Acute Coronary Symptoms

Diagnosis

Diagnosis of an acute coronary syndrome (ACS) involves consideration of symptoms and clinical history, ECG findings, and the results of cardiac enzyme tests.

Symptoms and signs

Acute-onset chest pain is the classic symptom suggestive of ACS. The patient may complain of new pain symptoms, chest pain at rest, or worsening of pre-existing angina.¹ The pain may be described as retrosternal pressure or heaviness, and may radiate to the jaw, neck or arms.² The symptoms of STEMI and NSTEMI are the same.³

Chest pain in patients with ACS is similar to angina pectoris, but is usually more severe and long-lasting, and is not usually relieved by sublingual glyceryl trinitrate (GTN; nitroglycerin).³ Other symptoms that may be present include diaphoresis, nausea, dyspnoea, abdominal pain and syncope.² Indeed, symptoms other than chest pain may predominate in some patients; for example, elderly patients with ACS are more likely to present with dyspnoea than chest pain.³ Other patients who may have an atypical presentation include younger patients (25-40 years), women, and those with diabetes, chronic renal failure, or dementia.²

Blood pressure is frequently low,4 and pulse may be thready, irregular, bradycardic or tachycardic.3,4 Cyanosis (central or peripheral) may be present.3 A third heart sound and rales may be heard on auscultation.3 When the right ventricle is affected, distension of the jugular veins (often with Kussmaul’s sign) is observed, in conjunction with clear lung fields and hypotension.3

Electrocardiography (ECG)

A 12-lead ECG should be performed in all patients in whom ACS is suspected within 10 minutes of first medical contact, and repeated a minimum of 6 and 24 hours later.² A working diagnosis of STEMI may be made when there is persistent (>20 min) ST-segment elevation of ≥1mm in 2 or more contiguous leads.^2,3 In STEMI, pathological Q waves (indicating transmural infarction) may appear over time, but are not necessary for the diagnosis.³ Figure 1 shows how the 12-lead ECG evolves over time in a typical patient with an anterior left ventricular STEMI.³

Patients who do not have persistent ST-segment elevation on ECG, with symptoms consistent with myocardial ischaemia, may be considered to have NSTE-ACS.² These patients tend to have persistent or transient ST-segment depression, T wave abnormalities (e.g. inversion), or no ECG changes.² ST-segment depression has prognostic significance; depression of ≥2mm is associated with a 6-fold increase in mortality at 1 year.⁵

Cardiac enzymes

A number of biomarkers are useful in the diagnosis of ACS, including creatine kinase (CK) and its isoenzyme CK-MB, and myoglobin. However, cardiac troponins (I and T) are now the preferred markers of myocardial injury because they have greater diagnostic specificity and sensitivity.²

Increased troponin levels are believed to reflect irreversible myocardial necrosis.² Additionally, there is good correlation between troponin I levels and mortality at 6 weeks.⁶ After acute MI, troponin levels rise rapidly, reaching a peak at around 18 hours post-event. Levels then gradually decline, becoming undetectable approximately 7-10 days post-MI.³

In patients with NSTE-ACS, cardiac enzyme tests enable the distinction between NSTEMI and UA; elevated levels indicate NSTEMI, while normal levels indicate UA.⁷

Definition of myocardial infarction

In 2007, a revised definition of MI was issued jointly by the European Society of Cardiology, American College of Cardiology, American Heart Association and World Heart Federation.⁸ Full details of the new definition can be found below.

Any one of the following criteria meets the diagnosis for MI:¹

1. Increase and/or fall in cardiac biomarkers (preferably troponins), with at least one value about the 99th percentile of the upper reference limit (URL), together with evidence of myocardial ischaemia (clinical symptoms, ECG, imaging). 
2. Sudden cardiac death in the presence of new ST-segment elevations or left bundle branch block, and/or evidence of coronary thrombosis (coronary angiography or autopsy). 
3. Increase in cardiac biomarkers to >3 times the 99th percentile of the URL during percutaneous coronary intervention (PCI). 
4. During coronary artery bypass grafting (CABG), increase in cardiac biomarkers to >5 times the 99th percentile of the URL, plus additional evidence of myocardial ischaemia (ECG, angiography, imaging). 
5. Pathological findings of an acute MI.

Figure 1. ECG tracings in patient with acute anterior left ventricular infarction: (a) within a few hours of symptom onset; (b) after 24 hours; and (c) several days later.

Figure 2. Schematic representation of normal ECG