I just realized that I had written "I did intend to bash PCPs" when I mean I did not. Fortunately, I think the context of the sentence makes it clear I meant not but it is now corrected.
Similar to you, my eldest daughter excelled in med school and chose primary care. Great primary care doctors like you and her are essential to quality health care but they are in short supply and at greater risk of burn-out due to many factors.
Hi. The PCP not knowing about ASCVD risk calculators would be a red flag against that clinician. Be careful with general PCP bashing though, as our role cannot be a luxurious deep dive into the nuances of each problem and medical decision. Most patients will not read through 5 articles you have constructed to help them, but they will read 5 articles that induce statin fear and undermine your expertise.
The doc who said “work harder on diet and exercise to get LDL<130” then probably went on to coordinate 10 other problems including a review of specialist letters, imaging studies, chronic medical problems like diabetes, cancer surveillance, htn, a recent hospitalization, anxiety and depression, OSA, etc. I think we all know from constant bombardment what “work harder on diet” means... don’t eat crap, eat more vegetables and healthy proteins and fats... and if the patient doesn’t, then suggesting a nutritionist consultation (which usually takes a whole hour we don’t have) or picking up a book on Mediterranean style diet would be a good idea for the truly motivated patient. The ones who’ve made it to see a cardiologist for primary prevention are already a highly engaged, educated, and motivated population unlike the baseline primary care population, many of whom are underinsured and can’t really afford CAC. I know it’s hard to imagine, but it’s true.
I recall an article about CAC testing and pitfalls published by the AAFP and written by John Mandrola. As family docs we really do depend on consensus guidelines- if we got tangled in the nuanced weeds of every decision we would need AI and 27 more hours per day (the amount of time already estimated a family doc would need to take care of everything that has been advised of them in patient care!). So we follow guidelines, and there is safety in that.
And the most frustrating thing about ASCVD calculators is that they do not include family history! Isn’t that one of the foundational risks?! Please let me know if there is such a calculator, assuming it’s been validated, so I don’t end up sounding ignorant like the PCP you’ve mentioned. Nonetheless, cut the rest of us some slack please 😉
Great points! And very happy you weighed in with the PCP perspective. I did not intend to bash PCPs because I know how tough their job is and I recognize that I have the luxury of focusing on one organ.
I agree with "The ones who’ve made it to see a cardiologist for primary prevention are already a highly engaged, educated, and motivated population unlike the baseline primary care population, many of whom are underinsured and can’t really afford CAC."
And I definitely have had patients tell me they can't afford a CAC or they are not interested in it.
And I have seen many many patients who have no interest in my diet or exercise advice and I recognize that I can't change their behavior no matter how much time I spend.
I agree with Mandrola and pretty much everything else he has written about but I think he's misguided on CAC. I'm in the process of updating my CAC guide (that triggered me updating the on the fence post) and I plan to write a point by point rebuttal of the arguments against CAC.
The MESA calculator does include family history and I think family history is very important.
Ok great and thanks for the validation - reading my own comment again maybe it came off a little defensive but that’s primary care for you! I was in the top quartile of my med school class but chose family medicine because it suited my personality and fledgling medical philosophy… but there is always the sense that by being jacks of all trades we can’t possibly master any. Fortunately we don’t have to and the generalist/specialist ecosystem finds a decent equilibrium so thanks for your expertise on behalf of your primary care referrers. And there are a lot mediocre PCPs I have to admit.
Will read more about the MESA calculator (wish they had a version without CAC, since the vast majority of patients in primary care have not had one).
I am a former patient of Dr P. My cholesterol was predictably high and was put on avoristatin (I think by my PCP at the time). I immediately had a severe reaction to the medication. I struggled to walk as my muscles were completely bound up. My pharmacist told me I was one of 5% to have this severe of a reaction and stop it immediately. After blood tests my muscle enzymes count was 3 times above normal. It took over a year for them to fall to normal range and pain to dissipate. Thankfully Dr P prescribed Praulent shots which works great and I tolerate very well. I for one will NEVER take ANY statin for ANY reason. Dr P also introduced me to the Kardia App which I use to this day to self monitor and for which I am very grateful!! Thanks for the chance to comment.
