I have recently had several patients who underwent this scan to look for early signs of coronary artery narrowings, and I wanted to relay my feelings on the value and risks of interpreting the test results.
Background:
A coronary calcium scan is a test that looks for specks of calcium in the walls of the coronary (heart) arteries. These specks of calcium are called calcifications. Calcifications in the coronary arteries are an early sign of coronary heart disease (CHD). CHD is a disease in which a hard substance called plaque builds up in the coronary arteries and narrows blood flow into the heart muscle.
Over time, plaque can harden or rupture (break open). Hardened plaque narrows the coronary arteries and reduces the flow of oxygen-rich blood to the heart. This can cause chest pain or discomfort called angina.
If the plaque ruptures, a blood clot can form on its surface. A large blood clot can mostly or completely block blood flow through a coronary artery. This is the most common cause of a heart attack. Over time, ruptured plaque also hardens and narrows the coronary arteries.
CHD also can lead to congestive heart failure and arrhythmias. Heart failure is a condition in which your heart can’t pump enough blood to meet your body’s needs. Arrhythmias are problems with the rate or rhythm of your heartbeat.
Overview:
Two machines can show calcium in the coronary arteries—electron beam computed tomography (EBCT) and multidetector computed tomography (MDCT).
Both use x rays to create detailed pictures of your heart. Your doctor will study the pictures to see whether you’re at risk for future heart problems.
A coronary calcium scan is a fairly simple test. You’ll lie quietly in the scanner machine for about 10 minutes while it takes pictures of your heart. The pictures will show whether you have calcifications in your coronary arteries. The question is how best to interpret the results and how best to assess your risk of CHD.
Coronary Calcium Scan
Some calcium (plaque) is found on the Coronary Calcium Scan in the majority of westeners above the age of 60 -65, and doesn’t necessarily correlate with important blockages or narrowings in the coronary arteries.
Why? Because, while may people have high LDL (bad) cholesterol, many also have elevated HDL (good) cholesterol, and markers of inflammation are often relatively low risk.
While high cholesterol leads to hardened arteries that can cause a heart attack or stroke, this view is simplistic and only partially accurate — cholesterol is part of the “total picture” when it comes to hardened arteries (atherosclerosis), but it gets a bad rap and in my opinion, is NOT the main culprit — inflammation is.
First and foremost, cholesterol does serve some very important purposes in our bodies, including these:
* It’s used to make hormones like estrogen, progesterone, testosterone, adrenaline and cortisol;
* It acts as a “healing salve” for injuries and tears in your tissues and blood vessels; and,
* It makes up the myelin sheath that surrounds and protects your nerves
Now, inflammation is part of your body’s repair process—it sends a signal for cholesterol and white blood cells to “come to the rescue” when you’re injured and that’s how the healing process is carried out.
But, the problem arises when inflammation in your body becomes chronic. Chronic inflammation in your arteries causes a repetitive “signal” for cholesterol to come on the scene and do its “repair work.” However, it’s not a cholesterol buildup exclusively that will clog an artery. On the contrary, when your body goes into overdrive trying to heal an inflamed artery, not only is cholesterol present, but that area also becomes a “magnet” for fibrous proteins called fibrinogens, calcium deposits, and wastes and toxins in your blood. All of these substances can keep building up and building up until eventually you have the blob called “plaque.” Plus when your arteries are inflamed, that interrupts your body’s cholesterol drop off/pick up cycle.
So, when your body is working the way it should, low-density lipoproteins (LDLs) carry cholesterol through your bloodstream and drop it off to your cells where it’s needed. Then high-density lipoproteins (HDLs) come through like a clean-up crew, “mopping up” excess cholesterol and bringing it to your liver to be recycled. But when this carefully orchestrated cycle is disturbed, that’s when you can get into inflammation trouble and become an attractive home for a clog.
In a nutshell, in my opinion, it’s INFLAMMATION that’s the most important culprit behind clogged arteries–not cholesterol. And, when one is not remarkably
inflamed, [which can be measured by a comprehensive battery of blood tests now routinely available], and can be treated with anti-oxidants, ozone therapy, stem cell therapy and natural medicines to resolve.
The statin drugs are not evil, but not all that helpful in preventing heart attacks and strokes. Only 1-2 events are prevented for every 100 patients treated. And, we know that now a growing number of patients are developing muscular symptoms with statin use; and more importantly, there is a growing concern of the relationship between long-term statin use and the development of dementia. If you modify your lifestyle to a more natural diet, and exercise 3 times a week and feel well during exercise, you likely don’t have significant coronary blockages, and you have time to reverse the process that leads to coronary blockages over time.
If you are concerned about your long-term risk for CHD, consult a physician that knows how to measure, identify and treat sources of inflammation. Your physician can then add this data to routinely used 10-year risk assessment tools from the National Institutes of Health, and come up with a more accurate assessment of your true risk.
If you already have CHD, I recommend considering chelation therapy, which has recently shown encouraging results, reducing risk in certain populations based on results from an NIH trial published in the Journal of the American Medical Association (JAMA) (Lamas GA et al. JAMA 2013 Mar 27. Bauchner H et al. JAMA 2013 Mar 27. Nissen SE. JAMA 2013 Mar 27). Read more in this New England Journal of Medicine article.