How Not to Age — Presentation

[AnUser]

@Davin8r

Ok, so just to be clear when you say the 0.2mm/10% criteria for “clinically relevant regression in the literature”, you are referring to a single paper when you say “in the literature”, not some firmly-established generally agreed-upon criteria established in cardiology.

It’s not one paper and I think that’s how it works.

@Davin8r

Because one could argue that a smaller degree of regression IS clinically significant, based on the positive clinical outcomes in the experimental group of the Ornish study.

No, since you are not using what is considered clinically significant reduction in the literature. Either way, in that case you would have to accept that a progression of disease is clinically significant reversal of ASCAD because it also can coincide with a reduction of outcomes. It makes no sense. It is not reversal of plaque and thus atherosclerotic coronary artery disease (ASCAD).

If you see my responses to @Neo you will see why you need an increase in minimum diameter as well and why it is included in the definition.

How Not to Age — Presentation

Oldest/most papers on heart disease where actual reversal of plaque/stenosis demonstrated No as there was no reversal of plaque demonstrated, a mere decrease in percent diameter stenosis does not mean so. There needs to be an increase in minimum diameter as well. [image]

How Not to Age — Presentation

The result in the graph is meaningless without minimum diameter as I said. If you increase the reference diameter without changing the minimum diameter then the percent stenosis decreases without any regression in plaque. That’s why you need both and it needed to be 200 times larger than it was, and with 7% more reduction in diameter stenosis.

[Davin8r]

@AnUser

It’s not one paper and I think that’s how it works

I’d recommend reading the review paper I posted. The cut-off point for “clinically significant” is subjective/unknown when applied to diameter stenosis and MLD based on the current state of the literature. Smaller changes can be clinically (i.e. real-world) significant, as suggested by outcomes in the Ornish study.

[AnUser]

@Davin8r

The cut-off point for “clinically significant” is subjective/unknown when applied to diameter stenosis and MLD based on the current state of the literature.

It’s not unknown and all definitions are subjective, unless you want me to argue for definitions being objective, and the Ornish study used Quantitative Coronary Angiography, so you need a definition for clinically relevant regression (or regression at all) pertaining to that.

@Davin8r

Smaller changes can be clinically (i.e. real-world) significant, as suggested by outcomes in the Ornish study.

Or rather an intervention can improve outcomes without regression of plaque, clinically relevant or not… There was no regression as a result of the intervention.

Read again why minimum lumen diameter has to increase.

If you accept that reversal is a decrease in percent stenosis without an increase in MLD (which can happen because the reference diameter increases, like vasodilation), then you’d have to accept that pomegranate juice reverses disease, which Ornish has studied, or nitrates, and a bunch of other interventions with similar results.

[Davin8r]

“…progression and regression should be related to an increase or decrease in risk of rupture as opposed to an increase or decrease in percent luminal stenosis (which has no direct relationship to events). For example, an increase in necrotic core volume with positive remodeling and fibrous cap thinning, regardless of change in luminal stenosis, could be considered plaque progression. Similarly, a decrease in necrotic core volume with a resultant increase in the fibrous cap thickness and calcification of the cap, even in the presence of a mild increase in luminal stenosis caused by negative remodeling, could be considered plaque regression”

https://www.jacc.org/doi/10.1016/j.jacc.2019.08.012

The Ornish study didn’t have access to new imaging modalities of plaque quality/quantity, but it stands to reason that the plaques regressed since LDL was decreased by 40% and the outcomes were so much better, even compared to those in the control group who went on statins. Regression/remodeling of plaques can be interpreted as “reversal”, although “cure” is admittedly an exaggeration (unless symptoms and clinical events were completely prevented/reversed, then “clinical cure” would be more appropriate).

[AnUser]

@Davin8r

The Ornish study didn’t have access to new imaging modalities of plaque quality/quantity, but it stands to reason that the plaques regressed since LDL was decreased by 40% and the outcomes were so much better, even compared to those in the control group who went on statins. Regression/remodeling of plaques can be interpreted as “reversal”, although “cure” is admittedly an exaggeration (unless symptoms and clinical events were completely prevented/reversed, then “clinical cure” would be more appropriate).

No it does not stand to reason because outcomes can improve without a clinically relevant regression in plaque.

Do you agree that the Ornish study cannot be said to be evidence that the intervention regresses plaque and ASCAD? Or do you believe that an improvement in outcomes is reversal of plaque?