Section 1 Definition and pathophysiology
Angina pectoris results from the failure of myocardial oxygen supply to keep up with demand.
When symptoms (usually chest discomfort) occur in proportion to exertion in a predictable and reproducible pattern, it is known as stable angina (pectoris).
Coronary heart disease
In the majority of cases, stable angina is a result of atherosclerotic coronary artery disease, which results in narrowing of the lumen and reduced coronary flow reserve (the increase in coronary blood flow above the resting level in response to exercise).
The normal two- to three-fold increase in coronary blood flow during exercise is significantly attenuated and the blood supply lags behind demand (see box).
According to British Heart Foundation statistics, 5 per cent of men and 3 per cent of women over the age of 35 years have (or have had) angina.
Approximately 100,000 patients are diagnosed with angina every year in the UK, and this incidence increases with age.
|Factors affecting myocardial oxygen demand|
|Heart rate||↑ myocardial work, |
↓ diastole length → ↓perfusion
|Contractility||↑ myocardial work|
|Afterload||↑ myocardial work (clinical indicator - systolic BP)|
|Wall Stress||Preload||↑ myocardial work|
↑ oxygen demand, ↓coronary perfusion pressure
CT scan of coronary stenosis: incidence increases with age
Section 2 Diagnosis
Rapid access chest pain clinic
The NSF for CHD recommends that patients with recent onset of symptoms (less than four weeks with no past history of coronary disease) should be assessed in a rapid access chest pain clinic (RACPC) within two weeks of referral from primary care.
This has resulted in a reduction in waiting times, early identification and risk stratification of coronary disease.
According to a recent survey, 27 per cent of referrals to RACPCs are diagnosed with incident angina, of whom 17 per cent have a primary endpoint event (death from coronary disease, non-fatal MI or admission with unstable angina) after three years compared with 3 per cent of those diagnosed with non-cardiac chest pain.1
Non-cardiac chest pain
Patients diagnosed at RACPC with non-cardiac chest pain who subsequently have a primary endpoint event account for a third of events and are more likely to be younger, south Asian, have atypical symptoms and/or have a normal ECG. Another survey revealed that 14 per cent of patients not referred to RACPCs fulfilled criteria for referral.2
|Canadian Cardiovascular Society (CCS) grading of angina3,4|
|Grade||Functional status||Onset of symptoms|
|1||No limitation of ordinary physical activity||Strenuous or prolonged exertion|
|2||Slight limitation of activity||Climbing stairs rapidly, brisk walking|
|3||Moderate limitation of activity||Climbing a flight of stairs, daily living activities|
|4||Inability to function without symptoms||Symptoms at rest|
Section 3 Treatment
The guiding principles of medical management are: reduction of future cardiovascular mortality and morbidity - secondary prevention - and alleviation of symptoms to enable a return to normal functional status.
Aspirin at a dosage of 75-325mg daily is beneficial in preventing future events.
Clopidogrel (75mg once daily) may be substituted for aspirin in patients with aspirin allergy or intolerance. Studies have not shown any beneficial role for dipyridamole in stable angina.5
Statins (simvastatin 40mg once daily), in addition to reducing LDL cholesterol, also have beneficial effects in reducing inflammation.
ACE inhibitors are recommended in the presence of hypertension or diabetes. However, they are not indicated in all patients with stable angina.
Alleviation of symptoms
Beta-blockers (atenolol 50-100mg or bisoprolol 5-10mg once daily) are first-line antianginal agents. They inhibit sympathetic stimulation, reducing heart rate and afterload, which helps to avoid or delay the onset of angina on exertion.
The predominantly beta-1 selective agents, such as atenolol, are generally well tolerated. Dosage may be titrated to achieve a resting heart rate of 50-60 beats/minute.
Calcium-channel blockers act either by decreasing peripheral vascular tone (dihydropyridines) or by reducing heart rate and contractility (verapamil, diltiazem).
They may be used in patients who are intolerant to beta-blockers, or in conjunction with other antianginals. Verapamil has very potent negative inotropic and chronotropic effects; hence concomitant use with a beta-blocker is contraindicated.
It is advisable to choose a second-generation dihydropyridine (amlodipine, felodipine) over short-acting preparations of nifedipine. The latter is associated with increased mortality in patients with previous MI and increased incidence of MI in hypertensive patients, possibly related to reflex tachycardia, which is rare in patients treated with agents such as amlodipine.