I was reading about the results with bempedoic acid. I am likely to remain statin-free, although I'll discuss bempedoic acid with my PCP... my total cholesterol and LDL are low enough, about the best recommendation for me is based on all-cause mortality. I guess, with an LDL of 75, and stable over the last 10+ years I could try to drop it to the 20s, but I'm not well-enough versed in the latest lipidology to have an opinion on the field overall, just on my own health.
Interesting post. My particular case was that with high cholesterol in my 50s, I was not prescribed statins due to a similar risk analysis matrix. While a grandfather had died of a heart attack in his 50s, my parents both succumbed to cancer quite young, so there was little info on their cardiovascular health in older age. I would be asked if my grandfather had high cholesterol. He died in 1955, before I was born and before such measurements were common (AFAIK). So who knows?
My cholesterol level was high enough that my optometrist noticed it during an eye exam. But my medical check-ups still resulted in recommendations to eat less fatty food and drink less and no statins.
By fortunate accident, I was visiting South Africa and needed some malaria prophylactics. I visited a doctor I knew, and he did a sort of wellness check where we decided to check my PSA level and a few other labs. The PSA was fine, but he was worried about my cholesterol level.
I had read (damn you Internet!) about a more-accurate test for lipids called ApoB, so I asked to have it as well. It was sky-high - much higher than my HDL/LDL levels would have implied.
I managed to get an appointment with a local cardiologist, whose opening line was "How are you still alive?" That gets your attention. He asked about my ancestry, which is Huguenot French. Many of the Huguenot also went to South Africa, and there is a genetic condition (Familial Hypercholesterolemia) common in those families, which I also appear to suffer from.
An ECG and stress test were normal (but I could be in better fitness - weight is fine). However an ultrasound showed 30% blockage in one carotid artery. I started on statins and a low-carb diet and my ApoB levels went from literally off-the-chart to extremely low. That was five years ago and subsequent ultrasound shows a reduction and smoothing of the visible plaque.
If I had not had a chat with a helpful GP and then asked for the ApoB test, plus chosen a cardiologist familiar with FH, I probably wouldn't be here to write this.
I've written about apo B (https://theskepticalcardiologist.com/2021/08/25/what-really-initiates-and-drives-atherosclerosis/) and consider it the primary driver of atherosclerosis. For most individuals LDL and apo B track pretty closely, however, I check apo B with the standard lipid parameters in the majority of my patients. It is especially important after drug treatment as apo B may respond differently than LDL to statin therapy.
Over the next few years, hopefully, more physicians will add apo B to their lipid panels. It is cheap and superior, IMO, to the more complicated and expensive NMR lipid particle analysis.
We should stop talking LDL, HDL, VLDL, Triglycerides. What matters is MI , Mortality and overall health. And no talk about relative risk. Some of the landmark studies had statistics done by the drug companies that were pushing their statin. These drugs can cause permanent muscle damage.
I'll freely admit that one of my areas of distrust re: statins stems from the plethora of Pharma-funded studies when they first came out. Mostly small (excluding the Phase II and III trials that were hard to come by at the time, most of the original work constituted poorly designed meta-analyses leading to strong statements of benefit and efficacy. My own statistical review of those early meta's wasn't pretty. There are better, large RCTs out now that continue to show benefit in lowering LDLa and APOb, but I'm not sure about the other effects. We see marked improvements in all-cause mortality, granted, but are we affecting other parameters, and we've been studying a group, typically, of older patients where mortality endpoints were not as long as if we had something like Framingham For Statins, and a much longer longitudinal database.
I've seen very little suggesting long-term muscle damage. That said, the short-term effects for me in muscle complains and perceived neurologic response were sufficient for me to decline after a planned and intended trial. As I noted below, my loss of memory and ability to focus were noted by my wife, a retired clinician, later in the simvastatin trial and within a couple of days in the atorvastatin trial.
Some of the statins, atorvastatin in particular, can also predispose or exacerbate T2DM. For a fairly long time, Pharma refused to concede this point, but in my case, within a week of starting atorvastatin, my well-controlled sugars skyrocketed, and I had to add an additional agent to eventually (over more than 2 months) get them down to something approaching "control" but not as well-regulated as pre-statin.
