Pulmonary Artery Thrombus Detection by Magnetic Resonance Imaging

temic embolization, and infective endocarditis. The incidence of pseudoaneurysm of the left ventricle following mitral valve surgery varies from 0.5 to 1 percent. 3 .8 Although infective endocarditis by itself can lead to submitral pseudoaneurysm, 4 in our patient, this probably resulted from extensive resection of the left atrium and mitral annulus during her first valve surgery. Demonstration of an echo-free space posteriorly or posterolaterally by echocardiography is seen in submitral pseudoaneurysms. 1-9 The presence of a narrow orifice differentiates a pseudo from a true left ventricular aneurysm. These findings are helpful in confirming the presence of pseudoaneurysm, but they are not specific. Pseudoaneurysm was not suspected clinically in our patient, and the initial echo interpretation was of a loculated pleural effusion. Color How Doppler clearly demonstrated Bow into the echo-free space and resulted in the correct diagnosis. Pulsed Doppler ultrasound may also have aided in the diagnosis, but the echo-free space of presumed pleural effusion was not interrogated by the pulsed Doppler probe. In conclusion, color flow Doppler enhances the echocardiographic and pulsed Doppler diagnosis of left ventricular pseudoaneurysms. Q

ACKNOWLEDGMENT: The authors would like to express their gratitude to Ms. Colleen Dusseau and Ms. Bobbie Murray for their assistance in typing this manuscript. REFERENCES

1 Van Tassel RA, Edwards JE. Rupture of the heart complicating myocardial infarction: analysis of 40 cases including nine examples of left ventricular false aneurysm. Chest 1972; 61:104-16 2 Martin RH, Almond CH, Saab S, Watson LE. True and false aneurysms of the left ventricle following myocardial infarction. Am J Med 1977; 62:418-24 3 Littler WA, Meade JB, Hamilton DI. Ventricular aneurysms after cardiac surgery. Br Heart J 1971; 33:962-69 4 Kessler KM, Kieval J, Saksena S, Sanderson TL, Myerburg RL. Echographic features ofposterior left ventricular wall pseudoaneurysm due to Escherichia coli endocarditis. Am Heart J 1982; 103:139-42 5 Aronstein CG, Neuman L. Syphilitic aneurysm of the heart case report with review of the literature. Am J Clin Path 01 1941; 11:128-37 6 Stewart S, Huddle R, Stuard I, Schreiner BF, DeWeese JA. False aneurysm and pseudo-false aneurysm of the left ventricle: etiology, pathology, diagnosis and operative management. Ann Thorax Surg 1981; 31:259-65 7 Davidson KH, Parisi AF, Harrington JJ, Barsamian EM, Fishbein MC. Pseudoaneurysm of left ventricle: an unusual echocardiographic presentation; review of the literature. Ann Intern Med 1977; 86:430-33 8 Carlson EB, Wolfe WG, Kisslo J. Subvalvular left ventricle pseudoaneurysm after mitral valve replacement: two-dimensional echocardiographic findings. J Am CoIl Cardiol 1985; 6:1164-66 9 Saner HE, Asinser R~ Daniel jA, Olson J. Two-dimensional echocardiographic identification of left ventricular pseudoaneurysm. Am Heart J 1986; 112:977-85 10 Smeal WE, Dianzumba SB, Joyner CR. Evaluation of pseudoaneurysm of the left ventricle by echocardiography and pulsed Doppler. Am Heart J 1987; 113:1508-10 11 Kupari M, Verkkala K, Maamies T, Hartel G. Value of combined cross sectional and Doppler echocardiography in the detection of left venticular pseudoaneurysm after mitral valve replacement. Br Heart J 1987; 58:52-56

232

Pulmonary Artery Thrombus Detection by Magnetic Resonance Imaging* Richard A. Szucs, M.D.; Roger B. Rehr, M.D.; and]ames L. Tatum, M.D.

We report a patient in whom cardiac magnetic resonance imaging detected a clinically unsuspected pulmonary artery thromboembolus. Follow-up MRI after surgical removal of the thromboembolus showed normal pulmonary arteries. This case illustrates the potential utility of MRI in the detection and follow-up of central pulmonary artery thromboembolism. (Chest 1989; 95:232-34)

W

e report a patient in whom magnetic resonance imaging detected the presence of a clinically unsuspected right pulmonary artery thromboembolus. CASE REPORT

