I have one of those snake scopes that I could put into the sewage line running under my massive front yard tree but I won't. Because I won't unsee it. If a problem or symptom arises then I'll take action. In the meantime, I won't let the tree grow too unruly and prune it back appropriately.
This is where more sensitive testing can create the illusion of better medicine. Finding more subclinical disease only helps if acting on what you find improves outcomes; otherwise you’ve mostly created a larger pool of abnormalities and downstream decisions. A CAC of zero missing plaque is interesting, but it doesn’t by itself make broader imaging a better screening strategy.
Now I have to admit that even NEJM can occasionally publish a worthwhile article. Despite the limitations of the imaging studies, it provides a valuable overview of the probable course of atherosclerosis. Dr. Mandrola's analysis is right on point although I disagree with his concluding statement that "Healthy living and exercise can slow the process, as can not smoking, and lipid-lowering therapy". There is, to my knowledge, no scientifically valid evidence for any of that. The article seems to confirm the theory of atherosclerosis put forward by Dr. William Stehbens---a pathologist that devoted most of his life and career to the study of it and literally "wrote the book"
on the subject. He described it as a nearly ubiquitous process common to all long-lived animal species. The "disease" doesn't really come into play until one suffers one of the common complications----mostly heart attack and stroke. We have no reliable measure for the incidence or severity of the underlying atherosclerosis nor any reliable way to gauge the risk of any of the complications. The fact that the incidence of atherosclerosis in men and women is roughly equal and that women may even progress a little faster while the rate of documented MIs is a multiple of at least 5 to 1 is a disconnect that demonstrates how little we actually know about causation and should lead us to suspect that "preventive" measures may be of questionable value.
Help me understand - "in younger adults with coronary plaque, roughly 40-48% had a coronary calcium score of zero". How did they know these younger adults had coronary plaque outside of the calcium score? It describes only carotid and femoral artery US testing. Was this a calcium score scan or a CCTA?
Landmark studies published in International Journal of Epidemiology revealed that nearly one-third of the historic decline in heart deaths was actually caused by the phase-out of leaded gasoline and environmental cleanup policies. As population blood lead levels dropped, the baseline incidence of MACE dropped with it.
This study provides interesting observations. Quite a bit of atherosclerosis in older people (to a large extent, duh), but more atherosclerosis in young people than I would’ve expected (actual good and new information).
But the cognitive leap of faith among the authors is (once again) where the science ends and their religion begins.
IF they were to show that such broad based screening and imaging as part of a diagnostic and management strategy reduced downstream outcomes…well….now THAT would be a story. And they are free to hypothesize that, and go out and try to prove it. But as noted, 2 RCTs have failed to demonstrate such benefits to date. They are welcome to give’er another go.
As it stands, “ primary prevention strategies informed by imaging” MIGHT do this/that/and the other, but the burden of proof is theirs, and it remains unmet.
But, jm, despite how good you are at your job, I don’t want my first encounter with atherosclerosis to be on the cath table while you open a previously occult critical lesion.
Dying of an MI, or surviving one with major cardiac morbidity, but for immediate access to an interventional cardiologist, is not something most Americans can count on.
The key question is whether primary prevention with a statin started years before we do now will significantly decrease the prevalence of silent atherosclerosis, because atherosclerosis is not a surrogate outcome: it IS the disease. Also, will the side effects of statins that worry so many be reduced in the young?
Alas, these 40 year randomized trials will never be done, unless the NIH bears the enormous cost.
You have not touched on the topic of statins in this review... is the consensus then that early statins is the only meaningful tool we have to delay cardiac events? and as such, should most people start medications prophylactically since disease begins early and progresses in all individuals regardless of screening/testing results? If anyone has any strong opinions on this topic please chime in...but I would love to hear from the experts :)
Statins themselves cause many terrible side effects. The emphasis should be on a healthy diet and exercise. Studies show starting statins at 50 or 60 (when cholesterol is usually tested and shown to be elevated) ) only lengthens life by 1 to 1 1/2 years, while causing many other issues. Everyone I know on statins is miserable because of it. No processed foods, cook from scratch a often as possible! Low sugar in your diet, a major cause of atherosclerosis. Or food is loaded with sugar! Read the labels. Including high fructose corn syrup.... in practically everything. Big food and big pharma have caused this disaster!