There's a lot going on in the background. I understand (to some small extent) the benefits of these drugs, especially in patients with familial hypercholesterolemia, and those with marked elevation of LDL and/or APO-b regardless of etiology. I with we had that Star Trek Tricorder that could look at an agent and tell us all the positive and adverse effects without having to wait 40 years to discover that some wonder drug was actually causing long-term harm.
You are correct. I don't give a hoot what my patient's lipid levels are and my sole goal is to reduce their risk of MI, sudden death, and stroke.
I feel the overall literature on the benefits of statins in select high risk patients is very solid and the evidence supporting a huge connection between lifelong apo b levels and atherosclerosis is even stronger.
As to permanent muscle damage from statins this is incredibly rare to the point where a causal relationship is suspect.
I admire what you are doing and enjoy reading your blog. I know how greedy big pharma can be as I worked for Parke Davis for 30 years. Their motto was medicamenta vera, truth in medecine. For the first 20 of my 30 yrs I would say that was true. But the companies research did not result in any new "blockbuster" drugs and things changed. And then one scientist in Parke Davis research in An Arbor was able to show that they had a very active statin. That drug was atoravastin. Pfizer made a hostile takeover and was able to get ownership of the Parke Davis drugs. They marketed the drug aggressively and spent a lot of money doing it.
It was all about LDL but according to many of the early studies LDL was only a weak risk factor. Somehow all of a sudden it was a risk factor. The latest studies that havent allowed the drug company to do the statistical work have shown very little benefit. One showed only one out 100 patients would not have a MI in a year of taking atoravastin. Meanwhile people were complaining of muscle pain and even difficulty walking.
The myopathy problem with Atoravastin is real and a gene has been identiifed in the approx 30 percent of patients who take it. Boston Scientific's Diagnostics company actually will sell you the test for your patients if you are an MD. The drop out rate with statins is quite high and I think most busy GP's would tell you that. There are two groups on facebook that discuss there experiences with myopathy and neuropathy.
I'm 74. Woman. Had a heart attack 4 years ago. Two stents put in I only took statins 1 month. Blood thinner 6 months. I take 4 to 6 grams Vitamin C/day plus a few other things (Linus Pauling protocol). Four months after the heart attack had eco test, cardiologist report "Dramatic improvement". Besides I feel great no problems. No meds.
Okay. I forgot the name. You made me go look in my files. Echocardiogram. "Compared to 12/6/2017 echo LV systolic function has dramatically improved". Dated 3/27/2018.
I'm in that curious component of the statin-intolerant. I've read the literature and assessed the quality of the studies (some early studies were rather poorly designed and the outcomes seemed predetermined). I've tried low-dose simvastatin and low-dose, alternating day atorvastatin.
Simvastatin did, according to my wife, induce a loss of short-term memory, and loss of attention to detail. Between her demand, and my significant myalgia (which resolved in 2 weeks after discontinuation) I managed 3 months of therapy.
Atorvatstatin was really worse. Fasting sugars popped up into the 200's from less than 110. myalgia was absolutely intolerable: I became an ibuprofen addict with acetaminophen as a kicker. This likely caused mood changes noted, again, by my wife. I couldn't concentrate on work-related issues.
Note that my 10 yr risk is about 13%, with T2DM, mild HTN, and excellent selection of grandparents with regard to lipids. Aside from the claims by lipidologists that they'd love to lower LDL to zero (mine's 75) I don't have much room to move on "fixing" my lipid status.
One concern I have with statins is I'm not exactly sure of the mechanism of action. We have studies that claim improvements in all-cause mortality, but if this is solely from lowering LDL, that claim's a little loose, at least to my way of thinking.
A generally excellent piece by ACP: However, it was not stressed strongly enough the 95% of elevated cholesterol (goal nonHDL cholesterol of 90 or less and triglycerices of 100 or less) is completely curable by a combination of diet and exercise. I did not say this was easy, convenient, or as comfortable as what people are used to. It is a simple statement of fact that some will grasp and act on. Here is my recent publication on that very subject :'Medical Research Archives 'January, 2023: "The Unhappening of Heart Disease."
