Key result
Selective MMP inhibition with PGE7113313 reduced LV peak wall stress (208 vs 319 g/cm2; P<0.05) in a porcine model of developing heart failure.
Why the study?
Does selective MMP inhibition improve hemodynamics and neurohormonal activation in a porcine model of developing heart failure?
RCT (n=32)
randomly assigned
Does selective MMP inhibition improve hemodynamics and neurohormonal activation in a porcine model of developing heart failure?
Absolute Event Rate: 208% vs 319%
p-value: p=<0.05
Selective MMP inhibition sparing MMP-1 improves LV mechanics and reduces neurohormonal activation in a porcine model of pacing-induced heart failure.
Hypothesis-generating for selective MMP inhibition in heart failure; leaves open clinical translation from this porcine model.
The matrix metalloproteinases (MMPs) are an endogenous family of proteolytic enzymes implicated to contribute to LV remodeling. However, broad-spectrum MMP inhibition (MMPi), particularly inhibition of interstitial collagenase (MMP-1), may not be clinically applicable. This study examined the effects of selective MMPi (sparing MMP-1) in a model of developing congestive heart failure. Pigs were randomly assigned to 3 groups: (1) rapid pacing for 3 weeks (240 bpm, n=10); (2) selective MMPi (20 mg/kg per day-PO;PGE7113313) and rapid pacing (n=12); and (3) controls (n=10). LV peak wall stress increased from controls with rapid pacing (140+/-6 versus 319+/-18 g/cm2; P<0.05) and was reduced with selective MMPi (208+/-9 g/cm2; P<0.05. Preload recruitable stroke work was reduced with rapid pacing (4.3+/-0.4 versus 1.2+/-0.2 dyne. cm/mm Hg; P<0.05) and was increased with selective MMPi (2.6+/-0.3 dyne. cm/mm Hg; P<0.05). Plasma norepinephrine increased by 6-fold in the rapid pacing group (P<0.05) and was reduced from untreated values with selective MMPi (P<0.05). At the myocardial level, myocyte cross-sectional area was increased with selective MMPi but fibrillar collagen volume fraction remained unchanged relative to control values. These results suggest that targeting a selective portfolio of myocardial MMP species for inhibition may provide a more rational therapeutic strategy in the setting of congestive heart failure.
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King et al. (2003) conducted an RCT in Developing congestive heart failure (n=32). Selective MMPi (PGE7113313) vs. Rapid pacing (untreated) and normal controls was evaluated on LV peak wall stress (p=<0.05). Selective MMP inhibition with PGE7113313 reduced LV peak wall stress (208 vs 319 g/cm2; P<0.05) in a porcine model of developing heart failure.
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