Need to know - Post-MI care
Community cardiologist Dr Jane Skinner answers questions on post-MI care from GP Dr Kathryn Griffiths
Community cardiologist Dr Jane Skinner answers questions on post-MI care from GP Dr Kathryn Griffiths
1 There is some confusion about the new definition of MI. Can you clarify this?
They recommend that the term MI be used when there is evidence of myocardial necrosis in a clinical setting consistent with myocardial ischaemia. For acute MI this is when there is a rise and/or fall in cardiac biomarkers – preferably troponin – with at least one value above the 99th percentile of the upper reference limit together with evidence of myocardial ischaemia with at least one of the following:
• ECG changes indicative of new ischaemia – new ST-T changes or new left branch bundle block (LBBB)
• Development of pathological Q-wave changes in the ECG
• Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality.
The definition also includes criteria for the diagnosis in the context of sudden cardiac death, after primary percutaneous coronary intervention (PCI) and CABG, and from pathological findings.
In practical terms, in primary care, the patients to target for secondary prevention are those who have an acute spontaneous MI because of a primary coronary event such as plaque erosion and/or rupture, fissuring or dissection, which is called a type 1 MI in the expert consensus document, as well as those with a prior MI.
There are other reasons why myocardial necrosis may occur and MI types 2 to 5 describe other presentations.
Patients with type 2 MI – when there is increased myocardial oxygen supply or reduced demand from causes other than spontaneous MI, for example an arrhythmia, anaemia or hypotension – are most likely to cause confusion. Patients with these presentations who fulfil the criteria for MI require appropriate specialist assessment to guide management.
2 Are there any important differences in the management of patients who have had primary PCI compared with patients following more traditional management?
Patients who present with a ST elevation MI (STEMI) are increasingly being managed with immediate primary PCI rather than thrombolysis to achieve reperfusion and there is evidence that this will lead to better outcomes.
But irrespective of how reperfusion is achieved, patients still need optimal secondary prevention treatment, including appropriate drug therapy, cardiac rehabilitation and lifestyle changes.
Further cardiological assessment is also similar, with an assessment of left ventricular function and – in those with significantly impaired left ventricular function – assessment for arrhythmic risk.
But unlike after thrombolysis, the coronary anatomy will be known, having been visualised at the time of the primary PCI. Patients who have had primary PCI with an uncomplicated recovery are usually discharged earlier than those who have had thrombolysis, and the post-infarct recovery period is shorter. Cardiac rehabilitation programmes need to recognise this and be tailored appropriately.
3 In May last year, NICE produced guidelines on secondary prevention after MI. What are the important messages for primary care?
These guidelines have set out measures to optimise secondary prevention after MI, and GPs may find it useful to structure management plans for individual patients along similar lines (see box below).
Lifestyle changes include dietary measures such as a Mediterranean-style diet, increasing oily fish consumption, physical activity, stopping smoking and reducing obesity.
If patients are within three months of an acute MI and are not consuming sufficient oily fish to amount to 7g omega-3 fatty acids per week, omega-3 acid ethyl ester supplements of at least 1g daily should be considered.
The guidelines also state what is not effective for secondary prevention, like folic acid and anti-oxidant vitamin supplements.
Cardiac rehabilitation should be available and accessible to all patients after an MI and although this is generally started before discharge, GPs should at least be aware of the arrangements and encourage their patients to attend.
Drug therapy is started early in acute MI and should be initiated before discharge – in the absence of contraindications. Aspirin, ß-blockers, ACE inhibitors and statins are recommended long term in all patients.
Patients will also be treated with clopidogrel, although will not usually continue the combination of aspirin and clopidogrel beyond 12 months after the MI, unless there are other indications to do so.
Eplerenone is a selective aldosterone antagonist initiated within three to 14 days of an acute MI if patients have or have had symptoms and/or signs of heart failure, and a left ventricular ejection fraction less than or equal to 40%. Drugs initiated in hospital may have to be titrated upwards in primary care and biochemical monitoring of patients treated with ACE inhibitors and eplerenone is mandatory.
Cardiological assessment includes assessment of left ventricular function, and assessment and appropriate management of ischaemic risk, as well as in patients with left ventricular dysfunction, arrhythmic risk. The guidelines also make recommendations for patients who have had an MI in the past.
