Emergency Cardiology

Karim Ratib, Gurbir Bhatia, Neal Uren, James Nolan

• Publisher: CRC Press
• Year: 2010
• ISBN:
  9781000218763
• Edition: 2
• Topic: Medizin
• Subtopic: Notfallmedizin & Intensivmedizin

This fully revised and updated second edition offers practical advice on the diagnosis and management of acute cardiac conditions. Throughout the book, the authors employ an evidence-based approach to clinical practice and provide detailed guidance for day-to-day practice in a wider variety of settings-from the emergency department to intensive care and the cardiac ward. Authored by four cardiologists with extensive experience in the emergency setting, it includes the results of the most groundbreaking clinical trials. Topics include arrhythmias, acute aortic syndromes, pericarditis, and cardiac trauma.

CHAPTER 1

ACUTE CORONARY SYNDROMES

Epidemiology

Definitions

Pathophysiology

Diagnosis

Initial treatment

Treatment of ST elevation MI

Primary PCI

Thrombolysis

Treatment of non-ST elevation ACS

Risk score s in NSTEACS

Revascularization strategies in NSTEACS

Bleeding risk in ACS

Adjunctive medical therapy

Complications of ACS

Early peri-infarction arrhythmias

Late post-infarction arrhythmias

Recovery and rehabilitation

Key points

Key references

EPIDEMIOLOGY

Coronary heart disease is the most common cause of death in the United Kingdom. In total, 220 000 deaths were attributable to ischaemic heart disease in 2007. It is estimated that the incidence of acute coronary syndrome (ACS) is over 250 000 per year.

Sudden death remains a frequent complication of ACS: approximately 50 per cent of patients with ST elevation myocardial infarction (STEMI) do not survive, with around two-thirds of the deaths occurring shortly after the onset of symptoms and before admission to hospital. Prior to the development of modern drug regimes and reperfusion strategies, hospital mortality after admission with ACS was 30–40 per cent. After the introduction of coronary care units in the 1960s, outcome was improved, predominantly reflecting better treatment of arrhythmias. Current therapy has improved outcome further for younger patients who present early in the course of their ACS. The last decade has seen a significant fall in the overall 30-day mortality rate. Most patients who die before discharge do so in the first 48 hours after admission, usually due to cardiogenic shock consequent upon extensive left ventricular damage. Most patients who survive to hospital discharge do well, with 90 per cent surviving at least 1 year. Surviving patients who are at increased risk of early death can be identified by a series of adverse clinical and investigational features, and their prognosis improved by intervention.

DEFINITIONS

The term ‘acute coronary syndrome’ (ACS) has been developed to describe the collection of ischaemic conditions that include a spectrum of diagnoses from unstable angina (UA) to non-ST elevation MI (NSTEMI) and STEMI. Patients presenting with ACS can be classified into two groups according to their electrocardiogram (ECG) (Figure 1.1): those with persistent STEMI and those without (non-ST elevation ACS or NSTEACS). The treatment of STEMI requires emergency restoration of blood flow within an occluded culprit coronary artery. Patients presenting with NSTEACS often have ECG changes including T-wave inversion, ST depression or transient ST elevation, although occasionally the ECG may be entirely normal. This group can be classified further according to the presence of detectable levels of cardiac proteins, troponins, in patients’ serum (see below). Thus, NSTEACS patients with undetectable cardiac troponins (UA) are distinguished from those in whom myocardial ischaemia is severe enough to cause myocardial necrosis, leading to troponin release into the circulation (NSTEMI). Detection of cardiac troponin following ACS is a strong predictor of recurrent ischaemia. However, it should be remembered that patients with UA are still at increased risk of further events, especially those with pain at rest or dynamic ST changes on their ECG.

Figure 1.1 Definition, diagnosis and management of ACS.

Myocardial infarction can also be classified with regards to underlying aetiology as defined by the European Society of Cardiology:

Type 1 Spontaneous myocardial infarction related to ischaemia due to a primary coronary event such as plaque erosion and/or rupture, fissuring or dissection.

Type 2 Myocardial infarction secondary to ischaemia due to either increased oxygen demand or decreased supply, e.g. coronary artery spasm, coronary embolism, anaemia, arrhythmias, hypertension or hypotension.

Type 3 Sudden unexpected cardiac death, including cardiac arrest, often with symptoms suggestive of myocardial ischaemia, accompanied by presumably new ST elevation, or new LBBB, or evidence of fresh thrombus in a coronary artery by angiography and/or at autopsy, but death occurring before blood samples could be obtained, or at a time before the appearance of cardiac biomarkers in the blood.

Type 4a Myocardial infarction associated with PCI (percutaneous coronary intrervention).

Type 4b Myocardial infarction associated with stent thrombosis as documented by angiography or at autopsy.

Type 5 Myocardial infarction associated with CABG (coronary artery bypass graft).