A 30-year-old man was hospitalized with painful swelling of the left leg and toes. Physical examination revealed a cold, pulseless foot and a grade 316 systolic ejection murmur at the left sternal border. Two-dimensional echocardiography showed right atrial and ventricular enlargement with a normal left ventricle, intact atrial and ventricular septa, and no valvular vegetations. An aortobifemoral arteriogram revealed a blunt occlusion of the left superficial femoral artery consistent with an embolus. The patient underwent endarterectomy, embolectomy and angioplasty. A postoperative chest radiograph showed a nodular density in the right lower lobe which subsequently cavitated. The patient was referred for magnetic resonance imaging to further evalute the possibility of an atrial septal defect. Cardiac gated MRI was performed using a Siemens Magnetom with a 1.0 Tesla superconducting magnet. Ten mm thick coronal and 5 mm thick axial images were obtained using a dual spin echo multislice technique with TEs of 28 and 56 ms and a TR of 520 ms. The transaxial images revealed a well-defined region of high signal intensity filling most of the main and virtually all of the proximal right pulmonary artery (Fig 1). The intensity of this abnormal intravascular signal decreased by 45 percent from the first to the second echo and did not vary as a function of the phase of the cardiac cycle. The extent and shape of the apparent mass remained constant from the first to the second echo and throughout the cardiac cycle. No intravascular signal was observed in other regions of the pulmonary artery. Coronal images also revealed the presence of this abnormal signal (Fig 2), although its location and extent \\'ere better delineated on the transaxial images. Both the interatrial and interventricular septa appeared intact and no intracardiac mass was observed. Additionally, MRI showed a pulmonary parenchymal process in the right lower lobe which appeared as a ring of high signal intensity surrounding a region of lower signal intensi~ We interpreted the MRI study as showing the presence of a large, probably thromboembolic mass within the main and right pulmonary arteries and a cavitating right lower lobe pulmonary infarct. Cardiac catheterization immediately following the MRI revealed mild pulmonary hypertension with a pulmonary artery pressure of 45125 mm Hg (mean 30 mm Hg). Pulmonary angiography confirmed complete occlusion of the right pulmonary artery by a thromboembolus projecting into the main pulmonary artery. No intracardiac *From the Department of Radiology, Medical College of Virginia Hospitals, Richmond. Reprint requests: Dr. Rehr, Box 1, MeV Station, Richrnond, VA

23298-0001

Pulmonary Artery Thrombus Detection by MRI (SZUCs, Rehr, Tatum)

FIGURE 1. This transaxial image shows high intensity signal 611ing the right and the adjacent main pulmonary artery (RPA = right pulmonary artery; MPA = main pulmonary artery).

FIGCRE 3. This postoperative transaxial image shows normal appearing right and main pulmonary arteries (RPA = right pulmonary artery; MPA = main pulmonary artery).

mass or septal defect was identi6ed. The patient was taken to the operating room and a large, organized thrombus extending from the main pulmonary artery distally into branches of the right pulmonary artery was removed. Histologic examination of the specimen revealed organizing 6brin thrombus with early calci6cation. Postoperative follow-up MRI and pulmonary angiography showed a patent right pulmonary artery without increased intravascular signal (Fig 3 and 4). The pulmonary artery pressure measured 27n mm Hg (mean 15 mm Hg).

on the initial MRI study. The disappearance of this abnormal signal on repeat MRI obtained using identical technique shortly after operation provides dramatic evidence that the abnormal signal was due to the pulmonary thromboembolus and underscores the striking nature of the original findings in this case of central pulmonary artery thromboembolism with minimally to mildly elevated pulmonary artery pressures. Because vascular structures containing normally flOWing blood have little or no intraluminal signal on MRI, cardiac gated MRI has proved to be a useful noninvasive means for detecting intravascular and intracardiac masses. Specifically, cardiac gated MRI has been used to evaluate atrial and ventricular thrombi and tumors' and to demonstrate thrombus within an aortic aneurysm and within the vena cava. 2 Detection of pulmonary artery emboli with MRI has been studied in an animal model, and in this setting even relatively small pulmonary emboli were detected.' There have been several clinical reports ofthe detection of pulmonary emboli using MRI, although these cases did not have surgical or

DISCUSSION

This report is unique because it provides unequivocal histologic documentation of the source of the increased intravascular signal emanating from the pulmonary arteries

FIGURE 2. This coronal image shows the high intensity signal611ing the right and projecting into the main pulmonary artery (RPA right pulmonary artery; MPA = main pulmonary artery).

FIGCRE 4. The postoperative anteroposterior pulmonary angiogram appears normal as well. CHEST I 95 I 1 I JANUARY, 1989

233

histologic confirmation of the diagnosis and postoperative follow-up studies. 4 ,5 These studies indicate that MRI can detect central pulmonary emboli. They suggest that it may be less useful in the detection of peripheral emboli. One of the potential problems in using MRI to evaluate suspected pulmonary embolism is the differentiation of thrombus from pulmonary arterial hypertension. In the setting of pulmonary arterial hypertension, slow Bow within the pulmonary arteries can produce intraluminal signal. A recent study by White et al6 using cardiac gated MRI addressed this problem of differentiating pulmonary embolus from pulmonary arterial hypertension. Their investigations suggested that thrombus appears as a discrete intraluminal signal which remains constant throughout the cardiac cycle and exhibits decreased signal intensity on the second echo image relative to the first echo image. Pulmonary arterial hypertension without thromboembolism produces an intraluminal signal which appears to change in distribution during the cardiac cycle, disappears at one phase of the cycle, and exhibits increased signal intensity on the second echo image. The surgically confirmed thromboembolus in our patient behaved on MRI precisely as suggested by White et al,6 with a signal constant in distribution and extent throughout the cardiac cycle and decreasing in intensity from first to second echo. Pulmonary embolism is an uncommon cause of unilateral absence of perfusion or unilateral massive perfusion defect 7 on pulmonary perfusion scintigraph~ Nevertheless, many patients with these scintigraphic findings undergo pulmonary angiography to rule out pulmonary embolus. Since MRI can detect not only central pulmonary artery thromboembolus but also other causes of massive unilateral perfusion defects such as bronchogenic carcinoma and mediastinal or hilar adenopathy, it may be a useful noninvasive alternative to angiography in evaluating these patients. This case illustrates the potential utility of cardiac gated MRI in the evaluation and follow-up of central pulmonary artery thromboembolism. REFERENCES

