Professor Bruce Campbell, a consultant neurologist and Head of Neurology and Stroke at the Royal Melbourne Hospital answers GPs questions.

What blood pressure and cholesterol targets do you aim for, particularly in younger patients?

Targets are slightly artificial because most of these risk factors do not really have threshold effects, so the lower the blood pressure the better, as long as you are not making the patient lightheaded and fainting or falling over.

For ischaemic stroke, we have evidence that less than 1.8mmol/L LDL is better than higher targets, so it is worth starting a high dose statin (80 mg of atorvastatin or 40 mg of rosuvastatin) and rechecking the lipids after a while. If the LDL remains greater than 1.8mmol/L and the stroke had an atherosclerotic component, I add ezetimibe.

We do not start statins for haemorrhagic stroke. We do not stop them if you have had a haemorrhage and you have got a good indication for a statin, but haemorrhages are not related to atherosclerosis. There is some suggestion that lowering cholesterol could actually worsen the risk of haemorrhage, though the evidence is inconsistent. There was one trial that showed atorvastatin 80mg reduced ischaemic stroke risk but there was a trend towards increased haemorrhage in that trial in people who had had a haemorrhage before. 

There is some biological plausibility that very low cholesterol levels might influence membrane stability and increase your risk of haemorrhage. But if someone has known coronary artery disease we continue their statin because that is of net benefit. In cardiology they target LDL less than 1.4mmol/L.

Do neurologists have a preferred class of antihypertensives?

Traditionally the evidence was from the PROGRESS study, in which an ACE inhibitor was used, perindopril, plus or minus indapamide. 

More recently the evidence has supported calcium channel antagonists as reducing blood pressure variability, which is thought to be important to stroke risk, so we use a lot of amlodipine and related medications.

We also use a lot of ACE inhibitors. Angiotensin II receptor antagonists tend to be a bit better tolerated without the cough, but ultimately the benefit seems to be about the blood pressure we achieve.  We are less likely to use beta-blockers because they increase blood pressure variability and are not particularly effective for lowering blood pressure.

The strategy for blood pressure lowering is dietary advice to reduce salt intake, exercise, weight reduction, ACE inhibitors or calcium channels. I tend to favour the calcium channel blocker or A2RA first up but the specific agent chosen is less important.

We aim to get the blood pressure as low as we can without making the patient dizzy. I commonly recommend a systolic BP target consistently less than 140mmHg, but there is reason to suspect 120mmHg is better for most patients if they do not have other comorbidities such as autonomic dysfunction.

It is about consistency as well, and the measures we take in the office may or may not be reliable. Some patients will measure BP at home and the numbers will vary, and some then worry why it varies. We have to explain that is normal for BP to vary to some degree with activity etc. 24 hour ambulatory blood pressure monitors are much easier to get now and can be helpful particularly to see if the patient has the normal dip overnight, versus an increase that might suggest they have obstructive sleep apnoea that you need to deal with.

Evidence is accumulating that you are more likely to slip into atrial fibrillation if you have obstructive sleep apnoea and it is part of the whole metabolic syndrome that is well worth treating if you find it.

Do you ever check Apolipoprotein A?

I do not currently. We do not have a specific therapeutic for that just yet, although I can see there are agents in trials.  Just recently there was a study published that looked quite promising for being able to lower Apo A with an agent but we would need to know whether that translates into cardiovascular benefits, so for the moment it is not routine.  I focus on the LDL.  If the statin is not enough to get the LDL less than 1.8mmol/L I will add ezetimibe.

I rarely use PCSK9 inhibitors (the monoclonal antibodies alirocumab and evolocumab). They are expensive and have restrictive eligibility criteria but are an option for patients who are having multiple territory vascular events and who genuinely cannot tolerate a statin, and you cannot achieve what you want to with ezetimibe. It is well worth considering whether a PCSK9 inhibitor is right for that patient and they are certainly effective.

Do neurologists use coronary artery calcium score before prescribing statins, or is that just something cardiologists do?

It is not something neurologists do. If I am prescribing a statin it is because someone has had a cerebrovascular event so my referral bias means I am not in the business of primary prevention and coronary calcium scores are not something we use when determining secondary prevention.  They have a role, certainly, in that primary prevention space for risk stratification but it is not something within my field of experience. I use statins after ischaemic stroke or TIA because the patients have demonstrated themselves to be at high risk and what their calcium score is doesn’t alter that.