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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).

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Part II of this three-part article on nonatherosclerotic causes of coronary heart disease focuses on myocardial bridges, coronary artery aneurysms, emboli, coronary dissection, and spasm as causes of luminal narrowing.

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Approximately 5% of patients with acute myocardial infarction do not have atherosclerotic coronary artery disease but have other causes for their luminal narrowing. The first part of this three-part review of nonatherosclerotic causes of coronary narrowing focuses on congenital coronary artery anomalies, coronary fistula, and high take-off position of coronary ostia.

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BACKGROUND: The omega-3 polyunsaturated fatty acids derived from fish oils have been shown to modulate many factors believed to affect the pathogenesis of atherosclerosis. Because certain features of restenosis following angioplasty mimic some of the early changes of atherogenesis, some researchers have suggested that fish oil might prevent restenosis following angioplasty. We report the effects of omega-3 fatty acids on the rate of restenosis following percutaneous intraluminal coronary angioplasty (PTCA). METHODS AND RESULTS: From August 1989 through September 1992, 551 patients were randomized to start receiving a daily dietary supplement of ten 1.0-g capsules containing 80.6% ethyl esters of omega-3 fatty acids providing 4.1 g eicosapentaenoic acid (EPA) and 2.8 g docosahexaenoic acid (DHA) for 6 months or an equal amount of an ethyl ester of corn oil. Four hundred seventy subjects who were well matched for risk factors completed successful angioplasty of one or multiple lesions in native coronary vessels and constituted the study cohort, of whom 447 were evaluable at 6 months after PTCA. The criteria for restenosis were that the quantitative coronary angiography at 6 months show a > 30% increase in narrowing at the stenosis site or loss of at least half of the gain achieved at the time of PTCA and final restenosis with < 50% luminal diameter remaining. In 93% of the patients, the end point was determined by angiography and in all except 1% of these by quantitative coronary angiography. Compliance with the fish oil supplement was good as judged by incorporation of EPA and DHA in plasma and red blood cell phospholipids. The restenosis rate among analyzable patients was 46% for corn oil and 52% for fish oil (P = .37). The addition of 200 mg alpha-tocopherol for all subjects during the study had no effect on restenosis rates. CONCLUSIONS: This was the largest of such trials to date, and a supplement of 8 g/d of omega-3 fatty acids failed to prevent the usual high rate of restenosis after PTCA. No adverse effects were attributable to this large daily supplement of omega-3 fatty acids.

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Various pathologic conditions producing atrioventricular block are reviewed. Calcific atrioventricular block (aortic stenosis, mitral valve annular calcium), active infective endocarditis ("ring" abscess), acute and healed myocarditis, various collagen-vascular diseases, amyloidosis, and tumors are reviewed as causes of atrioventricular block. Various diseases producing bundle-branch block are also discussed.

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Although morphologic findings in many of the cardiac arrhythmias of acute and chronic disease have been elusive, the correlates of heart block (particularly atrioventricular block) are abundant. Pathologic features of sinoatrial, atrioventricular, and bundle-branch block are reviewed. Lev and Lenegre diseases (idiopathic bilateral bundle-branch fibrosis) are also reviewed.

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Metastatic tumor involvement of the heart as a basis for the genesis of various cardiac arrhythmias is reviewed. The morphologic basis of pre-excitation syndromes and right ventricular dysplasia are also reviewed.

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The cardiac conduction system may be affected by various pathologic changes. Some of these changes are general and affect the nonconduction system tissues of the heart (atrophy, fibrosis, necrosis, segment deposition, mineral) and others are more localized to the conduction system (Lev and Lenegre disease). Pathologic conditions associated with atrial, junctional, and ventricular arrhythmias are reviewed.

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Normal anatomic and histologic features of the atrioventricular junction (transitional cell zone, atrioventricular node, penetrating portion of bundle) and the bifurcation of the penetrating portion into bundle branches are reviewed. Terminal ventricular Purkinje fibers are also discussed.

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Normal anatomic and histologic features of the sinus node, atrial myocardium, and interatrial conduction of the cardiac impulse are reviewed. The controversy surrounding atrial conduction via specialized atrial cells versus specific internodal tracts (between sinus and atrioventricular nodes) is discussed.

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Since the advent of echocardiography, embolus in transit, historically found during surgical exploration or on postmortem examination, has been found with increasing frequency on antemortem examination. There is an inherent high mortality rate with this condition and awareness of the association between deep venous thrombosis and embolus in transit is paramount. On echocardiography the embolus is typically seen as a pleomorphic mass moving in a tumbling fashion. The most frequent symptoms are dyspnea and near syncopal episodes. The most common signs are diastolic "tumor plop" and a systolic ejection murmur heard on auscultation. Despite the success of some medical interventions, surgery should be strongly considered in patients with embolus in transit.

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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 techniques. Part IV of this review will focus on congenital coronary artery anomalies, myocardial bridges, coronary aneurysm, emboli, and dissection and clinical implications regarding echocardiographic imaging techniques.

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In the last 15 years, intense interest has focused on various interventional, pharmacologic, and mechanical forms of therapy for the treatment of atherosclerotic 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 techniques. Part III of this four-part review focuses on eccentric and concentric plaques, formation of coronary thrombus, and status of the "infarct artery" after mechanical and pharmacologic forms of acute reperfusion therapy.

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In the last 15 years, intense interest has focused on various interventional, pharmacologic, and mechanical forms of therapy for the treatment of atherosclerotic 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 techniques. Part II of this four-part review will focus on aging changes seen in the epicardial coronary arteries and will review selected features of atherosclerotic plaque, including fissure and topography.

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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 techniques. 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.

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Pericardial heart disease is a common entity at necropsy. Frequently, focal areas of fibrin deposits or parietal-visceral pericardial adhesion are observed at necropsy without previous clinical evidence of pericardial dysfunction. Some of these instances are related to clinically silent acute or healed myocardial infarction but the vast majority of cases are incidental (idiopathic) findings. The purpose of this review is to summarize various morphologic responses of the pericardium and to provide an etiologic framework for these responses. Part II will review specific morphologic responses of pericardial layers to selected diseases.

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Pericardial heart disease is a common entity at necropsy. Frequently, focal areas of fibrin deposits or parietal-visceral pericardial adhesion are observed at necropsy without previous clinical evidence of pericardial dysfunction. Some of these instances are related to clinically silent acute or healed myocardial infarction, but the vast majority of cases are incidental (idiopathic) findings. The purpose of this review is to summarize various morphologic responses of the pericardium and to provide an etiologic framework for these responses. Part I will review general morphologic responses of pericardial layers.

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