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Related Subjects: |Atherosclerosis |Ischaemic heart disease |Assessing Chest Pain |ACS - General |ACS - STEMI |ACS - NSTEMI |ACS - GRACE Score |ACS - ECG Changes |ACS -Cardiac Troponins |ACS - Post MI arrhythmias |ACS: Right Ventricular Infarction

ST elevation changes everything - if you spot it act fast to establish coronary reperfusion through PCI or thrombolysis. Always check an ECG after any new episode of chest pain so as not to miss STEMI. Early intervention saves lives

Immediate assessment of Moderate to Severe Cardiac Chest pain

Introduction

• Acute coronary syndrome has become used to describe patients with chest pain of suspected cardiac origin.
• It is a general term for patients with new or increasing chest pain presumed due to myocardial ischaemia with symptoms with associated ECG changes.
• Stable angina is not included as an ACS and rarely presents acutely where it is more likely to be Unstable angina.
• ECG changes of ST-elevation separate the two forms of myocardial infarction as studies have shown that this separates those who benefit from PCI/thrombolysis and those that don't.
• Biomarkers separate the diagnosis of USA from NSTEMI and are not always available acutely.

Acute coronary syndromes include 

• Unstable angina (USA) : Symptoms + ECG changes Normal Troponin
• NSTEMI : Symptoms + ECG changes + raised Troponin
• STEMI: : Symptoms + ECG changes Raised Troponin

About

• Acute coronary syndrome is an important cause of sudden cardiac death
• Needs urgent reperfusion for STEMI, nitrates, antithrombotics, analgesia, oxygen
• Access to immediate defibrillation and arrhythmia and heart failure management

Aetiology

• Most cases of STEMI are caused by occlusion of a major coronary artery
• Effect depend on which artery and how proximal the lesion and how much myocardium is damaged
• Prompt treatment is very important as long delay times to Primary PCI are associated with a worse clinical outcome
• Primary percutaneous coronary intervention (PCI) is the term given to mechanical intervention to open the occluded artery.
• Fibrinolysis or thrombolysis is the term given to pharmacological reperfusion.

Pathophysiology

• Disruption or erosion of an atherosclerotic plaque within the coronary arteries
• Leads to Thrombosis which may cause total or subtotal occlusion of the vessel
• Thrombosis may embolise into distal coronary vessels
• Loss of normal flow leads to cardiac ischaemia

Classification of MI

Risk Factors

• These increase chance that chest pain is cardiac
• Age M > 40 yrs; F >50. Gender M > F
• Family IHD History especially premature <50 yr M, <60 F
• Smoking, Dyslipidaemia, Hypertension, Diabetes Mellitus IDDM, NIDDM

Clinical

• Take a careful history of the symptoms with relation to exertion.
• Chest/arm/jaw pain at rest is ominous and important.
• Assess clinical presentation in the light of risk factors.
• A similar history in a young risk free male is managed differently than in a 60 year old male smoker and hypertensive
• Patient with STEMI often pale, terrified and cold peripherally
• Examine for shock, murmurs, heart failure, and pulmonary disease.
• An S3 may be heard as well as a raised JVP and inspiratory crackles
• Look for ankle oedema. Pulmonary oedema is a poor prognostic sign.
• Clinical features that made IHD more likely
  • Radiation of pain to the arms or shoulders right or left
  • Pain associated with exertion, diaphoresis, nausea, or vomiting
  • Worse than previous angina or similar to a previous MI.
  • Hypotension or S3
• Atypical presentations
  • Breathlessness without pain
  • Delirium and confusion in the elderly
  • Falls and syncope also in elderly
  • Epigastric symptoms with inferior MIs
  • Elderly and diabetics are prone to atypical presentations
  • ECG is a screening test for the "silent MI".
  • New Arrhythmias
  • Acute Pulmonary oedema
• Clinical features that make Chest pain less likely to be IHD
  • Pleuritic, positional, or sharp chest pain
  • Inframammary location
  • Pain not associated with exertion
  • A normal exam

Poor Prognosis

• Ongoing and recurrent ischaemia
• Widespread ECG changes, Raised CK/Troponins
• Hypotension and Mitral regurgitation with ischaemia
• Pulmonary oedema, Cardiogenic shock

