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Arteriographie Anatomy and Mechanisms of Myocardial View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector JACC Vol. 9. No.6 1397 June 1987:1397-402 EDITORIALS Arteriographic Anatomy and Mechanisms of Myocardial Ischemia in Unstable Angina JOHN A. AMBROSE, MD, FACC , CRAIG E. HJEMDAHL-MONSEN, MD New York, New York Over the past 20 years, there has been considerable research stable angina; and 3) all ischemic rest pain without evidence into the pathogenesis of myocardial ischemia in unstable of myocardial infarction. angina. Early data (1-3) suggested that transient increases These catagories are not mutually exclusive . The cate­ in myocardial oxygen demand explained episodes of rest gory of rest pain would include some patients with previ­ pain in patients with unstable angina and severe coronary ously mild angina and a marked increase in symptoms (cres­ artery disease. In the 1970s this view changed and the con­ cendo angina) and also patients with previously severe angina cept of vasospasm became the most favored mechanism to and a slight increase in symptoms. Other proposed classi­ explain episodes of myocardial ischemia and rest pain, thus fications for unstable angina include the categories of sub­ changing the emphasis from the demand side to the supply endocardial infarction and postinfarction angina. The natural side of coronary dynamics (4,5). More recently, serial an­ history of patients with these conditions may be different giographic studies (6,7) have demonstrated that progression from that of patients classified in the preceding categories of coronary artery disease is extremely common in patients (14). More complex classifications have been proposed based with stable angina who are restudied after an episode of on clinical or angiographic criteria , or both (15,16). For the unstable angina . Angiographic, angioscopic and pathologic remainder of this discussion, we will classify unstable an­ data (8-13) have also incriminated thrombus in the patho­ gina as we did in the preceding paragraph . genesis of this condition. In this review we explore the relation between the coronary arteriographic anatomy in unstable angina and mechanisms of myocardial ischemia. Coronary Arteriographic Anatomy in Unstable Angina Definition of Unstable Angina Atherosclerotic disease. Eighty-five to 90 percent of patients with unstable angina have significant coronary ar­ A major difficulty in unraveling the cause of any con­ tery disease but in about 10 to 15% of patients, normal or dition occurs when that condition is not precisely defined. nonobstructed coronary arteries are found (17,18). Thus , Such is the case with unstable angina, which is a descriptive some patients with normal or nonobstructed coronary ar­ term for a spectrum of acute myocardial syndromes that teries have dynamic obstruction and myocardial ischemia clinically lie between stable angina and myocardial infarc­ related to coronary artery spasm or some other mechanism; tion. It generally includes the following categories: I) New other patients have a chest pain syndrome that is noncardiac onset of angina (1 to 2 months' duration) occurring at low in origin. work loads or at rest; 2) crescendo angina defined as a The majority ofpatients with unstable angina have mul­ marked increase in the frequency or severity of previously tivessel coronary artery disease. However, if one looks at only those patients with recent onset unstable angina, there *Editorials published in Journal ofthe American College ofCardiol ogy is a high incidence of one vessel disease (25 to 50%) (19,20) . rellect the views of the authors and do not necessarily represent the views of JACC or the American College of Cardiology. Significant obstruction of the left main coronary artery is From the Department of Medicine. Division of Cardiology. The Mount more common in unstable than in stable angina and occurs Sinai School of Medicine and The Mount Sinai Medical Center. New in up to 25% of patients with rest and exertional chest pain York, New York 10029. This work is supported by the New York Cardiac Center, Englewood Cliffs, New Jersey. and a previous history of stable angina (21). Manuscript received September 29. 1986; revised manuscript received Ischemia-producing artery. In patients with unstable December 10, 1986, accepted January 7. 