I completely disagree with your assessment. I can't think of anyone ON STATINS who is miserable and struggling with terrible side effects. And for anyone who did have some muscle side effects, switching to a different Statin olved the problem.The majority of people on statins are perfectly fine and have improved their lipid levels dramatically. I exercise regularly, i'm fit and eat a diet as prescribed by cardiologists specifically for reducing cholesterol. I have always been a very healthy eater (fish, nuts, heatly fats, legumes, grains, vegetables, no processed food and little sugar) but I still have high cholesterol (despite low Lpa). Unless someone is overweight and eats terribly, lifestyle modifications do very little to improve lipids. Lipids are affected by hormones, genetic and other comorbidities far more than diet or exercise. Like I said, those lifestyle changes can certainly help someone who lives a very unhealthy life but for the majority of health conscious people who are doing all the right things, no amount of dietary changes or exercise will help unfortunately.
Raison d'être Is not to be missed as a driver of happiness, quality of life and humanity. Seen many with orthorexia and hung up on Imaging and clinical lab tests, biometrics and extreme physical performance goals, causing them unwarranted concerns and anguish besides avoidable injuries. Be sensible …. Don’t forget to live.
So clear, thank you! I keep wondering what a person actually does with "you have plaque at 32" when the advice afterwards is the same advice as before - eat well, move, don't smoke. That's a lot to carry with nothing new attached to it.
What about fasting? My cardiologist thought I might have one or 2 clots. I fasted for 3 days before the scope to look for clots…there were none.
Great points but does screening at least make the myocardial infarction less severe even if it does not prevent it as referenced in the piece?
I have one of those snake scopes that I could put into the sewage line running under my massive front yard tree but I won't. Because I won't unsee it. If a problem or symptom arises then I'll take action. In the meantime, I won't let the tree grow too unruly and prune it back appropriately.
Please mention OMT vs revascularization when you write on this topic.
This is where more sensitive testing can create the illusion of better medicine. Finding more subclinical disease only helps if acting on what you find improves outcomes; otherwise you’ve mostly created a larger pool of abnormalities and downstream decisions. A CAC of zero missing plaque is interesting, but it doesn’t by itself make broader imaging a better screening strategy.
Now I have to admit that even NEJM can occasionally publish a worthwhile article. Despite the limitations of the imaging studies, it provides a valuable overview of the probable course of atherosclerosis. Dr. Mandrola's analysis is right on point although I disagree with his concluding statement that "Healthy living and exercise can slow the process, as can not smoking, and lipid-lowering therapy". There is, to my knowledge, no scientifically valid evidence for any of that. The article seems to confirm the theory of atherosclerosis put forward by Dr. William Stehbens---a pathologist that devoted most of his life and career to the study of it and literally "wrote the book"
on the subject. He described it as a nearly ubiquitous process common to all long-lived animal species. The "disease" doesn't really come into play until one suffers one of the common complications----mostly heart attack and stroke. We have no reliable measure for the incidence or severity of the underlying atherosclerosis nor any reliable way to gauge the risk of any of the complications. The fact that the incidence of atherosclerosis in men and women is roughly equal and that women may even progress a little faster while the rate of documented MIs is a multiple of at least 5 to 1 is a disconnect that demonstrates how little we actually know about causation and should lead us to suspect that "preventive" measures may be of questionable value.
Help me understand - "in younger adults with coronary plaque, roughly 40-48% had a coronary calcium score of zero". How did they know these younger adults had coronary plaque outside of the calcium score? It describes only carotid and femoral artery US testing. Was this a calcium score scan or a CCTA?
Continuing to decline a CAC, much to my physician’s chagrin.
Landmark studies published in International Journal of Epidemiology revealed that nearly one-third of the historic decline in heart deaths was actually caused by the phase-out of leaded gasoline and environmental cleanup policies. As population blood lead levels dropped, the baseline incidence of MACE dropped with it.
