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Posted on Tuesday May 28, 2024 in Health Screening
An article by Dr Edward Leatham, Consultant Cardiologist
Coronary artery calcification (CAC) is viewed with mixed feelings in the medical community. On one hand, its presence signals a history of coronary artery disease, which can be alarming. On the other, it also indicates a natural protective response of the body to harden and stabilise potentially dangerous coronary artery plaque.
In the early days, EBCT provided groundbreaking images but at very high capital cost, so only a few leading centres globally could afford the technology, however it was used enough for large prospective cohort studies to prove that CAC was a useful predictor of future coronary symptoms (angina) and events (heart attacks and cardiac death) [1]. The advent of spiral and multi-slice CT scanners revolutionised this field by offering similar diagnostic capabilities at a fraction of the capital cost and wider range of uses, so the test became more available and CAC screening gained acceptance and became more accessible.
CAC typically begins in individuals in their 40s, correlating with future cardiovascular events. It is said that on average only 10% of coronary plaque calcifies, so although this ratio unquestionably alters with age, coronary calcium can really be the tip of the iceberg. While it may be desirable to have zero CAC, hardening of non calcified plaque should equally be seen as a natural mechanism which helps heal non calcified plaques that might otherwise rupture, leading to heart attacks.
Initially, a standardised non-contrast CT scans became the primary tool for CAC detection, providing a reliable risk assessment through the Agatston score. However, the recognition that significant coronary artery disease could exist without calcification led to the wider user of contrast-enhanced CT scans to detect both calcified and noncalcified plaques. Even more advanced scans identify not only the non calcified plaques, but also areas of inflammation (using data processing to measure FAI) that a non-contrast CT (such as a CAC scan) would otherwise miss. Sequential CAC to follow up disease progression quickly established that an increase in CAC with age was inevitable in most patients and not linked to clinical course, so is not widely practiced.
In the figures below are representative images from contrast CTs of two 63 year old asymptomatic female patients. Whereas the second has zero CAC, she had the more clinically severe coronary artery disease. The top figure shows heavy coronary artery calcification of the left anterior descending artery (LAD) that has developed without significant stenosis; the lower figure shows a critical stenosis as a result of a non calcified plaque that has nearly occluded the LAD. In this case there zero coronary calcium in any vessel. Life threatening disease was confirmed in the zero CAC case by invasive angiography a week later (where the critical narrowing was immediately treated with a stent).
Case 1 The course of the LAD is shown by the contrast in grey, with focal coronary calcification in white. Workstation analysis showed no significant narrowing of the LAD.
Case 2
The course of the LAD is shown by the contrast in grey. Workstation analysis showed critical narrowing of the LAD. 
An image of the invasive angiogram of case 2, taken a week later, confirming the CT findings. There is a severe narrowing (stenosis) affecting the left anterior coronary artery (LAD).
These images illustrate that although a raised CAC for age is associated with higher future coronary event rates, the absence of CAC does not exclude important coronary heart disease.
Recent advancements have shown that coronary artery disease begins with inflammation, followed by plaque deposition and eventual calcification. Inflammation can persist for years, leading to scar tissue and calcification as part of the healing process. This understanding has shifted the focus from solely identifying calcification to recognising and managing inflammation. Its obvious why CTCA with FAI, which measures coronary inflammation[3}, is fast becoming the ‘go to’ test of choice for many preventative care physicians in this field.
One important insight from recent studies is that once calcification is present, it can indicate a stabilised phase of the disease. Statin therapy and other treatments often increase calcification, reinforcing plaque stability. This process, initially counterintuitive, is now understood as beneficial. Calcified plaques are less likely to rupture compared to their softer, more unstable counterparts, see another example [2] which illustrates this point.
Given the complexity of coronary artery disease, a comprehensive approach to risk assessment is necessary. While CAC scores remain a valuable tool, they should be part of a broader diagnostic strategy that includes evaluating inflammation and other risk factors. Advanced imaging techniques and AI-enhanced analysis are leading the way in this multifaceted approach.
In summary, i. although the presence of coronary calcification always means that there is coronary artery disease present, non calcified coronary plaque is common particularly under 65 years of age II. coronary artery calcification, once a marker of concern, is now recognized as a sign of stabilised disease in patients who have coronary atherosclerosis. The transition from soft, vulnerable plaque to calcified, stable plaque is likely to be a protective mechanism that reduces the risk of acute coronary events. For patients with coronary artery disease, promoting calcification through appropriate treatment may well become part of managing and mitigating risk.
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