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.
Antiatherosclerotically Yours,
-ACP