Key result
Left ventricular assist device support in dilated cardiomyopathy increased LV collagen cross-linking, type I to III ratio, and myocardial stiffness compared to unsupported hearts (P<0.05).
Why the study?
Does mechanical unloading with LVAD support alter left ventricular collagen cross-linking and myocardial stiffness in patients with idiopathic dilated cardiomyopathy?
Observational (n=51)
Does mechanical unloading with LVAD support alter left ventricular collagen cross-linking and myocardial stiffness in patients with idiopathic dilated cardiomyopathy?
p-value: p=<0.05
Mechanical unloading with LVAD support in failing hearts increases left ventricular collagen cross-linking and myocardial stiffness, likely driven by decreased collagen degradation and increased angiotensin levels.
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LVAD unloading was associated with increased myocardial stiffness in dilated cardiomyopathy; hypothesis-generating for remodeling effects, prospective studies needed.
Klotz et al. (2005) conducted an observational in Idiopathic dilated cardiomyopathy (n=51). Left ventricular assist device (LVAD) support vs. DCM without LVAD support and nonfailing hearts was evaluated on Left ventricular size, mass, myocyte diameter, collagen content/cross-linking, and myocardial stiffness (p=<0.05). Left ventricular assist device support in dilated cardiomyopathy increased LV collagen cross-linking, type I to III ratio, and myocardial stiffness compared to unsupported hearts (P<0.05).
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