I'm not sure I can concur with your statement, and will read your recent publication today, and possibly comment further. I've modified my own diet over the last 10 years, for weight loss. Increased my exercise as well. As a partially trained cook, with perhaps a little background in biochemistry, I can make a lot of things people think of as unpalatable taste pretty good, but identifying what will drive non-HDL cholesterol and triglycerides down using diet is a fairly tricky problem. Over the last 10 years, note the timeframe, and citing an "n of 1" of my own labs, I've succeeded in losing weight, my exercise level has increased, and my lipid panel is pretty well identical to what it was for the preceding 10 years: Diet and exercise did not lower my values. That said, I selected my grandparents pretty well. Were it not for the various risk calculators, with my lipid values, no one would have recommended I even consider statins. I'm relatively lucky in that regard.
I am not on the fence at all. I developed Auto Immune Hepatitis from the statins. I went on them and 6 months later almost needed a blood transfusion. LFT's were all over the place. He took me off statins. A month later LFT's almost back to normal and my blood count was almost normal. I personally think statins are over prescribed.
There are many ways we can present relevant information on risks/benefits to patients and your suggestion is reasonable. NNT and NNH can also be brought into the discussion. Lifelong risk versus 10 year risk is also important. Absolute risk versus relative matters. It is interesting that the MESA calculator comes up with lower risk estimates than the ACC/AHA. If you start at 5% risk the overall benefits will be lower than if you start at 8.4%.
Whether to begin a statin at the 5% risk level with average CAC is totally up to the individual as far as I'm concerned.
I just realized that I had written "I did intend to bash PCPs" when I mean I did not. Fortunately, I think the context of the sentence makes it clear I meant not but it is now corrected.
Ryan,
Similar to you, my eldest daughter excelled in med school and chose primary care. Great primary care doctors like you and her are essential to quality health care but they are in short supply and at greater risk of burn-out due to many factors.
Here's my post on the MESA app (https://theskepticalcardiologist.com/wp-admin/post.php?post=36905&action=edit&calypsoify=1)
It allows a calculation without the CAC score and it includes family history!
In the example I describe a 64 year old with a 175 score goes from 4.7% to 8% risk
Dr P
Hi. The PCP not knowing about ASCVD risk calculators would be a red flag against that clinician. Be careful with general PCP bashing though, as our role cannot be a luxurious deep dive into the nuances of each problem and medical decision. Most patients will not read through 5 articles you have constructed to help them, but they will read 5 articles that induce statin fear and undermine your expertise.
The doc who said “work harder on diet and exercise to get LDL<130” then probably went on to coordinate 10 other problems including a review of specialist letters, imaging studies, chronic medical problems like diabetes, cancer surveillance, htn, a recent hospitalization, anxiety and depression, OSA, etc. I think we all know from constant bombardment what “work harder on diet” means... don’t eat crap, eat more vegetables and healthy proteins and fats... and if the patient doesn’t, then suggesting a nutritionist consultation (which usually takes a whole hour we don’t have) or picking up a book on Mediterranean style diet would be a good idea for the truly motivated patient. The ones who’ve made it to see a cardiologist for primary prevention are already a highly engaged, educated, and motivated population unlike the baseline primary care population, many of whom are underinsured and can’t really afford CAC. I know it’s hard to imagine, but it’s true.
I recall an article about CAC testing and pitfalls published by the AAFP and written by John Mandrola. As family docs we really do depend on consensus guidelines- if we got tangled in the nuanced weeds of every decision we would need AI and 27 more hours per day (the amount of time already estimated a family doc would need to take care of everything that has been advised of them in patient care!). So we follow guidelines, and there is safety in that.
Here’s the counterpoint:
https://www.aafp.org/pubs/afp/issues/2019/1215/p734.html
And the most frustrating thing about ASCVD calculators is that they do not include family history! Isn’t that one of the foundational risks?! Please let me know if there is such a calculator, assuming it’s been validated, so I don’t end up sounding ignorant like the PCP you’ve mentioned. Nonetheless, cut the rest of us some slack please 😉
Ryan,
Great points! And very happy you weighed in with the PCP perspective. I did not intend to bash PCPs because I know how tough their job is and I recognize that I have the luxury of focusing on one organ.
I agree with "The ones who’ve made it to see a cardiologist for primary prevention are already a highly engaged, educated, and motivated population unlike the baseline primary care population, many of whom are underinsured and can’t really afford CAC."
