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4 Multislice CT in Coronary Heart Disease KCE Reports 82 1 SCOPE This Health Technology Assessment (HTA) report summarises current evidence supporting the use of multi slice computed tomography (MSCT) as a diagnostic aid in patients suspected for coronary artery disease (CAD). The technique has been available since 1998 but underwent substantial technical improvements during the last few years. Originally, MSCT systems were capable of acquiring only 4 sections of the heart simultaneously but in 2004, 64-slice devices were introduced on the market and have been studied in several diagnostic trials since. In 2006, the first trials using dual-source 64-SCT scanners were published and in 2007, 256- and 320-slice devices became available. Because of an increasing penetration of recent generation scanners into the radiological realm, and several trials being completed with them, this report will focus on the performance of 64 (or more) slices CT scanners. Computed tomography in evaluating CAD can be used (1) for risk stratification by assessing calcification of coronary arteries and (2) if coupled with intravenous contrast administration, as a diagnostic imaging technique to obtain a noninvasive coronary angiogram. This report does not address the use of MSCT for risk profiling based on calcium scoring, but is primarily concerned with the diagnostic use of MSCT as an imaging technique for native coronary arteries, by which coronary bypass grafts and intracoronary stents are excluded. Our major interest lies in the diagnosis of CAD in a population with no known heart disease, where an increase of the use of MSCT in the years to come is expected to be high. MSCT for screening in asymptomatic populations does not fall into the scope of the current report. No assessment was done of the diagnostic performance of MSCT in chest pain originating from extra-cardiac disease, such as pulmonary embolism, dissecting aneurysm of the aorta, or pleural effusion. Key point • This review is primarily concerned with the use of 64-SCT as an imaging technique for the diagnosis of obstructive CAD in native coronary arteries.
KCE Reports 82 Multislice CT in Coronary Heart Disease 5 2 BACKGROUND 2.1 CORONARY HEART DISEASE 2.1.1 Pathophysiology Coronary heart disease (CHD) or coronary artery disease (CAD) refers to any cardiac disease caused by an impaired blood flow and deficient oxygen supply to the myocardium, due to atheromatous narrowing of the coronary arteries. It is one of the main causes of mortality and morbidity in Western countries. It can be manifested by stable angina pectoris, acute coronary syndromes (ACS) - including myocardial infarction (MI) and unstable angina -, or sudden death. Loss of myocardial tissue due to MI can lead to heart failure and it can constitute the anatomical basis for arrhythmias, leading to “sudden death”. Cardiac disease may also be related to high blood pressure, valvular dysfunction, congenital abnormalities, primary cardiac muscle problems, or other rarer conditions. These are not part of the disease spectrum of CHD. Two separate arteries carry oxygenated blood to the heart muscle: the right and the left coronary artery. The first part of the left coronary artery, known as the “left main stem”, shortly after its origin divides into two branches: the circumflex artery (Cx) and the left anterior descending artery (LAD). Because the two branches of the left coronary artery are generally considered separately in clinical practice, it is common to refer to three coronary arteries instead of the anatomically more correct “two”. Depending on whether one, two or three coronary arteries are significantly involved in the atheromatous proces, the labels single, double, or triple vessel disease are attributed. Due to its prognostic significance, if the left main stem is involved in the atheromatous process in a given patient, it is stipulated as such. The underlying mechanism of CAD is a gradual build-up of fatty material into the coronary vessel wall that leads to the formation of atheromatous plaques. The pathophysiological mechanisms leading to stable angina pectoris or an ACS are different. It is traditionally accepted that a plaque has to reduce the internal diameter if a vessel by at least 50% (or >75% reduction in cross sectional area), in order to reduce blood flow through the coronary artery during exertion and provoke ischemia and angina pectoris. ACSs on the other hand result from a sudden blockage of coronary blood flow, due to rupture of a vulnerable atheromatous plaque, not necessarily involving flow-limiting stenoses. 1-3 The main risk factors for CAD development are tobacco use, high blood pressure, raised blood cholesterol, and diabetes mellitus. Several interventions aiming to prevent CAD have been well documented, ranging from lifestyle changes to a daily and lifelong intake of drugs. The best documented are smoking cessation, blood pressure lowering, anti-platelet aggregation therapy (low-dose aspirin) and pharmaceutical lipid management (statins). 2.1.2 Definitions Symptomatic CAD can be manifested either by stable angina pectoris, as an ACS or as sudden death. Loss of a substantial part of myocardial tissue can lead to heart failure, cardiogenic shock and death. Heart failure is a distinct clinical syndrome characterised by symptoms such as breathlessness and fatigue and signs such as fluid retention. The clinical spectrum of CAD is displayed in Table 1. Table 1: Clinical spectrum of CAD. Pathology Symptomatic CAD Asymptomatic CAD stable angina ACS Other Manifestations unstable angina AMI Sudden death, heart failure, …
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KCE reports 33 Effects and costs of
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