Over the past 2 to 3 years, I have become increasingly aware of the number of patients who are getting coronary artery calcium scores, (CAC) as well as seeing patients who are increasingly frightened about a comment written on chest x-rays or chest CT scans: namely the comment of “severe” coronary artery calcium” being present.
 
The fright these words create is intense, as the implication is that you have something really terrible and that you are at risk for a serious heart attack, or in need of an immediate heart bypass operation or a stent.
 
I cannot intervene with the choice of words that other doctors use, and the language and words doctors and other health care providers use can be misinformative and filled with undermining fear and anxiety.
 
Language can be used as a weapon or as a healing tool, and all too often it is used as a weapon.
In “cardiology world” there are a number of “expressions” used that undermine one’s confidence and well being:
Phrases such as “You are a walking time bomb”, “You have the widow maker”, “your heart is so weak I’m surprised you can breathe!” All these types of statements do no good at all to help to heal a human being. In fact, quite the opposite! These types of statements undermine the human soul. These are statements that do harm and may, in fact, contribute to making the health problem worse by stoking fear, anxiety, and a loss of self.
 
Patients are now commonly getting Coronary Calcium Scores and there can be the presence of the word “severe” in the report. Again, this word just creates degrees of fear and anxiety, and even panic.
AND, it misrepresents the nature of the problem!
Coronary atherosclerosis, or arterial sclerosis is a pathology of the artery wall that most people in the industrial world get.
 
It is a “disease” that actually can start early in life and it “Smolders” through the decades.
It is a very, very complicated phenomenon that includes the sciences of molecular biology, biochemistry, physiology, pathology, and histology, and the breadth and depth of this complexity is often undermined by information in social media, or “30-second” TV commercials.
It continually mystifies people invested in the study of this complex problem, namely cardiologists, lipidologists, endocrinologists, cardiovascular surgeons and scientists with PhD degrees doing research in these various disciplines.
The wall of an artery is made of a triple layer of muscle!. The largest is the aorta, at about an inch in diameter, then many of the larger arteries: carotids to your brain, femorals down your legs are about 1 to 1.5 cm in diameter, and the coronary arteries are about 2 to 5 mm in diameter.
 
Through the reasons of genetics and the usual things you know about; being overweight, having high blood pressure , diabetes, smoking , much of our nutrition leads to a process where the triple layer of smooth muscle cells of the artery wall gets infiltrated by substances through the years of life-even starting in early childhood!
 
These substances are atherogenic lipoproteins and inflammatory cells that cross through the “endothelium” which is the lining on the inside of the tubes of the artery wall, and these then work on displacing the muscle cells, and then there is a very complex situation with the leaking of toxic inflammatory substances and chemicals that over time degrade the architectural integrity of the artery wall, and atherosclerotic plaque starts to evolve. SO…the disease itself is a disease within the artery wall, and eventually the plaque can break through into the Lumen which is the hollow part of the tube where the blood flows.
 
The development of plaque, is a combination of “cholesterol products” bleeding and clotting products, and inflammatory chemicals. Plaques then develop and over time can get harder and “calcified” and they may also be “mushy and soft” and combinations of both with a lot of complexity.
I could go on endlessly talking about the complexity of atherosclerosis. I’ve referred many of you to read my essays on my website at Chesniehearthealth.com in the Cardio Topic section.
I suggest that you revisit this and read the essay on Heart Disease and it will talk to you about the disease of atherosclerosis and how it crosses over to coronary artery disease.
 
Therefore, the disease process of atherosclerosis, leads to calcium build-up in the coronary artery wall, and also in the plaque itself.  When a radiologist reports “severe” calcification in the coronary artery it means that you have an atherosclerotic disease process present, but it doesn’t make any implication with the word “severe” that there is any degree of “blockage” present! So, in my opinion it is a bad and stupid word to use, because all it does is create fear, without further explanation.
Also with the coronary calcium score: the usual implication is that the higher the score, the worse the blockage! That is not true!
  