And I definitely have had patients tell me they can't afford a CAC or they are not interested in it.
And I have seen many many patients who have no interest in my diet or exercise advice and I recognize that I can't change their behavior no matter how much time I spend.
I agree with Mandrola and pretty much everything else he has written about but I think he's misguided on CAC. I'm in the process of updating my CAC guide (that triggered me updating the on the fence post) and I plan to write a point by point rebuttal of the arguments against CAC.
The MESA calculator does include family history and I think family history is very important.
I hereby cut some slack
Dr .P
Ok great and thanks for the validation - reading my own comment again maybe it came off a little defensive but that’s primary care for you! I was in the top quartile of my med school class but chose family medicine because it suited my personality and fledgling medical philosophy… but there is always the sense that by being jacks of all trades we can’t possibly master any. Fortunately we don’t have to and the generalist/specialist ecosystem finds a decent equilibrium so thanks for your expertise on behalf of your primary care referrers. And there are a lot mediocre PCPs I have to admit.
Will read more about the MESA calculator (wish they had a version without CAC, since the vast majority of patients in primary care have not had one).
Cheers 😊
I am a former patient of Dr P. My cholesterol was predictably high and was put on avoristatin (I think by my PCP at the time). I immediately had a severe reaction to the medication. I struggled to walk as my muscles were completely bound up. My pharmacist told me I was one of 5% to have this severe of a reaction and stop it immediately. After blood tests my muscle enzymes count was 3 times above normal. It took over a year for them to fall to normal range and pain to dissipate. Thankfully Dr P prescribed Praulent shots which works great and I tolerate very well. I for one will NEVER take ANY statin for ANY reason. Dr P also introduced me to the Kardia App which I use to this day to self monitor and for which I am very grateful!! Thanks for the chance to comment.
Larry Scales
Despite our disagreements here and there, I still consider your insights and writings excellent
Gerry,
Fortunately, we have some great options for patients like you who are at high ASCVD risk but have significant intolerance to statins.
Ezetimibe has an excellent side effect profile and has shown improved outcomes.
The PCSK9 inhibitors are very effective with good outcome data and minimal side effects.
Yesterday, we heard at the ACC that bempedoic acid lower MAC in stat in-intolerant high risk patients.
All of these drugs, by the way, work by one method or another to lower apo B and LDL levels.
Dr. P
Skep,
I was reading about the results with bempedoic acid. I am likely to remain statin-free, although I'll discuss bempedoic acid with my PCP... my total cholesterol and LDL are low enough, about the best recommendation for me is based on all-cause mortality. I guess, with an LDL of 75, and stable over the last 10+ years I could try to drop it to the 20s, but I'm not well-enough versed in the latest lipidology to have an opinion on the field overall, just on my own health.
Thanks!
gerry
Interesting post. My particular case was that with high cholesterol in my 50s, I was not prescribed statins due to a similar risk analysis matrix. While a grandfather had died of a heart attack in his 50s, my parents both succumbed to cancer quite young, so there was little info on their cardiovascular health in older age. I would be asked if my grandfather had high cholesterol. He died in 1955, before I was born and before such measurements were common (AFAIK). So who knows?
My cholesterol level was high enough that my optometrist noticed it during an eye exam. But my medical check-ups still resulted in recommendations to eat less fatty food and drink less and no statins.
By fortunate accident, I was visiting South Africa and needed some malaria prophylactics. I visited a doctor I knew, and he did a sort of wellness check where we decided to check my PSA level and a few other labs. The PSA was fine, but he was worried about my cholesterol level.
I had read (damn you Internet!) about a more-accurate test for lipids called ApoB, so I asked to have it as well. It was sky-high - much higher than my HDL/LDL levels would have implied.
I managed to get an appointment with a local cardiologist, whose opening line was "How are you still alive?" That gets your attention. He asked about my ancestry, which is Huguenot French. Many of the Huguenot also went to South Africa, and there is a genetic condition (Familial Hypercholesterolemia) common in those families, which I also appear to suffer from.
An ECG and stress test were normal (but I could be in better fitness - weight is fine). However an ultrasound showed 30% blockage in one carotid artery. I started on statins and a low-carb diet and my ApoB levels went from literally off-the-chart to extremely low. That was five years ago and subsequent ultrasound shows a reduction and smoothing of the visible plaque.
