Acute Coronary Syndrome

A spectrum of conditions caused by acute myocardial ischaemia, comprising unstable angina, non ST elevation myocardial infarction and ST elevation myocardial infarction. The unifying pathology is atherosclerotic plaque rupture or erosion with superimposed thrombus, and the classification depends on whether the resulting occlusion is complete and on whether myocardial necrosis has occurred.

Pathophysiology and the classification it produces

• Plaque rupture exposes the lipid core and subendothelial collagen, activating platelets and the coagulation cascade.
• A partially occlusive, platelet rich white thrombus produces unstable angina if no necrosis occurs, or non ST elevation myocardial infarction if troponin rises. The electrocardiogram shows ST depression, T wave inversion, or is normal.
• A completely occlusive, fibrin rich red thrombus produces transmural ischaemia and ST elevation, and requires immediate reperfusion.

The clinical importance of the distinction is that ST elevation myocardial infarction requires immediate reperfusion within minutes, while non ST elevation acute coronary syndrome is managed with antithrombotic therapy and risk stratified invasive assessment over hours to days, and immediate thrombolysis in the latter is harmful.

Occlusion without ST elevation

A significant minority of patients with complete coronary occlusion do not show ST elevation and are misclassified. These patterns must be actively sought:

• Posterior infarction: ST depression of 1 mm or more in V1 to V3 with upright T waves and a prominent R wave, which is the mirror image of posterior ST elevation. Record posterior leads V7 to V9.
• Right ventricular infarction: ST elevation in V1 with ST depression in V2 in the context of an inferior infarct. Record right sided leads, particularly V4R.
• Left main or proximal left anterior descending occlusion: ST elevation of 1 mm or more in aVR and in V1 with widespread horizontal ST depression, most marked in leads I, II and V4 to V6. This indicates severe global subendocardial ischaemia and requires immediate interventional cardiology involvement.
• De Winter pattern: upsloping ST depression at the J point in the precordial leads with tall symmetrical T waves, indicating proximal left anterior descending occlusion.
• Wellens pattern: deeply inverted or biphasic T waves in V2 and V3 in a pain free patient, indicating critical proximal left anterior descending stenosis, in whom stress testing is dangerous.
• Left bundle branch block: use the Sgarbossa criteria, that is concordant ST elevation of 1 mm or more, concordant ST depression of 1 mm or more in V1 to V3, or excessively discordant ST elevation, with the modified criterion using a ratio of ST elevation to S wave depth of 0.25 or more.

• Chest discomfort, typically central, described as pressure, tightness, heaviness or squeezing rather than sharp pain, lasting more than 20 minutes in infarction.
• Radiation to the jaw, neck, shoulder, arm, back or epigastrium.
• Anginal equivalents, which are atypical presentations and which are the reason infarction is missed: exertional pain in the ear, jaw, neck, shoulder, arm, back or epigastrium without chest pain; exertional dyspnoea; nausea and vomiting; diaphoresis; syncope; and profound unexplained fatigue.
• Diaphoresis, which is a useful and objective feature.
• Associated features: pallor, nausea, anxiety and a sense of impending doom.

Groups in whom presentation is atypical and infarction is missed

Women, patients with diabetes in whom autonomic neuropathy blunts pain, the elderly who present with confusion, breathlessness or a fall, patients with chronic kidney disease, and postoperative patients. A low threshold for an electrocardiogram in these groups is the single most effective countermeasure.

Examination

Often normal, which is important to recognise. Look for signs of complications and of alternative diagnoses: hypotension, bradycardia or tachycardia, new murmurs of mitral regurgitation or ventricular septal rupture, a third heart sound, pulmonary crackles, raised jugular venous pressure with clear lungs suggesting right ventricular infarction, unequal blood pressures or pulses suggesting dissection, and a pericardial rub.

Life threatening alternative diagnoses that must be considered in every chest pain

• Pulmonary embolism: pleuritic pain, dyspnoea, hypoxia, sinus tachycardia, T wave inversion in leads III and V1 to V3, and the S1Q3T3 pattern in a minority.
• Aortic dissection: tearing pain radiating to the back, pulse or blood pressure differential, a new aortic regurgitant murmur, and neurological deficit. Giving antiplatelets and anticoagulants to a dissection is catastrophic, which is why it is considered before treatment is started.
• Cardiac tamponade: hypotension, raised venous pressure, muffled heart sounds, pulsus paradoxus and electrical alternans.
• Tension pneumothorax.
• Oesophageal rupture: severe pain after vomiting, subcutaneous emphysema, pleural effusion.

Immediate actions

• Manage in the resuscitation area with continuous monitoring, prepared to provide cardiopulmonary resuscitation, defibrillation and reperfusion. Ventricular fibrillation is most likely in the first hours.
• Obtain and interpret a twelve lead electrocardiogram within 10 minutes of arrival. This is the single most time critical action in chest pain and its delay is the commonest system failure.
• Add V4R when ST elevation is present in V1 with ST depression in V2, and V7 to V9 when there is ST depression of 1 mm or more in V1 to V3 with upright T waves.
• Check vital signs including blood pressure in both arms, pulse, respiratory rate, oxygen saturation, temperature and blood glucose.
• Give oxygen only if the saturation is below 90 percent or the patient is dyspnoeic, targeting 90 percent or above. Routine oxygen in the normoxic patient causes coronary vasoconstriction, increases infarct size and does not improve outcome.
• Brief targeted history and examination, recording the time of symptom onset, which determines the reperfusion strategy.
• Establish intravenous access and send blood for urea and electrolytes and high sensitivity troponin.