Investigations

• FBC:Haemoglobin : anaemia can exacerbate ACS
• U&E:Baseline renal function
• Glucose and lipids: Diabetes
• Troponin T/I
• CK(MB)/AST/LDH - historical biomarkers superseded by Troponin
• Echocardiogram - if available acutely may show wall movement abnormalities suggesting ischaemia/infarction. An estimation of LV function and valve function is useful.
• Exercise stress test: If pain settles and ECG changes equivocal and troponin negative then consider diagnostic EST. See topic
• Tests to assess hibernating myocardial whose viability will improve with revascularisation by PCI or CABG. Try Cardiac MRI or PET scan. Dobutamine stress echo, Thallium. Most give a sensitivity of over 90% except stress echo (70%)
• Electrocardigram - always repeat with new symptoms
  • ECG is recorded. Comparison with previous ECGs, if available, is very valuable, particularly in those with pre-existing cardiac pathology such as LVH or established coronary disease. The ECG splits patients with a suspicion of ACS in two categories requiring different therapeutic approaches:
  • ST-segment elevation signifies complete occlusion of a major coronary artery and immediate reperfusion therapy is usually indicated. ST-elevation due to STEMI is associated with ST depression in opposing leads as well as T wave changes.
  • ST-segment changes but without persistent ST-segment elevation or a normal ECG. Will need an estimation of biochemical markers.
  • In a small number there are undetermined ECG changes such as bundle branch block or pacemaker rhythm. Will need an estimation of biochemical markers.
• Assessing Troponin
  • Normal (hs Troponin T < 14ng/l) A result of <14ng/L more than 6 hours after symptoms rules out MI.
  • Possible MI (hs Troponin T 14-30 ng/l) especially if there is +7ng/L rise 3 hrs later
  • Probable MI (hs Troponin T > 30 ng/l)

Differentials

• Syndrome X:  Recurrent chest pain suggestive of IHD. Worse with exertion. Normal coronary arteries. Recurrent symptoms but a good prognosis
• Coronary spasm : "Printzmetal's angina". ST-segment elevation seen sometimes. Coronary arteries normal. Given nitrates and calcium channel blockers - good prognosis
• Takotsubo Cardiomyopathy - Also known as "broken heart syndrome". Possibly due to elevated catecholamine response to stress leading to myocardial stunning. Anginal chest pain, dyspnoea and evidence of heart failure often in a setting of severe emotional or physiological stress. ECG ST elevation, Q wave and T wave changes, Long QT. Troponin may be raised. Echo - generalized akinesis of the apex and mid ventricle with hypokinesis and wall motion problems beyond the area of one coronary artery. The left ventriculogram shows apical ballooning. Supportive management and the condition resolves over several months.
• Aortic dissection: central chest pain may be into back
• Acute pericarditis: can have saddle-shaped ST elevation and chest pain

Unstable Angina

• Chest pain that is of unlimited duration and/or increasing severity and occurs after a fixed site of exertion or at rest and may be worsening.
• Cardiac biomarkers are normal. ECG - Normal or ST depression and T wave changes associated with symptoms
• Management same as NSTEMI

Non STEMI Management (Subocclusive thrombus)

• See Topic

STEMI Management (Occlusive thrombus)

