Left ventricular hypertrophy due to volume overload versus pressure overload

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.