Q: Are the NICE guidelines designed for primary or secondary prevention?
Both. These guidelines update the relevant sections of the NSF for CHD and are the latest guidance on CHD for the NHS.
Recommendations for primary prevention include the identification and assessment of cardiovascular risk to include a determination of an individual's absolute risk of developing cardiovascular disease (CVD).
Recommendations for lipid modification are made for patients identified at high risk and for those with established CVD (acute coronary syndrome, stroke and peripheral artery disease).
Interventions to modify lipids were only considered when there was evidence that they could reduce the risk of CVD events. Both pharmacological and non-pharmacological interventions were considered.
Q: The draft guidance identified QRISK as a more accurate method of estimating cardiovascular risk. What was behind the decision not to use this but to retain use of the older, Framingham risk assessment?
The guideline development group (GDG) recommended that healthcare professionals be aware that risk tools give only approximate results on risk, that they are blunt instruments to be used as the starting point for a discussion between clinicians and patients.
The strengths and weaknesses of Framingham are known and it is already widely used. Although there is a strong demand for a risk equation developed and validated in a UK population, the GDG decided that a number of issues needed clarification.
The GDG went to some length to assess QRISK. When the revised QRISK paper was published, because of the particularly advanced statistical techniques used to account for missing data, the GDG members requested specialist statistical advice from leading experts.
Then, having received positive recommendations, the GDG provisionally recommended QRISK subject to a stakeholder consultation.
Many broader issues were raised by the general medical community. The GDG reviewed issues such as the ascertainment of outcomes, importance of independent validation, validation of QRISK other than in general practice records and comparisons with other risk tools.
Other issues considered included the over-estimation and under-estimation of risk with specific tools. The GDG considered that, as statins were known to have benefits below the thresholds currently used, under-estimation might have greater morbidity consequences than over-estimation.
Q: How does this fit in with the government's cardiovascular screening programme, announced earlier this year?
This guideline describes cardiovascular risk assessment and the modification of blood lipids; ultimately it is a guideline not a programme.
The vascular risk assessment programme is looking at simultaneously targeting a much wider range of conditions, including diabetes, which obviously aren't dealt with by this guideline. The full details of the programme are currently undergoing consultation.
Q: The systematic approach, promises to identify an additional 1.5 million patients who should be taking statins. How should GPs support these previously 'well' patients?
Firstly, it is important to use jargon-free language to communicate information on risk. Adequate time should be set aside during the consultation to provide information on risk assessment and to allow any questions to be answered.
Patients should be offered information about their absolute risk of CVD and about the absolute benefits and harms of an intervention over a 10-year period in a form that presents individualised risk and benefit scenarios and uses appropriate diagrams and text.
Clinicians should also find out what the patient has been told about their CVD risk and explore their beliefs about what determines future health as this may affect their attitude to changing risk.
Many patients take aspirin for primary prevention of CHD and I think this provides a good analogy for the aftercare of patients receiving statins for the primary prevention of CVD. The 1.5 million at-risk patients eligible for statins equates to about 45 patients per GP, notwithstanding the likelihood that practice nurses will be taking up the substantial part of this workload.
Q: The new guidelines do not give a cholesterol target for primary prevention. Why is this?
The clinical effectiveness of higher-intensity statins and combining statins with other drugs has not been shown for primary prevention.
Because of this lack of evidence, the GDG agreed that this guideline would not recommend the use of a cholesterol target.
Also, the absolute benefits of statins in primary prevention are considerably less than in secondary prevention - benefit is proportional to risk and the lower the risk of the adverse prognosis, the lower is the potential to benefit.
The target here is a patient who agrees to treatment, putting lifestyle advice into practice and taking a statin regularly.
Q: What is implementation of these new guidelines going to cost the average practice? Is there extra funding available for GPs to implement a primary prevention strategy?
GPs routinely ration the delivery of primary healthcare to manage an increasing workload, but we have been performing risk assessment ever since the NSF for CHD in March 2000.
