6th March 2024

Acute coronary syndrome

Pathophysiology

The term acute coronary syndrome includes a spectrum of conditions ranging from unstable angina, non-ST-segment-elevation myocardial infarction (NSTEMI) and ST-segment-elevation myocardial infarction (STEMI). Much like stable angina, the underlying cause of acute coronary syndrome is coronary artery disease caused by atherosclerosis, the build-up of fatty plaques within the wall of the coronary arteries. Once a plaque has formed, it can cause a physical blockage inside the coronary artery, or the plaque can rupture and cause occlusion of a coronary artery (thrombosis). Partial occlusion of a coronary artery will affect the sub endocardium and may cause unstable angina or NSTEMI. Total occlusion of a coronary artery will cause transmural infarction leading to STEMI. 

Presentation

The classic feature of acute coronary syndrome is chest pain. This pain is usually described as ‘heavy’ or ‘constricting’, left sided and can radiate to the jaw or arm. This can be accompanied by diaphoresis, dyspnoea, nausea and vomiting. Certain patients will present with epigastric sounding pain, whereas other patients, such as the diabetic or elderly, may not experience any chest pain. 

Investigations

The two most important investigations that will lead to the diagnosis are ECG and cardiac enzymes (high sensitivity troponin). ST segment elevation in at least two contiguous leads or new left bundle branch block and raised troponin will confirm diagnosis of STEMI. 

The distinguishing feature between unstable angina and NSTEMI is the presence of elevated troponin in NSTEMI which implies cardiac damage. Both will have non-ST segment changes (ST segment depression or inverted T waves) or nonspecific changes on ECG. 

The correlation between ECG changes and coronary territories are explained in the table below: 

Troponin I serum levels will usually be elevated 2-3h after the onset of chest pain and reach their peak levels around 12-48h. Levels will normalise 4-10 days post event. They have the highest sensitivity and specificity compared to other cardiac markers. 

CK-MB (creatine kinase myocardial band) are less sensitive and specific than troponin but will normalise 48-72h post MI. Continued rise of CK-MB after 72h is diagnostic of myocardial reinfarction. 

The correlation between ECG changes and coronary territories are explained in the table below: 

 Troponin I serum levels will usually be elevated 2-3h after the onset of chest pain and reach their peak levels around 12-48h. Levels will normalise 4-10 days post event. They have the highest sensitivity and specificity compared to other cardiac markers. 

CK-MB (creatine kinase myocardial band) are less sensitive and specific than troponin but will normalise 48-72h post MI. Continued rise of CK-MB after 72h is diagnostic of myocardial reinfarction. 

Management 

The management of acute coronary syndrome is divided into two subtypes: 

1. STEMI 
2. NSTEMI and unstable angina 

All patients with acute coronary syndrome should receive aspirin 300mg in the absence of contraindications. Routine administration of oxygen is no longer recommended, and oxygen should be administered if SpO2 < 94% in keeping with the British thoracic guidelines. Routine administration of IV morphine has been shown to have adverse effects and is recommended for patients with severe pain. If the patient has ongoing pain or hypertension, nitrates can be administered intravenously. 

STEMI

In patients with acute STEMI, NICE guidelines recommend the following: 

• If the patient presents within 12h of onset of symptoms, a coronary angiogram with follow-on primary percutaneous coronary intervention (PPCI) is the first management option if PPCI can be delivered within 120 mins where fibrinolysis could have been administered. 
• If PPCI is possible, then the patient should be loaded with prasugrel if they are not taking an oral anticoagulant or clopidogrel if they are. 
• When PPCI is possible, access through the radial artery is preferred and, in that case, NICE recommends the administration of unfractionated heparin with bailout glycoprotein IIb/IIIa inhibitor.  
• If radial access is not possible and femoral access is being used, then NICE recommends bivalirudin with bailout glycoprotein IIb/IIIa inhibitor. 
• If stenting is indicated, NICE recommends the use of a drug eluting stent.
• If the patient presents within 12 hours of onset of symptoms and PPCI is not possible, then fibrinolysis should be offered. The preferred agents are tenecteplase and alteplase and they should be given together with an antithrombin drug.  
• An ECG should be repeated 60-90 mins after administration of fibrinolysis. If this fails to show > 50% resolution of ST segment elevation, then PCI should be offered to the patient as rescue PCI is superior to repeat fibrinolysis.
• NICE also recommends considering coronary angiography during the same admission for patients who have successfully been treated with fibrinolysis. 

NSTEMI

In patients with acute NSTEMI or unstable angina, NICE guidelines recommend the following: 

• Patients presenting with NSTEMI should be offered fondaparinux in the absence of contraindications if there is no immediate PCI planned. 
• NICE recommends using a 6-month mortality risk using an established scoring system (e.g: GRACE score) to determine who should be offered coronary angiography with follow-on PCI.  As a rule of thumb, patients with a 6-month intermediate to high mortality risk should be offered coronary angiography with follow on PCI within 72h whereas patients with low mortality risk can be managed conservatively. 
• For those patients undergoing coronary angiography, NICE recommends giving unfractionated heparin and a second antiplatelet agent (if taking an oral anticoagulant, clopidogrel is the drug of choice; if not taking an anticoagulant, then prasugrel or ticagrelor is advised). 
• If the patient has a low risk of cardiovascular adverse events and is stable, NICE recommends conservative management with dual antiplatelet therapy (aspirin + ticagrelor (low bleeding risk) or aspirin + clopidogrel (high bleeding risk). 

Secondary prevention

The following classes of medication are used to reduce the risk of further cardiac events following an MI:   

• Dual antiplatelet therapy unless contraindicated 
• ACE inhibitor 
• Beta blocker 
• Statin 

Complications

Following a myocardial infarction, patients are at risk of several complications. Early complications include: 

• Cardiac arrest commonly caused by ventricular fibrillation, the most common cause of death following MI 
• Cardiogenic shock is usually dependent on the myocardial infarct size 
• Bradyarrhythmia and heart block are common following inferior myocardial infarction 
• Tachyarrhythmias, including ventricular tachycardia and ventricular fibrillation, as mentioned above 

Late complications include: 

• Chronic heart failure due to dysfunctional myocardium following infarct
• Left ventricular aneurysm due to weakened myocardium. This is associated with persistent ST elevation and left ventricular failure. There is an increased risk of stroke therefore, patients need anticoagulation
• Left ventricular free wall rupture is most common with anterior myocardial infarction. Presentation is with acute heart failure secondary to cardiac tamponade and is a medical emergency 
• Mitral regurgitation is common with inferoposterior infarction and occurs due to ischaemia or rupture of the papillary muscle 
• Pericarditis / Dressler syndrome may present following a large transmural infarct. It is thought to be due to an autoimmune reaction against antigenic proteins formed as the myocardium recovers. 

References

• Acute coronary syndrome. NG185. Published 18 November 220. Available at: https://www.nice.org.uk/guidance/ng185/chapter/Recommendations#dual-antiplatelet-therapy-for-people-with-acute-stemi-having-primary-pci 
• 2017 ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation – Web Addenda. Published 2017. Available at: https://www.escardio.org/static-file/Escardio/Guidelines/2017%20STEMI%20ehx393_web%20addenda%20-%20FOR%20WEB.pdf