The topic of plaque regression is a complicated one. Conveying the nuance of what is going on with atherosclerotic plaque with aggressive treatment (which many consider plaque regression) was beyond the scope of this article. With high intensity statin therapy , complicated coronary imaging studies have shown regression. Some components of the plaque, however, increase (like calcium). Overall, though the components we are most worried about decline significantly.
"Statins induce plaque regression in a dose-dependent manner and proportionally to reductions in low-density lipoprotein (LDL) cholesterol. With statins, fibrous and calcified plaque volume appear to increase, while noncalcified fibrofatty and necrotic core volumes decrease. Several studies demonstrated greater plaque regression with ezetimibe compared to optimal medical therapy, but the differences were not significant. The impact of each of the PCSK9 antibody classes of drugs was evaluated with intravascular ultrasound (IVUS) in relatively large studies: one stable coronary heart disease (CHD) and the other following an ACS. The impact was modest possibly because of the impact of high-intensity statins on plaque in all patients in both studies.
"...the more effective we can be at stopping and reversing the build-up of atherosclerotic plaque; modifying plaque so that is less likely to cause MI..." I was under the assumption there was yet no way to reduce plaque; how is this accomplished?
“Due to advances in medical therapy, lifestyle and device therapy, deaths from cardiovascular disease declined by 70% between 1980 and 2009.....In the last 10 years, however, the rate of decline of ASCVD has slowed and sudden cardiac death rates have remained constant. “
The decline in rate is perhaps because many of those with ASCVD have died, but those remaining who have a sudden attack still die at the same rate. The low-hanging fruit, so to speak, have been scythed, leaving far less higher available.
The point you made regarding CAD being a silent disease really should be stressed. My cholesterol was always under 200, however my elevated LDL was never addressed. I smoked for 25 years and had no known history of CAD in my family. However, I suffered an MI at age 46 and underwent a quadruple bypass. I was not overweight and exercised regularly. I later discovered my Liproprotein (a) level was "off the charts" so I was unknowingly at severe high risk for a major cardiac event. I didn't fit the "profile" of a candidate for CAD except for being a light, intermittent smoker. I worked in cardiac step down units as an RN for almost 10 years and did not know all the current facts and diagnostic tests and criteria that could have been addressed earlier in my life that might have prevented the severity of my disease at such an early age. Thanks for your knowledge and expertise in this area.
"Remarkably, one-quarter of the centenarians had high Lp(a) serum levels even though they never suffered from atherosclerosis-related diseases." 1998 G. Baggio.
What was your Lp(a) and HDL level? Maybe that was not really the cause. Did you ever get the lipid inflammation tests for Myeloperoxidase, Lp-PLA 2, hs-CRP, ADMA, OxLDL, F2-Isoprostane/Creatinine, Microalbumin/Creatinine, IR score, sdLDL, HDL-P, Large HDL-P and HDL size? Did you ever get a non invasive, no radiation CIMT test which will check both soft and hard plaque?
I don't remember what my HDL level was at the time of my heart attack since it was almost 15 years ago. I did not have any of those other tests you mentioned. My Lp (a) was 350!
Thank you for the clear explanations - very helpful!
I'm hopeful that you would consider including in your series of stories on “Profiles in Coronary Artery Disease” how a 60 year old male, in good health and no known risk factors could have a Calcium CAC score of 618. In particular, this male is not overweight, exercises regularly, eats what is typically considered a very healthy diet (according to the AHA guidelines for a healthy heart), consistently healthy blood pressure (at or below 110/70), resting pulse consistently below 50, has very good cholesterol numbers (LDL, HDL, triglycerides and relevant ratios), is not diabetic, has no know genetic dispositions (both parents lived well into their 90's, siblings are all still living and healthy) and no apparent markers for inflammation according to blood tests. Based on a few sources, it appears that one factor that could be contributing is chronic insomnia - no problems falling asleep, but waking typically occurs after 5-6 hours of sleep and trouble falling back to sleep. Sleep studies show no evidence of sleep apnea.
Any insights you could provide in your upcoming series would be greatly appreciated.
