An acute coronary syndrome (ACS) is the clinical picture produced when a coronary artery suddenly narrows or closes; it covers myocardial infarction and unstable angina. Recognition comes before testing. An occluded coronary artery is diagnosed only if the possibility is considered, and the features that raise or lower that suspicion are gathered in the first minutes, from the history and the examination, before any result returns.
The typical description
The classic description is prolonged pressure or tightness in the centre of the chest, lasting more than 20 minutes, occurring at rest or on minimal exertion, radiating to the arm, jaw, back or epigastrium, and accompanied by sweating, nausea or breathlessness. Unlike stable angina, the predictable exertional chest pain of chronic coronary disease, it is not reliably relieved by rest.
Anginal equivalents and silent infarction
Not every patient describes chest pain. Anginal equivalents are symptoms of ischaemia that take the place of the pain, and they matter because they are easy to dismiss: dyspnoea, profound fatigue, epigastric discomfort or sudden pulmonary oedema without chest pain. Older patients, women and people with diabetes are more likely to present this way, and in the same groups associated symptoms such as breathlessness, nausea or vomiting, lightheadedness, confusion, presyncope or syncope, and vague abdominal symptoms are more frequent.
The same groups are more likely to have their pain attributed to something else, so an atypical presentation is a reason to lower the threshold for an ECG and a troponin (the blood marker of heart-muscle injury) rather than to raise it. In people with diabetes, autonomic neuropathy — nerve damage from diabetes — makes truly silent infarction possible. Unexplained dyspnoea in an older patient with diabetes is a reason to obtain an ECG and troponin, not a reason to relax.
Some patients arrive without pain at all and without an obvious trigger to look for: syncope, acute pulmonary oedema or a cardiac arrest can be the first contact with the medical system, and the ECG taken afterwards is what reveals the infarction.
The four pain patterns of a non-ST-elevation presentation
When the ECG does not show ST elevation, the pain history often takes one of four shapes:
- prolonged rest pain;
- new-onset angina of Canadian Cardiovascular Society class II or III, meaning angina that limits ordinary activity slightly (class II) or markedly (class III);
- crescendo angina in previously stable disease, where the angina becomes more frequent, more severe or easier to provoke;
- angina recurring soon after a previous infarction.
None of these patterns proves infarction on its own; they set the level of suspicion that the ECG and troponin then test.
Separating ischaemic pain from its alternatives
The history that matters captures the nature of the pain, its onset and duration, its location and radiation, what precipitates and relieves it, and the associated symptoms. Those elements do most of the discriminating work, and two findings move probability further than any other: chest-wall tenderness on palpation, and pain that worsens with inspiration, both markedly reduce the probability of an acute coronary syndrome.
The alternatives fall into three groups. Non-ischaemic cardiac causes include myopericarditis (inflammation of the heart muscle and pericardium), aortic dissection, severe aortic stenosis and anomalous coronary anatomy. Immediately life-threatening non-cardiac causes include pulmonary embolism, tension pneumothorax, oesophageal rupture and sickle-cell chest crisis. The third group — musculoskeletal, gastro-oesophageal and anxiety-related pain — is where most of the patients who are eventually discharged come from, and the difficulty is that it also produces convincing chest pain.
| Alternative | Feature that points to it |
|---|---|
| Acute pericarditis | sharp pain that worsens with inspiration and when lying flat, and eases on sitting forward |
| Aortic dissection | tearing pain radiating to the back, with a pulse or blood-pressure difference between the arms — present in only about 30% of cases, so its absence is not reassurance |
| Tension pneumothorax | breath sounds absent on one side |
| Oesophageal rupture | forceful vomiting followed by subcutaneous emphysema (air under the skin), with pneumothorax in about 20% of cases |
| Musculoskeletal or chest-wall pain | pain that is positional, or reproducibly tender on palpation |
One mimic cannot be separated at the bedside at all. Stress cardiomyopathy (Takotsubo syndrome) produces chest pain, ECG changes and troponin release with normal or non-obstructive coronary arteries, so it presents exactly like an acute coronary syndrome and is identified during the angiography performed for suspected occlusion (see MINOCA, Takotsubo and Other Non-Atherothrombotic ACS).
Two further traps are worth naming. Relief of pain by nitroglycerin does not confirm ischaemia, because oesophageal spasm and several other causes also respond to it. And a normal or non-diagnostic ECG does not exclude an acute coronary syndrome, which is why the ECG is repeated rather than treated as a final answer.