If I had not had a chat with a helpful GP and then asked for the ApoB test, plus chosen a cardiologist familiar with FH, I probably wouldn't be here to write this.
CanAmSteve,
I've written about apo B (https://theskepticalcardiologist.com/2021/08/25/what-really-initiates-and-drives-atherosclerosis/) and consider it the primary driver of atherosclerosis. For most individuals LDL and apo B track pretty closely, however, I check apo B with the standard lipid parameters in the majority of my patients. It is especially important after drug treatment as apo B may respond differently than LDL to statin therapy.
Over the next few years, hopefully, more physicians will add apo B to their lipid panels. It is cheap and superior, IMO, to the more complicated and expensive NMR lipid particle analysis.
Dr. P
We should stop talking LDL, HDL, VLDL, Triglycerides. What matters is MI , Mortality and overall health. And no talk about relative risk. Some of the landmark studies had statistics done by the drug companies that were pushing their statin. These drugs can cause permanent muscle damage.
I am a very skeptical retired Pharmacist.
I'll freely admit that one of my areas of distrust re: statins stems from the plethora of Pharma-funded studies when they first came out. Mostly small (excluding the Phase II and III trials that were hard to come by at the time, most of the original work constituted poorly designed meta-analyses leading to strong statements of benefit and efficacy. My own statistical review of those early meta's wasn't pretty. There are better, large RCTs out now that continue to show benefit in lowering LDLa and APOb, but I'm not sure about the other effects. We see marked improvements in all-cause mortality, granted, but are we affecting other parameters, and we've been studying a group, typically, of older patients where mortality endpoints were not as long as if we had something like Framingham For Statins, and a much longer longitudinal database.
I've seen very little suggesting long-term muscle damage. That said, the short-term effects for me in muscle complains and perceived neurologic response were sufficient for me to decline after a planned and intended trial. As I noted below, my loss of memory and ability to focus were noted by my wife, a retired clinician, later in the simvastatin trial and within a couple of days in the atorvastatin trial.
Some of the statins, atorvastatin in particular, can also predispose or exacerbate T2DM. For a fairly long time, Pharma refused to concede this point, but in my case, within a week of starting atorvastatin, my well-controlled sugars skyrocketed, and I had to add an additional agent to eventually (over more than 2 months) get them down to something approaching "control" but not as well-regulated as pre-statin.
There's a lot going on in the background. I understand (to some small extent) the benefits of these drugs, especially in patients with familial hypercholesterolemia, and those with marked elevation of LDL and/or APO-b regardless of etiology. I with we had that Star Trek Tricorder that could look at an agent and tell us all the positive and adverse effects without having to wait 40 years to discover that some wonder drug was actually causing long-term harm.
Pmyron1,
You are correct. I don't give a hoot what my patient's lipid levels are and my sole goal is to reduce their risk of MI, sudden death, and stroke.
I feel the overall literature on the benefits of statins in select high risk patients is very solid and the evidence supporting a huge connection between lifelong apo b levels and atherosclerosis is even stronger.
As to permanent muscle damage from statins this is incredibly rare to the point where a causal relationship is suspect.
Dr. P
I admire what you are doing and enjoy reading your blog. I know how greedy big pharma can be as I worked for Parke Davis for 30 years. Their motto was medicamenta vera, truth in medecine. For the first 20 of my 30 yrs I would say that was true. But the companies research did not result in any new "blockbuster" drugs and things changed. And then one scientist in Parke Davis research in An Arbor was able to show that they had a very active statin. That drug was atoravastin. Pfizer made a hostile takeover and was able to get ownership of the Parke Davis drugs. They marketed the drug aggressively and spent a lot of money doing it.
It was all about LDL but according to many of the early studies LDL was only a weak risk factor. Somehow all of a sudden it was a risk factor. The latest studies that havent allowed the drug company to do the statistical work have shown very little benefit. One showed only one out 100 patients would not have a MI in a year of taking atoravastin. Meanwhile people were complaining of muscle pain and even difficulty walking.
The myopathy problem with Atoravastin is real and a gene has been identiifed in the approx 30 percent of patients who take it. Boston Scientific's Diagnostics company actually will sell you the test for your patients if you are an MD. The drop out rate with statins is quite high and I think most busy GP's would tell you that. There are two groups on facebook that discuss there experiences with myopathy and neuropathy.