Electrocardiographic classification

• New or presumed new ST elevation of 1 mm or more in two or more anatomically contiguous leads: ST elevation myocardial infarction.
• New or presumed new, usually dynamic, horizontal or downsloping ST depression of 0.5 mm or more in two or more contiguous leads, or T wave inversion of more than 1 mm in two contiguous leads with a prominent R wave or an R to S ratio above 1, or transient ST elevation: high risk unstable angina or non ST elevation myocardial infarction.
• Normal or non diagnostic ST segment or T wave changes: intermediate or low risk unstable angina.

Territories and culprit vessels

• V2 to V5: anterior, left anterior descending.
• V1 to V2: septal, septal branches of the left anterior descending.
• II, III and aVF: inferior, right coronary artery in around 80 percent and left circumflex in around 20 percent.
• V1 to V4: anteroseptal.
• V3 to V6, I and aVL: anterolateral.
• I, aVL, V5 and V6: lateral, left circumflex.
• V7, V8 and V9: posterior, left circumflex or right coronary.
• V1 and V4R: right ventricle, right coronary artery.

Serial electrocardiography

Fewer than half of patients with acute myocardial infarction have clearly diagnostic changes on the first tracing, and around 10 percent of proven infarcts never develop ST elevation or depression. Repeat the twelve lead electrocardiogram at 30 minutes, with any change in symptoms, and use continuous ST segment monitoring where available. The evolving sequence is hyperacute tall wide T waves, then ST elevation, then Q wave formation with T wave inversion, then resolution of ST elevation and normalisation of T waves with persistent Q waves.

Troponin

• Obtain a high sensitivity troponin, and obtain it at least 4 hours after symptom onset rather than earlier, since a sample taken too early cannot exclude infarction.
• Where the first sample is taken under 4 hours from symptom onset, repeat it at least 4 hours after onset.
• Interpret with the clinical picture. Troponin is a marker of myocardial injury, not of infarction, and rises in pulmonary embolism, myocarditis, sepsis, renal failure, tachyarrhythmia, heart failure, cardiac contusion and subarachnoid haemorrhage.
• The pattern matters: a rise and fall indicates acute injury, while a stable elevation suggests chronic injury as in renal disease.
• Do not wait for troponin before treating ST elevation myocardial infarction. Reperfusion is decided on the electrocardiogram and the history.

Risk stratification with the HEART score

Scored 0 to 2 in each of five domains:

• History: highly suspicious 2, moderately suspicious 1, slightly or non suspicious 0.
• Electrocardiogram: significant ST depression 2, non specific repolarisation change 1, normal 0.
• Age: 65 or above 2, above 45 to under 65 1, 45 or below 0.
• Risk factors: three or more risk factors or known coronary disease 2, one or two 1, none 0. Risk factors are diabetes, current or recent smoking within a month, hypertension, hyperlipidaemia, family history of coronary disease and obesity.
• Troponin: three times the normal limit or above 2, above one to under three times 1, at or below normal 0.

Interpretation: 0 to 3 gives approximately 1.7 percent major adverse cardiac events over 6 weeks; 4 to 6 gives approximately 16.6 percent; 7 to 10 gives approximately 50.1 percent.

Chest radiography

Consider for pulmonary oedema, a widened mediastinum suggesting dissection, pneumothorax and alternative diagnoses. It must not delay reperfusion in ST elevation infarction.

Initial therapy common to all acute coronary syndrome

• Aspirin 300 mg to chew, unless already given by prehospital services, unless allergic, and unless there is active upper gastrointestinal or retinal bleeding or haemophilia. Chewing rather than swallowing achieves faster absorption.
• Nitroglycerin sublingual spray 0.4 mg for pain, repeated every 5 minutes to a maximum of three doses or until the discomfort resolves.
• Do not give nitroglycerin if the systolic pressure is below 90 mmHg, or 30 mmHg below the patient's known baseline; if the heart rate is above 100 or below 50 per minute; in right ventricular infarction, which is preload dependent and in which nitrates cause profound hypotension; or where sildenafil or vardenafil has been taken in the previous 24 hours or tadalafil in the previous 48 hours.
• The right ventricular point is critical. In any inferior infarction, record right sided leads before giving nitrates, since the combination of an inferior infarct and nitrates is a well recognised cause of catastrophic hypotension.
• Fentanyl 25 to 50 micrograms intravenously if pain is not relieved by three doses of sublingual nitroglycerin, repeated once after 5 minutes if pain persists. Morphine 2 to 5 mg intravenously in titrated increments is an alternative, recognising that opioids delay the absorption of oral antiplatelet agents.
• For persistent pain, consult a cardiologist or physician and consider an intravenous nitroglycerin infusion, subject to the same contraindications.
• Continuous cardiac monitoring and defibrillator availability.
• Consider a chest radiograph.

Where the electrocardiogram shows ST elevation: proceed immediately to the ST elevation myocardial infarction pathway.

Where the electrocardiogram shows high risk changes or the troponin is raised: proceed to the non ST elevation pathway with consultation of a cardiologist or physician, and consider immediate transfer to a facility with interventional capability.

Where the electrocardiogram is normal or non diagnostic and the troponin is negative: risk stratify, observe, repeat the electrocardiogram and troponin, and discharge only if the discharge criteria are met.

Immediate consultation and transfer

Consult a cardiologist or physician and consider immediate transfer to an appropriate facility for all ST elevation infarction and all high risk non ST elevation acute coronary syndrome. The transfer decision is made at the moment of diagnosis rather than after treatment has been given, since transfer time is part of the reperfusion clock.