Please understand I'm not saying the veins are *identical*. What I'm saying is that if all of these considerations ("sicker" vs "healthier" vs "comorbidities) make an impact on the way a relatively simple enzyme digests elastin when dripped on a vessel, then why are none of the underlying surrogates for improved AVF impacted?
Vein diameter data, blood flow rate and hemodynamically significant stenosis are all unchanged with treatment of RCF or BCF. So if the underlying mechanics of the AVF are unchanged, how do you reconcile a magical subgroup popping out of the data?
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