I'm 74. Woman. Had a heart attack 4 years ago. Two stents put in I only took statins 1 month. Blood thinner 6 months. I take 4 to 6 grams Vitamin C/day plus a few other things (Linus Pauling protocol). Four months after the heart attack had eco test, cardiologist report "Dramatic improvement". Besides I feel great no problems. No meds.
What is an eco test?
Dr P
Okay. I forgot the name. You made me go look in my files. Echocardiogram. "Compared to 12/6/2017 echo LV systolic function has dramatically improved". Dated 3/27/2018.
I have been on a statin since A-Fib June 2018, Elequis also...numbers fine no side effects.
I am curious as to whether you have written any articles on statins for those of us 75 years old or older? If not, would you.
No I am not on the fence. I refuse.
I'm in that curious component of the statin-intolerant. I've read the literature and assessed the quality of the studies (some early studies were rather poorly designed and the outcomes seemed predetermined). I've tried low-dose simvastatin and low-dose, alternating day atorvastatin.
Simvastatin did, according to my wife, induce a loss of short-term memory, and loss of attention to detail. Between her demand, and my significant myalgia (which resolved in 2 weeks after discontinuation) I managed 3 months of therapy.
Atorvatstatin was really worse. Fasting sugars popped up into the 200's from less than 110. myalgia was absolutely intolerable: I became an ibuprofen addict with acetaminophen as a kicker. This likely caused mood changes noted, again, by my wife. I couldn't concentrate on work-related issues.
Note that my 10 yr risk is about 13%, with T2DM, mild HTN, and excellent selection of grandparents with regard to lipids. Aside from the claims by lipidologists that they'd love to lower LDL to zero (mine's 75) I don't have much room to move on "fixing" my lipid status.
One concern I have with statins is I'm not exactly sure of the mechanism of action. We have studies that claim improvements in all-cause mortality, but if this is solely from lowering LDL, that claim's a little loose, at least to my way of thinking.
Suggestions?
A generally excellent piece by ACP: However, it was not stressed strongly enough the 95% of elevated cholesterol (goal nonHDL cholesterol of 90 or less and triglycerices of 100 or less) is completely curable by a combination of diet and exercise. I did not say this was easy, convenient, or as comfortable as what people are used to. It is a simple statement of fact that some will grasp and act on. Here is my recent publication on that very subject :'Medical Research Archives 'January, 2023: "The Unhappening of Heart Disease."
I'm not sure I can concur with your statement, and will read your recent publication today, and possibly comment further. I've modified my own diet over the last 10 years, for weight loss. Increased my exercise as well. As a partially trained cook, with perhaps a little background in biochemistry, I can make a lot of things people think of as unpalatable taste pretty good, but identifying what will drive non-HDL cholesterol and triglycerides down using diet is a fairly tricky problem. Over the last 10 years, note the timeframe, and citing an "n of 1" of my own labs, I've succeeded in losing weight, my exercise level has increased, and my lipid panel is pretty well identical to what it was for the preceding 10 years: Diet and exercise did not lower my values. That said, I selected my grandparents pretty well. Were it not for the various risk calculators, with my lipid values, no one would have recommended I even consider statins. I'm relatively lucky in that regard.
More after I binge on another article...
HRS,
We will have to agree to disagree on this point ( as usual.)
Dr P
I am not on the fence at all. I developed Auto Immune Hepatitis from the statins. I went on them and 6 months later almost needed a blood transfusion. LFT's were all over the place. He took me off statins. A month later LFT's almost back to normal and my blood count was almost normal. I personally think statins are over prescribed.
Steve,
There are many ways we can present relevant information on risks/benefits to patients and your suggestion is reasonable. NNT and NNH can also be brought into the discussion. Lifelong risk versus 10 year risk is also important. Absolute risk versus relative matters. It is interesting that the MESA calculator comes up with lower risk estimates than the ACC/AHA. If you start at 5% risk the overall benefits will be lower than if you start at 8.4%.
Whether to begin a statin at the 5% risk level with average CAC is totally up to the individual as far as I'm concerned.
Dr. P