Cardiologists often make the mistake of assuming their patients have a greater understanding of heart function, physiology, anatomy, terminology, and pathology than is realistic. I am frequently guilty of such faulty assumptions but in the last decade, I’ve made a determined effort to listen more closely when laypeople tell me about the heart or reveal their understanding of heart disease and adjust the way I communicate with patients accordingly.
I’ve written extensively on the diagnosis and treatment of the complications of atherosclerosis on the skeptical cardiologist but I haven’t really sat down and created a layperson-directed overarching synthesis of this complicated disease.
I will be initiating a series of stories on “Profiles in Coronary Artery Disease” and thought before posting the first such profile it would be useful to provide a background on coronary artery disease and heart disease in general and hopefully get everyone “up to snuff” as it were.
What is Heart Disease?
Heart disease kills nearly 700,000 people in the United States annually, more men and more women than any other disease.
The majority of these deaths (nearly 400,000) are due to heart damage caused by disease in the arteries that supply blood to the heart, something doctors usually term coronary artery disease and abbreviate by writing or saying CAD.
When the man (or woman) on the street mentions being concerned about heart disease they are usually thinking about CAD, a disease caused by a process called atherosclerosis (aka arteriosclerosis aka hardening of the arteries).
If you read about prevention of heart disease on a website the discussion is going to be about preventing atherosclerosis and thereby preventing CAD and heart attacks. The risk factors typically mentioned on these websites (high blood pressure, high cholesterol, smoking, diabetes) are risk factors for atherosclerosis.
There are, of course, lots of other forms of heart disease, ranging from abnormal rhythm disturbances (some of which are caused by CAD) to valve abnormalities (some of which are caused by CAD) to congenital heart disease to heart failure (often caused by CAD) which can also result in death but summed together these non-CAD forms of heart disease cause less death and disability than does atherosclerosis.
Atherosclerosis: Insidious and Ubiquitous
Atherosclerosis is an insidious and ubiquitous process in modern humans. Although we are born with a smooth, unblemished lining to our arteries (the endothelium), small fatty streaks in that lining develop as early as our 20s. They are caused by a complex interplay between lipoproteins, white blood cells (macrophages), the immune system and the arterial wall’s normal elements.
This complex interplay appears predominantly driven by particles of apolipoprotein B which pass through the endothelium and initiate a chronic inflammatory process within the arterial wall. I wrote about this and provide a link to my lecture on this topic here.
The disrupted, blemished, and inflamed areas are found throughout our blood vessels but are more common at areas of high pressure and turbulence in the circulation where arteries branch.
When they become large enough to be visualized by imaging techniques we call these localized areas, atherosclerotic plaques. In the attempt to help patients understand atherosclerosis, an analogy to household plumbing (see my post on the superiority of the pimple analogy here) is often used with graphics like this one:
Atherosclerosis attacks all the arteries in our body not just the ones to the heart (the coronary arteries). The problems and diseases it causes are related to disruption of the blood supply in the vascular blood conduits (arteries) to various body organs (heart, brain, legs, and kidneys being the organs most affected).
Currently, the term in vogue for all the havoc that atherosclerosis wreaks on our bodies is atherosclerotic cardiovascular disease, abbreviated ASCVD. The three areas most dependent on a consistent arterial blood flow are the heart, the brain and the kidneys, thus ASCVD predominantly consists of CAD, ischemic strokes, and chronic kidney disease,
The majority of diseases caused by ASCVD are heart attacks (myocardial infarction or MI in doctor-speak), ischemic strokes, and kidney failure. In addition, ASCVD can attack arteries to the legs or arms and other organs, obstructing blood flow.
This piece is focused on heart disease but cardiologists have extended their purview beyond the immensely important organ sitting in your chest and pumping blood out to the rest of your body. Indeed, the techniques for treating atherosclerotic disease in the coronary arteries developed primarily by cardiologists (including stenting to open blocked arteries without surgery and the medications which can prevent atherosclerosis) have a major beneficial impact on all forms of ASCVD.
Thus, I received board certification in Cardiovascular Disease in 1987 and many cardiology groups use the word cardiovascular in their titles.
Asymptomatic Heart Disease, The Silent Killer
Long before ASCVD manifests, however, the process of atherosclerosis begins and it is totally silent. Like a thief in the night, those fatty streaks begin; inflammation progresses, large plaques develop and we are totally unaware that we have been robbed of our smooth and naturally compliant vasculature.
The actual complications of ASCVD don’t generally manifest until later in life: typically in the fifties or sixties for men and the sixties and seventies for women. For those with strong risk factors, either inherited (like lipoprotein (a) or familial hyperlipidemia) or acquired (like cigarette smoking or diabetes) heart attacks and strokes can occur as early as the thirties.
