Acute coronary syndromes

Introduction

Acute coronary syndrome (ACS) is the most common life-threatening condition in emergency medicine. Failure to identify and treat it promptly risks avoidable morbidity and mortality.

The spectrum of disorders comprised by ACS is represented in Fig. 5.2.1 . They range from the acute myocardial infarction (AMI) patterns of ST elevation acute myocardial infarction (STEMI) to non–ST-elevation elevation acute myocardial infarction (NSTEMI) and non–ST-elevation elevation ACS (NSTEACS), which broadly includes both NSTEMI and unstable angina (UA). A new left bundle branch block (LBBB) with the diagnosis of AMI may be categorized as STEMI, as this condition requires the same treatment pathway. AMI is defined in pathological terms as myocardial cell death due to prolonged ischaemia.

Box 5.2.1 contains the Third Universal Definition of Myocardial Infarction. It is worth noting the breadth of the current diagnostic spectrum in the age of high-sensitivity biomarkers.

See Chapter 5.1 for a more detailed description of the process of diagnosis and risk stratification for possible ACS.

Patients presenting with possible ACS should undergo formal risk stratification and receive further care guided by a suspected ACS-AP. An example of this can be found at: https://www.heartfoundation.org.au/images/uploads/publications/Assessment_protocol_for_suspected_ACS_using_a_highly_sensitive_lab-based_assay-2016.pdf . Suspected ACS-APs use a combination of validated risk-stratification tools (such as TIMI (Thrombolysis in Myocardial Infarction) or HEART (History, ECG, Age, Risk factors, Troponin) score), with electrocardiograph (ECG) and biomarker features to determine an appropriate clinical pathway for the patient. This includes repeat cardiac biomarker testing, safe disposition and outpatient investigation. Pathways such as the ADAPT (2-hour accelerated diagnostic protocol) have demonstrated a negative predictive value (NPV) of greater than 99% for major adverse cardiac events (MACE), and enable the identification of patients who are suitable for early discharge. Emergency departments should develop their suspected ACS-APs in collaboration with their cardiology and laboratory colleagues.

With regard to risk factors for ischaemic heart disease (IHD), both clinicians and patients are generally aware of those derived from the Framingham study ; these also feature in the aforementioned risk-stratification tools and therefore in many suspected ACS-APs. There is increasing evidence demonstrating the association between human immunodeficiency virus (HIV) and IHD, so this information should also be sought from the patient presenting with possible ACS.

Table 5.2.1 summarises evidence-based recommendations on the assessment and treatment in suspected and confirmed ACS.

Pathology

ACS is nearly always caused by a coronary artery atheroma or disruption of its endothelial layer resulting in thrombotic occlusion, which impairs blood flow and myocardial oxygen delivery. This occlusion leads to myocardial ischaemia or infarction depending on a number of factors including duration and extent of occlusion, myocardial oxygen demand and antecedent physiological conditions such as anaemia and circulating catecholamine levels.

The nature of the presentation reflects the pathophysiology of the coronary occlusion. Many people have coronary atheromas but are asymptomatic because it is not extensive enough to occlude coronary blood flow. Others have a degree of coronary occlusion that does not cause symptoms unless myocardial oxygen demand is increased by exertion or acute illness. Fissuring or rupture of a coronary atheroma leading to rapid vessel obstruction and STEMI may present with the classic presentation of AMI, with a sudden onset of severe crushing chest pain. Cardiac chest pain that occurs in a fixed and predictable pattern of exertion and is rapidly relieved by rest is known as stable angina and is not classified as an ACS.

Not all coronary artery occlusion is due to an atheroma. Prinzmetal or variant angina is a syndrome in which myocardial ischaemia is associated with coronary artery spasm; it is characterized by transient ST-elevation on the ECG and may be seen in cocaine use. Coronary angiography may show a minor atheroma or normal coronary arteries.

Other rare causes of coronary artery occlusion include Kawasaki disease, in which occlusion is due to inflammation in the coronary artery, aortic dissection that involves the ostia of the coronary arteries—in particular the right coronary artery (RCA)—and spontaneous coronary artery dissection.

