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LDL cholesterol – one size does not fit all…

LDL cholesterol – one size does not fit all…

As one of the consultants dealing with prevention of heart disease at London Medical, I see many patients with the genetic condition Familial Hypercholesterolaemia. Inheritance of one or both of some 5 genes accounts for most cases here and the condition is characterised by very high levels of the LDL cholesterol (low-density lipoprotein), sometimes called “bad” cholesterol. High levels of LDL cholesterol are associated with a propensity to early coronary artery disease – out of proportion sometimes to the level of cholesterol. Intense treatment is rewarding not only because young members of the family carrying the gene can be treated early but also because there are now excellent medicines to control and even reverse the atherosclerosis. The concern is that so many of these families remain undiagnosed.

There is also an additional larger group of people who have benefited considerably from consulting with our lipid specialists. This is the group of patients who have had a raised LDL cholesterol either treated with a low dose of a statin by their primary care doctor (something that became routine the moment statin drugs became generic and cheap) or patients who have refused or stopped treatment with this medication. This often leaves people who are at severe risk of early cardiovascular events (heart attack, stroke, erectile dysfunction, vascular dementia) effectively untreated.

The risk of future cardiovascular disease, which is what really matters, is more commonly assessed using “scores”. The best of these are the QRisk3 score used in the NHS (which predicts the 10 year risk of developing a coronary event) and the European Society of Cardiology HeartScore which is country specific. These take time to use in a clinic, and further, 10 year risks are poorly understood by both doctors and patients, and they are never tailored to the individual risks of a patient. Many of the parameters that feed these risk scores give a general population based assessment – which may not apply to an individual patient. In our clinic, we take account of family history, smoking, diabetes and hypertension but all measurements are surrogate – they do not directly reflect the propensity of a coronary artery to have a heart attack (a thrombosis or clot in the artery) but they DO identify a patient vulnerable to such an event. This has been the basis of London Medical's approach to managing cardiovascular risk for the last 30 years where we aim to identify the vulnerable patient and grade their risk crudely – low, average or high risk.

We use NMR (nuclear magnetic resonance) analysis for the size and number of the LDL and HDL particles, cardiovascular markers such as lipoprotein (a), Lp-PLA2 , myeloperoxidase, oxidised LDL and the apolipoproteins. This approach is particularly important when patients have raised triglyceride as happens in diabetes with an excess of lipoprotein remnants.

We also use imaging with coronary artery calcium scores and quantitative ultrasound measurements of carotid artery intima media thickening and 3D volumetric measurements of plaque size.

These additional tests make it easier to explain to a patient their risk and why two patients with the same level of raised LDL cholesterol do not necessarily have the same risk and need to be treated very differently.

Modern treatment algorithms for the high risk patient have changed substantially with the advent of stronger more effective drugs and we now know that we can reverse atherosclerosis with very low levels of LDL cholesterol. So a patient with a strong family history of heart disease, showing plaque in their common carotid arteries in their sixties, whose coronary artery calcium score places them at the 90th percentile of the population, does not only need standard treatment with just a statin. He/she will need much more medication. The target LDL cholesterol should be as low as possible and this is particularly relevant if there has been a lifetime of no or inadequate treatment of the LDL cholesterol and there is need to play “catch up” as we can now reverse atherosclerosis.

But how can we know that this approach works or benefits our patients? When we set up the protocol for our quantitative carotid intima media and plaque studies 30 years ago, we did not have the 3D probe and it was then believed that the intima media thickness was the main prognostic factor for future cardiovascular disease. It is, in the young, as plaques will not have developed yet in most people – but later on, changes in plaque size give one a lot of information on progression or regression of atherosclerosis. Our being the first in Europe to start assessing plaque size volumetrically with a 3D probe was a signal advance in our practice. The most useful measurements made in our clinic are the repeat carotid studies done over our patients’ lifetimes. We have been able to follow worsening arterial thickening and plaque disappearance and use this information to guide treatment – and fortunately, the advent of strong drugs has enabled us to learn that LDL lowering remains the key to opening up arteries. Different patients require different LDL lowering strategies. So our patients have seen changes in LDL lowering in their lifetime with attendant slowing or even improvement in their carotids dictating the intensity of LDL lowering. What is gratifying is to see guidelines shift with lower LDL cholesterol now an aim for all patients with advanced cardiovascular disease risk. There are guidelines for the masses but the individual patient in our clinic can still share in decision making with knowledge of what is happening in their own arteries and get timely intervention before cardiovascular events have already occurred.

Dr Ralph Abraham
August 2021

+44 (0)800 0483 330

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