Before those complications develop and long before any symptoms develop, however, the volume, frequency, and severity of the atherosclerotic plaques within your arterial walls, something we term the atherosclerotic burden, can increase to dangerous levels.
What is dangerous, you might ask, about these innocent and silent plaques as long as they aren’t causing chest pain or haven’t caused a heart attack or stroke?
The danger, my friend, is that the first symptom of high atherosclerotic burden in the coronary arteries is often a heart attack. Although we have an amazingly effective tool to stop an acute heart attack (coronary stenting), many sufferers suddenly collapse with cardiac arrest and die (Jim Fixx ) or are found dead in their beds (like Bill Bryson’s dad and Darryl Kile) and don’t survive.
With the advent of CPR and AEDS we can resuscitate some of these so-called sudden cardiac deaths (like Bob Harper) but most don’t survive and < 10% make it out of the hospital and live a normal life.
Diagnosing and Treating Subclinical and Clinical Atherosclerosis
The optimal approach to the detection and treatment of CAD has evolved substantially over the 3 decades that I have been a practicing cardiologist. Due to advances in medical therapy, lifestyle and device therapy, deaths from cardiovascular disease declined by 70% between 1980 and 2009.
Much of this decline I believe can be ascribed to three factors:
- the development of safe and effective LDL cholesterol-lowering medical therapy (predominantly statins.)
- the ability to stop acute heart attacks quickly using coronary stenting.
- a progressive decline in cigarette smoking. Smoking is by far the biggest lifestyle factor contributing to ASCVD.
In the last 10 years, however, the rate of decline of ASCVD has slowed and sudden cardiac death rates have remained constant. There were 356,000 out-of-hospital cardiac arrests in 2017 and only 10% of them survived and left the hospital.
I feel that the majority of these deaths could have been prevented if underlying ASCVD had been identified early and effective medical treatment started. Detection of a high atherosclerotic burden before symptoms, before an MI or stroke, and before any coronary stenting or bypass surgery is imperative.
The earlier we can diagnose subclinical high atherosclerotic burden, 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, and stopping the downstream ASCVD events that cause death and disability.
Over the last 10 years, I have written extensively on the skeptical cardiologist about the ways to identify the silent build-up of plaque in the arteries, something doctors call subclinical atherosclerosis.
We’ve also stressed the importance of utilizing imaging techniques like coronary artery calcium scanning and advanced lipid biomarkers to more precisely determine an individual’s risk for heart attack and stroke.
The standard risk factors are a useful crude first step to assessing an individual’s short and long-term risks for ASCVD but they frequently underestimate (especially in those with a strong family history) or overestimate the true risk.
We can blame a lot of heart disease on the standard lifestyle risk factors: poor diets and lack of exercise are huge factors leading to obesity, diabetes, hypertension and hyperlipidemia, but in many patients I see who develop heart disease at an early age, lifestyle is not the issue, it is the genetic cards that they have been dealt.
Risk estimates using standard age, gender and lifestyle factors will significantly underestimate the risk of ASCVD in individuals with really bad genetic CAD cards.
In my Profiles in Coronary Artery Disease series we will hear the stories of individual patients who have gone through the panoply of complications that atherosclerosis can cause and and variety of cardiovascular procedures that cardiologists have in their tool kit. These patients are now undergoing secondary prevention.
We will also hear the stories of patients with large atherosclerotic burdens at a young age who have had none of these complications and none of these procedures thanks to early identification and aggressive treatment. These patients are classified as primary prevention.
Hopefully, by the end of this decade, all of our new profiles in heart disease due to CAD will be cases of primary prevention and secondary prevention will have become a historical curiosity.
17 thoughts on “A Primer on Heart Disease: Atherosclerosis is Numero Uno”
Always enjoy reading your articles. Leaving a comment to say that you have a stray apostrophe “but cardiologist’s have extended”
Thanks, got that and a few other typos.
Robert, not sure why but my reply is listed as a separate response entirely.
