Presentation on Acute coronary syndrome

Presentation of Acute coronary syndrome by Doctor practicing in the NHS, UK.

1. Acute Coronary Syndrome Dr Sanam RAj

2. A spectrum of acute myocardial ischemia and/or infarction from acute obstruction of a coronary artery. Unstable angina NSTEMI STEMI P resence or absence of ST-segment elevation on the initial ECG T ogether with measurement of myocardial biomarkers, such as high-sensitivity cardiac troponins. Symptoms

3. STEMI ST elevation, elevated cardiac enzymes. NSTEMI ST depression, T wave inversion, elevated cardiac enzymes. Unstable angina Non-specific ECG changes ( or no changes at all), normal cardiac enzymes.

4. Acute coronary syndrome defined as myocardial ischaemia at rest or on minimal exertion in the absence of acute cardiomyocyte injury/necrosis. [1]   It is characterised by specific clinical findings of prolonged (>20 minutes) angina at rest; new onset of severe angina; angina that is increasing in frequency, longer in duration, or lower in threshold; or angina that occurs after a recent episode of myocardial infarction. [1]   Unstable angina should be suspected based on: P resence of symptoms suggestive of myocardial ischaemia (e.g., acute chest pain) ECG findings (no evidence of ST-elevation myocardial infarction) T roponin testing (no dynamic elevation of cardiac troponin above the 99th percentile). Unstable angina

5. Risk Factors Non-modifiable risk factors : Gender Age F amily history of CVD D iabetes H uman immunodeficiency virus (HIV).

6. Pathophysiology Ischaemic heart disease is a complex process which develops over a number of years. initial endothelial dysfunction is triggered by a number of factors such as smoking, hypertension and hyperglycaemia . this results in a number of changes to the endothelium including pro-inflammatory, pro-oxidant, proliferative and reduced nitric oxide bioavailability fatty infiltration of the subendothelial space by low-density lipoprotein (LDL) particles monocytes migrate from the blood and differentiate into macrophages. These macrophages then phagocytose oxidized LDL, slowly turning into large 'foam cells'. As these macrophages die the result can further propagate the inflammatory process. smooth muscle proliferation and migration from the tunica media into the intima results in formation of a fibrous capsule covering the fatty plaque.

7. ACS generally develops in patients who have ischaemic heart disease. It describes the gradually build up of fatty plaques within the walls of the coronary arteries. This leads to two main problems: 1. Gradual narrowing less blood and therefore oxygen reaching the myocardium at times of increased demand angina, i.e. chest pain due to insufficient oxygen reaching the myocardium during exertion 2. The risk of sudden plaque rupture. The fatty plaques which have built up in the endothelium may rupture leading to sudden occlusion of the artery. This can result in no blood/oxygen reaching the area of myocardium.

8. Complications of atherosclerosis

9. Diagram showing the progression of atherosclerosis in the coronary arteries with associated complications on the right

10. Ruptured coronary artery plaque resulting in thrombosis and associated myocardial infarction.

11. Clinical features Symptoms typically, central/left-sided may radiate to the jaw or the left arm often described as 'heavy' or constricting, 'like an elephant on my chest'. Anxiety and fear of impending death. Nausea and vomiting, breathlessness, collapse/syncope. Physical signs Signs of sympathetic activation. Pallor, sweating, tachycardia. Signs of vagal activation. Vomiting, bradycardia. Signs of impared myocardial function Hypotension, oliguria, cold peripheries, raised JVP, third heart sound, diffuse apical impulse, lung crepitations.

12. Uncommon symptoms Marked sweating epigastric pain dyspnoea syncope backpain Painless or silent MI may also occur and is particularly more common in older people and those with diabetes mellites.

13. Investigations The two most important investigations when assessing a patient with chest pain are: ECG Cardiac markers e.g. troponin CXR , FBC , U&E , LFT , blood glucose , CRP , lipid profile, coagulation profile. Investigations to consider: ECHO Invasive coronary angiogragraphy functional stress test coronary CT angiogram

14. ECG in unstable angina Be aware that the ECG may be normal in more than 30% of patients. [1]  Furthermore, unstable angina is generally not associated with ECG changes (based on the opinion of our experts).  However, abnormal findings that suggest non-ST-elevation ACS include: [1]   ST depression; this indicates a worse prognosis Transient ST elevation T-wave changes.

