April 15, 2022

Cardiovascular Disease

Preventing Atherosclerosis: 2 Fatal Flaws with the “10 Year Risk” Approach

Read Time 5 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

Problems with the current 10-year risk assessment of cardiovascular disease (CVD) and the implications for prevention [4:30]

Understanding atherosclerosis/ cardiovascular disease

Figure 1. Book cover Herbert Stary’s Atlas of Atherosclerosis Progression and Regression showing plaque rupture “rings”. Image credit: Amazon.com

  • Peter asks him why he gave him this last book
    • Atherosclerosis, it’s a disease in the tissue, yet almost everything that lipid people talk about is in plasma
    • One must understand the natural history of the disease to learn how to construct a strategy to prevent it
  • Although much of Allan’s work has been on apoB, the more important part has been on understanding how the natural history of atherosclerosis should direct a prevention strategy
    • What this leads to is that every major guideline in the world bases their selection of subjects for statin prevention on the ten-year risk of disease
      • This was a huge step forward in 1980 and 1990
      • But it fundamentally makes prevention of premature disease almost impossible

Problems with the 10-year risk approach

  • When one plugs in the numbers to calculate a patient’s risk for any of the risk algorithms, one expects the output to be the patient’s risk of cardiovascular disease (CVD) but it isn’t 
    • The American College of Cardiology ASCVD Risk Estimator Plus
    •  The calculation is driven by the age and sex of the patient
    • Things like cholesterol and blood pressure contribute minimally to the actual calculation of ten-year risk
      • So if the patient is 35, there isn’t a risk calculator for them
      • If the patient is 40, everyone’s risk is low at age 40
      • It isn’t until age 55 or 60 that the risk gets over the threshold for the American Prevention Guideline treatment
        • So prevention really starts at 55 to 60, but almost half of all infarcts and strokes occur before the age of 60
  • Stary and colleagues established that for the first three decades or so of life, the disease gets a foothold in the artery, but it’s only in the fourth decade that one starts to develop the lesions that can actually precipitate a clinical event
    • Risk is low, yet the event rate is high — How could that possibly be?
  • Allan says the answer is “stunningly obvious” — Allan has published on how this can be explained; there are 2 problems:
    • 1) There are a ton more people under 60 than over 60; so the rate of events is low, but the absolute number of events is high
    • 2) Say a patient gets to their 60’s without a cardiac event, but the disease was developing and extending during their 30’s-50’s
      • So by the time a doctor tries to prevent an event, the disease is well advanced in the arteries
    • These are the 2 fatal flaws in the 10-year risk approach
  • Risk is a good concept but Allan realized doctors should be selecting people based on causes of CVD
  • For example, if Peter’s risk is 4.1%, what does this number mean?
    • Is his risk 4.1%?  ⇒ No, it means 4.1 people out of 100 will have an infarct
      • But within this category, there is tremendous variance in real risk
      • Not everyone is at 4.1; some are higher; some are lower; some are dead on
  • The philosopher AJ Ayer (known for logical positivism) was actually darn good on probability
  • There’s a real challenge predicting singular events
    • One is either going to have an infarct in the next year or not; it’s not really a probability
    •  If one algorithm said a patient has a 10% risk and another one said a patient has a 15% or 20%, whether they have an infarct or not, both algorithms were right because they said there was sort of a chance the patient would have an infarct
      • There is also a far greater chance that the patient won’t have an infarct
  • When the advice is to treat patients with a risk abouve 7.5%, that means 92.5% of the time nothing will happen to these patients
    • That’s not a great incentive for helping people understand what’s truly going to happen

A 30-year model of risk that focuses on cause of CVD

  • What Allan has done is develop what’s called a casual benefit model
  • When Allan gave Peter the book on atherosclerosis he was starting his own journey on trying to construct an alternative to the present risk model in which with the help of my colleague here at McGill, George Thanassoulis, and Michael Pencina from Duke, and Karol Pencina from Harvard we have done
  • Peter remembers from pathology class in med school something the professor said, “No doctor has more experience with what it is to have heart attacks than pathologists because 50% of the people who have a heart attack die on their first heart attack.
    • So 50% of people who have a heart attack, their first presentation is death
    • It’s a very sobering fact
    • He doesn’t think this is true today, but it was 25 years ago
    • Maybe now one third of first events are fatal; sobering nonetheless
  • The textbook went through, in great detail, the pathological staging of atherosclerosis; it was also littered with autopsy sections of coronary arteries from people who had died for other reasons
    • Notably, many of these people who died from other causes, but their coronary arteries were studied in autopsy, these people were quite young
      • A 26-year-old male victim of a gunshot wound; or a 27-year-old female who died in a motor vehicle accident, etc.
    • Looking at their coronary arteries, one realizes they already have atherosclerosis; they have oxidized apoB-bearing particles engulfed by macrophages and thickened intima
      • While they may not have calcification in their arteries yet or the types of plaque that would rupture within the ensuing weeks or days or months, they nevertheless had atherosclerosis
      • Now what Peter’s professor said some 20 years earlier made sense
  • Allan remarks that cardiologists are so used to looking at angiograms

“Well, there’s an LAD lesion, but the whole damn artery is diseased. And when you destroy the normal architecture of the artery, you can’t restore it.” – Allan Sniderman

  • Much of statin prevention therapy is to prevent complication of disease not actually prevent disease
  • Statins lower apoB particle number; that’s how they work
  • With fewer apoB particles in plasma, fewer get into the arterial wall, fewer get trapped
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]

Disclaimer: This blog is for general informational purposes only and does not constitute the practice of medicine, nursing or other professional health care services, including the giving of medical advice, and no doctor/patient relationship is formed. The use of information on this blog or materials linked from this blog is at the user's own risk. The content of this blog is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Users should not disregard, or delay in obtaining, medical advice for any medical condition they may have, and should seek the assistance of their health care professionals for any such conditions.
Facebook icon Twitter icon Instagram icon Pinterest icon Google+ icon YouTube icon LinkedIn icon Contact icon