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.
Brian Chesnie M.D.