Thoracic Imaging 2003 - Society of Thoracic Radiology

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MONDAY 130 Pulmonary Hypertension Aletta Frazier, M.D. Pulmonary hypertension is an extensively investigated but complex spectrum of diseases with insidious clinical onset and often devastating cardiorespiratory consequences. The condition is defined as a mean pulmonary artery pressure greater than 25 mm Hg at rest, or greater than 30 mm Hg during exercise. These hemodynamic parameters, combined with appropriate clinical history and histologic findings, confirm the diagnosis. The profoundly altered hemodynamics reflect underlying vascular remodeling, intravascular thrombosis, and/or extravascular constriction within the pulmonary circulation. In the case of severe, chronic pulmonary arterial hypertension, the sustained pressure or volume overload leads to changes in right heart mass and function. Additional notable complications of longstanding pulmonary hypertension include aneurysmal dilatation of the central pulmonary arteries, pulmonary elastic arterial thrombosis or dissection, and premature pulmonary arterial atherosclerosis. In accordance with the established approach at the Armed Forces Institute of Pathology, the spectrum of pulmonary hypertension may be categorized for optimal clarification as either “precapillary” (with histologic changes limited to the arterial side of the pulmonary circulation) or “postcapillary” (with primary vascular changes within the pulmonary venous circulation, between the capillary bed and the left atrium). The histologic changes may be the ultimate consequence – and final common pathway - of an identifiable cause or a coexistent disease state. When no clear etiology is identified, the condition may be termed “idiopathic”. SPECTRUM OF DISEASES Well-recognized causes of precapillary pulmonary hypertension include Eisenmenger syndrome, chronic thromboembolic disease, chronic hypoxic states, collagen vascular disease, mediastinal fibrosis or tumor, and widespread pulmonary embolism secondary to agents such as circulating tumor cells, talc injection, and parasitic infestation. Associated conditions include human immunodeficiency virus (HIV) infection, pregnancy, portal hypertension, anorexigenic drug use, hyperthyroidism, and obstructive sleep apnea. Primary pulmonary hypertension (PPH) is a diagnosis reached when no clear etiology is identified and specific histologic features are observed. In the rare familial form of PPH, a gene mutation has been identified. Etiologies of postcapillary pulmonary hypertension include mediastinal fibrosis or tumor, left atrial mass, left ventricular failure, left-sided cardiac valvular disease, and more rarely, pulmonary venous occlusion, congenital venous stenosis, and anomalous pulmonary venous return. The postcapillary counterpart to PPH is pulmonary veno-occlusive disease (PVOD), a rare idiopathic condition that widely affects the small pulmonary veins. Conditions associated with PVOD include HIV infection, pregnancy, bone marrow transplantation, and chemotherapeutic drug toxicity. HISTOLOGIC FEATURES The muscular arteries are predominantly affected in precapillary pulmonary hypertension with histologic changes of intimal cellular proliferation and medial smooth muscle hypertrophy. Features of necrotizing arteritis and plexiform lesions are observed exclusively in patients with PPH or Eisenmenger syndrome. A plexiform lesion is the hallmark of sustained and irreversible pulmonary arterial hypertension, recognized by pathologists as the focal disruption of the internal elastic lamina of small muscular arteries by a proliferative plexus of endothelial channels. Venous medial hypertrophy and intimal proliferation, with secondary findings of capillary congestion and interlobular septal edema and fibrosis, characterize postcapillary hypertension. Recanalized channels and webs within the pulmonary veins are features specific to PVOD and suggest that thrombosis is the central pathogenic factor. RADIOLOGIC MANIFESTATIONS The radiologic manifestations of pulmonary arterial hypertension reflect central pulmonary arterial dilatation, sharply diminished peripheral vascular markings, and right-sided hypertrophy with or without chamber dilatation. In cases of chronic thromboembolism or mediastinal fibrosis, findings may be limited to a few segmental or subsegmental vessels. Mosaic perfusion, dilated bronchial arteries and collateral vessels, subpleural pulmonary infarcts, calcified plaques lining larger pulmonary arteries, and arterial thrombosis may be evident on computed tomography. Magnetic resonance imaging is well-suited to demonstrate abnormalities in right ventricular configuration, as well as ventricular and valvular dysfunction. Postcapillary pulmonary hypertension classically reveals the features of interstitial edema, including Kerley B lines, thickened pleural fissures, and small pleural effusions. In addition, the radiologic evaluation of longstanding postcapillary pulmonary hypertension may demonstrate evidence of secondary pulmonary arterial hypertension, due to retrograde transmission of elevated pressures across the capillary bed.