1987. angina and single vessel disease, it can be assumed that the Address for reprints: John A. Ambrose, MD, Division of Cardiology . The Mount Sinai Medical Center, One Gustave L. Levy Place, New York. ischemia-producing artery is that vessel with the significant New York 10029. obstruction . In rare instances, however, ergonovine testing ©1987 by the American College of Cardiology 0735-1097/87/$3.50 1398 AMBROSE AND HJEMDAHL-MONSEN JACC Vol. 9, No.6 EDITORIAL June 1987:1397-402 has indicated spasm (with reproducibility of clinical symp­ toms) of a normal-appearing artery in the presence of sig­ nificant obstruction in other vessels (22). Whereas multi­ vessel disease is common in unstable angina, it is often possible to identify an ischemia-producing artery. By a care­ ful assessment of both the distribution of lesions within the coronary arteries and segmental wall motion analysis as well as electrocardiographic (ECG) changes during pain, we (8) were able to localize the presumed artery responsible for symptoms in about 40% of patients with either stable or unstable angina and multivessel coronary artery disease. The presence of an "acute" coronary lesion as determined by analysis of coronary morphology will increase the likelihood of localizing the ischemia-producing artery in unstable an­ gina and multivessel disease (see later). Figure 1. Left coronary artery angiogram intheleftanterior oblique Progression of coronary artery disease. In previously projection showing a type II eccentric lesion in the left anterior catheterized patients with a history of stable angina pectoris, descending artery (arrow). progression of coronary artery disease is seen in approxi­ mately 75% who are recatheterized after an episode of un­ stable angina (6,7). On the other hand, only about 33% of farction in comparison with patients with one vessel disease patients recatheterized with little or no increase in symptoms and unstable angina. The lack of more quantitative data show such progression. This progression can be seen to makes it difficult to assess the role of the degree of stenosis, occur in lesions that at the time of the first angiogram were the minimal diameter or the cross-sectional area of the coro­ either significant (>50% diameter obstruction) or "non­ nary lesion in the ischemia-producing artery as a sole de­ obstructive" «50% diameter obstruction) (6,7). We found terminant of the particular clinical syndrome. Therefore, (7) that in unstable angina, progression in the ischemia­ more quantitative data are required to compare unstable producing artery usually originated from a previously in­ angina with other acute coronary syndromes. significant lesion or even from a normal-appearing artery. Qualitative analysis of coronary lesions in unstable This pattern of progression from previously insignificant angina. In either acute presentations of unstable angina (8), disease was seen less commonly in the study of Moise et recent non-Q wave infarction (26), acute infarction with ST al. (6). Although quantitative techniques for analyzing coro­ segment elevation or recent Q wave myocardial infarction nary stenoses were not utilized in these studies of coronary (27), a characteristic coronary lesion is found in the majority disease progression, approximately 25% of patients in both of cases in which an ischemia-producing artery < 100% studies did not appear to have any progression of disease occluded is identified. An eccentric stenosis in the form of despite the symptomatic progression to unstable angina. a convex intraluminal obstruction with a narrow neck due Quantitative analysis of coronary lesions in unstable to one or more overhanging edges, or borders that are scal­ angina. There are ample data, (18,23) suggesting that the loped (type II eccentric lesion) is found in approximately extent and location of coronary artery disease are similar two-thirds of such patients (Fig. 1). This type II eccentric for patients with stable and unstable angina except for the lesion is also common in coronary artery disease progres­ higher incidence of left main coronary involvement in un­ sion. It is rarely found in patients with stable angina. In the stable angina. However, there are few data that quantita­ remaining one-third of ischemia-producing arteries in these tively analyze the degree of stenosis or the minimal diameter acute syndromes, other types of morphology can be seen. of the ischemia-producing lesion in unstable angina versus Symmetricand smooth (concentric)or asymmetric and smooth other acute coronary syndromes. Although visual analysis (type I eccentric) narrowings are the most common lesions of the degree of coronary stenosis has been shown to be in those ischemia-producing arteries that contain non-type similar in the acute coronary syndromes (23), this method II eccentric lesions. is inaccurate for precise comparison. Raffenbeul et al. (24) Other angiographic studies have assessed the importance found similar degrees of stenosis in patients with either of intracoronary filling defects in unstable angina (9,10). unstable angina or stable angina when lesions were quan­ Filling defects located either within or distal to a lesion have titatively
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