1 Winkler M, Higgins CB. Suspected intracardiac masses: evaluation with MR imaging. Radiology 1987; 165:117-22 2 Hricak H, Amparo EG, Fisher MR, Crooks LE, Higgins CB. Abdominal venous system: assessment using MR. Radiology 1985; 156:415-22 3 Gamsu G, Hirji M, Moore E, Webb WR, Brito A. Experimental pulmonary emboli detected using magnetic resonance. Radiology 1984; 153:467-70 4 Thickman 0, Kressel HY, Axel L. Demonstration of pulmonary embolism by magnetic resonance imaging. AJR 1984; 142:921-22 5 Moore E, Gamsu G, Webb WR, Stulbarg MS. Pulmonary embolus: detection and follow-up using magnetic resonance. Radiology 1984; 153;471-72 6 White RD, Winkler ML, Higgins CB. MR Imaging of pulmonary arterial hypertension and pulmonary emboli. AJR 1987; 149:1521 7 Cho SR, Tisnado J, Cockrell CH, Beachley MC, Fratkin MJ, Henry DA. Angiographic evaluation of patients with unilateral massive perfusion defects in the lung scan. Radiographies 1987; 7:729-45 234

Severe Pulmonary Hypertension with Diffuse Smooth Muscle Proliferation of the Lungs* Pulmonary Tuberous SClerosis? Osvaldo E. Wagener, M.D.;t Aquiles J Roncoroni, M.D., F.C.C.R;+ and Juan A. Barcat, M.D.§

A 49-year-old man with normal intelligence and no cutaneous lesions had symptoms and signs of cor pulmonale. The chest roentgenogram showed an interstitial pattern. Hemodynamic studies revealed increased pulmonary arterial and wedge pressures. The patient died in shock, and the postmortem findings were a diffuse smooth muscle proliferation in the lungs as the cause of the pulmonary hypertension. We presume that this is a form of pulmonary tuberous sclerosis of which few cases are reported with such severe pulmonary hypertension as shown by our measurements. (Chest 1989; 95:234-37)

D

iffuse smooth muscle proliferation involving ~lveola~, bronchiolar, and vessel walls and pulmonary InterstItium is uncommon. Since the report of Berg and Vejlens, I it has been recognized that such proliferation may represent the pulmonary component of tuberous sclerosis, a disease characterized by epilepsy, mental retardation, and adenoma sebaceum. Similar pulmonary lesions may be found in patients without other evidence of this last disease. Muscle proliferation may affect intrapulmonary lymphatic vessels, mediastinal lymph nodes, and the thoracic duct, producing chylous effusions in pulmonary lymphangiomyomatosis. 2 In the absence of lymphatic involvement, the condition is named diffuse pulmonary leiomyomatosis. Many cases of diffuse pulmonary leiomyomatosis show one or more signs oftuberous sclerosis, a fact which induced ValensP to propose that diffuse pulmonary leiomyomatosis may represent a "forme fruste" of the disease. The present report details the findings in a man without clinical or family history oftuberous sclerosis who had severe cor pulmonale and elevated pulmonary and wedge pressures which induced his death. CASE REPORT

The patient was a 49-year-old man, a physician, referred because of dyspnea on minimum exertion. Symptoms started four years prior to admission with exertional dyspnea. Three years later, the patient developed dyspnea on mild exertion, edema of the lower extremities, and ascites. He received digoxin and diuretics, with symptomatic relief. An echocardiogram showed enlarged rightsided chambers. Two months later, the patient complained of cough and sudden dyspnea. With a presumption of pulmonary thromboembolism, he was treated with anticoagulants. T"ro months prior to admission, dyspnea on minimum exertion appeared. The patient had smoked 40 cigarettes daily for 27 years and met clinical criteria *From the Instituto de Investigaciones Medicas "Alfredo Lanari," Facultad de Medicina, U niversidad de Buenos Aires, Buenos Aires, Argentina. tChief Medical Resident. +Professor of Medicine and Medical Director. §Chief Pathologist. Reprint requests: Dr. Roncoroni, Av. Donato Alvarez 3150, Buenos

Aires, Argentina 1427

Severe Pulmonary Hypertension (Wagener, Roncoroni, Barcat)