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Dr. Neeraja Yedlapati University Tennessee, Memphis [email protected] CORONARY CALCIUM SCORE THE PAST, PRESENT AND FUTURE

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Page 1: Coronary Calcium Score The Past, Present and Futuretnacc.org/wp-content/uploads/2017/04/Coronary-Calcium...For a patient with an ASCVD risk of 7.5%, his or her benefit from statin

Dr. Neeraja Yedlapati

University Tennessee, Memphis

[email protected]

CORONARY CALCIUM SCORE

THE PAST, PRESENT AND FUTURE

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• Early autopsy showed that patients who died of CAD had 2-5

times as much calcium as those who died of other causes

• Calcium deposition was believed to be the result of a

degenerative process

• Evidence now suggests an active process, perhaps related to

inflammation and repair process seen in atherosclerotic lesions

• Inflammation, propagated by apolipoproteins and oxidized

phospholipids in the artery wall, is critical to the development of

both atherosclerosis and vascular calcification.

PATHOPHYSIOLOGY

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ATHEROSCLEROTIC BURDEN

• CAC quantification was found to be an excellent anatomic

measure of atherosclerotic plaque burden

• The close correlation between the atherosclerotic plaque burden

and the extent of CAC has been confirmed both by

histopathology and intravascular ultrasound

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MDCT

• Faster gantry rotation and multiple detectors is able to provide a

quantitative CAC (Volume score/ Agatston Scoring)

• It takes about 10-15 mins

• Noncontrast, gated study

• Radiation dose – 1mSv

• Screening mammogram

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CALCIFIED LESIONS BY CT

• Calcific lesion by CT -minimum of 3 contiguous pixels with an

attenuation threshold of 130 Hounsfield units (HU)

• Area of each lesion was multiplied by a density factor based on

the maximum HU within the area (1 for lesions with peak

attenuation of 130–199, 2 for 200–299, 3 for 300–399, and 4 for

400 or greater).

• CAC score was obtained by summing individual lesion scores

from each of the four arteries where calcium was assessed: left

main, left anterior descending, left circumflex, and right coronary

artery

• Calcium volume scores and Agatston scores

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FRAMINGHAM 10YR RISK SCORE

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ACC/AHA 2013 guideline which uses

ASCVD risk score and a cut off of

≥7.5% for initiation of moderate to

high intensity statin

Does not account for Family History of

CAD

In those patients with pooled cohort

risk score <7.5%, about two-thirds of

these patients have a FRS of >10%.

This was because of the events

predicted in FRS in comparison to

ASCVD risk estimator giving a

magnified view of the risk.

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ENDPOINTS ASSESSED IN FRAMINGHAM

GENERAL CVD RISK SCORE (2008)

• CHD death

• Nonfatal MI

• Coronary insufficiency or angina

• Fatal or nonfatal ischemic or hemorrhagic stroke

• Transient ischemic attack

• Intermittent claudication

• HF

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ENDPOINTS ASSESSED IN ACC/AHA POOLED

COHORT HARD CVD RISK CALCULATOR (2013)

• CHD death

• Nonfatal MI

• Fatal stroke

• Nonfatal stroke

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Statins in general reduce the risk by 30%.

For a patient with an ASCVD risk of 7.5%, his or her benefit from statin therapy will be an

absolute benefit of about 2.5% (ie, reduced risk from 7.5% to 5%, number needed to treat of 40).

