Ian Jones, BSc (Hons), RN, PGCLT, DPSN.
Lecturer in Cardiac Nursing, School of Nursing, University of Salford
Professional Nurse 2003 Jan;18(5):289-92.
Coronary heart disease remains the single biggest killer in the western world, accounting for over 135 000 deaths in the UK alone (British Heart Foundation, 2000). A number of strategies have been introduced in an attempt to reduce the mortality of this disease and the latest figures suggest that these strategies have started to have an effect (British Heart Foundation, 2002).
The results of a number of groundbreaking clinical trials have revolutionised the care that cardiac patients now receive. However, a large proportion of these studies have concentrated on the management of myocardial infarction (MI) in the acute setting and, while these developments have been crucial, the author argues that the care of a significant percentage of people suffering from other forms of unstable coronary artery disease now deserve further debate and exploration.
The following paper discusses the concept of acute coronary syndromes, highlighting their identification, classification and subsequent management, in an attempt to broaden the debate on the management of acute cardiac care.
What are acute coronary syndromes?
The term acute coronary syndrome has recently been adopted to include the three main clinical presentations of unstable coronary artery disease:- Acute ST-elevation MI (STEMI)- Non-ST-elevation MI (NSTEMI replaces the more traditional terms of non-Q-wave MI or sub-endocardial MI)- Unstable angina (Fox, 2000).The reason for this umbrella term is that it is now accepted that the three conditions share a very similar pathology. Unstable angina occupies the beginning of this spectrum, causing disability and a risk greater than stable angina but less than that of NSTEMI (Braunwald et al, 1994); although NSTEMI for many years was thought to have a similar prognosis to unstable angina some studies indicate that the prognosis for this group is similar to STEMI (Aguire et al, 1995; Zareba et al, 1994), which occupies the end of the spectrum.
The terminology used to classify MI relates to the presence, or not, of ST-segment elevation on an electrocardiograph (ECG). The presence of such ECG changes often indicate prolonged coronary artery occlusion, which initially causes acute myocardial injury and, if left untreated, progresses to infarction. However, transient occlusion of a coronary artery can also lead to small areas of MI without elevation of the ST segments being noted on a 12-lead ECG. This may be due to spontaneous re-cannulisation of the artery before the ECG is recorded. However, the use of more sensitive and specific biochemical markers and precise imaging techniques mean that patients with small areas of MI are now more likely to be diagnosed correctly (Joint European Society of Cardiology/American College of Cardiology (JESC/ACC), 2000).
Pathophysiology of coronary heart disease
To understand acute coronary syndromes it is necessary to appreciate the underlying pathophysiology of coronary heart disease and how progression can occur. The term coronary heart disease is used to describe ‘the effects of a reduction or complete obstruction of the blood flow through the coronary arteries as a result of narrowing (atherosclerosis) or a blood clot (thrombus)’ (Quinn et al, 2002). Atherosclerosis occurs as a result of the lining of the artery becoming penetrable to lipids and, over time, altering the integrity of the vessel (Todd, 1997). This disease process is characterised by raised fatty plaques protruding into the arterial lumen. The plaques themselves are composed of a combination of a lipid core and a fibrous cap.
Plaques that have a small lipid core tend to produce larger but more stable lesions. Conversely, plaques that consist of a larger lipid mass tend to be unstable and have an increased propensity to rupture (Libby, 1995). There have been many theories on the origin of atherosclerosis but the most accepted hypotheses are: damage to the arterial wall, lipid infiltration and monoclonal ageing (Dinarevic, 1984). A number of factors are thought to contribute to the progression of the disease, including infection (Cheng and Rivera, 1998), increased cholesterol levels (Pekkanen et al, 1990), hypertension (Kannel, 1990) and cigarette smoking (Daly et al, 1983).
Pathophysiology of acute coronary syndromes
Acute coronary syndromes share a common anatomical substrate (Bertrand et al, 2000) and occur as a result of the rupture or erosion of the atheromatous plaque (Forrester, 2000). Disruption of the plaque wall initiates a clotting mechanism with subsequent thrombus formation. Such a rapid change in the shape of the plaque may result in total or partial occlusion of the artery.In unstable angina a small fissuring of an atheromatous plaque leads to a change in plaque geometry and coronary flow resulting in exacerbation of angina (Fuster et al, 1992a; 1992b).
A platelet-rich thrombosis at the site of plaque rupture may occur (Figure 1), resulting in temporary occlusion or partial occlusion of the affected artery lasting around 10 to 20 minutes. This temporary occlusion results in areas of surrounding myocardium becoming ischaemic, which may transpose onto the ECG as ST-segment depression and/or abnormalities of the T wave. Unfortunately, even in the acute phase a percentage of people will present with a normal ECG (JESC/ACC, 2000).
In NSTEMI more severe plaque damage occurs, resulting in thrombus formation and coronary occlusion for up to one hour (Fuster et al, 1992a; 1992b). If coronary blood flow is obstructed for longer than 20 minutes then a growing area of cell necrosis develops in the affected part of the muscle (Figure 2). However, at this point it may not affect all the muscle layers (Quinn et al, 2002), hence the term partial thickness MI. Once again the ECG recorded may show abnormalities of the T wave and/or ST-segment depression.In STEMI larger plaque fissures result in the formation of a fixed and persistent thrombus (Fuster et al, 1992a; 1992b).
