Summary:In the last 15 years, intense interest has focused on various interventional pharmacologic and mechanical forms of therapy for the treatment of atherosclerosis coronary artery disease. Many techniques and devices (dilating balloons, perfusion catheters, thermal probes and balloons, lasers, atherectomy devices, stents, intravascular ultrasound) have been used or are under study for future use. Many of these techniques and devices require an understanding of histologic and pathologic features of the coronary arteries and diseases which affect them. This article reviews selective areas of anatomy, histology, and pathology relevant to the use of various new interventional Part I of this review will focus on anatomic aspects of the epicardial coronary artery system, coronary arterial distribution, myocardial supply, and histologic features of the normal coronary artery. Key words: coronary artery, coronary ostium, high takeoff position Epicardial Coronary Artery SystemThe epicardial coronary artery system consists of the left and right coronary arteries, which normally arise from 0s-tia located in the left and right sinuses of Valsalva, respec- tively ( Fig. 1). In about 50% of humans a "third coronary artery" ("conus artery") arises from a separate ostium in the right sinus. Additional smaller ostia may be found in the right sinus, which give rise to multiple right ventricular branches (Fig. 2). Up to five separate coronary ostia have been described (Figs. 2+.3 The left main coronary artery ranges in length from 1-25 mm before bifurcating into the left anterior descending and left circumflex bran~hes.~ The left anterior descending coronary artery measures from 10-13 cm in length, whereas the usual nondominant left circumflex artery measures about 6-8 cm in length. The usual dominant right coronary artery (supplying posterior descending and/or atrioventricular nodal artery) is about 12-14 cm in length before giving rise to the posterior descending artery. The luminal diameters of the major coronary arteries in adults range as follows: left main, 2.0-5.5 mm (mean 4 mm); left anterior descending, 2.0-5.0 mm (mean 3.6 mm); left circumflex, 1.5-5.5 mm (mean 3.0 mm); and right, 1.5-5.5 mm (mean 3.2 mm)? Although the left anterior descending and left circumflex arteries generally taper in diameter as each extends from the left main bifurcation, the right coronary artery maintains a fairly constant diameter until just before the origin of its posterior descending branch. The subepicardial coronary arteries run on the surface of the heart embedded in various amounts of subepicardial fat. Portions of the epicardial coronary arteries may dip into the myocardium ("mural artery" or "tunneled artery") and be covered for a variable length (1 to several mm)5 by ventricular muscle ("myocardial bridge") ( Coronary OstiaThe left and right coronary ostia arise normally within the sinus of Valsalva or at the junction of the sinus and tub-
This report describes clinical, morphologic and histologic findings at necropsy late (range 1.6 to 24.1 months [average 8.2 months]) after clinically successful coronary balloon angioplasty in 20 patients with coronary angioplasty restenosis. Clinical evidence of restenosis occurred in 14 patients (70%), including 6 patients with sudden coronary death. Of the 20 patients, 14 (70%) had a cardiac cause of death and 6 (30%) had a noncardiac cause of death. Two major subgroups of histologic findings were observed: 1) intimal proliferation (60%), and 2) atherosclerotic plaque only (40%). Of the eight sites with atherosclerotic plaque only, six were eccentric lesions and two were concentric lesions. No morphologic evidence of previous angioplasty injury (cracks, breaks, tears) was observed in the eight patients with atherosclerotic plaque only. Proposed mechanisms for the development of intimal proliferation involve the reaction of smooth muscle cells and platelets, whereas elastic recoil of overstretched eccentric or concentric atherosclerotic lesions represents the most likely explanation for the findings in the latter subgroup. On the basis of these morphologic findings at angioplasty restenosis sites, specific treatment strategies for restenosis after coronary artery balloon angioplasty are proposed.
Summary: Approximately 5% of patients with acute myocardial infarction do not have atherosclerotic coronary artery disease but have other causes for their luminal narrowing. The third part of this three-part review of nonatherosclerotic causes of coronary narrowing focuses on coronary vasculitis, infectious diseases, Kawasaki's disease, metabolic disorders, metastatic disease, and substance abuse (cocaine).Key words: coronary vasculitis, Kawasaki's disease, cocaine, metastatic tumor coronary arteritis: (1) focal artery necrosis with or without calclfication, (2) acute coronary artery thrombosis or recanalized thrombus unassociated with underlying atherosclerotic plaque, (3) rupture of the vessel wall unassociated with trauma or an interventional procedure, (4) coronary artery wall thickening with secondary luminal narrowing, and (5) wall thinning with aneurysm formation.3 Specific coronary lesions also may be seen in specific systemic diseases (e.g., polyarteritis nodosa). Tbberculosis Coronary Artery Arteritis (Vasculitis)Epicardial coronary arteritis (vasculitis) is a rare event that has been reported in several conditions . The resulting coronary injury may directly lead to myocardial ischemidinfarction (MI) with or without associated coronary artery thrombosis.' Baroldi2 provides a useful classification of the arteritis conditions based upon type of coronary artery route of entry. Coronary arteritis may result From direct extension from adjacent organ or tissue infections (e.g., epicardial or myocardial abscess from aortic valve endocarditis, pericardial tuberculosis). In this situation, the coronary artery adventitial layer is initially involved. Coronary arteritis may result from a hematogenous spread through the coronary lumen or through vasa vasorum. In this situation, the intimal layer is initially involved. In other vasculitides, the exact mechanism of vascular origin is not understood. Baroldi2 also considers the following morphologic-histologic findings as signs of Tuberculosis arteritis is seen chiefly in patients with pencardial or myocardial lesions. Specific coronary artery granuloma may involve the adventitia, the intima, or the entire wa11.234 Polyarteritis NodosaPolyarteritis nodosa is probably the most common cause of coronary angitis. It is a systemic necrotizing vasculitis that affects medium and small vessels. Of 66 cases studied by Holsinger et al.? 41 (62%) had involvement of the epicardial coronary arteries and 4 1 also had myocardial infarcts of varying size. The coronary lesions resemble the necrotizing vascular lesions elsewhere, with an acute cellular phase with destruction of the media and internal elastic membrane and subsequent intimal proliferation and scar in the healed phase. The coronary artery may dilate to form small berry-like aneurysms, become occluded by thrombus, or rupture (producing fatal pencardial tamponade Systemic Lupus ErythematosusPericardial and myocardial involvement are common complications in systemic lupus erythematosus. Several young patients with lupus ...
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