In our locality, an audit showed that 60 per cent of statin prescribing was for primary prevention, so it's already been going on for quite a while.
This guideline informs ongoing care that was set in motion by the NSF for CHD, in addition to updating aspects relevant to identification of high risk primary prevention patients, risk assessment and lipid modification.
Some PCTs have set in place local enhanced services for the primary prevention of CVD and there is always the possibility that the issues may also be raised within future quality framework.
Q: The secondary prevention targets are tighter than the quality framework. What should GPs aim for given it is difficult and expensive to achieve the NICE target?
Guidelines need to be realistic. Up-titration of initial statin treatment to achieve the recommended cholesterol levels will only be successful in 37 per cent of patients.
Therefore, cholesterol levels of 5mmol/l for total cholesterol and 3mmol/l for LDL-cholesterol have been adopted for audit purposes, as although all patients should be considered for optimisation of their recommended treatment, the hard reality is that the majority of these patients will not achieve total cholesterol of 4mmol/l or 2mmol/l for LDL-cholesterol.
The audit standard is the minimum level of acceptable performance.
In an identical way, we use audit targets for BP in the quality framework, which are the minimum level of performance. In clinical practice I would consider reducing BP below the audit figure where appropriate.
Q: Why should we measure LFTs with simvastatin, when the Heart Protection Study (HPS) didn't endorse it?
Patients that we see in practice are undifferentiated and the patients that clinical triallists enrol are not representative.
Patients in trials tend to be younger, male and have fewer co-morbid conditions.
Patients in the HPS trial and many other statin studies were given a small dose of the statin before the real trial got under way.
These 'run-in periods' result in a statin-tolerant population that you can't rely on for judging safety.
The 'lower is better' philosophy is based on studies like these, but disregards the safety issues that these studies obscure.
The licence for simvastatin still includes the need for measuring LFTs, which is sensible given that GPs' patients don't undergo a run-in period in real life.
This guideline recommends that LFTs are measured at three months and one year and do not need to be measured again if normal.
Q On what were the Framingham adjustment factors (increase risk by a factor 1.4 if the patient is a south Asian man; and by a factor of 1.5 to 2.0 if the patient has affected relatives) based?
The 1.4 inflation factor for south Asian men is based on the Standardised Mortality Ratio (SMR), which is the age- and sex-adjusted death rate compared with the reference population. This is where the frequently-quoted statistic that south Asians have a 40 per cent increased risk of having a heart attack comes from. It has been traditionally been used to adjust the risk calculated in the white reference population to a level that corresponds with the south Asian population. It’s imperfect, but has been the best there is.
The inflation factors of 1.5 to 2.0 for family history come from a variety of studies that explored risk of cardiovascular disease, such as the MALMO Preventative Project, Women’s Health Study and several others. The studies gave different figures based on how the exact relationships between relatives (ie siblings versus parents and children, for instance) and the age at which the event occurred.
Generally speaking, the younger the event in the family member, the greater the risk.
Q The NICE guidelines advise calculating BMI – weren’t we all supposed to be measuring waist circumference these days?
The NICE clinical guideline on obesity recommends that BMI should be used in adults, supplemented with waist circumference. BMI is height standardised and more reproducible than waist circumference. Waist circumference adds some value as a direct measure of adiposity. Where one is weak, the other is strong. Remember also that the indications for weight loss drugs are all specified in terms of BMI too.
Q How should GPs estimate left ventricular hypertrophy? Are all potential at-risk patients expected to have an ECG/echo?
Presence of LVH should be factored into the equation where this is known. This does not mean that there should be general screening of LVH for patients undergoing risk assessment.
- Dr Minhas is a GPSI in cardiology in Gillingham, Kent, and a member of the NICE guideline development group. The guideline was developed by the National Collaborating Centre for Primary Care (NCC-PC). Any views expressed in this article are those of the author and not necessarily those of NICE or the NCC-PC.