The clot formed will by now consist of the original platelet plug but, in addition, a fibrin mesh will also have trapped red blood cells (Figure 1). This leads to coronary occlusion in excess of two hours (unless thrombolysis occurs) resulting in trans-mural or full-thickness MI (Willerson et al, 1986) (Figure 2). This injured tissue is represented on an ECG as ST-segment elevation. After a period of time any resultant necrotic area manifests itself by the formation of deep Q waves on the ECG.
Diagnosis of acute coronary syndrome
Theoretically, diagnosis of acute coronary syndrome can be made either prospectively or retrospectively. A diagnosis of acute evolving MI can be made when the patient presents with one of the following criteria:- Typical rise and gradual fall (troponin) or more rapid rise and fall (CK-MB) of biochemical markers of myocardial necrosis with at least one of the following:- ischaemic symptoms, for example chest pain- development of pathological Q waves on ECG- ECG changes indicative of ischaemia (ST segment elevation or depression) or- Coronary artery intervention- Pathologic findings of an acute MI (JESC/ACC, 2000).However, while these criteria are comprehensive, they may be used only in retrospect. Biochemical markers can take several hours to be released into peripheral blood and, in reality, due to the critical nature of the illness, every attempt is made to determine a working or provisional diagnosis on presentation. The ECG is used in the acute phase to aid diagnosis and assist in risk stratification.Diagnosis of acute STEMI
In a healthy subject the ST segment of an ECG complex will be located on the baseline. However, the position of the ST segment may alter in the presence of ischaemia, injury and/or infarction. Prolonged obstruction of a coronary artery can lead to the ST segment becoming elevated above the baseline; during ischaemia the ST segment may fall below the baseline. This movement of the ST segment guides the clinician towards a diagnosis, while confirmation, utilising biochemical markers, is awaited (Figure 3).A diagnosis of acute STEMI is suspected if the ST segment is elevated in excess of:- 1mm in two or more consecutive limb leads or- 2mm in two or more consecutive chest leads or- New left bundle branch block (JESC/ACC, 2000).Patients who present in the acute stages with a STEMI should (as long as no contraindications exist) receive thrombolytic therapy in an attempt to dissolve the fibrin-rich clot. If ST elevation is not present on the ECG then thrombolysis is not indicated (Fibrinolytic Therapy Trialists’ Collaborative Group, 1994).Diagnosis of unstable angina
A diagnosis of unstable angina is essentially a clinical one, made on the basis of a clinical history and ECG (Unstable Coronary Artery Disease Council, 1998). A normal ECG does not exclude unstable angina but the following all support the diagnosis:- ST-segment depression >0.5mm- Transient ST-segment elevation >1mm- T-wave inversion (Unstable Coronary Artery Disease Council, 1998).Patients with unstable angina are at high risk of MI and death (Hamm et al, 1992). Indeed, patients who present with >1mm ST depression on their ECG have a high early mortality rate (Antman et al, 1996; Holmvang et al; 1998). Hyde et al (1999) even argue that as little as 0.5mm of ST elevation can reduce a patient’s long-term survival rate. In order for the clinician to ensure patients are given appropriate care there is a need for risk stratification.
Diagnosis of acute NSTEMI
When the patient presents in the acute stage it can be extremely difficult to distinguish between a NSTEMI and unstable angina. The presenting symptoms and ECG patterns are often identical. Only when biochemical markers are raised can the clinician confidently diagnose a NSTEMI. Therefore the treatment options and risk stratification are identical in the acute stage.
Risk stratification in acute coronary syndromes
Unfortunately, the treatment for unstable angina/NSTEMI is rather more complex than the treatment for STEMI because of the heterogeneous nature of the group. In STEMI the gold standard is the dissolution of a persistent thrombus by the use of thrombolytic therapy (ISIS II, 1988). Unfortunately, these drugs have been shown to be ineffective and in some cases harmful when given to patients without ST elevation (Boden et al, 1998).
Patients with unstable angina are categorised into order of risk. These categories are important for the choice of pharmacological and interventional treatment as the relation between risks and outcome have been defined in a number of clinical trials (Fox, 2000). These risk groups have been developed following the study of a number of databases and the outcomes of patients within these databases (Boersma et al, 2000; Savinotto et al, 1999).
Some drugs are available to all patients regardless of categorisation, for example aspirin, whereas other drugs, such as GPIIb/IIIa inhibitors and indeed other forms of therapy, may be prescribed only to the more high-risk groups. A number of risk stratification formulae are available from the databases and share common themes including age (Boersma et al, 2000), severity of ST depression (Boersma et al, 2000; Cannon et al, 1995; GUSTO IIB, 1996), elevated troponins (Hamm et al, 1998; Lindahl et al, 1997), heart failure (Boersma et al, 2000), prior coronary heart disease (Boersma et al, 2000; GUSTO IIB, 1996) and diabetes (Antman et al, 2000).
Risk status requires regular review as a patient’s condition changes or their risk status changes in light of new information such as cardiac enzymes (Fox, 2000). One such risk stratification formula is that devised by the European Society of Cardiology (2000) (Figure 4).
In the past 20 years there has been an explosion in the number of therapies available for patients with acute STEMI. Nurses have been at the forefront of these developments in acute coronary care and A&E. The debate now needs to move forward to consider other groups of cardiac patients with similar mortality figures in order to provide a more equitable service.
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