Coronary Artery Disease

How the disease develops

Fatty deposits, called plaque, build up gradually within the wall of a coronary artery. This process begins decades before symptoms appear and is driven by cholesterol, blood pressure, diabetes, smoking, inflammation and inherited susceptibility. In South Asian patients it tends to present earlier and more diffusely than in Western populations, which is why screening thresholds that were designed elsewhere often apply poorly here.

As plaque accumulates, the artery narrows. Below a certain point, blood flow during exertion becomes insufficient for the heart muscle, and this shortfall is experienced as angina — typically a pressure or tightness in the chest brought on by effort and relieved by rest.

What the tests can and cannot tell you

An angiogram is an anatomical picture. It shows where the narrowings are and how tight they look. It does not show whether a given narrowing is limiting blood flow, and the correlation between the two is weaker than most patients assume.

Functional testing — treadmill testing, stress echocardiography, perfusion imaging — asks the more useful question: is any part of the heart muscle short of blood when it is working hard? Where the answer is uncertain in the catheter lab, physiological measurement across the lesion itself, such as fractional flow reserve, resolves it directly. The FAME 2 trial established that lesions selected this way are a materially different set from lesions selected by appearance.

Treatment: what the evidence supports

For stable coronary disease, the randomised evidence is unusually consistent. COURAGE (2007), BARI 2D (2009), ISCHEMIA (2020) and REVIVED-BCIS2 (2022) each compared a stent-first strategy against optimal medical therapy, and none found a reduction in death or heart attack from the stent.

Stents do relieve angina — ORBITA-2 (2023) demonstrated that against a placebo procedure. But relief of symptoms and prevention of death are different goals, and a patient is entitled to know which one is on offer.

Optimal medical therapy in this context means high-intensity statin therapy titrated to a lipid target, blood pressure controlled to goal, antiplatelet therapy where indicated, glucose control in diabetes, structured exercise, complete tobacco cessation, and follow-up that actually happens. It is more demanding than a procedure, not less.

When intervention is the right answer

During a heart attack, immediately and without debate. Also in high-risk acute coronary syndromes, in significant left main stem disease, in angina that persists despite properly optimised medical therapy, and where objective testing shows a large ischaemic burden with symptoms limiting daily life.

Treating stable disease conservatively and treating an acute event urgently are not opposing philosophies. They are the same principle — match the intervention to what the evidence says it achieves — applied to two very different situations.