Coronary calcium scoring – it’s not just about one number!
Atherosclerotic vascular disease remains the biggest killer worldwide. Over the past two decades, there have been highly effective preventative strategies for this condition. One of the major breakthroughs has been early detection of atherosclerosis and, to date, the simplest and most accurate predictive test is the coronary calcium score.
Many cardiologists around the world have replaced this test with the intravenous CT coronary angiogram, using the same technology, but involving a greater cost, typically higher radiation protocols, often pre-treatment with beta blockers & always, an intravenous injection with the potential for anaphylactic reactions & also renal dysfunction.
There is not one paper in the peer-reviewed literature suggesting any prognostic benefits of CT coronary angiography over coronary calcium scoring as a screening test in asymptomatic patients.
In conjunction with the Sydney Adventist Hospital and Dr David Grout, a fellow cardiologist, I introduced coronary calcium scoring into Australia in 1999. It has become my practice to perform this test in all males at age 50 and females at age 60 (because of the moderate protection from female hormones in women, delaying the onset of significant atherosclerotic disease in most cases by around 10 years). This test is not for people with known existing heart disease. It is my opinion that CT Coronary Angiography should only be performed in very high-risk symptomatic patients presenting to an A & E with chest pain or with non-specific symptoms as an outpatient & equivocal stress imaging results.
If a person has major risk factors for heart disease, such as hypercholesterolaemia, hypertension, cigarette smoking, clinical diabetes or prediabetes and, in particular, a very strong family history of premature vascular disease, I would consider performing a coronary calcium score at an earlier age.
Around 50% of males age 50 and females aged 60 will have a coronary calcium score above zero. Although coronary calcium in itself is not the problem, it is a very strong and accurate surrogate marker for atherosclerosis. The coronary calcium score is formulated by taking the area (a 2-D estimate of volume) of individual coronary plaques multiplied by a density factor of calcium from 1 to 4. Thus, as an example, if the area of an individual’s plaque is 100mm2 and there are a few flecks of calcium within the plaque (i.e. low density), then the score is 100 X 1. As another example, if the area of the plaque is 50, but the plaque is densely calcified, the score would be 50 X 4. This would represent a more stable plaque because of the lower volume but denser calcification.
Calcium is deposited within plaques as a reparative response by the body. Calcium is used throughout the body to strengthen structures. Most of the calcium in our body is in the bones to make them strong. With pathologic, atherosclerotic plaques, a degree of calcium is protective until the plaque calcification becomes excessive.
The presence of a significant amount of coronary calcium should prompt the treating doctor to introduce aggressive risk factor modification. A recent study presented at the European Society of Cardiology meeting in Paris in 2019 demonstrated that in patients over 50 years of age with a coronary calcium scores over 100, there is a significant benefit from taking statin therapy. If the coronary calcium score is below 100 then there is no statistically significant benefit from prescribing a statin.
Interestingly, the MORGEN trial from Holland demonstrated that following the five keys of being healthy i.e. quit all addictions, 7 to 8 hours of good quality sleep, following sound nutritional habits (basically a Mediterranean diet), exercising 3 to 5 hours on a weekly basis, cultivating happiness and managing stress, there is a reduction in risk for a vascular event, such as a heart attack, by 83%. Standard statin therapy reduces vascular risk by around 20 to 30% and with more aggressive doses, up to 50%. But, the stronger the dose, the stronger the potential side-effects. We, therefore, must have strong justification to introduce chronic pharmaceutical therapy in our patients.
Thus, the frequent use of coronary calcium scoring. But, if you are in the lower risk ranges (0-100) or the moderate risk range (100 to 400), it is also my practice to repeat the coronary calcium score every five years to determine the progression of the disease. It is a little known fact that the coronary calcium score should not be considered alone as any good software program also gives a measurement of volume. Over the 21 years using coronary calcium scoring, I have seen multiple patients who have followed my prescribed therapeutic strategies, including strong lifestyle principles and taking appropriate therapies, demonstrate a significant reduction in the coronary volumes despite variable increases in coronary calcification.
It is these follow up scores that are vital in determining whether the treatments are working. In particular, it is the reduction in coronary volume that suggests some degree of regression of the plaque. If over time, the coronaries become more calcified, this is purely stabilisation of the plaque or even a degree of regression, if there is a concomitant reduction in volume.
Over the past 10 years, I have been using in all my patients over the age of 50, BPF 99, the desiccated juice of Bergamot oranges grown in Calabria. Although I have no published data in this regard, I have seen numerous patients in my clinical practice who have followed sound lifestyle principles and have taken BPF99. This particular group of patients either could not tolerate statin therapy or purely did not want to be on statins because of significant negative “press” outside the medical profession.
In a number of patients, I have seen a significant reduction in coronary volumes with variable rises in coronary calcification. In all of these patients, there have been no clinical events and I have often seen a significant drop in triglycerides and elevations in HDL cholesterol. There is published data showing BPF99 increases the particle size of LDL and HDL which is the healthy pattern associated with plaque regression.
There are a number of studies showing increased coronary calcification with chronic statin therapy. I would suggest this is not because statins make the arteries worse but purely make them more stable, for all the above reasons. Around 20 years, there was a major paper published by Paulo Raggi et al demonstrating significant reductions in coronary volumes after 12 months of statin therapy.
Unfortunately, at present many doctors still manage their patients with clinical parameters and measurements of basic lipid values. It is my view that this is not enough to determine the stabilisation and, at times, regression of coronary artery disease. The patients in my practice that appear to have the best clinical course are those that follow strong lifestyle principles, are compliant with appropriate pharmaceutical therapy along with high quality supplements such as BPF99, attend for regular follow-up every 1-2 years and also, just as importantly, are educated to report any new symptoms if they occur.
Over the next few decades, we will see enormous advances in the management of atherosclerotic coronary artery disease but regardless, with our current therapeutic strategies, we can still offer our patients enormous longevity and an excellent quality of life.