Caused by, or associated with? A big difference.
This study feels like the Boogeyman
This study provides interesting observations. Quite a bit of atherosclerosis in older people (to a large extent, duh), but more atherosclerosis in young people than I would’ve expected (actual good and new information).
But the cognitive leap of faith among the authors is (once again) where the science ends and their religion begins.
IF they were to show that such broad based screening and imaging as part of a diagnostic and management strategy reduced downstream outcomes…well….now THAT would be a story. And they are free to hypothesize that, and go out and try to prove it. But as noted, 2 RCTs have failed to demonstrate such benefits to date. They are welcome to give’er another go.
As it stands, “ primary prevention strategies informed by imaging” MIGHT do this/that/and the other, but the burden of proof is theirs, and it remains unmet.
A thoughtful evaluation of a great article!
But, jm, despite how good you are at your job, I don’t want my first encounter with atherosclerosis to be on the cath table while you open a previously occult critical lesion.
Dying of an MI, or surviving one with major cardiac morbidity, but for immediate access to an interventional cardiologist, is not something most Americans can count on.
The key question is whether primary prevention with a statin started years before we do now will significantly decrease the prevalence of silent atherosclerosis, because atherosclerosis is not a surrogate outcome: it IS the disease. Also, will the side effects of statins that worry so many be reduced in the young?
Alas, these 40 year randomized trials will never be done, unless the NIH bears the enormous cost.
Do the 52-60% of younger adults with a POSITIVE CAC score greater than zero have a worse prognosis than those the test "missed?"
You have not touched on the topic of statins in this review... is the consensus then that early statins is the only meaningful tool we have to delay cardiac events? and as such, should most people start medications prophylactically since disease begins early and progresses in all individuals regardless of screening/testing results? If anyone has any strong opinions on this topic please chime in...but I would love to hear from the experts :)
Statins themselves cause many terrible side effects. The emphasis should be on a healthy diet and exercise. Studies show starting statins at 50 or 60 (when cholesterol is usually tested and shown to be elevated) ) only lengthens life by 1 to 1 1/2 years, while causing many other issues. Everyone I know on statins is miserable because of it. No processed foods, cook from scratch a often as possible! Low sugar in your diet, a major cause of atherosclerosis. Or food is loaded with sugar! Read the labels. Including high fructose corn syrup.... in practically everything. Big food and big pharma have caused this disaster!
I completely disagree with your assessment. I can't think of anyone ON STATINS who is miserable and struggling with terrible side effects. And for anyone who did have some muscle side effects, switching to a different Statin olved the problem.The majority of people on statins are perfectly fine and have improved their lipid levels dramatically. I exercise regularly, i'm fit and eat a diet as prescribed by cardiologists specifically for reducing cholesterol. I have always been a very healthy eater (fish, nuts, heatly fats, legumes, grains, vegetables, no processed food and little sugar) but I still have high cholesterol (despite low Lpa). Unless someone is overweight and eats terribly, lifestyle modifications do very little to improve lipids. Lipids are affected by hormones, genetic and other comorbidities far more than diet or exercise. Like I said, those lifestyle changes can certainly help someone who lives a very unhealthy life but for the majority of health conscious people who are doing all the right things, no amount of dietary changes or exercise will help unfortunately.
A trial to test that will never be done imo
yes thats likely true so then the questions becomes....what,when, and who do we treat and with what interventions?
I was going to ask the same question. Thank you!
Raison d'être Is not to be missed as a driver of happiness, quality of life and humanity. Seen many with orthorexia and hung up on Imaging and clinical lab tests, biometrics and extreme physical performance goals, causing them unwarranted concerns and anguish besides avoidable injuries. Be sensible …. Don’t forget to live.
Is it better to “do without so you can live longer to “do without “???🫤
As stated by a very wise physician before : “ the patient died in electrolyte balance “
So clear, thank you! I keep wondering what a person actually does with "you have plaque at 32" when the advice afterwards is the same advice as before - eat well, move, don't smoke. That's a lot to carry with nothing new attached to it.