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6 Multislice CT in Coronary Heart Disease KCE Reports 82 2.1.2.1 Typical stable angina Typical angina has three characteristics: (1) discomfort in the chest, jaw, shoulder, back or arms, that is (2) provoked by exertion or emotional stress and (3) relieved by rest or nitroglycerin. 4, 5 In most cases, it is caused by a temporary imbalance of the blood supply to the heart muscle combined with the increased demand induced by exercise or emotion. A grading system of angina pectoris has been proposed by the Canadian Cardiovascular Society and is generally adopted. 6 It attributes a higher, i.e. more severe class of angina, depending on the intensity of exercise that elicits chest pain: • Class I: Ordinary physical activity does not cause angina. Angina occurs with strenuous work. • Class II: Slight limitation of ordinary activity. Angina occurs on walking or climbing stairs rapidly, walking uphill, … • Class III: Marked limitations of ordinary physical activity. • Class IV: Inability to carry on any physical activity without discomfort. Angina symptoms may be present at rest. Angina is “stable” when the symptoms remain unchanged, i.e. there is no change in the usual pattern of the discomfort, such as an alteration in its frequency or the occurrence with less exertion or at rest. “Unstable” angina is discussed under the heading “acute coronary syndromes”. 2.1.2.2 Atypical angina Atypical angina has only two of the three characteristics of typical angina. Very often, these patients have significant CAD 7 and sometimes, it is referred to as “probable angina” in contrast to “typical angina”. 8 The term “atypical angina” is not commonly used in Belgian cardiological practice where the epithet “atypical” most often is applied in combination with “chest pain” suggesting a noncardiac origin of the complaints as discussed below. 2.1.2.3 Atypical chest pain Atypical or nonanginal chest pain is diagnosed in patients with only one or none of the characteristics of typical angina. 9 Such as the other types of chest pain, it is a descriptive term resulting from clinical history taking and is sometimes referred to as nonanginal, atypical or noncardiac chest pain. By assuming this diagnosis, the physician involved indicates his belief in a noncardiac origin of the patient’s chest pain. 2.1.2.4 Non-acute vs. acute chest pain Non-acute chest pain typically refers to stable angina or chest pain that exists since several weeks or more and that is not experienced as severely discomforting, thus excluding ACS. Acute chest pain refers to pain for which the patient is admitted to an emergency department. 2.1.2.5 Myocardial infarction A myocardial infarction is a condition in which myocardial tissue is damaged and lost because of prolonged ischeamia induced by an abrupt occlusion (mostly due to thrombus formation) of a coronary vessel. Whereas traditionally a substantial amount of myocardial tissue had to be destroyed before the diagnosis of MI could be made, recent developments in the detection of small quantities of myocardial necrosis using serum biomarker levels, such as cardiac troponin, have lead to a more sensitive diagnosis of MI. A universal definition of MI has been proposed to be used whenever there is evidence of myocardial necrosis in a clinical setting consistent with myocardial ischemia. 10 Chest pain is a major symptom of acute myocardial infarction (AMI), mostly occuring at rest and usually lasting at least 20 min. 10
KCE Reports 82 Multislice CT in Coronary Heart Disease 7 2.1.2.6 Acute coronary syndromes Acute coronary syndromes (ACS) encompass a heterogeneous spectrum of acute ischemic heart diseases, extending from acute MI, through minimal myocardial injury to unstable angina. In MI, per definition, there is loss of myocardial tissue. Unstable angina refers to a syndrome of cardiac ischemia clinically manifestating itself as prolonged chest pain, in which no myocardial necrosis can be documented. As opposed to stable angina, unstable angina is also diagnosed when the chest pain started recently, when it becomes more easily provoked or when it occurs with increased frequency, severity or duration. 5, 9 Patients with an ACS may have chest discomfort that has all the qualities of typical angina except that the episodes are more severe and prolonged, may occur at rest, or may be precipitated by less exertion than in the past. 11 2.1.2.7 Obstructive CAD Obstructive CAD in this report is defined as CAD in which at least one coronary stenosis exceeding 50% in luminal diameter is present, mostly as documented by invasive coronary angiography. Key points • The underlying mechanism of CAD is a gradual build-up of fatty material into the coronary vessel wall, leading to the formation of atheromatous plaques. These may cause narrowing of the coronary arteries leading to angina pectoris, or they may suddenly rupture and induce thrombosis of the vessel giving rise to an acute MI. • Chest pain can be induced by several non-cardiac conditions as well, originating from the lungs, other intrathoracic structures or the chest wall. It may also be psychosomatic in origin, e.g. caused by anxiety. 2.2 DIAGNOSIS OF CAD IN NON-ACUTE CONDITIONS 2.2.1 Baseline clinical investigations Diagnosis of CAD can often be made by history taking alone, based on the pain characteristics, taking into account the patient’s age, gender and cardiovascular risk profile. If other risk factors exist, such as smoking, hypertension, family history, hypercholesterolaemia, diabetes, the probability of CAD increases. 5 Physical examination can further increase the likelihood of CAD when signs of peripheral atheromatosis or heart failure are found. Very often however, especially in younger patients with angina pectoris, the physical examination is normal. Sometimes, other causes of chest pain may become apparent (pericarditis, pleuritis, orthopaedic disease, …). In a much-referred to paper, Diamond and Forrester describe how the probability of CAD can be estimated in a given patient from information readily obtainable by clinical evaluation. 7 In 4952 patients with different types of chest pain (as defined earlier), the prevalence of angiographic CAD was 90% in patients with typical angina, 50% in patients with atypical angina and 16% in patients with nonanginal chest pain. By combining data from different patient subgroups with disease likelihoods from autopsy studies, probability estimates for angiographic CAD for a set of combinations of age, sex and symptoms were calculated as shown in Table 2.
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KCE reports 33 Effects and costs of
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