April 15, 2022

Cardiovascular Disease

When CAC Tests Are Useful and When They Are Not

Read Time 3 minutes

This video clip is from episode #185 – Allan Sniderman, M.D.: Cardiovascular disease and why we should change the way we assess risk, originally released on November 29, 2021.

Show Notes

Using the coronary artery calcium (CAC) score as a predictive tool [1:03:15]

  • The coronary artery calcium score (CAC)
  • Coronary calcium is an important step forward in cardiovascular imaging
  • It uses x-ray techniquest to accurately and safely determine whether there’s calcium (bone) in the coronary arteries 
  • Calcification is a feature of advanced atherosclerosis
  • There’s very strong evidence that people who have coronary calcification are at higher risk of a heart attack or stroke than people who do not have coronary calcification
  • There are several facts to consider:
    • 1) The frequency of a positive coronary calcium goes up as we age (so does the risk of disease)
      • All American men by age 60 are at high risk according to current guidelines; women are five to 10 years later
  • At age 60 the CAC test isn’t helpful
  • In most people arteries become substantially transformed in bad ways by age 60
  • But in people younger than 60, this can give extra information that is helpful, should the doctor be on the cusp of treatment
  • This test would be for the patient who wants more information to help them decide about intervention
  • 2) There is a problem with the corollary, if the coronary calcium is negative concluding that the patient is okay
  • From Allan’s interpretation of the literature, coronary calcification is associated with advanced disease
  • When people have a heart attack, they don’t just have one little area of their arteries that are abnormal; that’s simply the area where the plaque broke or the endothelium eroded, but the whole artery is diseased
    • This means there’s a chance of an event a cm down or a cm closer
  • If a patient has high apoB, the fact that their coronary calcium is negative doesn’t mean they don’t have a lot of disease and that the disease isn’t developing at a rapid rate; it could be there
  • There’s an argument saying, if the coronary calcium is negative, nothing’s going to happen to in the next five or 10 years
    • Maybe this is true; but the disease is developing and doctors can’t make the disease go away
    • Doctors can modify the effects of the disease, modify the consequences
  • For a patient who has been treated and their LDL, cholesterol, and apoB levels are brought low, remember that they still have an artery that is destroyed; they’re going to have a substantial number of events
  • John Wilkins, and Don Lloyd Jones from Northwestern, they have a paper in JAMA but it’s terribly complicated (they’re Allan’s friends so he can be honest)
  • Allan is conservative when it comes to protecting patients
    • He wants to give  them the option to have the best outcome possible when they appear to be in danger
    • So he wouldn’t use a negative coronary calcium to change his clinical decision for patients who have high apoB or another cause of vascular disease present
    • He thinks CAC is a good test, but has relatively limited utility for him 
  • Peter uses a 2 x 2 matrix to explain this to patients; he considers the patient’s age and CAC score
    • A 70-year old who has a calcium score of 50 doesn’t tell him much
    • An older patient with a calcium score of 0 who is adamant about not getting treatment; this is an easier decision to accept
      • It would be fortunate to have a calcium score of 0 at age 73 with an apoB of 140 mg/dL
  • On the flip side of things is a young patient who has a positive calcium score; really that’s a 4-alarm fire
    • Allan agree’s, treating this patient is a no-brainer
  • Regardless of apoB, for a patient under 50 who has a speck of calcium in their coronary arteries, that’s utterly unacceptable 
    • Allan agrees; if it’s positive, it’s only going to go up
    • Peter notes it says something about the entire system, that might be the one area in the middle of the patient’s left, anterior descending artery where it’s at an advanced stage, and calcium is laid down

“It’s like looking at the concrete that’s been poured over Chernobyl and trying to infer what’s going on in the 10 miles around Chernobyl. It’s all bad.” – Peter Attia

§
Allan Sniderman, M.D.

Allan Sniderman obtained his MD from the University of Toronto in 1965 and then moved to Montreal, where he did his clinical training in Internal Medicine and Cardiology at McGill University. In 1971, he went to the University of California at San Diego to study lipoprotein metabolism with Dr. Daniel Steinberg. He returned to McGill and, with the passage of time, became the Edwards Professor of Cardiology and a Professor of Medicine at McGill University.

With colleagues within and outside McGill, he began and has continued a series of studies, which identified the commonest dyslipoproteinemia associated with coronary artery disease- hyperTg hyperapoB. Study of the pathophysiology of hyperTg hyperapB led to studies of the regulation of hepatic apoB secretion and the uptake and release of fatty acids by adipose tissue. He has conducted an extensive series of epidemiological studies, which have demonstrated apoB to be superior to LDL-cholesterol as a marker of the risk of vascular disease. His current research interests are: to understand the regulation of plasma LDL, to create simplified but advanced diagnostic algorithms to recognize and treat those with and those at high risk of vascular disease, and to develop new models to determine the absolute value of different strategies to identify and treat those at risk of vascular disease.

Dr. Sniderman, father of five, grandfather of four, is a committed, but not very skilful, golfer. His most joyful moments have come from learning with his students and colleagues.

Allan D. Sniderman, MD, is the Edwards Professor of Cardiology and Professor of Medicine at McGill University. He is Director of the Mike Rosenbloom Laboratory for Cardiovascular Research at Royal Victoria Hospital in Montreal and was elected a Fellow of the Royal Society of Canada in 2009. [McGill University Health Centre]

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