (LVBW) (5.0 +/- 0.2 MR, 5.2 +/- 0.2 ASHy) were studied. SW was greater in the MR group, suggesting more SW overload was required to produce similar amounts of hypertrophy in MR vs. AS. Contractile function was depressed in the MR group but not in the AS. These findings indicate that the hypertrophic response to a similar SW demand is less in MR than AS, a response associated with contractile dysfunction in the MR group.