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• Overestimate or underestimate the risk of initial CHD events in

other populations such as Japanese American and Hispanic

men, Chinese patients, Native American women, European and

Asian populations, and African American patients

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Age and Race seem to

increase the risk score with no

risk factors

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RISK FACTORS NOT CAPTURED BY THE

ASCVD POOLED COHORT EQUATIONS

Family history

• Higher LDL >190mg/dlt

• Sedentary lifestyle

• Poorly controlled diabetes

• Obesity

• CKD

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• Racially diverse participants of the MESA cohort (42

percent white, 26 percent African American, 20 percent

Hispanic, 12 percent Chinese)

• Ages 50 to 74 years

• Without CVD or diabetes at baseline

• Follow-up 10.2 years

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• Of participants eligible (recommended or considered) for statins

with ASCVD score > 5-7.5% , 44% (1,316 of 2,966) had CAC 0

at baseline

• Observed 10-year ASCVD event rate was 4.2 per 1,000 person-

years

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Coronary Artery Calcium Score for Long-term Risk Classification in Individuals With Type

2 Diabetes and Metabolic Syndrome From the Multi-Ethnic Study of Atherosclerosis

44.8% of those with MetS and 37.3% of those with diabetes have no evidence of CAC at

baseline, associated with observed 10-year CHD event rates of only 2.3% among those with

MetS and 3.7% among those with diabetes

“Warranty period” of a CAC score of 0, as previously discussed, can be extended to 10 years

in those with MetS or diabetes

Moreover, in our adjusted analyses, a CAC score of 0 was associated with low CHD and

ASCVD risk among those with diabetes that was independent of diabetes duration, insulin

use, or glycemic control

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RISK PREDICTION

• Studies have suggested strong risk predictive value of CAC over

traditional factors.

• Adding CAC > 400 or CAC =0 improved risk stratification by

Framingham score

• CAC further re-risk stratified intermediate risk patients by

Framingham risk score

• The incremental risk value of CAC is extended to younger, older

subjects, diabetics and smokers too

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ENDPOINTS ASSESSED IN MESA RISK SCORE

(2015)

• CHD death

• Nonfatal MI

• Resuscitated cardiac arrest

• Coronary revascularization in patient with angina

• STROKE is not an end point

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• -Stroke is not studied

as an outcome

• -Radiation exposure

• -Involves additional

cost

• -May lead to additional

testing

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? SYMPTOMATIC PATIENTS

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IS THERE VALUE OF REPEATING THE TEST ?

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• CAC 0 ----> 85% have CAC 0-> Lower rates of progression ->

lower risk over time

• The absolute 10yr risk is still <5%

• CAC > 0 ----> CAC continued to increase over years-> >100U/yr

-> Higher events

• Even though patients with CAC 0 increased their score slightly,

their risk is still lower than CAC >0 to begin with

• Management probably does not change other than adding high

intensity statins

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? OTHER PLAQUES BY CCTA

Coronary Atherosclerosis Imaging by Coronary CT Angiography

Current Status, Correlation With Intravascular Interrogation and Meta-Analysis

JACC: Cardiovascular Imaging : Volume 4, Issue 5, May 2011

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HIGH RISK PLAQUES

SPOTTY CALCIFICATION

POSITIVE REMODELLINGRING ENHANCING LESIONS

Multislice Computed Tomographic Characteristics of Coronary Lesions in Acute Coronary Syndromes

JACC Volume 50, Issue 4, July 2007

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NONCALCIFIED PLAQUES

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CCTA FOR RISK STRATIFICATION IN

ASYMPTOMATIC PATIENTS

NOT USEFUL !!!

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Statins - slowed progression of overall coronary atherosclerosis volume

Increased plaque calcification and reduction of high-risk plaque features

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SUMMARY• When risk factors including family history of CAD, higher LDL >190mg/dlt, sedentary lifestyle,

poorly controlled diabetes, obesity are present traditional risk scores fall apart

• CAC further re-risk stratified intermediate risk group patients

• In symptomatic patients –

CAC is found to be zero, the chance of having events is <1 %

High CAC score does not imply ischemia -

Aggressive lifestyle therapy

High-intensity statin therapy

Aspirin

BP goals

• If CAC is zero, when patients are followed the CHD events are still going to be low and the

risk of future disease is still < 5%

• CAC only estimates plaque burden but not plaque rupture