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Posted on Friday March 15, 2024 in Diagnostic & Health Screening
An article by Dr Edward Leatham, Consultant Cardiologist
Coronary heart disease (CHD) remains one of the leading causes of premature death worldwide and is a major contributor to morbidity across developed countries. One of the most important facts about CHD is that the disease process begins silently and often decades before symptoms appear.
Pathological studies have shown that early changes may start as early as a person’s twenties. At this stage, fatty streaks develop within the coronary arteries — findings commonly observed by pathologists during autopsy studies, even in young individuals who died from non-cardiac causes such as accidents. These early changes highlight that coronary disease is not an abrupt event but a long, progressive biological process.
Modern cardiology increasingly recognises atherosclerosis as a chronic inflammatory disease rather than simply a passive build-up of cholesterol. Over many years, inflammatory cells — including foam cells within the arterial intima — interact with LDL cholesterol, leading to the gradual formation of focal plaques within the coronary arteries.
Initially, these plaques are non-calcified and soft in composition. They tend to develop in predictable locations, particularly in the proximal segments of the coronary arteries. During this early phase, the disease is invisible to most traditional tests and can only be detected using high-resolution imaging modalities such as intravascular ultrasound or advanced CT techniques.
As inflammation continues, plaques slowly evolve. The soft, lipid-rich material gradually calcifies, transforming into harder, more stable plaques. Although calcification is often viewed negatively, it frequently represents a stabilisation phase of plaque biology, reducing the likelihood of acute rupture.
Importantly, it is only at this stage — when calcification appears — that coronary artery disease becomes visible on a non-contrast CT calcium scan. By the time coronary calcification is detected using a coronary artery calcification (CAC) score, the disease has usually been present for many years.
In earlier stages, the coronary artery can compensate for plaque growth by expanding outward — a process known as positive remodelling. Eventually, however, this compensatory mechanism reaches its limit. At this point, plaques begin to encroach upon the arterial lumen, producing flow-limiting areas of scar tissue.
It is only at this relatively advanced stage that symptoms typically arise, including:
Many of the traditional diagnostic tests used in cardiology — such as stress ECG, stress echocardiography, nuclear perfusion imaging, and myocardial perfusion scans — often only become abnormal when disease has progressed to this stage.
Over the past decade, advances in cardiac computed tomography (CT) have transformed our understanding of coronary artery disease. CT imaging now allows cardiologists to look beyond simple obstruction and explore the biological activity of disease within the artery wall itself.
CAC scoring remains a valuable and widely used tool for risk assessment. It provides a simple measure of overall calcified plaque burden and helps estimate long-term cardiovascular risk. However, calcium scoring detects only one phase of disease — the later calcified stage.
CT coronary angiography offers a more comprehensive assessment, allowing visualisation of both calcified and non-calcified plaque. This makes CTCA particularly useful for detecting patients who may have significant non-calcified disease despite low or absent calcium scores.
A major recent advancement is the development of the CaRi heart score, pioneered by researchers in Oxford. This approach applies artificial intelligence and machine-learning analysis to cardiac CT images to measure the Fat Attenuation Index (FAI) — an indirect marker of inflammation around the coronary arteries.
FAI analysis evaluates subtle changes in CT grey-scale values within the adipose tissue surrounding each coronary artery. These tissue changes reflect inflammatory signals originating from the artery wall itself.
When combined with age and traditional risk factors, FAI allows clinicians to:
In clinical practice, this represents a significant shift — moving from simply detecting existing disease to identifying biological activity that may predict future events.
The growing range of CT-based tools has led to a more individualised approach to screening and risk assessment.
By identifying early inflammation and non-calcified disease, cardiologists can intervene earlier with lifestyle modification, preventive therapies, and risk-factor optimisation.
Cardiac CT has moved beyond simply identifying blockages. Modern imaging now allows us to understand where a patient sits along the spectrum of coronary disease — from early inflammation to calcified plaque and obstructive disease.
This shift supports a more proactive model of care focused on:
Through detailed pre-consultation assessment and careful selection of imaging strategies, cardiologists can tailor investigations to each patient’s age, symptoms, and risk profile — improving both accuracy and outcomes.
Coronary heart disease is a long-term process that often begins silently early in life. Advances in CT imaging — particularly CT coronary angiography, FAI analysis, and the CaRi heart score — now allow clinicians to detect disease much earlier than ever before.
The aim is no longer simply to diagnose disease once symptoms occur, but to identify risk earlier, intervene sooner, and prevent future heart attacks before they happen.
In cardiometabolic medicine, muscle is not a cosmetic tissue but a metabolic organ. Evidence consistently shows that strength, not muscle mass, predicts insulin resistance, cardiovascular risk, and survival. Many older adults are not losing muscle tissue — they are losing muscle function, and that is the pathology that matters.
Ten minutes of strength training, five days a week, is enough to change metabolic health. Like brushing your teeth, it works because it’s sustainable. Keep the time fixed, increase the weights gradually, and focus on strength, not scales. Small daily habits protect muscle, reduce visceral fat, and support long-term health.
When blood sugar levels are consistently high, causing prediabetes and diabetes, the risk of conditions such as heart disease and type 2 diabetes increase in the long-term. It is easy to understand why the phenomenon of glucose spiking, where blood sugar levels surge and then fall back into the normal range after a meal, is also widely considered to be harmful.
For much of modern cardiology, in its battle against coronary artery disease—one of mankind’s greatest threats—the “enemy” seemed clear. When I trained, the diagnostic armoury was focused on accurately identifying flow-limiting narrowing of one or more coronary arteries. Yet in the last decade, a profound paradigm shift has unsettled these foundations—and in some respects, turned them on their head.