When the Calcium Score CT scan came out in the late 1980’s, and into the early 90’s, we, as cardiologists, were taught that a score of over 200 meant that atherosclerotic plaque was present and it was important to take note of it and to discuss the basis of risk with patients and decide on medical treatment. If the score was over 400, it was considered more serious, and the implication was that the patient was in harm’s way and that they needed to be put on medication to hopefully prevent calamity. In fact, if the score was over 400, many cardiologists, including me, took patients to the cath lab and we did coronary angiography in the expectation that the patient would likely need a bypass operation. (PTCA was just getting started and this was before the development of coronary stenting).
Not one patient that I did an angiogram on showed sufficient blockage that required them to be sent for a coronary bypass operation! Yes, we would see the calcium tracking down the coronary artery, and there were irregularities of plaque in the lumen (the tube where the blood flows) but there was no presence of tight narrowing impairing flow.
 
The higher the number does not predict the degree of narrowing in an artery. It just indicates that there is a higher density of calcification present in coronary plaque. It does not mean that your coronary atherosclerotic disease is worse or more critical.
I will share with you that my own coronary calcium score number is greater than 800 and has been for years!
That’s a pretty high number, yet, I continue to be fit and strong, I feel well, and I’m active with physical activity and career fulfillment. I also have numbers of patients who have scores greater than 1000, or 2000, and even up to 4000!- and they have not had a coronary blockage, nor have they had a stent or a bypass operation, and they continue to be active, and feel well.
Of course, we all take medications to specifically optimize blood pressure and lipid profile.
  
So… here’s “the crunch”-
Atherosclerotic coronary disease, arterial disease, is not curable! And it smolders through the decades, and it can be unpredictable and can “bite you” with a sudden acute coronary blockage, a myocardial infarction, or an acute coronary event that can severely impair the flow of blood in the artery, requiring emergency stenting or bypass surgery.
 
The job of the cardiologist is to ongoingly assess with a patient if there is any impairment of coronary artery blood flow, which is why I like to see my patients at least annually to question the presence of any symptoms, such as various types of chest discomforts, difficulty with breathing mainly with exertion, but sometimes at rest, and other things…and we do exercise treadmill stress testing with an EKG, or we do nuclear imaging scans with treadmills or medications, or stress echoes with a treadmill-all to try and determine if there is any evidence of flow impairment in the artery or not.
 
If there is evidence of flow impairment, we then proceed to look at the flow in the artery with a coronary CT angiogram, or with a catheter-based angiogram with the possibility of placing a balloon to open a blockage and stent (or brace) to keep the artery open and restore normal flow. At times and with degrees of complexity, a coronary artery bypass operation may be recommended.
 
The other job is to provide advice around lifestyle: encouraging physical activity, good nutrition (I advocate the Mediterranean diet), control of blood pressure, control of blood sugar, and lowering of lipids (cholesterol and atherogenic subparticles. In addition to the lifestyle guidance, is the use of medications including statins, other lipid lowering drugs, blood pressure meds, diabetes meds, etc.
  
In conclusion, I say this every day to many of my patients:
We are all on the planet for only so long, and every day you have to wake up lucky. Most importantly, you have to have great respect for the unpredictable!
 
I hope this letter has been of benefit to you!

I had two patients send me this article from the New York Times written by Dr. Haider Warraich, M.D., who is a cardiologist. I found it interesting and wanted to share it with you. Click the button below!

I would like to try and clarify the misunderstanding that exists, even among health care professionals, of how the blockage of a coronary artery (which creates a heart attack, or “Myocardial Infarction”) relates to the smoldering underlying disease of “Atherosclerosis”. The tragedy of Coronary Artery Disease is that it is essentially an “after the fact” diagnosis. This means that a clinical event has had to have happened: anginal chest discomfort, acute coronary syndrome, heart attack, placement of a stent, or having a coronary bypass operation. Once any of these have occurred, you now have the diagnosis of Coronary Artery Disease.
 
