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sts66

07/13/20 1:56 PM

#285828 RE: funnygi2 #285681

Big diff is that Nelson spelled out the RRR's and Budhoff did not - compare the impact of reading:

there was a significant, 42% slowing of progression of total plaque volumes (non-calcified +calcified plaque)(15% versus 26%,p=0.0004),a significant 19% slowing in progression of total non-calcified plaque(sum of LAP,fibrofatty and fibrous plaque) volumes(35% versus 43%,p=0.010) and a significant 57% slowing of progression fibrous plaque volumes(17% versus 40%,p=0.011).Surprisingly,and very interesting was the 89% reduction in progression of calcified plaque volumes(-1% versus 9%,p=0.001)



To this much blander statement lacking RRR's:

there was slowing of total non-calcified plaque (sum of LAP, fibrofatty, and fibrous plaque)(35% v. 43%,p=0.010), total plaque (non-calcified + calcified plaque)(15% v. 26%,p=0.0004), fibrous plaque (17% v. 40%,p=0.011) and calcified plaque (-1% v. 9%,p=0.001)




He posted this tidbit in the comments section, they found a connection between HDL and plaque - I think he's saying that raising HDL decreased plaque in women but not men:

There are many exciting secondary endpoints we will be evaluating.Check out my LinkedIn Post on 7/7/20.We just published from baseline EVAPORATE data for the first time in patients with coronary atherosclerosis on statin therapy with elevated triglycerides that increasing HDL-c levels were independently associated with lower volumes of baseline coronary plaque on CCTA including total non-calcified plaque(p=0.042) and total plaque(p=0.035) in all trial participants.We also made a novel observation regarding women. We showed for the first time ,in an exploratory analysis,that high HDL-c levels were independently associated with decreasing plaque volumes on CCTA in females when compared with male-statin treated participants with elevated triglycerides.