• See Topic

Secondary Prevention medications

• Beta-blockers
  • All patients should receive a beta-blocker as soon as clinically stable unless contraindicated. Contra-indicated in: bradycardia <60bpm 2nd or 3rd degree AV block systolic BP <100mmHg severe heart failure, bronchospasm or asthma significant peripheral vascular disease concomitant use of verapamil.
  • Continue current beta-blocker or start Bisoprolol 2.5mg daily titrating up to a maximum 10mg daily as tolerated as per heart rate and blood pressure. For patients who have LVSD (EF<40%) or subsequently develop LVSD consider bisoprolol, nebivolol or carvedilol. A lower starting dose of 1.25mg daily for bisoprolol/nebivolol or carvedilol 3.125mg twice daily should be initiated. Monitor BP, pulse rate, for conduction disturbances or worsening of heart failure.
• Nitrates
  • Glyceryl trinitrate (GTN) infusion (ready diluted 50mg/50ml vial) or isosorbide dinitrate 1mg/ml infusion. Consider for all patients with the acute coronary syndrome with ongoing or persistent pain.
  • Not given if a patient has systolic BP < 100 mmHg known nitrate sensitivity. known severe aortic stenosis. Up-titrate as per local policy every 30 minutes until a satisfactory response. Measure BP and HR after each dose titration and then hourly.
• Statins
  • Start Atorvastatin 80mg daily in all patients (consider 40mg daily if very elderly, frail with multiple co-morbidities as appropriate). Check LFTs prior to therapy, within 1-3 months after starting therapy then 6 months thereafter up to 1 year. LFTs should then be checked yearly. Patients should be warned to report any unexplained muscle pain, tenderness or weakness.
  • It is recommended to start high-intensity statin therapy as early as possible unless contraindicated, and maintain it long term. In patients with LDL cholesterol >70 mg/dL (>1.8 mmol/L) despite a maximally tolerated statin dose, further reduction in LDL cholesterol with a non-statin agent should be considered.
• ACE inhibitors (ACEi)
  • Once clinically and haemodynamically stable, start Ramipril at 2.5mg once or twice daily dependent on BP and renal function. Increase every 1-3 days in the hospital to a maximum of 5mg BD or 10mg daily.
  • Patients with LVSD EF<40% and/or NYHA class IV should be started on Ramipril 1.25mg daily and titrated gradually every 1-2 days to 10mg daily.
• Angiotensin II Receptor Blockers (ARBs)
  • Should ONLY be used where patients truly intolerant of ACEI due to an ACEi induced cough (persistent, intolerable cough - not just dry cough)
  • Start Candesartan 8mg daily post MI and uptitrate.
  • If LVSD with EF<40% start Candesartan 4mg daily increasing up to a maximum 32mg daily as tolerated.
  • Monitor as per ACE inhibitors
• Eplerenone (Aldosterone antagonist/ mineralocorticoid receptor antagonist)
  • For patients with signs and/or symptoms of heart failure post-myocardial infarction who are not already on an aldosterone antagonist. Started 3-14 days post-myocardial infarction if indicated. Initially, 25mg daily, increased preferably within 4 weeks to 50mg daily
  • Check potassium levels prior to initiation, during the 1st week and at 1 month after the start of treatment and each dosage change. Potassium levels should be monitored periodically after this. Patients with potassium levels >5 should not be started on eplerenone. After initiation, the dose should be adjusted based on the serum potassium.
  • Patients admitted on spironolactone may be continued on spironolactone instead of starting eplerenone (never use eplerenone and spironolactone together).
• PPI
  • A proton pump inhibitor in combination with DAPT is recommended in patients at higher than average risk of gastrointestinal bleeds (i.e. history of gastrointestinal ulcer/haemorrhage, anticoagulant therapy, chronic NSAID/corticosteroid use or two or more of the following
  • Age =65 years, dyspepsia, gastro-oesophageal reflux disease, Helicobacter pylori infection, chronic alcohol use).
  • Avoid Omeprazole and Esomeprazole in patients taking Clopidogrel.
• Antithrombotic strategies in NSTEMI and non-valvular AF
  • In patients with a firm indication for OAC (e.g. atrial fibrillation with a CHA2DS2-VASc score =2, OAC is recommended in addition to antiplatelet therapy.
  • An early invasive coronary angiography (within 24 h) should be considered in moderate- to high-risk patients, irrespective of OAC exposure, to expedite treatment allocation (medical vs. PCI vs. CABG) and to determine the optimal antithrombotic regimen.
  • Initial dual antiplatelet therapy with Aspirin plus a P2Y12 inhibitor in addition to OAC before coronary angiography is not recommended.
• Coronary Angiography
  • In the setting of NSTEACS management, coronary angiography is performed partly for diagnostic reasons to confirm the presence of coronary artery disease, but more importantly as a means of identifying patients in whom coronary revascularization by PCI or CABG would be appropriate.
  • Coronary artery disease. Significant CAD on invasive coronary angiography is = 70% diameter stenosis of at least one major epicardial artery segment or =50% diameter stenosis in the left main coronary artery
  • It is important to recognise that the assessed risk of death or further cardiac event on its own does not always equate with a patients capacity to benefit from coronary revascularisation. It is very important in making the decision as to whether to embark on the pathway of coronary angiography +/- coronary revascularisation, to take into account other factors such as clinical context, co-morbidity, contraindications and, importantly, patient preference.
  • Assess Patient Suitability after careful evaluation of potential risks and benefits, o Clinical context: pre-morbid functional status, frailty etc. Co-morbidity: including known severe peripheral vascular disease, COPD, renal impairment, previous strokes, co-existent malignancy etc
  • Careful attention should be given to ensuring that patients understand the potential benefits and risks of the treatment options proposed and why other options are not proposed. It is important that realistic estimates of risk, discomfort and benefits are given in order to avoid unrealistic expectations.
• Patient selection for angiography +/- coronary revascularisation
  • Very high risk An immediate invasive strategy (<2 h) is recommended in patients with at least one of the following very-high-risk criteria: Haemodynamic instability or cardiogenic shock. Recurrent or ongoing chest pain refractory to medical treatment. Life-threatening arrhythmias or cardiac arrest. Mechanical complications of MI. Acute heart failure with refractory angina or ST deviation. Recurrent dynamic ST- or T-wave changes, particularly with intermittent ST elevation.
  • High Risk An early invasive strategy (<24 h) is recommended in patients with at least one of the following high-risk criteria: Rise or fall in cardiac troponin compatible with MI. Dynamic ST- or T-wave changes (symptomatic or silent) GRACE score >140.
  • Intermediate Risk An invasive strategy (<72 h) is recommended in patients with at least one of the following intermediate-risk criteria: Diabetes mellitus, Renal insufficiency (eGFR <60 mL/min/1.73 m2), LVEF <40% or CHF, Early post-infarction angina, Recent PCI, Prior CABG, GRACE risk score >109 and <140, or recurrent

References

• SIGN 148 Acute coronary syndrome 2016