REFERENCES Bergin CJ, Rios G, King MA, Belezzuoli E, Luna J, Auger WR. Accuracy of high-resolution CT in identifying chronic thromboembolic disease. AJR 1996; 166:1371-1377. Botney MD. Role of hemodynamics in pulmonary vascular remodeling. Am J Respir Crit Care Med 1999; 159;361-364. Burke A, Virmani R. Mini-symposium: pulmonary pathology – evaluation of pulmonary hypertension in biopsies of the lung. Curr Diagn Pathol 1996; 3:14-26. Burke AP, Farb A, Virmani R. The pathology of primary pulmonary hypertension. Mod Pathol 1991; 4:269-282. Dalen JE, Haffajee CI, Alpert JSIIII, Howe JP, Ockene IS, Paraskos JA. Pulmonary embolism, pulmonary hemorrhage, and pulmonary infarction. N Engl J Med 1977; 296:1431-1435. Frazier AA, Galvin JR, Franks TJ, Rosado de Christenson M. From the archives of the AFIP: Pulmonary vasculature: hypertension and infarction. RadioGraphics 2000; 20:491-524. Primack SL, Muller NL, Mayo JR, Remy-Jardin M, Remy J. Pulmonary parenchymal abnormalities of vascular origin: highresolution CT findings. RadioGraphics 1994; 14:739-746. Rubin LJ. Approach to the diagnosis and treatment of pulmonary hypertension (clinical conference). Chest 1989; 96:659- 664. Wagenvoort CA. Vasoconstrictive primary pulmonary hypertension and pulmonary veno-occlusive disease. In: Brest AN, ed. Cardiovascular clinics. Philadelphia, Pa: Davis, 1972; 98-113. Worthy SA, Muller NL, Hartman TE, Swensen SJ, Padley SPG, Hansell DM. Mosaic attenuation pattern on thin-section CT scans of the lung: differentiation among infiltrative lung, airway, and vascular diseases as a cause. Radiology 1997; 205:465-470. 131 MONDAY TUESDAY
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The Society of Thoracic Radiology T
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Dear Friends, Welcome to Miami Beac
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Continuing Medical Education Credit
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Warren B. Gefter, MD University of
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Ernest M. Scalzetti, MD SUNY Upstat
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Registration Hours Saturday, March
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Program Committee Ella A. Kazerooni
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Small Airway Disease Americana 3 Mo
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Benjamin Felson Memorial Lecture Am
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Session 2-B Concurrent Session Clin
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Workshops (choose 1) 1:00 - 1:45 D1
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Sunday
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March 2, 2003 General Session Sunda
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SUNDAY 46 One type of direct-readou
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CT-PET Imaging Suzanne Aquino, M.D.
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SUNDAY 58 an accompanying decreased
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SUNDAY 60 Radiofrequency Ablation i
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SUNDAY 62 17. Sewell PE, Vance RB.
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SUNDAY 64 cal ventilation will be r
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SUNDAY 66 radiologic, and histopath
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SUNDAY 68 application. The untreate
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SUNDAY 70 The Expanded Spectrum of
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SUNDAY 72 Hypersensitivity Pneumoni
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Page 49 and 50: SUNDAY 76 The “Head-cheese Sign
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Page 53 and 54: SUNDAY 80 Pleural Effusions Gerald
Page 55 and 56: SUNDAY 82 Asbestos Related Pleural
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Page 59 and 60: SUNDAY 86 Image-Guided Therapy of M
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Page 63 and 64: March 3, 2003 General Session 7:00
Page 65 and 66: Cardiac MRI: Established Indication
Page 67 and 68: Cardiac MRI: New Developments Gauth
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Page 71 and 72: Acute Aortic Syndrome Ernest M. Sca
Page 73 and 74: as well as separation of the cusps
Page 75 and 76: Pulmonary Veins: Imaging for Radiof
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Page 103 and 104: March 4, 2003 General Session 7:00
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Page 109 and 110: Imaging of the Pericardium Paul L.
Page 111 and 112: Cardiomyopathy Martin J. Lipton, M.
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Page 131 and 132: Multidetector Pediatric Chest CT: P
Page 133 and 134: The Spectrum of Pulmonary Infection
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March 5, 2003 General Session Wedne
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WEDNESDAY 208 principle is that “
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WEDNESDAY 210 years and a current o
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WEDNESDAY 212 lesions generally mim
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WEDNESDAY 214 capable of studying t
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WEDNESDAY 216 Small T1 Lung Cancer:
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WEDNESDAY 218 REFERENCES Seely JM,
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WEDNESDAY 220 Therefore, radiologis
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WEDNESDAY 222 sectional area varies
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WEDNESDAY 224 Lung Cancer Staging A
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Metastatic Disease to Lung Gordon L
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Thoracic Metastates from Osteosarco
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STR tutorial: Use of MD CT reconstr
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ogenic edema, fat embolism, heroin
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WEDNESDAY 236 Pulmonary Arterial Hy
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WEDNESDAY 238 pathological process,
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Thursday
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THURSDAY 250 Pulmonary Tuberculosis
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THURSDAY 252 1. Clinical criteria:
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THURSDAY 254 AIDS patients are also
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THURSDAY 256 Viral Infection on HRC
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THURSDAY 258 Imaging of Coccidioido
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THURSDAY 260 from the laryngeal sur
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THURSDAY 262 Inflammatory Diseases
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Virtual Endoscopy in the Thorax: Pr
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Notes 269 THURSDAY
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SECOND LEVEL THIRD LEVEL
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