LVH-BM ACC '21

Hi and thank you so much for joining me today

for a short audio tour of our project entitled left

ventricular hypertrophy and biomarkers of cardiac damage and stress and

aortic stenosis.

My name is Elliot Stein and I am a second

year internal medicine resident at Vanderbilt.

I'm really excited to apply for fellowship in cardiology This

coming summer I've had the distinct honor of working with

my P.

I. Dr brian lemon and the rest of this fabulous

cadre of co authors on this project.

We studied the relationship between left and curricular hypertrophy, cardiac

damage and stress and the probability of survival at five

years after Tavern.

So we'll start with a little background.

Left ventricular hypertrophy often develops in response to pressure overload

from aortic stenosis and it is already well known that

there is an adverse association between greater LVE me left

ventricular mass index and worse clinical outcomes among patients with

severe as treated with Tavern.

But what is not yet known is whether preoperative biomarkers

of cardiac damage and stress namely plasma troponin and anti

pro BMP can further risk stratify those with severe A.

S. And left ventricular hypertrophy.

Going on to receive Tavern.

We used a multi center prospective registry of patients with

severe A.

S. Undergoing Taber which yielded 674 subjects with a mean

age of 82 years and was approximately 44%.

Female Patients had a mean sts score of 5.3.

We use core lab measured LV mass index.

In addition to other standard echocardiogram thick dimensions, We also

obtained preoperative plasma troponin Anti Pro Bmp on bank specimens

which were all quantitative ana rocha say we then used

adjusted cox proportional hazard models and restricted cube explains to

evaluate associations between L.

V. H.

And biomarkers and all cause death.

We made adjustments for age sex Bme sts, core hemoglobin,

creating clearance Taber approach left ventricular ejection fraction, presence of

oxygen dependent lung disease, mitral regurgitation severity, presence of a

fib or flutter and presence of active cancer.

So now let's take a look at figure one.

This figure shows the proportion of biomarker elevation among females,

males and both.

And it also stratified biomarker levels by L.

V. H.

Severity. Looking for some troponin, which is represented by the

blue graphs.

You can see that in females, males in both sexes

together, there is a statistically significant up trend in the

proportion of patients with elevated troponin.

Moreover, absolute troponin concentration increases as L.

V. H severity increases, which is represented in the box

and whisker plots now moving over to anti pro Bmp,

represented by the green group graphs.

We can observe the same findings hold true as with

your opponent.

Finally, when combining troponin and anti pro Bmp as expected,

increasing L.

V. H.

Results in a statistically significant increase in the fraction of

patients who had elevations in both biomarkers.

So we can conclude from this figure that elevations in

these biomarkers are both common and they are also correlated

with worsening L.

V. H.

Now I'd like to return our attention to the table.

This table describes each of the four adjusted cox proportional

hazard models that we studied in the first model.

We compared moderate severe LDH to know and mild L.

V. H.

We found that the five year mortality rate for moderate

severe LDH trended higher than with no mild L.

V. H.

With a P value of 0.059.

However, this effect was attenuated after adjustment as you can

see in model one of the table for context.

Partner trial data showed an independent association between increased LDH

and five year mortality with a similar point estimate as

our study.

But the partner trial had higher power with a sample

size around 4000 patients moving to model to.

We compared moderate severe LV.

H. As sub classified by biomarker elevations to know mild

and LDH.

Which serves as the reference.

You can see here that only when patients had both

moderate severe LV H and have an elevation in troponin

or anti pro BNP, is there a statistically significant hazard

of all cause death at five years?

1.4 fold for troponin and 1.3 fold for anti pro

Bmp. Since we observed a high percentage of patients with

no mild L.

V. H.

Having elevated biomarkers.

As I showed in figure one, we also asked whether

biomarkers could risk stratify patients with no mild LDH, which

is shown in Model three.

Here we separate the no mild and moderate severe LV.

H groups into those with elevated biomarkers versus those with

normal biomarkers.

And then compare them to the reference of no mild

L. V.

H. Without biomarker elevation.

Here we observed that even among those without significant L.

V. H.

There is an excess hazard of death on the order

of 1.78 fold for troponin And 1.37 fold for anti

pro bmp.

Expectedly this result holds true and the relationship is even

stronger among those who have both moderate severe LV.

H. And biomarker elevation.

You can see that the elevated hazard that the hazard

of all cause death is 2.2 for troponin elevation and

1.7 for anti pro BMP elevation, importantly, the deleterious effect

of L.

V. H was completely attenuated when comparing those who had

modern severe LV.

H. Without a biomarker elevation to the reference, suggesting that

the excess risk is captured by biomarkers.

Finally, model for Model four looks at the hazard of

all cause death among those with and without biomarker elevations.

When controlling for L.

V. H.

We observe that the hazard of all cause death as

1.94 and 1.45 for for cardiac troponin, anti pro BMP

elevation respectively.

Furthermore, there is no interaction between troponin and anti pro

BMP, suggesting that biomarker elevations are associated with all cause

death independent of L.

V. H.

And independent of each other.

To conclude this point, the bottom of the table says,

is the interaction between L.

V. H.

Severity and biomarker concentration, finding that there is no interaction

between these variables, suggesting again that the excess risk seen

in those with biomarker elevations is independent of LDH severity.

As you can see, there are several more figures.

But in the interest of time, I will not go

over them.

During this brief tour, I'm of course happy to answer

any questions about them during the chat.

So to summarize the bottom line is this, we used

a multi center prospective registry yielding 670 for patients with

severe A.

S. Who received Tavern.

We showed several key things.

First, the majority of subjects with severe A.

S. And her cohort had elevations in plasma levels of

cardiac troponin and anti pro BMP.

These elevations became more common as the amount of left

ventricular hypertrophy increased.

Second, the biomarkers cardiac troponin and anti pro Bmp were

able to robustly risk stratify patients with moderate severe LV.

H. Undergoing tavern, but also risk stratified patients with known

mild LVMH.

In other words, the presence of L.

V. H.

Did not alter the increased hazard of death conferred by

elevated cardiac troponin and anti pro BMP.

When examined together, troponin and anti pro BMP reached independently

associated with mortality after tavern.

Whereas L.

V. H.

Was not, I'll finish with a few points of discussion

First, the limitations one our sample size was likely too

small to show that L.

V. H.

Severity is related to all cause death to.

We did not have follow up echocardiogram phycor biomarker data

to assess for regression Three, we could not report rehospitalization

rates among each group because that data was not available

for our cohort was unfortunately highly biased towards white individuals

and five all patients in the study had symptomatic s.

Nevertheless, to our knowledge, this is the largest study incorporating

core lab red echo and centrally measured biomarker concentrations.

To date to conclude the increased hazard of mortality associated

with greater LDH observed in prior studies appears to be

due at least in part two more frequent and severe

cardiac damage and stress, rather than increased LV mass per

se. These findings may have important implications for risk stratification

and treatment of patients with S.

Thank you so much for joining me.

LVH-BM ACC '21

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