4 Both NICE guidelines and the QOF recommend the use of ACE inhibitors in all patients after a MI. But are there any circumstances where you feel this may be contraindicated or inappropriate?
There is good evidence that ACE inhibitors reduce future cardiovascular events. But obviously, patients with contraindications should not be treated. One that comes to immediately to mind for ACE inhibitors is known renal artery stenosis.
Of course some patients may not tolerate ACE inhibitors. But it's important not to overdiagnose problems like cough and there are many other causes of a cough that should be considered before ascribing it to the ACE inhibitor. If the cough is truly a side-effect, though, an ARB could be considered as an alternative.
There has also been some debate about whether the absolute benefit warrants treatment in some patients with preserved left ventricular function.
In one placebo-controlled trial of patients with stable coronary disease and preserved left ventricular function who had received other intensive secondary prevention measures, there was no significant benefit from ACE inhibitor treatment, which the researchers suggested could be due to the low baseline risk of the population2.
But post-hoc analysis of another trial of patients with stable coronary disease and preserved left ventricular function showed there was still a benefit, albeit small, in patients at low absolute risk3.
In practical terms, all patients after MI should be considered for long-term ACE inhibitor treatment. In a small proportion, the absolute benefit may be small and patients with preserved left ventricular function, particularly those who are developing side-effects, may wish the opportunity to discuss what impact treatment is likely to have.
This requires a full assessment of risk factors, left ventricular function, ischaemic burden and any prior coronary revascularisation, to determine the likely impact of treatment, and then discussion with the patient in an understandable way.
5 Are some patients aspirin-resistant and should they be given a larger dose?
A number of clinical studies have investigated the importance of aspirin resistance, but there is a lot that still needs to be understood and further prospective studies are needed. But there are factors that may be causes of aspirin resistance that can be addressed in primary care.
Aspirin resistance may be due to inadequate dosage and reduced bioavailability, and in some cases this could be because of poor patient concordance with treatment, co-administration of NSAIDs or even reduced absorption.
Poor concordance is not unique to aspirin, but we should make sure patients are not only prescribed treatment, but are also taking it. Co-administration of NSAIDs should be reviewed.
Although there may be reduced absorption in some patients, there is currently insufficient evidence to justify recommending long-term treatment with higher doses routinely.
However, there might be an argument for a temporary dose increase in conditions where there is increased platelet turnover, although this is at present unproven. For example, it is standard practice for patients with acute coronary syndrome to be given a loading dose of aspirin of 300mg on presentation, even if they are already treated with prophylactic therapy.
It is also possible that maximising treatment of other possibly confounding conditions, such as diabetes, hyperlipidaemia and smoking, will also increase aspirin efficacy. This should be part of any secondary prevention management plan anyway.
6 Which patients need the combination of aspirin and clopidogrel after an MI?
Nowadays, virtually all patients will be treated with the combination of aspirin and clopidogrel after an acute MI. After a non-STEMI there is evidence to continue this combination for 12 months.
In patients with STEMI the evidence is restricted to short-term trials of no longer than four weeks, and from which patients treated with primary PCI for reperfusion were excluded. It is in this group of patients that there is greatest debate.
It's not that clinical trials have shown a lack of efficacy of longer-term combination therapy, but rather that trials have only been of limited duration. Many patients will be treated for longer than four weeks and many cardiologists would argue that since both types of spontaneous MI are a result of a primary coronary event that the combination of aspirin and clopidogrel should be used for 12 months in both.
But the combination should not usually continue beyond 12 months after the MI, unless there are other indications to do so.
It is important that the planned duration of combination therapy is known in all patients and recorded, and that GPs review the indications for the combination to confirm cessation of clopidogrel is appropriate before doing so.
7 A recent publication suggested there is an increase in death and MI in the 90 days after clopidogrel therapy has stopped. Do you believe this ‘rebound' effect is clinically important and should this have an effect on how long the drug is used for?
This comes from a retrospective study published in JAMA earlier this year and supports the hypothesis of a rebound phenomenon when patients after acute coronary syndrome treated with aspirin and clopidogrel stop the clopidogrel. But it is important to remember it was a retrospective study. Also, it didn't report aspirin use after clopidogrel was stopped, although 91% were taking aspirin at hospital discharge.