This man is an interesting case and should have lipoprotein (a) checked first.
If that is normal (and assuming no smoking history) most likely he has some form of genetic mutation predisposing him to cholesterol build up that has yet to be identified.
Does he engage in ultra-endurance sports?
I don't think the insomnia is causing this, even if he had sleep apnea.
I'm curious why you asked if he engaged in high endurance sports? This question could have been about me, except I know that I have the apoe4 gene, double copy, suffered an mi I 3 years ago without any previous symptoms. I was a triathlete until about age 53.
Thanks for your prompt response!! I will recommend that he get lipoprotein (a) checked.
He was very involved in ultra-endurance sports as a younger adult (up until about age 35) - mostly triathlons, bicycle racing and long-distance touring (e.g., across the country) via bicycle. Do you think this could be a contributing factor?
Thanks for the questions. According to his 23andMe reports - there was no variant detected for APOB (although with a disclaimer that they don't test all possible variants). Not sure about the others you mentioned and will have to check. Thanks again!
A very interesting read, and easily understood and correct paths for optimum health benefits...most [we] already know, but need to be reminded. This venue is a handy reminder.
I actually understood all that! Thank you so much for taking the time to write such an edifying post for us newbies to the ins-and-outs of heart disease!
There is no fixed relationship between those parameters.
But those all convey a similar level of risk.
Dr. P
And that risk level is?
Are these results consistent across tests?: LDL-C 121; APOB 102; LDL-P 1598. I am thinking they are not. 72 yo/f who want to prevent a cardiac event.
Gorgo,
A careful reading of my current article and all of my writing on the skeptical cardiologist on diet and exercise would inform you that
1. I constantly expound he virtues of healthy living
2. I am not on the "cholesterol causes heart disease soapbox"
3. As a preventive cardiologist I am devoted to minimizing the use of cardiovascular procedures
4. There are tens of thousands of patients who have excellent diet and lifestyle but it is not enough to prevent or reverse CAD in them.
Dr. p
Do you have a link for this reference from 25 years ago?
Dr. P
Dennis,
The topic of plaque regression is a complicated one. Conveying the nuance of what is going on with atherosclerotic plaque with aggressive treatment (which many consider plaque regression) was beyond the scope of this article. With high intensity statin therapy , complicated coronary imaging studies have shown regression. Some components of the plaque, however, increase (like calcium). Overall, though the components we are most worried about decline significantly.
This article summarizes current thinking in the area (https://www.acc.org/latest-in-cardiology/ten-points-to-remember/2022/01/10/23/23/coronary-atherosclerotic-plaque-regression).
And here is a point from the link I provided.
"Statins induce plaque regression in a dose-dependent manner and proportionally to reductions in low-density lipoprotein (LDL) cholesterol. With statins, fibrous and calcified plaque volume appear to increase, while noncalcified fibrofatty and necrotic core volumes decrease. Several studies demonstrated greater plaque regression with ezetimibe compared to optimal medical therapy, but the differences were not significant. The impact of each of the PCSK9 antibody classes of drugs was evaluated with intravascular ultrasound (IVUS) in relatively large studies: one stable coronary heart disease (CHD) and the other following an ACS. The impact was modest possibly because of the impact of high-intensity statins on plaque in all patients in both studies.
Dr P
"...the more effective we can be at stopping and reversing the build-up of atherosclerotic plaque; modifying plaque so that is less likely to cause MI..." I was under the assumption there was yet no way to reduce plaque; how is this accomplished?
Christine,
Good to hear from you! Your story is the classic example of the insidious nature of CAD.
Dr. p
“Due to advances in medical therapy, lifestyle and device therapy, deaths from cardiovascular disease declined by 70% between 1980 and 2009.....In the last 10 years, however, the rate of decline of ASCVD has slowed and sudden cardiac death rates have remained constant. “
The decline in rate is perhaps because many of those with ASCVD have died, but those remaining who have a sudden attack still die at the same rate. The low-hanging fruit, so to speak, have been scythed, leaving far less higher available.