The anatomical location of coronary artery occlusion in ACS determines the clinical presentation, ECG findings and likelihood of complications. The most common site for myocardial infarction (MI) is the anterior or antero-septal region. It usually results from occlusion of the left anterior descending (LAD) artery and has a worse prognosis than other types of MI; complications are also more common, including sudden cardiac death. Lateral infarction is usually caused by occlusion of the circumflex artery or the diagonal branch of the LAD artery. Inferior MI is usually caused by occlusion of the RCA or the circumflex artery. It has a better prognosis than anterior infarction, and ventricular dysfunction is less likely, although heart block due to involvement of the atrioventricular node is more common. Posterior infarction is usually due to occlusion of the RCA or, less commonly, the circumflex artery in patients with dominance of the left coronary circulation. Posterior or inferior MI may result in right ventricular (RV) infarction, leading to RV failure. Further details are provided in the sections titled Investigations and Complications.

The Third Universal Definition of Myocardial Infarction describes five categories of MI ( Box 5.2.2 ). Types 1 and 2 are most relevant to the ED setting.

Epidemiology

Although coronary heart disease (CHD) mortality rates have declined over the past four decades in western countries, this condition remains responsible for about one-third of all deaths in individuals over age 35. Nearly half of all middle-aged men and one-third of middle-aged women in the United States will develop some manifestation of CHD.

In Australia,

• The age-standardized rate for acute coronary events is twice as high in men as in women; the rate of acute coronary events increases rapidly with age, with the rate among the 85-and-over age group (3005 per 100,000 population) more than three times that for the 65-to-74 age group (854 per 100,000 population) and six times the rate for the 55-to-64 age group (502 per 100,000 population).

• The rate of acute coronary events fell by 24% from an age-standardized rate between 2007 and 2012.

Clinical features

Clinical assessment of suspected ACS is described in detail in Chapter 5.1 , and Table 5.1.2 details the features on clinical assessment that have the most discriminatory value in diagnosing ACS. In short, patients presenting with chest pain radiating to the right or both shoulders, diaphoresis, dyspnoea, vomiting or pain, as in a previous MI, are more likely to have ACS, and those with pleuritic pain or pain that is reproducible to palpation are less likely. Note that no single assessment feature is particularly useful in ACS diagnosis.

Clinical assessment of cardiac pain is required to distinguish between stable angina and ACS. Stable angina is characterized by pain that is predictable, precipitated by exertion, relieved promptly by rest or glyceryl trinitrate (GTN) and is not becoming more frequent or severe. The symptoms of UA, a form of ACS, are unpredictable or occur with increasing severity or decreased effort. It is useful to grade the level of exertion a patient needs to experience angina symptoms so as to assist in the diagnosis of UA; the New York Heart Association (NYHA) grading is commonly applied ( Table 5.2.2 ), although its original use was in the description of dyspnea relating to heart failure.

Clinical examination is generally unhelpful in making the diagnosis of ACS, which should be based on clinical history and investigations. However, clinical examination is essential to identify complications of ACS and to rule out differential diagnoses. Heart failure may be identified by poor peripheral circulation, tachycardia, pulmonary crepitations, elevated jugular venous pressure and a third heart sound on cardiac auscultation. The additional finding of hypotension may suggest cardiogenic shock. A systolic murmur raises the possibility of papillary muscle rupture or ventricular septal defect secondary to MI, although pre-existing aortic or mitral valve disease are much more common.

Differential diagnosis

Alternative diagnoses and their differentiation from ACS are described in Chapter 5.1 . The most potentially serious alternative diagnoses are pulmonary embolus and aortic dissection. These should be considered in all patients presenting with atraumatic pain between the jaw and upper abdomen.

Clinical investigations

The ECG is the critical test to perform on patients with suspected ACS and should be undertaken and interpreted by a clinician within 10 minutes of the patient arriving. If there is uncertainty over interpretation, senior assistance should be sought immediately. Repeating the ECG as the patient’s clinical picture evolves is important, and again, once the patient is pain-free to examine for Wellen syndrome.