The actual blockage in the artery, or the limitation of blood flow in the artery is NOT the actual disease. It is a consequence of the disease. The underlying disease, the root cause is a disease process called Atherosclerosis. This disease is an insidious culprit, located within the wall of the artery, smoldering over decades until it may unpredictably disrupt through the wall into the Lumen (where the blood flows) and compromise the flow of blood.
 
Lets begin this way: the ventricles are the pumps of the heart (the lower chambers) that pump the “fuel” to all the cells in the body. The “fuel” is oxygenated blood, as well as nutrients, vitamins, hormones, chemicals, enzymes, proteins, amino acids, etc.  that are carried by a series of tubes, getting smaller and smaller to where the blood may be transferred into organs and into cells. These tubes are the arteries, the largest of which is the aorta (the diameter is about 20 to 30 millimeters), to the smallest which are the first 2 that come off the aorta above the aortic valve and left ventricle: the coronary arteries (diameter of 2 to 4 millimeters). The right and left coronary arteries and their branches sit on the surface of the heart and wrap around the heart, delivering oxygenated blood and other substances to the heart muscle.
 
An artery is like a hose. It is circular, and the structure like the plastic of the hose is actually a three- layered muscle. The inner wall where the blood flows, is called the endothelium which is the lining into the artery, like your skin is the lining into your body.  The inner layer of muscle is called the “intima”, the middle layer is called the “media”,  and the outer most layer is called the “adventitia”. Think of the lining, or endothelium, as the bricks and mortar, though this “mortar” is permeable, meaning that “things” such as cells, proteins, cholesterol, etc. can pass through the lining into the inner arterial structure.
 
The arteries do not maintain the same diameter, nor the same direction. They vary in caliber size, they change direction, and they have bifurcating branches that twist and turn as well; and the flow of blood is by no means constant! With the contraction of every heart beat from the left ventricle, there is a sudden, rapid, bolus amount of blood ejected through the artery.
 
(When your blood pressure is checked, this is what the upper number is, the systolic number of your blood pressure: the bolus (amount) of blood traveling through the artery against the tension in that muscular tube, while the lower number, the diastolic number, is the absence, or relaxation phase of wall tension in that muscular tube.)
 
Therefore, arteries, particularly coronary arteries, which are smaller size arteries, are subject to great stresses throughout life; High velocity spurts of blood shooting into tubes that twist and change direction, changing diameter size, with branches  that bifurcate, and a lining that is vulnerable to penetration into the interior of the arterial structure… and the penetration of substances includes good things as well as bad things! If a person lives to 80, there will be about 4 billion heart beats!
 
I like to explain the insidious nature of atherosclerosis with the analogy of termites penetrating into the wood structure of your home. Termites penetrate into the wood structure and eat the wood from the inside out. Much the same with the atherosclerotic process…and the atherosclerotic process often begins in childhood and in some cases, in infancy! There have been studies of autopsies on babies who have died, demonstrating the presence of fatty streaking and infiltration of cholesterol onto the coronary artery wall. These babies were born to overweight mothers in poor areas of the country who ate poor food very rich in saturated fats.
 
The science of atherosclerosis is extremely complicated. It involves biochemical pathways, molecular and cellular biology, histological changes of cells, physiological pathways of food absorption and pathways through the liver. It simply cannot be realistically communicated in “sound bites”. I can tell you that I have practiced cardiology now for over 30 years, and in the last 10 years undertook intense study, writing of exams, and became board certified in clinical lipidology, which is the science of atherosclerosis, and I can tell you that it is staggering in its complexity and variability.
 
