Understanding “plaque” and evolution of coronary heart disease: Insights from Dr. Simon Binny

Why is plaque Important?

Everyone develops atherosclerosis (“plaque”) and is spread across their arteries leading to progressive hypertension, dementia, kidney disease, visual loss as the organs all depend on normal blood flow.

The risk of sudden vascular events can lead to strokes and heart attacks from a plaque rupture and can be often catch people by surprise.

Understanding plaque tends to develop in the normal population in males in their late 20s and females in early 30s but current cardiac assessments are not routinely happening until 45.

In Tasmania 5% (or 1 in 20) of heart attacks across the state occur before 40 years.

Once you form plaque it CANNOT be removed, but it can be slowed from getting worse.

“The stenosis theory”

As a training cardiologist everything was taught and based around the principle of identifying when someone has developed severe stenosis and then deciding how best to fix it with stenting or bypass and if no option to manage just with medicines.

This lead to GPs referring patients to clinics or presenting to emergency to assess their story of chest pain and either book then directly for a coronary angiogram or first do a functional test like a treadmill stress test (+/- echo) or a nuclear perfusion scan to identify if there was a flow limitation and where.

The angiogram would then confirm or exclude a severe narrowing and it would typically be stented or sent for bypass surgery.

The problem with the stenosis theory.

There was never actually any evidence fixing a severe narrowing reduced either heart attacks or death in patients presenting with “stable chest pain”, being pain on limited or increased exercise.

And evidence provided in the Courage trial in 2007 confirmed this was the case but did not assess the higher risk arteries and so was questioned.

However in 2018 the much larger ISCHEMIA trial was published that assessed patients with stable angina, who underwent and failed stress testing and was confirmed to have a severe stenosis on angiography showed between medical/tablet management and stenting/bypass there was no difference in death rates out to at least 7 years and there was no significant difference in heart attack but there was a signal of higher heart attack initially with stent and bypass but at 5 years there was a trend to a reduction in heart attack but only small.

Unstable plaque and heart attack stenting.

There was however data that placing a stent at the site of an unstable plaque (with a heart attack) it did reduce the rate of further plaque rupture at that site over simply adding multiple blood thinners (medical management).

Hence arises the “plaque characteristics theory”.

The “plaque characteristics” theory.

This is the new prevailing theory since the ISCHEMIA trial and the advent of CT coronary imaging.

Large imaging datasets now spanning over 18 years has allowed the retrospective assessments of coronary plaques on CT in patients who subsequently have had a heart attack and a plaque rupture in those specific plaques.

This has allowed for the identification of specific plaque characteristics that predict whether a plaque will rupture or not.

High risk plaque characteristics.

A high burden of the early phase, non-calcified plaque along the arteries.

Bulky, individual non-calcified plaques.

Eccentric plaques that grow outwards off the side of the artery rather than those that grow inwards narrowing the artery.

Low attenuation, peri-coronary fat near the plaque (inflammatory).

Location at the start of an artery, at a branching point or at a tortuous curve.

Spotty calcification within the centre of a non-calcified plaque, or with a non-calcified inner cap.

Management of vulnerable/high risk plaque

Studies have only now just started in the pre-emptive stenting of plaques deemed to be high risk and not flow limiting as to whether we are accurate enough to identify a plaque that will rupture and recommend targeted stenting to prevent a heart attack.

Until we get to this being allowed practice or for plaques not quite meeting the future criteria for stenting we use lifestyle and medical management to reduce the risk of an event.

Reducing blood pressure, limiting exercise intensity/heart rate.

Caution with inflammatory conditions, flu/covid shots.

Reducing clotting risks (HRT, smoking) and using blood thinners: aspirin/clopidogrel.

Adding statin therapy, actively stabilises the plaques, which is its main but seemingly unknown benefit and effectively cleans up the non-calcified high risk plaques into stable calcified plaques.

Management of “safe” calcified but stenosed plaques

Based on the plaque characteristics theory these severely narrowed but “safe” calcified plaques do not need to be stented as there is no evidence of heart attack or death benefit.

There was presumed benefit in stenting the artery if there was heart failure or reduced muscle function in the areas inadequately provided, however the REVIVE study showed identical improvement in function by simply using heart failure medications.

There is still presumed benefit in patients having concerning ventricular arrhythmias due to muscle not getting adequate blood flow to reduce the risk of a cardiac arrest.

There is still presumed benefit in reducing angina/chest pain although the ORBITA 1 and 2 trials using sham stenting vs actual stenting has shown mixed angina benefit but is likely still true.

So what should we be doing now with this new theory?

We need to acknowledge many patients are presenting with heart attacks at an early age, often in young, fit, “healthy” patients before they would have been traditionally thought to be high risk and on treatment.

We need to assess patients at an early age for risk of developing plaque, and with it possible high risk plaques.

We need to integrate the use of coronary imaging earlier in a patient’s journey and well before they start to develop chest pain.

Consider a much earlier and across the board use of statins to both reduce plaque formation to much more rapidly reduce and stabilise high risk plaques.