Acute coronary syndromes

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Chapter 7 Acute coronary syndromes

Symptoms and signs which may indicate an acute coronary syndrome (ACS) need to be identified as soon as possible, ideally by the patient, so that treatment can be initiated to avoid or minimise myocardial damage and to avert the risk of life-threatening complications. A defibrillator must be immediately available with staff trained in its use. Assign a high priority at triage to patients with a history of chest pain, breathlessness, syncope or palpitations. Provide ECG monitoring and supplemental oxygen and insert an intravenous cannula as soon as possible. Send blood samples for testing and provide analgesia (nitrates and/or morphine) and, unless contraindicated, give oral aspirin (300 mg).

Cardiac risk factors increase the likelihood of cardiac disease, particularly in those under the age of 40; however, their absence does not exclude the diagnosis. Atypical pain or even the absence of pain is also relatively common (e.g. in diabetics and the elderly), and observation and investigation over a period of time may be required in some cases.

ASSESSMENT

The patient should be assessed in a safe environment with oxygen, monitoring and a cannula in situ. Look for ACS with ECG changes, known as ST-segment elevation myocardial injury (STEMI), indicating recent coronary artery occlusion, or ACS without new ECG changes, now known as ‘non-ST-segment elevation acute coronary syndrome’ (NSTEACS). NSTEACS patients can then be stratified as high risk, medium risk or low risk.

In some cases no ACS can be demonstrated and an alternative diagnosis is established, such as aortic dissection, pericarditis or pulmonary embolism

Table 7.1 Initial patient assessment and stratification

STEACS	NSTEACS
ST-elevation acute coronary syndrome usually referred to as STEMI (ST–segment elevation myocardial injury)	Non-ST-elevation acute coronary syndrome Stratify: → HIGH RISK → INTERMEDIATE RISK → LOW RISK

or a non-cardiovascular cause such as pneumonia, musculoskeletal pain or gastro-oesophageal disease may be identified. In a significant subgroup of presentations, immediately serious illness can be excluded and, although no diagnosis is reached, the patient can be discharged for follow-up outpatient assessment.

DIAGNOSING AND STRATIFYING ACUTE CORONARY SYNDROMES

History, examination, investigation and management proceed rapidly and concurrently and senior staff should be contacted as soon as possible (see Figure 7.1).

Figure 7.1 Chest pain pathway

Typical presentations of ACS involve chest discomfort at rest or for prolonged periods (prolonged is defined as > 10 minutes, not relieved by sublingual nitrates) or recurrent chest discomfort or discomfort associated with syncope or acute heart failure.

Some important points of immediate history include the time of onset of pain, exertionally-related pain, risk factors and comorbidities, allergies and contraindications to treatments.

Physical examination may show tachycardia or bradycardia, hyper- or hypotension, sweating, nausea or evidence of heart failure (dyspnoea, basal crepitations, third heart sound, poor peripheral perfusion). Importantly there may be no specific physical findings in some patients with ACS.

Note that although cardiac myonecrosis is demonstrated by increased levels of cardiac biomarkers (troponins, creatine kinase-myocardial band (CK-MB)) and can occur in ACS with or without ECG changes, the indication for initial urgent reperfusion therapy is acute ECG change.

Tests to include are listed in Table 7.2.

Table 7.2 Tests to aid in the diagnosis and stratification of patients with ACS ^∗

Test	Comment
Full blood count	Anaemia or polycythaemia may need treatment, baseline platelet count (particularly if heparin is to be used)
Coagulation PT and APTT	Guides anticoagulant therapy
Serum chemistry	Hypokalaemia increases the risk of arrhythmia. Hypomagnesaemia may be present if patient taking some diuretics or has liver/renal disease

Renal function

Creatinine (and, if elevated, eGFR calculation).

Kidney disease is a risk factor for high- and intermediate-risk NSTEACS

Troponin I or T^∗∗ May take up to 6 hours to rise, two or more measurements over time may be required; remains elevated 5–14 days Serum lipids Initiating treatment of hyperlipidaemia within the first few days may be required Blood glucose Diabetes may be undiagnosed (especially mild NIDDM); close control of blood glucose levels improves outcomes Chest X-ray May show heart failure, cardiomegaly. Do not delay urgent treatment to obtain a CXR. Do not send potentially unstable patient out of resuscitation monitoring area for CXR

APTT, activated partial thrombin time; CXR, chest X-ray; eGFR, estimated glomerular filtration rate; NIDDM, non-insulin dependent diabetes mellitus; PT, prothrombin time

∗ Additional tests such as high-sensitivity C-reactive protein (CRP) and B-type natriuretic protein (BNP) or Pro-BNP are still being evaluated. In some settings bedside cardiac echocardiography can be valuable as it may be able to provide information on wall motion (myocardial ischaemia or infarction), ejection fraction (heart failure, systolic or diastolic dysfunction), valvular disease (aortic stenosis, acute mitral valve chordae disruption), free wall rupture, aortic or pericardial disease. Drug screening (cocaine, amphetamines) may be relevant. An alternative diagnosis of pulmonary embolism can sometimes be made when significant right heart abnormality is seen on echo.

∗∗ Elevated or rising troponin T and I measurements indicate myocardial damage and are predictors of increased risk of cardiac mortality. It may take several hours for troponin levels to rise and a series of tests may be required with an initial measurement at presentation and subsequent testing at 6 or more hours from the time of onset of the pain. Troponin may sometimes also be elevated in patients with heart failure, tachycardia, myocarditis, pericarditis or other non-ischaemic cardiac injury.