Simply put, it is an infiltration process with cholesterol products, mainly LDL, penetrating through the lining and into the interior of the artery wall. This is associated with the attachment of inflammation cells, called macrophages, that enter the vessel wall and displace and disrupt the integrity of the muscle cells. Associated with this displacement is also a leaking out of “poisonous toxins” that further cause degradation and destruction to the architectural integrity of the arterial wall. This interior disruption eventually breaks through the arterial lining and causes bleeding and further inflammation of the vessel wall, into the lumen where the blood flows. The bleeding of the vessel wall, as well as the inflammation process, causes clotting products to accumulate with the creation of “Plaque” which is a combination of clotting products, fibrin and thrombin, and cholesterol products, and inflammatory cells. It is not a “linear process” but accumulates sporadically and unpredictably with shear stress, flow stress, and variable plaque rupture.
 
This may lead to a gradual growth of plaque that becomes hardened and calficifed and may block the interior lumen to 70, 80, 90 percent and interfere with the flow of blood through the artery.
 
These are the types of plaques and narrowing that we look for in cardiology practices, and these will often be associated with the onset of chest discomfort, often with exertion (angina), or with the presentation of an abnormal exercise stress test, or an abnormal nuclear stress test. When angiography is done we will see one or more narrowing in the coronary arteries, and depending on location, number, degree of narrowing, it will usually lead to opening up the vessel ( angioplasty) and placement of a stent, or possibly the consideration of coronary artery bypass surgery. Interestingly these plaques are firm, rigid, and calcified and they tend to be stable. I compare them to the Rock of Gibraltar: they are not going anywhere! They certainly interfere with fuel delivery to the engine, and if the heart is working hard and not getting enough fuel delivery, terrible things can happen including sudden death. But they tend not to completely close off, and tend not to cause acute heart attack (myocardial infarction).
 
The task at hand with these very significant narrowing that interfere with coronary blood flow, is to utilize medications that improve flow, that stabilize the heart, and slow or stop the process of further plaque accumulation. The procedures discussed above do NOT AT ALL cure the disease, or control the development of the disease, but restore flow through or around the artery (stent of bypass) to deliver the appropriate amount of blood to the heart muscle and protect it.
 
However, there is even more of an insidious problem to atherosclerotic coronary disease! A plaque may be present that is small and “mushy”. It may encroach into the artery lumen by 20 or 30 percent, not interfering with flow delivery at all. And it is not at all like the Rock of Gibraltar, it is much more like Creme Brûlée!… A soft mushy plaque filled with fatty cholesterol and toxic byproducts covered by a thin cap, that can unpredictably rupture and then clot off and block the artery. In fact, these insidious smaller plaques are considered to be “vulnerable” or “unstable” and their unpredictable rupture causes about 60 to 70 percent of acute coronary syndromes, or heart attacks (myocardial infarction)
 
These plaques do not present with chest discomfort, or abnormal exercise stress tests, or abnormal nuclear stress tests. And if an angiogram is done, a stent is not provided, nor is a bypass operation because the narrowing does not interfere with blood flow delivery.
 
The task at hand is to either slow the further build up of plaque, stop the process of plaque build-up, or even reverse the process and try to aim for plaque regression.
 
This is the domain of clinical lipidology, or preventative cardiology.
The placement of stents, particularly within the context of rushing the patient to the cath lab to open the artery during an acute heart attack is hard, stressful, heroic work. To try and prevent that from happening at all, so that a person never knows what it means to rush to the hospital in the throes of an acute heart attack, or to be brought in, in cardiac arrest, or to end up with severe heart failure, is what the goal is of preventing all of this from happening.
 
This is an initial conceptual overview of the topic.  The next discussion will be to talk about the issues of lifestyle, and diet, and medication to prevent the tragedy of coronary artery disease.
 
Remember: this is an “after the fact diagnosis”. This means that a clinical event has had to have happened: anginal chest discomfort, heart attack, stent, bypass. When this has happened the person is labeled as having Coronary Artery Disease.
The underlying disease before clinical presentation is the insidious “termite infested” hidden disease process call Atherosclerosis, and this is what we in Preventative Cardiology work so hard on trying to control.