CHEST pain is an extremely common symptom in secondary care but relatively uncommon in primary care, amounting to about 1-2 per cent of consultations.
The vast majority of patients with chest pain will not have symptoms caused by myocardial ischaemia. In one study of 35,075 GP consultations in Sweden, only 1.5 per cent were for chest pain and only 8 per cent of these were due to underlying ischaemic heart disease1. In a Swiss study of 24,620 GP consultations, 2.7 per cent were for chest pain, with coronary artery disease accounting for 12 per cent of these2.
However, when chest pain is due to myocardial ischaemia there are potentially fatal consequences if action is not taken to reduce the risk for myocardial infarction.
Studies of large populations of patients with chest pain have identified those characteristics and symptoms which predict the presence of underlying coronary artery disease. Positive and negative predictors are shown in the table below.
Although considering the characteristics of the pain can help, so can the context in which this pain has occurred.
Consider these two case histories:
Case history 1
A 66-year-old man and ex-miner experiences chest tightness on walking up hill to the paper shop every morning. He has smoked 20 cigarettes a day since age 14 years and is overweight (BMI 29), hypertensive and suffers from diabetes. The likelihood that this man has significant underlying coronary artery disease is very high. He has four important risk factors and a typical history.
Case history 2
A 22-year-old female and non-smoker has an argument with her boyfriend, panics, feels breathless and develops tingling in the lips and fingers and then severe central chest tightness with pain in the left arm. The history of the pain is characteristic of angina, but she has no risk factors so is very unlikely to have underlying coronary artery disease. In fact the history strongly suggests panic disorder and hyperventilation which can cause myocardial ischaemia because of coronary artery spasm.
Both patients have chest pain of cardiac origin, but the underlying cause of their symptoms and the mechanism behind their generation is different. The clinical implication of their symptoms, prognosis and management is very different.
Also apart from the characteristics of the pain and the circumstances around its occurrence, other factors have also been shown to have predictive value.
Positive predictive factors
• Age (> 55 years in men and > 65 years in women)
• Gender (male)
• Presence of risk factors (more present greater risk)
• Previous history of coronary disease
Coronary artery disease occurs progressively with age. However, in some individuals it starts earlier. There are a number of factors which have been shown to encourage the development of premature coronary disease.
These risk factors include:
• Genetic factors – the tendency can run in families.
• Sex – men develop coronary artery disease earlier.
• Smoking (especially cigarettes) – there is a dose response also with the more cigarettes smoked the higher the risk.
• Diabetes mellitus.
• Psychosocial factors –weak social links, low socio-economic status, north versus southeast
Types of angina
When angina only occurs with exercise and it is reproduced by the same degree of exercise, this is called chronic stable angina. The pattern of angina may change with time over years, but can occur more abruptly over days. When the pattern changes so that it occurs more easily than previously, but still only on exercise it is called crescendo angina.
When angina occurs at rest this means that the myocardium is ischaemic even in the absence of an increase in workload and implies critical myocardial perfusion. These latter two patterns of angina represent unstable angina. This is usually due to the development of a thrombus on the surface of an atheromatous plaque within the artery. Thrombus development is rapid and so symptom deterioration is sudden.
In patients with rest angina the pain lasts for less than 30 minutes and then is relieved. If the pain from myocardial ischaemia persists for longer than 30-45 minutes then cardiac muscle damage occurs – this constitutes a myocardial infarction.
These facts must also be taken into account when considering the presentation in primary care. Crescendo and unstable angina are pre-infarction syndromes and require urgent action. The early mortality of chest pain in this situation is about 10 per cent. Admission is mandated for aggressive medical and, nowadays, interventional therapy (angiography and angioplasty).
If a patient presents late, say days after having rest pain, then it is possible to use simple diagnostic tests to determine whether the pain was of cardiac origin. If the pain was ischaemic in origin and lasted longer than 30 minutes then myocardial damage would have been caused which would result in an increase in blood troponin level. This is a very sensitive test and is nearly always raised in patients with unstable angina. It persists for about 2 weeks after an event. Similarly, if the pain lasted for hours then the only cardiac syndrome that could account for the pain is a myocardial infarction and this would usually cause a change on the resting 12-lead electrocardiograph which evolves over time after an infarction.
It is essential to make a diagnosis of coronary artery disease because the treatments available significantly reduce the risk of death or infarction. Avoiding or preventing infarction is also very important as myocardial damage reduces life expectancy; a damaged heart will not survive as long as a normal heart.
In patients with a typical history of angina and risk factors for the premature development of ischaemic heart disease, immediate treatment with risk-modifying drugs is indicated to minimise the risk of infarction or death, pending more definitive investigations or treatments. Thus, any patients in whom there is a suggestion that the presenting symptom is of cardiac origin should be given aspirin (75mg daily), a statin and a beta blocker.
The risk of developing an infarction is reduced by these treatments but the size of the risk reduction is important. The single most valuable risk reduction strategy is to stop smoking. This reduces the chance of developing an infarction after presentation with unstable angina by about 30 per cent. Aspirin is also very important and reduces risk by about 40 per cent. By comparison, statins do not reduce risk immediately and there is a lag time of up to 12-18 months before risk is reduced by these drugs. Beta blockers reduce risk by about 10 per cent.
Early angiography and angioplasty reduce the chance of developing myocardial infarction (by about 20 per cent) but death is not significantly reduced by this strategy.
Reducing medico-legal risk
Below are some important points to remember in reducing medico-legal risk in patients presenting with chest pain in primary care:
• Chest pain is uncommon in primary care.
• The history is the most valuable tool in the diagnosis of chest pain of cardiac origin.
• Simple tests like ECG and blood troponin are useful in the diagnosis of infarction.
• Unstable angina is a medical emergency and demands admission to hospital.
• Early confirmation of the diagnosis of angina is important as there is a 10 per cent mortality in the first year after diagnosis which then falls to an annual mortality of 3 per cent thereafter. Refer to a Rapid Access Chest Pain clinic.
• In patients suspected of having angina, advise stopping smoking and give aspirin, a statin and a beta blocker if not contra-indicated.
• Consistent relationship with exercise
• Squeezing, crushing, burning, tightness or heaviness
• Central, substernal or left-sided
• Relieved with rest
• Relieved with GTN
• Radiation to neck and arms
• Pain lasting longer than 30 minutes
• Unprovoked pain at rest > with exercise
• Right-sided location in chest
• Single spot
• Not radiating
• Inducible by local pressure
• Position, respiration or cough dependent
Professor Kevin Channer is a consultant cardiologist at the Royal Hallamshire Hospital in Sheffield and Honorary Professor of Cardiovascular Medicine at Sheffield Hallam University
1 Nilsson S et al Br J GP 2003; 53: 378-82
2 Verdon F et al Swiss Med Weekly 2008; 138: 340-47
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