Further prospective studies are needed to confirm the findings, and to determine the efficacy of longer-term treatment, taking into account the risks of long-term treatment as well as potential benefits.
For now, the current recommendations are valid and most patients will continue combination therapy for no longer than 12 months. But there are some caveats and the indications for combination therapy should be reviewed in all patients before stopping clopidogrel to make sure no new indications have developed.
It's also vital that patients understand the importance of continuing other secondary prevention therapies, including aspirin, after stopping clopidogrel.
There have been particular concerns about the risk of stent thrombosis in patients with drug-eluting stents. This was addressed in a recent NICE technology appraisal4 which has endorsed the views of the American and British professional bodies that patients with these stents should be treated with clopidogrel for at least 12 months.
After this, continuation of clopidogrel should be reviewed, taking into account the risk for further events on an individual patient basis.
8 Some centres start high-dose statins after an acute event. Should this be for long-term use and if so what is the evidence for this?
Two randomised trials have compared high-intensity statins with lower intensity statins in patients with acute coronary syndrome, and two trials in patients with more stable coronary disease.
Meta-analysis of these four trials has shown a reduction in the composite outcome of coronary death or MI, and in the composite outcome of coronary death or any cardiovascular event – MI, stroke, hospitalisation for unstable angina or any revascularisation – in those given high-intensity statins.
There was a trend for significance in reduction of cardiovascular death, although no effect on total mortality.
NICE has reviewed the studies and examined the cost-effectiveness of high-dose statins in patients after acute coronary syndrome. Its lipid modification guidelines5 concluded that treatment with a high-dose statin is both clinically- and cost-effective and recommended for people with acute coronary syndrome. High-intensity statins should be continued long-term if patients can tolerate them.
9 How do we promote significant lifestyle changes when it is so much easier just to prescribe a tablet?
This is a difficult one – but it's worth remembering that secondary prevention is not a case of either making lifestyle interventions or taking medication, but doing both.
Individualised advice, taking into account past habits, may improve compliance with healthy eating advice and increasing physical activity. Referring smokers to cessation services improves the chances that patients will quit.
It may be easier to prescribe a tablet, but we also need to remember that these will only be effective if patients take them.
A holistic approach to secondary prevention with clear and consistent information and advice for patients is most likely to be successful, both for lifestyle changes and encouraging concordance with medication.
10 Is nicotine replacement therapy (NRT) safe to use after an MI, and how quickly will a patient benefit from smoking cessation?
Patients can use NRT after an MI, providing it does not exacerbate any cardiac symptoms. It will do far more good than harm, providing of course it actually helps the patient quit smoking.
But to maximise the benefits, patients should be strongly advised to use behavioural support in their attempt to quit, and patients who quit smoking in hospital and are discharged with NRT should have very clear arrangements for ongoing support and follow-up.
The risk of further major coronary events is reduced by about half within a year of an MI and continues to decline thereafter if smokers quit and remain abstinent.
Dr Jane Skinner is consultant community cardiologist at the Royal Victoria Infirmary in Newcastle-upon-Tyne and was the clinical adviser for the NICE guideline for secondary prevention after MI.
Competing interests: None declaredTake home points What I will do now
Dr Griffiths responds to the answers to her questions
• It's useful to read about the new MI classification and that a type 1 MI is associated with erosion, rupture or dissection of a plaque in the coronary artery.
• Primary PCI is an increasingly common first-line treatment and I'll make sure patients who have had it get the same secondary prevention and rehabilitation programme as those who are given thrombolysis.
• I'll consider treatment with omega-3 fatty acids in patients who are not consuming enough oily fish.
• I'll carry on encouraging all post-MI patients to take part in a rehabilitation programme.
• Patients will not usually be treated with the combination of aspirin and clopidogrel for more than 12 months unless they have had a further event during that time.
• Assessment of left ventricular function identifies patients at high risk and if the ejection fraction is 40% or less eplenerone may be indicated.
• It's useful to know that all acute MI patients should be considered for an ACE inhibitor or ARB, but the patients who gain the most benefit from treatment are those with evidence of left ventricular dysfunction.
• Patients with acute coronary syndrome should receive high-intensity statin therapy, found by NICE to be clinically- and cost-effective. Treatment should be continued long term if tolerated.