Dr Martin Day ( left ) Basic physician trainee , Concord Repatriation General Hospital , Concord , NSW .

Professor David Brieger ( right ) Head of cardiology , Concord Repatriation General Hospital , Concord , NSW .

First published online on 7 July 2023

BACKGROUND

ACUTE coronary syndrome ( ACS )

is defined as a sudden reduction in the blood supply to the heart , most commonly due to thrombotic atherosclerotic coronary disease . ACS is an umbrella term that encapsulates a continuum of coronary presentations with varying degrees of severity . These include ST-elevation myocardial infarct ( STEMI ), non-ST elevation myocardial infarction ( NSTEMI ) and unstable angina .

ACS has a significant impact on Australia ’ s health system and on the general population . The Australian Institute of Health and Welfare ( AIHW ) reports that an estimated 580,000 Australians have had coronary heart disease ( CHD ) at some time in their lifetime . 1 In 2018-19 there were 161,000 hospitalisations for CHD , with the condition the primary cause of death in 17,700 individuals ( representing 11 % of all deaths ) in 2019 . 1

Given its scope , it is vital that GPs are familiar with both the acute management and long-term care of those with ACS , as this condition is almost certain to feature within their spectrum of practice . The National

Heart Foundation of Australia and Cardiac Society of Australia and New Zealand released clinical guidelines relating to the management of acute coronary syndromes in 2016 . 2 These guidelines are currently being updated and should be available in the first quarter of 2024 .

This How to Treat draws on the latest local and international recommendations in the hope of familiarising GPs with the management of ACS . It focuses on the acute presentations of chest pain , indications for referral to hospital , which patients require biochemical testing ( that is , a troponin ), and longterm antiplatelet therapy . The article aims to ensure GPs can identify ACS and refer and manage patients appropriately .

AETIOLOGY

ACS represents a continuum of disease ; a STEMI is the result of a complete coronary artery occlusion , while an NSTEMI is caused by partial or intermittent occlusion of the artery . STEMIs represent 30 % of ACS , with NSTEMIs representing a further 25 % ( older data ). 3 The underlying pathogenesis of the ACS is

the development of atherosclerotic plaque ( see figures 1 and 2 ) within the coronary vasculature .

Risk factors implicated in the development of coronary artery disease ( CAD ) may be broadly categorised into traditional and additional . Traditional risk factors include older age , diabetes mellitus , hypertension , hypercholesterolaemia , obesity , smoking and family history of premature coronary disease . 4 , 5 Additional risk factors include chronic inflammatory conditions like rheumatoid arthritis , HIV / AIDS , chronic kidney disease , non-alcoholic fatty liver disease , mental health disorders , ethnicity and a history of premature menopause or high-risk conditions during pregnancy such as pre-eclampsia .

Community medicine and general practice form the critical task force for the primary prevention of CAD through appropriate risk factor modification .

PATHOPHYSIOLOGY

IT is well established that the development of atherosclerosis takes many decades , but the clinical consequences of the disease ( thrombosis

and acute ischaemia ) occur suddenly and potentially fatally . Progressive advancements in cross-sectional imaging have allowed greater appreciation of the pathology associated with disease progression .

Ultrasonography and CT angiography have demonstrated that outward expansion of atherosclerotic arteries accommodates for the growth of plaque , and subsequently luminal narrowing occurs relatively late in the disease process . 6

At this point , the growth of the plaque occurs at a capacity greater than that at which the artery can compensate . This helps explain why some patients do not present with the typical symptoms of angina before plaque rupture .

There are two major mechanisms by which atherosclerotic plaque can lead to acute thrombosis . First , rupture of a thin fibrous cap , and second , superficial erosion of the intimal surface . 6 Inflammatory pathways have been recognised as important drivers in both processes . The accumulation of LDL particles within the intima of the arterial wall has been identified as a major antigenic factor in the propagation of an