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LVAD unloading associated with increased microvascular density, fibrosis
Drakos S. J Am Coll Cardiol. 2010;56:382–91.
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Left ventricular assist device unloading led to increased microvascular density and was accompanied by increased fibrosis and no indication of cardiomyocyte atrophy in patients with chronic HF, according to new study results.
Researchers collected hemodynamic data and LV tissue from patients with chronic end-stage HF at LVAD implant and explant (n=15), as well as from normal donors (n=8).
“New advances in digital microscopy provided a unique opportunity for comprehensive whole-field, endocardium-to-epicardium evaluation for microvascular density, fibrosis, cardiomyocyte size and glycogen content,” the researchers said.
Hemodynamic data indicated significant pressure unloading with LVAD and was accompanied by a 33% increase in microvascular density (P=.001) and a 36% decrease in microvascular lumen area (P=.028). Researchers also identified ultrastructural and immunohistochemical evidence of endothelial cell activation. Additionally, interstitial and total fibrosis increased in failing hearts vs. normal donor hearts and increased further after LVAD unloading by 61% (P<.001) in interstitial fibrosis and 35% (P=.001) in total fibrosis.
“The LVAD-induced unloading of the failing human heart increased microvascular density and was accompanied by endothelial cell activation, increased fibrosis and no structural, ultrastructural or metabolic changes compatible with cardiomyocyte degeneration and atrophy,” the researchers concluded. “These clinical findings might guide future studies aimed at unloading-induced reverse remodeling of the failing human heart.”
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