It’s weird, most of my numbers were fine. Total cholesterol stayed below 200, trigs were never a concern. Like a lot of thirty-somethings who felt like they were in great shape I had a few years where I just forgot to get my annual physical, but going back to 2008, and including 8 physicals between then and 2021, the only really stand-out thing is that around 2012 my LDL went past 100, by the middle of the ’10’s it was consistently in the 120s, then it peaked at 140 and stayed in the high 120s and low 130s. All it took was 10 mg of crestor to crash it from 127 to 78 as of December, so I’m happy about that and excited to see what the bump to 20 mg will do. I want to crater that number as low as possible! I do recall asking my PCPs back then if I should be concerned and they always said to just exercise more and eat healthy. I recall being told that several years and thinking, “I do eat healthy, and I’ve been a runner and gym rat all my life! I really can’t do much more on these fronts than I’m already doing!” But I never really pushed back, and I never did enough research on my own. My dad died rather suddenly in 2010 from an aggressive form of pancreatic cancer and I can’t help but think that If he’d been alive when those LDL numbers started to jump he’d have ordered more tests and would have started me on a statin. It wasn’t until I stumbled on Attia’s podcast in late 2020 and started hearing really in-depth discussions about ASCVD, lipidology, Apo(b), the difference between LDL-C and LDL-P, etc… that I started to read a lot about this stuff. When I went to my PCP in 2021 I had a battery of tests I was demanding. She had no idea what Apo(b) or Lp(a) even was (I had to explain them as best as I could) and she thought the CAC would be a waste of money, but she approved them all. Turns out those all should have been done years ago, but they’re just not standard practice and like I said, I just wasn’t informed enough to take matters into my own hands. I agree with Attia…at the first signs of ASCVD (such as consistently unfavorable LDL-C) this disease should be tested for aggressively and treated aggressively. I just didn’t know that back then, and I suppose my PCPs didn’t either.
Super article, thank you for writing it.
It’s weird, most of my numbers were fine. Total cholesterol stayed below 200, trigs were never a concern. Like a lot of thirty-somethings who felt like they were in great shape I had a few years where I just forgot to get my annual physical, but going back to 2008, and including 8 physicals between then and 2021, the only really stand-out thing is that around 2012 my LDL went past 100, by the middle of the ’10’s it was consistently in the 120s, then it peaked at 140 and stayed in the high 120s and low 130s. All it took was 10 mg of crestor to crash it from 127 to 78 as of December, so I’m happy about that and excited to see what the bump to 20 mg will do. I want to crater that number as low as possible! I do recall asking my PCPs back then if I should be concerned and they always said to just exercise more and eat better. I recall being told that one year where I’d gone largely carb and sugar free and was sporting a noticeable six-pack and thinking, “You’ve got to be kidding me, do you see the shape I’m in?” But I never pushed back, and I never did enough research on my own. My dad died rather suddenly in 2010 from an aggressive form of pancreatic cancer – diagnosis to death was about four months. If he’d been alive when those LDL numbers started to jump I have to think he’d have ordered more tests and would have started me on a statin. It wasn’t until I stumbled on Attia’s podcast in late 2020 and started hearing really in-depth discussions about ASCVD, lipidology, Apo(b), the difference between LDL-C and LDL-P, etc… that I started to really read a lot about this stuff. When I went to my PCP in 2021 I had a battery of tests I was demanding. She had no idea what Apo(b) or Lp(a) even was (I had to explain them as best as I could) and she thought the CAC would be a waste of money, but she approved them all. Turns out those all should have been done years ago, but they’re just not standard practice and like I said, I just wasn’t informed enough to take matters into my own hands. I agree with Attia…at the first signs of ASCVD (such as consistently unfavorable LDL-C) this disease should be tested for aggressively and treated aggressively. I just didn’t know that back then, and I suppose my PCPs didn’t either.
I’m glad you finally got things figured out and are now on the right track.
Your observation “When I went to my PCP in 2021 I had a battery of tests I was demanding. She had no idea what Apo(b) or Lp(a) even was (I had to explain them as best as I could) and she thought the CAC would be a waste of money, but she approved them all. Turns out those all should have been done years ago, but they’re just not standard practice ”
is why I keep hammering on these things in my writing and practice.
CAC scans should be as well known and promoted as colonoscopies for men over 40 and women over 50. I’ve got a strong family history of heart disease on both sides going back generations. Knowing the cards I was dealt, and having a dad who was a cardiologist, I started taking diet, exercise, and lifestyle really seriously as far back as my teens. Not saying I’ve been a flawless saint every day of my life, I’ve enjoyed a few plates of barbecue and spent more than a few nights in my twenties closing down bars, but overall, diet and exercise have been VERY important parts of my life for a good thirty years. In 2021 I thought I was in ridiculously good shape for a 46 year-old…hell, I thought I was in ridiculously good shape for a 26 year-old. However, I learned about CAC scans through Peter Attia’s podcast, thought it might be a good idea to take one, and was shocked when it came back with a score of 107, putting me in the top 3% for my age group. I’m still trying to come to grips with it, but the point is, without that scan, there is no way I would have believed I had moderately advanced CAD. I was running 5ks with ease, powering through intense weight lifting sessions, doing hill-sprint HIIT workouts to exhaustion, and had a body-fat percent in the low teens. My cardiologist has me on 20mg Crestor with the goal of getting up to 40mg in a few months, and a daily low-dose aspirin before bed, and he’s basically said the only explanation he can think of for such a high number is genetics, which is something my late father, the cardiologist, also told me many times that I’d have to deal with later in life. No symptoms…none whatsoever…and without that CAC scan the CAD would have just gotten worse and worse. I was very likely headed for one of those out-of-the-blue heart attacks. I probably still am, but at this point I at least know what I have. I have a cardiologist, I’ve adjusted my exercise routines to be safer, I take my statins religiously, I read a lot about this disease, I have blood work done multiple times a year, and I’m even more fanatical about my diet, but still…the damage is done. A CAC at 40 would likely have turned up a single or low double-digit number and would have allowed me to start fighting this thing earlier. More folks like me should know about CAC scans and should be having them when they’re younger.
