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Cardiology experts Dr Alistair Cormack and Dr Adrian Brady tackle common primary care dilemmas from GP Dr Mike Fitzpatrick

Cardiology experts Dr Alistair Cormack and Dr Adrian Brady tackle common primary care dilemmas from GP Dr Mike Fitzpatrick

1. We learned as medical students that if chest pain is not related to exertion, it's not angina. Is this still true?

Of course most cases of angina are related to exertion but a small minority experience symptoms at rest, following meals or during emotional rather than exertional stress.

As a rule, young people with no risk factors are very unlikely to have intermittent 'angina' at rest but clinical suspicion should increase in the presence of cardiovascular risk factors. In general, a negative exercise test is a reliable and robust indicator of patent coronary arteries.

2. Given continuing difficulties of access, should every patient with stable angina have an echocardiogram? How often should cardiac investigations be repeated once the diagnosis is made? Or are symptoms a good enough guide to disease progression?

Echocardiography is not a regular cardiac investigation for those with uncomplicated angina. Situations where echocardiography is required would include patients with concomitant murmurs, symptoms of heart failure, those with an abnormal ECG and those with a fall in blood pressure during exercise testing.

The only interventions with proven prognostic benefit in uncomplicated chronic stable angina are anti-platelets, statins and blood pressure control (in particular blockade of the renin-angiotensin system) and as such, unless there is a change in symptoms, there is no need to repeat investigations if secondary prevention is adequately addressed.

3. Patients often ask about B vitamins, homocysteine and minerals. What do you advise them?

Homocysteine associates with CHD as a risk factor. Yet there is no conclusive evidence to support or refute lowering homocysteine with folic acid. There is reasonably good evidence that neither vitamin supplementation nor mineral ingestion has any effect on CHD. In general we support complementary therapies if the patient is insistent, since such patients usually comply with conventional therapy also. Long-term trials are awaited, but we are not holding our breath.

4. Which ß-blocker is best to prescribe?

All ß-blockers are anti-anginals and atenolol, metoprolol and bisoprolol are the most commonly prescribed. In renal disease, metoprolol is preferred given its hepatic metabolism. Carvedilol, bisoprolol and nebi-volol have evidence of benefit if there is concomitant heart failure and should be the drugs of choice. Other ß-blockers should not be used in heart failure.

5. Which calcium channel blocker should I prescribe? Verapamil is one of the great survivors and diltiazem still has its advocates. Given their profile of risks and side-effects, do they still have a role?

In the ß-blocker intolerant patient, the rate-limiting calcium channel blockers verapamil and diltiazem are standard substitutes, usually in their slow-release forms. These drugs are contraindicated in patients with bradycardia and in those with heart block. The non-rate limiting calcium channel blockers – amlodipine and extended-release nifedipine preparations – can be added as second-line agents to ß-blockers.

With their negatively inotropic and fluid retention side-effects these drugs should not be used in those with heart failure. For hypertension, amlodipine has abundant evidence, once-daily nifedipine and felodipine have good evidence, and the rest have no supportive evidence whatsoever. So amlodipine, Adalat LA or felodipine should be chosen.

6. In what circumstances is isosorbide mononitrate to be preferred to dinitrate?

Neither drug carries a prognostic benefit in angina so one looks at these drugs purely for symptom control. The mononitrate preparations have better bioavailability and can be used as once- or twice-daily preparations.

7. What is nicorandil good for?

Nicorandil is a useful vasodilator with both nitrate donor properties and potassium channel activator properties. It is usually added as a third- or fourth-line agent after a ß-blocker (if tolerated), calcium channel blocker and possibly oral nitrate.

Often patients with nitrate headache experience headache with nicorandil too. Mucosal ulceration is appearing now as a particular side-effect, and the drug should be discontinued if this occurs.

8. For men with angina and erectile dysfunction, is there any hope?

These are two common co-morbidities. Erectile dysfunction in those with angina may be due to the existing 'vasculopathy' and have the same risk factors – dyslipidaemia, hypertension, smoking, diabetes. In addition, many of the drugs commonly used in angina, classically ß-blockers, have erectile dysfunction as a side-effect.

There may be an anxiety component in addition, in either partner. As first-line, men (couples) should be reassured that in the absence of a high-risk exercise tolerance test intercourse is safe if the man is pain free. Second-line is to address pharmacotherapy.

Risk factors should be addressed as usual. Anti-ischaemics can then be altered, for instance swapping ß-blockers for calcium channel blockers/nicorandil/nitrate or even the new rate-limiting anti-anginal ivabradine. No anti-ischaemic agent carries prognostic benefit in uncomplicated angina (those patients with no previous MI/heart failure) so there is scope to find the right drug by trial and error.

Beyond this sildenafil may be tried if the patient does not take any nitrate preparation or oral nicorandil. If a patient can be rendered angina-free by, for example, calcium channel blockade or through mechanical intervention then sildenafil may be used safely. Our usual practice is to recommend sildenafil or its brother compounds for individuals who do not require GTN frequently for angina attacks.

9. In view of the effect of statins on plaques, what lipid levels should we aim for and what dose of statin?

QOF targets still use total cholesterol =5mmol/l and LDL cholesterol =3mmol/l as a target but evidence indicates that 4mmol/l and 2mmol/l respectively should be our target in those with proven disease. The dose of statin is a balance between cholesterol achieved and tolerability, usually starting with generic simvastatin 40mg and increasing if necessary, or switching to the more powerful statins, atorvastatin or rosuvastatin.

It should be remembered that doubling the dose of any statin increases the cholesterol lowering by only 6 per cent. Ezetimibe 10mg may be added in at any point, either if LDL targets are not achieved or if higher dose statins are not tolerated.

10. Are we now able to do more percutaneous coronary intervention (PCI) on patients that might have previously needed CABG? Have stents altered the picture much?

CABG rates have been falling by about 10 per cent per year and most of this is due to a rise in PCI, in particular multi-vessel PCI. Stents have radically altered the picture with plain old balloon angioplasty being reserved for certain lesions with particular anatomy.

Bare metal stents are associated with an in-stent restenosis rate in the order of 10 per cent but this restenosis rate has been reduced to low single figures with the introduction of drug-eluting stents.

Alistair Cormack is a research fellow in cardiology at Glasgow Royal Infirmary

Competing interests None declared

Adrian Brady is a consultant cardiologist at Glasgow Royal Infirmary and is one of the main authors of the SIGN guideline on CHD

Competing interests Adrian Brady has received research grant support and consultancy fees from a number of companies that produce, or are developing, drugs for cardiovascular disease

What I will do now

Dr Fitzpatrick comments on the answers to his questions

• It is reassuring to know an echocardiogram is not mandatory – and that it is unnecessary to repeat investigations if symptoms remain stable

• I will continue to discourage patients from taking vitamins and other complementary therapies which may impose a substantial burden of cost – because of the lack of evidence for them in this setting

• For ß-blockers, I will stick to atenolol for uncomplicated angina, falling back on bisoprolol in patients with heart failure and metoprolol in renal failure

• It is good to know that there is still a place for verapamil and diltiazem; though the recent ASCOT study and NICE guidelines have boosted amlodipine, it is not without side-effects

Mike Fitzpatrick is a GP in north London

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