The point you made regarding CAD being a silent disease really should be stressed. My cholesterol was always under 200, however my elevated LDL was never addressed. I smoked for 25 years and had no known history of CAD in my family. However, I suffered an MI at age 46 and underwent a quadruple bypass. I was not overweight and exercised regularly. I later discovered my Liproprotein (a) level was "off the charts" so I was unknowingly at severe high risk for a major cardiac event. I didn't fit the "profile" of a candidate for CAD except for being a light, intermittent smoker. I worked in cardiac step down units as an RN for almost 10 years and did not know all the current facts and diagnostic tests and criteria that could have been addressed earlier in my life that might have prevented the severity of my disease at such an early age. Thanks for your knowledge and expertise in this area.
"Remarkably, one-quarter of the centenarians had high Lp(a) serum levels even though they never suffered from atherosclerosis-related diseases." 1998 G. Baggio.
Interesting to know!
What was your Lp(a) and HDL level? Maybe that was not really the cause. Did you ever get the lipid inflammation tests for Myeloperoxidase, Lp-PLA 2, hs-CRP, ADMA, OxLDL, F2-Isoprostane/Creatinine, Microalbumin/Creatinine, IR score, sdLDL, HDL-P, Large HDL-P and HDL size? Did you ever get a non invasive, no radiation CIMT test which will check both soft and hard plaque?
I don't remember what my HDL level was at the time of my heart attack since it was almost 15 years ago. I did not have any of those other tests you mentioned. My Lp (a) was 350!
Thank you for the clear explanations - very helpful!
I'm hopeful that you would consider including in your series of stories on “Profiles in Coronary Artery Disease” how a 60 year old male, in good health and no known risk factors could have a Calcium CAC score of 618. In particular, this male is not overweight, exercises regularly, eats what is typically considered a very healthy diet (according to the AHA guidelines for a healthy heart), consistently healthy blood pressure (at or below 110/70), resting pulse consistently below 50, has very good cholesterol numbers (LDL, HDL, triglycerides and relevant ratios), is not diabetic, has no know genetic dispositions (both parents lived well into their 90's, siblings are all still living and healthy) and no apparent markers for inflammation according to blood tests. Based on a few sources, it appears that one factor that could be contributing is chronic insomnia - no problems falling asleep, but waking typically occurs after 5-6 hours of sleep and trouble falling back to sleep. Sleep studies show no evidence of sleep apnea.
Any insights you could provide in your upcoming series would be greatly appreciated.
This man is an interesting case and should have lipoprotein (a) checked first.
If that is normal (and assuming no smoking history) most likely he has some form of genetic mutation predisposing him to cholesterol build up that has yet to be identified.
Does he engage in ultra-endurance sports?
I don't think the insomnia is causing this, even if he had sleep apnea.
Dr P
I'm curious why you asked if he engaged in high endurance sports? This question could have been about me, except I know that I have the apoe4 gene, double copy, suffered an mi I 3 years ago without any previous symptoms. I was a triathlete until about age 53.
Thanks for your prompt response!! I will recommend that he get lipoprotein (a) checked.
He was very involved in ultra-endurance sports as a younger adult (up until about age 35) - mostly triathlons, bicycle racing and long-distance touring (e.g., across the country) via bicycle. Do you think this could be a contributing factor?
Has this person checked their LP(a) or APOB for a genetic issue? Also APOE4 can increase cholesterol levels.
Thanks for the questions. According to his 23andMe reports - there was no variant detected for APOB (although with a disclaimer that they don't test all possible variants). Not sure about the others you mentioned and will have to check. Thanks again!
Lipoprotein (a) genetics will not be reported by 23 and Me. it is a simple, cheap blood test that you can get at any Quest or Labcorp
Apolipoprotein B , the primary driver of atherosclerosis is highly related to LDL-C concentrations but adds additional information on risk
A very interesting read, and easily understood and correct paths for optimum health benefits...most [we] already know, but need to be reminded. This venue is a handy reminder.
Thank you🙏. Really appreciate the commentary. Your writing helped me advocate for further investigation (for myself) with CAC and advanced lipids.
I actually understood all that! Thank you so much for taking the time to write such an edifying post for us newbies to the ins-and-outs of heart disease!