MANAGEMENT OF ACS WITH DIAGNOSTIC ECG CHANGES (STEMI)

Time-critical reperfusion therapy

Time-critical reperfusion therapy should be immediately considered when diagnostic ECG changes are present and the patient has presented within 12 hours of symptom onset. Logistics and local protocols will strongly influence the decision between percutaneous coronary intervention (PCI) and fibrinolysis, unless contraindications are present.

When PCI can be commenced within 2 hours of the onset of symptoms, this is the treatment of choice based on current evidence. The benefits of PCI over fibrinolysis are still present up to 12 hours after the onset of symptoms if PCI can be performed within a further 2 hours (including transfer times).

PCI is the preferred treatment for unstable patients or those with ongoing symptoms or evidence of failed fibrinolytic therapy on ECG, i.e. ‘rescue PCI’ (refer to the reference by Kastrati et al). This is seen as persistent (> 50% of initial) ST elevation 90 minutes after administration of the agent. Fibrinolysis can be repeated if PCI is not available. Early coronary artery bypass graft (CABG) surgery may also be considered for some patients, especially if they have an anatomy that is unsuitable for stenting or have associated cardiogenic shock, valve injury or other structural complications.

Fibrinolytic agents

Fibrin-specific bolus agents such as tenectaplase or retaplase are now the usual choices although streptokinase can be used unless the patient is an Indigenous Australian or Torres Strait Islander or has received streptokinase before.

Contraindications to fibrinolysis

Absolute—acute haemorrhage is likely to cause death or severe disability

• Current—

• Significant uncontrollable bleeding or major bleeding diathesis

• Suspected aortic dissection

• Past history—

• Any past proven intracranial haemorrhage

• Known structural cerebral vascular lesion

• Intracranial neoplasm

• Major head injury within the past 3 month

• Ischaemic stroke within the past 3 months

Relative—clinical judgement is required to gauge the relative risk, particularly if PCI may be possible, even with some delay

• Past history—

• Ischaemic stroke more than 3 months ago, dementia, other intracranial abnormality that is not an absolute contraindication

• Long-term poorly controlled hypertension

Adjunctive reperfusion therapy

Safety and resuscitation are paramount. Reperfusion confers outcome benefit, particularly aspirin and PCI or fibrinolysis. Additional therapies also convey incremental improvement, although not as marked, and will add to the risk of adverse events.

1. Give oral antiplatelet agents (aspirin, clopidogrel) as well as heparin early, whether the patient has PCI or fibrinolysis.

Note: Patients who have been given clopidogrel can still have urgent CABG surgery although this is not ideal.

2. Glycoprotein IIb/IIIa inhibitors (abciximab) are of most benefit in patients undergoing PCI.

Additional treatment

1. Optimise the heart rate. Significant bradycardia or tachycardia—associated with poor cardiac output (e.g. hypotension, syncope/presyncope heart failure or oliguria) —requires treatment with appropriate antiarrhythmics or pacing (see Chapter 12, ‘Clinical electrocardiography and arrhythmia management’). When not contraindicated, use beta-blockade.

2. Hypotension may require careful intravenous fluid volume optimisation, titration of therapeutic drugs and, in some patients, inotropes. Hypertension may resolve with analgesia (nitrates and morphine) or beta-blockers when appropriate but, rarely, if unresponsive potent agents (diazoxide, sodium nitroprusside) with close monitoring may be required.

3. Treat heart failure, if present, with diuretics, angiotensin-converting enzyme (ACE) inhibitors and other standard therapy.

4. Medical therapy (usually a statin) is now recommended for most patients with ischaemic heart disease unless contraindicated.

Although only a minority of patients (less than 6%) with chest pain associated with cocaine use will have proven cardiac myonecrosis, cocaine (a vasoconstrictor) has multiple effects that can contribute to the development of myocardial ischaemia hours or days after ingestion. Even small doses have been associated with vasoconstriction of coronary arteries, which may be more accentuated in patients with preexisting coronary artery disease. Cocaine users have been shown to have accelerated atherosclerosis as well as elevated levels of C-reactive protein, von Willebrand factor and fibrinogen. Anterior and inferior infarctions are equally likely and most are non-Q wave. Initial typical ischaemic ECG changes are relatively uncommon. In general, beta-blockers should be avoided; benzodiazepines are often used. Mortality overall is relatively low.

Table 7.3 Additional treatment in STEMI

Therapy	Dose	Comments
Oxygen	6 L (non-rebreather)	Issues (uncommon) with patients retaining CO₂
Aspirin	300 mg PO (soluble or rapidly absorbable)	True allergy or bleeding risks may contraindicate
Nitrates	SL or spray or titrated IV	Headache, flushing, hypotension may occur with higher doses
Morphine	2.5–5.0 mg IV increments	Nausea, decreased LOC and ventilation, hypotension
Metoprolol	2.5–5.0 mg IV increments	Asthma, bradycardia, heart block, other side effects and contraindications
Clopidogrel	600 mg PO loading	Increased bleeding risk
Heparin	Low-MW or unfractionated protocols	Bleeding risk, HITS
Tenectoplase	Dose per kg, max 10,000 U	Bolus
Abciximab	IV protocol	Not with fibrinolytics (or at least reduce dose)
Frusemide	40–80 mg IV	Higher doses needed if renal impairment present