coronary calcium score the past, present and...
TRANSCRIPT
Dr. Neeraja Yedlapati
University Tennessee, Memphis
CORONARY CALCIUM SCORE
THE PAST, PRESENT AND FUTURE
• 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
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
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
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
FRAMINGHAM 10YR RISK SCORE
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.
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
ENDPOINTS ASSESSED IN ACC/AHA POOLED
COHORT HARD CVD RISK CALCULATOR (2013)
• CHD death
• Nonfatal MI
• Fatal stroke
• Nonfatal stroke
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).
• 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
Age and Race seem to
increase the risk score with no
risk factors
RISK FACTORS NOT CAPTURED BY THE
ASCVD POOLED COHORT EQUATIONS
Family history
• Higher LDL >190mg/dlt
• Sedentary lifestyle
• Poorly controlled diabetes
• Obesity
• CKD
• 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
• 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
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
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
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
• -Stroke is not studied
as an outcome
• -Radiation exposure
• -Involves additional
cost
• -May lead to additional
testing
? SYMPTOMATIC PATIENTS
IS THERE VALUE OF REPEATING THE TEST ?
• 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
? 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
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
NONCALCIFIED PLAQUES
CCTA FOR RISK STRATIFICATION IN
ASYMPTOMATIC PATIENTS
NOT USEFUL !!!
Statins - slowed progression of overall coronary atherosclerosis volume
Increased plaque calcification and reduction of high-risk plaque features
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