The diagnostic criteria of a STEMI are a clinical history of typical chest discomfort or pain of greater than 20 minutes duration (which may have resolved by the time of presentation) and ECG criteria with persistent (>20 minutes) ST elevation in ≥2 contiguous leads of:

• ≥2.5 mm ST elevation in leads V2–V3 in men under 40 years, or

• ≥2.0 mm ST elevation in leads V2–V3 in men over 40 years, or

• ≥1.5 mm ST elevation in V2–V3 in women, or

• ≥1.0 mm in other leads, or

• Development of new onset LBBB.

With regard to new LBBB, diagnosis can often be challenging due the need to access prior ECGs and patient records. The Sgarbossa criteria can assist the diagnosis of STEMI in the setting of prior LBBB or when it is not known if the observed LBBB is new. They are:

• ST elevation ≥1 mm concordant with QRS (5 points);

• ST depression ≥1 mm in leads V1–V3 (3 points); and

• ST elevation ≥5 mm discordant with the QRS (2 points).

Three or more points is 90% specific for MI, but only 36% sensitive. The modified Sgarbossa criteria perform better, and replace ST elevation ≥5mm discordant with the QRS with ST elevation to S-wave depth (ST/S ratio) of ≤0.25. In diagnostically difficult cases, an echocardiogram can be performed to assess for regional wall motion abnormalities and specialist opinion can be sought on the need for urgent revascularization. These criteria can also be applied to those who have ventricular pacing.

The location of ischaemic changes on ECG reflects the anatomy of the affected coronary vessel. LAD artery typically produces anteroseptal changes, left circumflex (LCx) artery anterolateral changes, RCA inferior changes and the posterior descending artery (PDA)—which may arise from either the LCx or the RCA—resulting in posterior changes.

The presence of anterior ST depression with prominent R waves in the right precordial leads should prompt consideration of a posterior MI, and a posterior ECG should be performed accordingly. Inferior MI with ST elevation greater in III than II may indicate RV infarct. These complicate up to 40% of inferior STEMIs and render the patient highly preload sensitive and at risk of hypotension, particularly in response to GTN. Other findings in RV infarct include ST elevation in V1 (especially with ST depression in V2) and ST elevation in V1 > V2. Performing right-sided leads will demonstrate V4R abnormality, with ST elevation of greater than 1 mm being 100% sensitive and 87% specific for RV infarction.

De Winter sign and Wellens syndrome are two eponymous characteristic ECG findings in proximal LAD occlusion. De Winter sign or de Winter T waves describe an upsloping ST depression in leads V1–V6 with associated symmetrical and prominent T waves, often with ST elevation in aVR. Wellen’ syndrome is perhaps even more fascinating, as the characteristic biphasic (type A) or deeply inverted (type B) T wave inversion is typically only seen when the patient is pain free, and often cardiac biomarkers are normal. Both entities should be considered as STEMI equivalents with regards to management.

There are many other ECG findings that may be seen in ACS, not forgetting that ECG may also be completely normal or benign in appearance. Less specific ECG features which suggest ACS include peaked or hyperacute T waves, T wave inversions or biphasic T waves, loss of R wave progression and pathological Q waves.

The ECG should also be inspected for the consequences of MI, such as conduction blocks and dysrhythmias and antecedent factors such as left ventricular (LV) hypertrophy associated with hypertension.

Other ECG changes may be useful in diagnosing AMI and are described in Chapter 5.1 and Table 5.1.2.

Biochemical markers are discussed in detail in Chapter 5.1 . Their role is to identify patients with probable ACS and to rule out ACS if negative. However, it should be remembered that a negative cardiac biomarker, even high sensitivity troponin (hsT) performed within an optimal time frame, does not exclude underlying coronary vascular disease.

Outpatient functional and anatomical testing is discussed in Chapter 5.1 . Institution specific variability in the choice of further cardiac testing reflects the mixed evidence in this area, and should prompt the reader to familiarize themselves with their local practice.

Treatment

All patients with possible ACS should be assessed and observed in an environment which permits physiological monitoring, repeat ECGs and access to advanced resuscitation equipment. The workup and treatment for ACS should occur in parallel to minimize potential delays.