Acute coronary syn.

BASIC Instructor & Provider Course, October 2008, Sydney. Registration deadline 27th September.
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Charles Gomersall and Sarah Ramsay

Spectrum of conditions which includes:

Unstable angina
Non-ST segment elevation MI (non-STEMI)
ST elevation MI (STEMI)

The syndrome is characterized by a clinical syndrome of acute ischaemic chest pain with either rest pain or a crescendo pattern of pain on minimal exertion, associated with ECG changes of ischaemia (ST elevation or depression or T inversion). STEMI is then distinguished from other forms of acute coronary syndrome (ACS) by the presence of persistent ST elevation. Patients with often present in a similar manner. The distinction between non-STEMI and unstable angina is based on the presence or absence of a rise in cardiac enzymes or troponin.

Pathophysiology

in majority of cases syndrome occurs when an atherosclerotic plaque ruptures, fissures or ulcerates and precipitates thrombus formation. This results in sudden total or near-total arterial occlusion. Alternatively thrombus may break off from a ruptured plaque and occlude a downstream vessel.
systemic factors and inflammation also contribute to alterations in haemostatic and coagulation pathways and may play a part in the initiation of the intermittent thrombosis that is a characteristic of unstable angina. Inflammatory acute phase proteins, cytokines, chronic infections and catecholamine surges may enhance production of tissue factor, procoagulant activity or platelet hyperaggregability.
in the case of Q wave infarct results in a spreading area of necrosis that reaches epicardium in 4-6 h – full thickness infarct
in rare cases may be due to coronary artery occlusion by emboli, congenital abnormalities, coronary spasm and a wide variety of systemic (particularly inflammatory) diseases
initially infarcted muscle is softened leading to an increase in ventricular compliance but, as fibrosis takes place, compliance decreases
poor correlation between angiographic severity of coronary stenosis and chance of acute occlusion
Other causes of reduced myocardial blood flow include mechanical obstruction (e.g. air embolus), dynamic obstruction (e.g. vessel spasm), and inflammation or infection.

Diagnosis

Figure 1. Investigation and treatment algorithm. If initial troponin is measured <6 h from onset of pain test should be repeated 4 h later.

STEMI

Management

NSTEMI & unstable angina

Risk stratification

Based on risk of ischaemic complications and risk of failure of medical therapy. Patients can be classified as being high, intermediate or low risk on the basis of a number of clinical features and the results of simple investigations (see table 1).

The most important risk factors are:

Acute ST depression on the presenting ECG
Elevated cardiac troponin
Advanced age
Pain at rest
Haemodynamic instability

Treatment

aspirin
- 160-325 mg of non-enteric coated aspirin to chew and swallow as soon as the diagnostic impression of ACS formed (patients presenting within 24 h). Thereafter daily oral dose indefinitely
clopidogrel
low molecular weight heparin
- enoxaparin is preferred agent
glycoprotein IIb/IIIa inhibitor
- give IV to high risk patients
- oral form contraindicated - associated with increased mortality
angiography ± revascularization for high risk patients
low and intermediate risk patients can be treated conservatively or invasively

Site of action of anti-platelet and anti-thrombotic agents

Adjunctive treatment

ACE inhibition

indicated in first 24 h for all patients who have had an episode of LV failure associated with MI, regardless of whether it persists or not or for patients with LV dysfunction or failure within 3-16 days after MI
early initiation of treatment is important because much of the survival benefit is realised in the first 48 h

ß -blockade

IV ß blockade followed by oral early after infarction decreases mortality following STEMI (ISIS 1). (However patients not given thrombolysis).
Give cardioselective ß blocker eg atenolol or metoprolol
- as soon as possible and preferably within 2 hours of ACS
- reactive airways disease and left ventricular dysfunction are not absolute contra-indications

Nitrates

no benefit demonstrated from routine use after STEMI
safe and effective for the treatment of ischaemic chest pain during and after MI
indicated for high risk non-STEMI and unstable angina patients
GTN should NOT be used within 24 hours of use of sildenafil (Viagra)

Calcium antagonists

short acting dihydropyridines, particularly nifedipine, contraindicated
no survival benefit from administration of longer acting agents or other calcium antagonists (eg diltiazem or verapamil)

Statins

reduced incidence of recurrent ischaemic events with early treatment after NSTEMI
no data related to STEMI

Differential diagnosis

aortic dissection
gastro-oesophageal disease including oesophageal rupture
musculoskeletal disease
mediastinitis

Early complications

arrhythmias
cardiogenic shock
- acute ventricular septal defect
- acute mitral regurgitation
acute pulmonary oedema
ventricular free wall rupture

Prognosis

mortality approx 8% of patients who survive to reach hospital

RV infarction

has clinical significance out of proportion to amount of muscle damage
relatively poor prognosis
? consider acute angioplasty
volume load patient despite high RV filling pressures in order to increase cardiac output