Nitrates are predominantly peripheral venodilators and coronary arteriolar dilators. In stable angina, their therapeutic effect is likely to be due to a reduction in preload from venodilation (and the resultant decrease in left ventricular wall stress). Sublingual preparations improve exercise tolerance if used prior to a period of physical activity.
Oral nitrates may be administered in short-acting twice daily doses or as once daily sustained-release preparations.
Phosphodiesterase-5 inhibitors (e.g. sildenafil) are best avoided in patients on nitrates because of the risk of profound hypotension.
Nicorandil (10-30mg twice daily) is a potent antianginal that acts as a vasodilator achieving both coronary and peripheral vasodilation. It also aids ischaemic preconditioning of the myocardium, which is likely to explain the reduction in coronary events seen in the IONA study.6
Ivabradine is a novel agent that achieves heart rate reduction (by modifying the sinus node If current) without negative inotropy or effects on coronary vasculature. It is suitable for patients who are intolerant to beta-blockers.
Visual side-effects have been reported in the first three months of therapy.
Section 4 Referral and prognosis
A significant proportion of patients with stable angina are managed in primary care after initial RACPC assessment.
Recent studies have shown that optimum monitored medical therapy alongside lifestyle modifications prevents future events in the majority of patients, including those with multi-vessel disease.7
An angiogram of stenosis in the left coronary artery (narrowing arrowed)
Further specialist review is usually indicated for those refractory to optimum/maximum tolerated medical therapy. In addition, those with high risk features at the time of diagnosis are usually offered further invasive assessment with or without revascularisation. However, a recent multicentre study identified underuse of diagnostic angiography, associated with a higher risk of coronary events in older patients, women, south Asians and those in the lowest socioeconomic class.8
'Real world' data from RACPCs show an annual mortality rate of 3 per cent in treated patients with stable angina.1 Older age, diabetes mellitus, past history of MI, left ventricular dysfunction and reduced exercise capacity (<6 minutes of the standard Bruce protocol for exercise testing) are associated with a poor prognosis.
Non-cardiac chest pain
The changes to the care pathway, especially RACPC assessment, have led to a significant number of patients being diagnosed with 'non-cardiac chest pain'.
A study has identified significantly higher levels of anxiety in such patients after assessment, probably due to a lack of explanation about their symptoms. 9
This highlights the importance of reassurance to identify other causes, keeping in mind that a minority may still have undiagnosed coronary disease.
1. Sekhri N, Feder G, Junghans C, Hemingway H, Timmis A. How effective are rapid access chest pain clinics? Prognosis of incident angina and non-cardiac chest pain in 8762 consecutive patients. Heart 2007; 93: 458-63.
2. Sekhri N, Feder G, Junghans C, Hemingway H, Timmis A. Rapid-access chest pain clinics and the traditional cardiology out-patient clinic. QJM 2006; 99: 135-41.
3. Campeau L. Letter: Grading of angina pectoris. Circulation 1976; 54: 522-3.
4. Campeau L. The Canadian Cardiovascular Society grading of angina pectoris revisited 30 years later. Can J Cardiol 2002; 18: 371-9.
5. Picano E. Dipyridamole in chronic stable angina pectoris: a randomized, double blind, placebo-controlled, parallel group study. Eur Heart J 2001; 22: 1,785-93.
6. IONA study group. Effect of nicorandil on coronary events in patients with stable angina: the Impact Of Nicorandil in Angina (IONA) randomised trial. Lancet 2002; 359: 1,269-75.
7. King S, 3rd. Five-year follow-up of the Medicine, Angioplasty, or Surgery Study (MASS-II): prologue to COURAGE. Circulation 2007; 115: 1,064-6.
8. Sekhri N, Timmis A, Chen R et al. Inequity of access to investigation and effect on clinical outcomes: prognostic study of coronary angiography for suspected stable angina pectoris. BMJ 2008; 336: 1,058-61.
9. Robertson N, Javed N, Samani N, Khunti K. Psychological morbidity and illness appraisals of patients with cardiac and non-cardiac chest pain attending a rapid access chest pain clinic: a longitudinal cohort study. Heart 2008; 94: e12.
SIGN guideline: Management of stable angina. A national clinical guideline (www.sign.ac.uk/pdf.sign96.pdf)
British Heart Foundation: www.bhf.org.uk