I’d be very interested to know what your other relevant numbers were (e.g., LDL-C) before you had the scan. I
A nice summary. I would decline of cigaret use at the top of the list.
Would you please give a citation of recent research which shows a mortality benefit from scenting?
I assume you mean coronary stenting.
What I said in the article and what I’ve written about a lot is that stenting greatly benefits those who are having an acute heart attack. The results are dramatic and immediate.
For those with stable CAD the situation is entirely different. For the most part, stenting should be withheld in stable CAD patients and utilized only if symptoms are refractory to medical treatment.
“Overall, in these unstable scenarios PCI was associated with a significant reduction in mortality (RR, 0.84 [95% CI, 0.75–0.93]; P=0.02). In unstable CAD, PCI also reduced cardiac death (RR, 0.69 [95% CI, 0.53–0.90]; P=0.007) and MI (RR, 0.74 [95% CI, 0.62–0.90]; P=0.002). For stable CAD, PCI did not reduce mortality (RR, 0.98 [95% CI, 0.87–1.11]), cardiac death (RR, 0.89 [95% CI, 0.71–1.12]; P=0.33), or MI (RR, 0.96 [95% CI, 0.86–1.08]; P=0.54).”
Not sure how to break this to you, but vegans, health nuts, and workout enthusiasts with great “numbers” drop dead of infarction and get bypass surgery etc with the “general public”….I believe Dr Pearson discusses this as well. Where is your data that risk “regresses to zero” if you follow this protocol? Your site also indicates following a “low fat diet” which is completely not aligned with current research. You’re presenting a “magic bullet” which doesn’t reflect any type of reality or data as some type of magic bullet.
Atherosclerosis, (which killed my father), will always be a major cause until Internists and Cardiologists start preaching diet and warning of Metabolic Syndrome. It’s the Standard American Diet, SAD, that is killing people. We’re sugar addicts with Insulin flooding our arteries. Eliminate all sugars and processed carbs. Shop on the periphery of the grocery store. Eliiminate snacks and adopt intermitent fasting. I was pre-diabetic with my Internist saying, let’s monitor this…(and I’ll prescribe metformin when you get to a certain level). I took charge of my helath and after two years, I got rid of 15 lbs., I weigh 155 lbs. for the first time since college, my beer belly is gone and my A1C is 5.6, Trigliceride to HDL is 1.8, LDL 77.
Food is medicine.
Very nicely written and explained. Quite logical and correct. I offer just a couple of clarifying points: You said ” … the development of safe and effective LDL cholesterol-lowering medical therapy (predominantly statins.) …” That should have been slightly clarified to discussing the adequate dose of statin or other medication to reach a non-HDL cholesterol of 90 or less in the well and 75 or less in those with ASCVD.
I have a problem in being simply straightforward: so here goes. Your statement that people develop ASCVD without risk factors is absolutely wrong. There are numbers for every risk factor where future risk regresses to 0. Those people who have a lifestyle that includes being trim, highly (90%) whole and unprocessed and ideally organic foods vegan, do not smoke, exercise significantly, have a positive-serving attitude, accept and persevere thru the difficulties of reality, limit alcohol to 4 drinks a week or less and drink essentially only water and weak herbal tea do not, let me repeat ‘do not’, develop ASCVD. The goal numbers are BP 110-115/60-70, non-HDL cholesterol of 90 or less, triglycerides of 100 or less, A1c of 6.2 or less at age 62 and down to 4.4 at age 44, hemoglobin about 14, having abdominal clear lines of demarcation = “trim”, etc. These values are listed in the “Wellness Protecting Numbers” at http://www.thepmc.org. These previous statements are not an advertisement, they are a discussion of reality. With respect, and once again to ACP, well done.
I tend to follow the advice of my good friend Barry Sears. He recommends taking a high quality omega 3 supplement to keep your AA/EPA ratio between 1 and 3, along with a polyphenol supplement like one made from maqui berries. So far, so good at the age of 74!
Do you think heart valve calcification involves the same or a different process than atherosclerosis? I note that several studies have found that statins do not help with valvular disease, although they clearly help with atherosclerosis.
What are your thoughts on possible cardioprotective effects ofPDE-5i inhibitors? https://academic.oup.com/jsm/article/20/1/38/6986842