15. ECG in NSTEMI Abnormal findings that suggest NSTEMI include: [1] [7] ST depression; this indicates a worse prognosis Transient ST elevation T-wave changes. Be aware that the ECG may be normal in more than 30% of patients

16. ECG in STEMI STEMI is diagnosed in the appropriate clinical context (a patient with chest pain or other symptoms consistent with myocardial ischaemia ) when there is new (or increased) and persistent ST-segment elevation in at least two contiguous ECG leads of ≥1 mm in all leads other than leads V2-V3 where the following cut-off points apply: 2.5 mm ( i.e ≥ 2.5 small squares) ST elevation in leads V2-3 in men under 40 years, or ≥ 2.0 mm ( i.e ≥ 2 small squares) ST elevation in leads V2-3 in men over 40 years 1.5 mm ST elevation in V2-3 in women 1 mm ST elevation in other leads new LBBB (LBBB should be considered new unless there is evidence otherwise)

17. ST-elevation myocardial infarction (STEMI): ST-segment elevation + elevated biomarkers of myocardial damage. Non ST-elevation myocardial infarction (NSTEMI): ECG changes but no ST-segment elevation + elevated biomarkers of myocardial damage ECG showing a ST elevation myocardial infarction (STEMI). Note by how looking at which leads are affected (in this case II, III and aVF ) we are able to tell which coronary arteries are blocked (the right coronary artery in this case). A blockage of the left anterior descending (LAD) artery would cause elevation of V1-V4, what is often termed an 'anterior' myocardial infarction.

18. ECG showing a non-ST elevation myocardial infarction (NSTEMI). On the ECG there is deep ST depression in I-III, aVF , and V3-V6. aVR also has ST elevation. Deep and widespread ST depression is associated with very high mortality because it signifies severe ischemia usually of LAD or left main stem.

19. The table below shows a simplified correlation between ECG changes and coronary territories: ECG changes Coronary artery Anterior V1-V4 Left anterior descending Inferior II, III, aVF Right coronary Lateral I, V5-6 Left circumflex

20. Diagram showing the correlation between ECG changes and coronary territories in acute coronary syndrome

21. H igh-sensitivity troponin Measure high-sensitivity cardiac troponin ( hs-cTn ) immediately after presentation and obtain results  within 60 minutes  in all patients with suspected acute coronary syndrome to rule out acute myocardial infarction. T here will be no dynamic rise above the 99th percentile in patients with unstable angina. [1]  . NSTEMI dynamic elevation above the 99th percentile. STEMI acute MI is definitively confirmed by a rise and/or fall in cardiac troponin (with  at least one value >99th percentile of the upper reference limit ) in a patient who has symptoms or signs of ischaemia [1] [68]

22. Practical tip Reassess the patient if they have a raised hs-cTn . Troponin can be acutely raised due to other causes such as myocarditis, aortic dissection, or acute pulmonary embolism. Chronic elevation of high-sensitivity troponin is also common in patients with renal dysfunction and heart failure. Troponin levels may remain elevated for 1-2 weeks following recent myocardial infarction and/or percutaneous coronary intervention. Interpret hs-cTn in the context of the clinical scenario.

23. Management Prevent worsening of presentation (i.e. further occlusion of coronary vessel) Revascularise (i.e. 'unblock') the vessel if occluded (patients presenting with a STEMI) Treat pain A commonly taught mnemonic for the treatment of ACS is MONA: Morphine Oxygen (British Thoracic Society guidelines are now widely adopted and oxygen should only be given if the oxygen saturations are < 94%.) Nitrates Aspirin

24. Common management of all patients with ACS Initial drug therapy aspirin 300mg oxygen should only be given if the patient has oxygen saturations < 94%  in keeping with British Thoracic Society oxygen therapy guidelines morphine should only be given for patients with severe pain previously IV morphine was given routinely evidence, however, suggests that this may be associated with adverse outcomes nitrates can be given either sublingually or intravenously useful if the patient has ongoing chest pain or hypertension should be used in caution if patient hypotensive

25. Once a STEMI has been confirmed the first step is to immediately assess eligibility for coronary reperfusion therapy. There are two types of coronary reperfusion therapy:

26. Percutaneous coronary intervention for patients with STEMI

27. Secondary prevention Patients who've had an ACS require lifelong drug therapy to help reduce the risk of a further event. Standard therapy comprises the following as a minimum: aspirin a second antiplatelet if appropriate (e.g. clopidogrel) a beta-blocker an ACE inhibitor a statin

28. Complications of ACS Arrythmias Ventricular fibrillation Ventricular tachycardia ventricular ectopics Atrial fibrillation Sinus bradycardia particularly after inferior MI Atrioventricular block Post infarct angina Acute heart failure Pericarditis Dressler syndrome Papillary muscle rupture Ventricular septal rupture Ventricular rupture Embolism Ventricular aneurysm

29. Case • 60 year old male with history of DM2 for 20 years, HTN, HLD who presented to the ED with 4 hour onset of chest pain which was described as in the anterior chest without radiation. The pain seemed to improve when he sits down and worsening when he walked upstairs. • VS: T 36.9, HR: 95, BP: 84/56, RR 22, O2 sat. 99% RA. What would you do?

30. ECG Findings: Normal Sinus Rhythm (NSR) Anterior Wall ST Segment Elevation Myocardial Infarction (STEMI)

31. Case 2 62 year old male with history of HTN who presented to the ED with sudden onset of chest pain which was described as in the anterior chest radiating to left arm. Unabl e to walk. ECG Trops 6 >> 26 Diagnosis ? Managemen t ?

32. Reference: BMJ best practice https://bestpractice.bmj.com/topics/en-gb/3000100#referencePop1