PATHOPHYSIOLOGY

ACSs are caused by an imbalance between myocardial oxygen demand and supply that results in cell death and myocardial necrosis. Primarily, this occurs due to factors affecting the coronary arteries, but may also occur as a result of secondary processes such as hypoxaemia or hypotension and factors that increase myocardial oxygen demand. The commonest cause is rupture or erosion of an atherosclerotic plaque that leads to complete occlusion of the artery or partial occlusion with distal embolization of thrombotic material.

Atherosclerosis is a disease of large and medium-sized arteries, affecting predominantly the arterial intima. The precise mechanism responsible for the generation of atherosclerotic arterial disease remains open to debate, but it is likely that arterial endothelial injury is an initiating factor. It is clear that the extent and stability of atherosclerotic lesions is influenced by the common riskfactors of smoking, hypertension, hyperlipidaemia and diabetes. There are a large number of other modifiable risk factors, such as homocysteine, oxidative stress, fibrinogen and psychosocial factors, which may play an important role in atherogenesis in some individuals. Individual susceptibility to the adverse effects of riskfactors may relate to genetic predisposition.

Atherosclerotic plaques are complex structures consisting of a fibrous cap and a core of lipid, connective tissue and inflammatory cells. The morphology of plaques is variable, and those with a thin fibrous cap, a large lipid core and an increase in inflammatory activity are highly unstable. An increase in inflammatory activity within plaques may be triggered by systemic infections (Chlamydia, cytomegalovirus (CMV), Helicobacter or chronic dental sepsis) or stimuli such as stress, severe exercise and temperature change. ACS is initiated when the fibrous cap of an unstable atherosclerotic lesion ruptures (in 75 per cent of cases) or the overlying endothelium erodes (in 25 per cent of cases). Plaque erosion is more common in females. Both mechanisms expose highly thrombogenic subendothelial and core components of the unstable plaque to the blood, leading to localized platelet adhesion, activation of the clotting mechanism, and formation of an intraluminal thrombus that occludes the coronary artery. Prior to plaque rupture or erosion, other conformational changes may occur as a result of endothelial injury. This causes a proliferation of smooth muscle cells leading to a reduction of the luminal diameter, which increases shear stress, and causes further endothelial injury. Intravascular ultrasound studies have confirmed that unstable coronary plaques are associated with more expansive arterial remodelling compared to stable coronary lesions, which may imply a more marked recent progression in extent and severity of plaque at the site of rupture/erosion. Angiographic and intravascular ultrasound studies of culprit lesions have demonstrated complex eccentric morphology consistent with ruptured plaque and superimposed thrombus. Vulnerable plaques that fissure or rupture are characterized by large eccentric lipid pools with foam cell infiltration and tend to rupture at the border of the fibrous cap and adjacent normal intima. This weakness in the integrity of the plaque is initiated by matrix metalloproteinases secreted by macrophages, and ultimately rupture occurs through an acute change in wall shear stress.

The lipid core is a potent substrate for platelet-rich thrombus formation with the initiation of the coagulation cascade through the interaction of tissue factor with factor VIIa. Platelet adhesion to subendothelial collagen through the release of tissue factor and the expression of the vitronectin (α_vβ₃) receptors leading to platelet activation and aggregation through the expression of the glycoprotein IIb/IIIa receptor is an important event in the development of thrombus. Platelet-rich thrombus is associated with cyclical reductions in coronary blood flow with additional coronary vasoconstriction resulting from endothelial disruption, and thromboxane A₂ (TXA₂) and serotonin production leading to reduced nitric oxide (NO) production. Inflammatory acute phase proteins, cytokines and systemic catecholamines stimulate the production of tissue factor, procoagulant activity and platelet hypercoagulability.

A number of factors that can trigger the onset of ACS have been identified, acting by initiating plaque rupture or promoting thrombus formation. Some patients report heavy physical exertion or mental stress shortly before the onset of ACS. Circadian variation in coagulation and autonomic nervous system activity contribute to an increased incidence of ACS in the morning. Irrespective of this, the risk of an individual episode of exercise or stress precipitating the onset of ACS is low, and most episodes have no identifiable direct triggers.

Other non-athersclerotic causes for ACS include arteritis, trauma, spontaneous coronary dissection, thromboembolism, cocaine use and congenital abnormalities such as anomalous coronary arteries. Patients who present as a result of these rare causes will usually not have the classical risk factors associated with atherosclerosis; typically the diagnosis is not established until after coronary angiography.

Acute STEMI usually results from total occlusion of a coronary artery, with subsequent myocardial cell necrosis occurring in as little as 15 minutes. Continued occlusion results in a wavefront of necrosis spreading from the subendocardium to the subepicardium. The amount of myocardial injury depends on the duration of occlusion, the presence of collateral blood flow and the degree of preconditioning of the myocytes to ischaemia. In animal models, persistent occlusion of a coronary artery will usually result in complete infarction of the area subtended after 6 hours. Subendocardial and full thickness or transmural mycocardial infarction can be well demonstrated with cardiac magnetic resonance imaging (MRI) using late gadolinium enhanced images. These images correlate well with macroscopic histological findings.

NSTEACS are usually associated with partial or transient occlusion of the coronary artery that may result in ST depression or T-...