Pulmonary angiography in acute pulmonary embolism: Indications, techniques, and results in 367 patients

Pulmonary embolism: results

angiography Indications, in

367

in acute techniques,

pulmonary and

patients

James E. Dalen, M.D. Harold L. Brooks, M.D. Lewis W. Johnson, M.D. Steven G. Meister, M.D. Murrill M. szucs, Jr., M.D. Lewis Dexter, M.D. Boston, Mass.

A

lthough angiographic techniques were first used to visualize the pulmonary vasculature more than 30 years ago,.L,2 this technique has been adapted to the detection of acute pulmonary embolism in man only in the past few years. The first angiographic studies relating to pulmonary embolism in man were reported in patients being evaluated for primary pulmonary hypertension and/or car pulmonale of unknown cause.3-6 In these studies, contrast medium was injected into the superior vena cava, and various angiographic abnormalities consistent with pulmonary vascular disease and/or recurrent pulmonary embolism were noted. The first large series of patients to be studied by angiography because of suspected acute pulmonary embolism was reported by Williams and Wilcox’ in 1963. Sasahara and associates8 and Alexander and co-workers9 were the first to report the use

of selective pulmonary angiography in the detection of acute pulmonary embolism. At the present time selective pulmonary angiography is widely accepted as the most specific test available for the detection of pulmonary embolism. In addition to detecting pulmonary embolism, hemodynamic studies performed at the time of angiography permit evaluation of the severity of pulmonary vascular obstruction by the emboli. Correlation of angiographic findings with hemodynamic and clinical tindings in acute pulmonary embolism has greatly enhanced our understanding of the pathophysiology of this common disorder. At the Cardiovascular Laboratory of the Peter Bent Brigham Hospital, we have utilized selective pulmonary angiography to assess patients suspected of having acute pulmonary embolism since 1964. The results of our experience with 367 angiographic studies of the pulmonary vascula-

From the Cardiovascular Laboratory, Peter Bent Brigham Hospital, and Harvard Medical School, Boston, Mass. Supported in part by grants (1 ROl-HE12439-01 and 5 TOl-HE05234.12) from the National Heart Institute, National Institutes of Health, United States Public Health Service. Received for publication April 9, 1970. Reprint requests to: Dr. James E. Dalen, 721 Huntington Avenue, Boston, Mass. 02115.

Vol. 81, No. 2, pp. 175185

February,

1971

American Heart Journal

175

Table I.

Irljection site

Results _I-

Number of studies Poor

sutis1 factory

’ Excelj lent

28 190

14 2

86 75

0 23

133

5

75

20

j Right atrium Right ventricle Main pulmonary artery

(70) ___-

ture during the six-year period from I964 to 1970 will be discussed. Techniques

Selective pulmonary angiography is performed by introducing a No. 7F or No. 8F closed-tip angiographic catheter with multiple side holes via a cutdown of an antecubital vein. Under fluoroscopic control the catheter tip is placed in the main pulmonary artery. Cardiac output is determined by the Pick or indicator dilution technique. Pressures in the pulmonary artery, right ventricle, right atrium, and a systemic artery are measured. After collection of these hemodynamic data the catheter is positioned in the main pulmonary artery or in the right ventricular outflow tract. Forty to 60 ml. of contrast medium is injected with a power injector at a rate of 20 to 30 ml. per second. A total of 12 chest x-rays are taken in the anterior-posterior position during held inspiration, at time intervals appropriate to visualize the passage of contrast medium through the peak pulmonary arterial phase, pulmonary venous phase, and the left heart. The contrast media used in these studies has been Hypaque-M 75 per cent” or Renografin-76 per cent.t We have noted no significant differences in the technical quality of studies or a difference in patient reaction to these two media. The earlier techniques of pulmonary angiography utilized injection of contrast medium in a peripheral vein, the superior *Sodium and rneglumine diatri~oates, Winthrop Labs., York, N. Y. tMethylglucamine Diatrizoate, I?. R. Squibb & Sons. York, N. Y.

New New

vena cava, or the right atrium.1s2.7 In our experience, injection into the pulmonary artery or right ventricle results in a more detailed and more complete visualization of the pulmonary vasculature. The technical quality of pulmonary angiograms performed from three different injection sites is shown in Table I. As noted, 14 per cent of the studies performed by injection in the right atrium were of poor quality, as opposed to only 2 per cent and 5 per cent with injection in the right ventricle or main pulmonary artery. We have encountered no complications related to the more central injection sites. Whereas premature ventricular contractions frequently occur during injection, no arrhythmias requiring treatment occurred in 190 studies in which injection was made in the right ventricle. The only two arrhythmias related to this procedure in 367 patients occurred when the catheter entered the right atrium (Table III). Furthermore, we have observed no evidence that passage of the catheter through the right heart to the pulmonary artery has dislodged thrombi or emboli. he! normal

pdmonary

~ngiQgr~m

In patients without pulmonary embolism or pulmonary vascular disease, contrast medium injected proximal to or at the pulmanic valve visualizes each lobe of the lung at the same time (Fig. 1) A). Using conventional techniques, the main left and right pulmonary arteries, lobar arteries, segmental branches, and the first two subdivisions of the segmental arteries are visualized. When contrast medium is injected into the right ventricular outflow tract or the main pulmonary artery at an injection rate of 20 to 30 ml. per second, the peak arteriai phase occurs three to four seconds after injection, As shown in Table II, the presence of pulmonary embolism per se does not delay visualization of the peak arterial phase. The factors that are associated with a delay in the circulation of contrast medium are clinical evidence of left heart failure, low cardiac index, and pulmonary hypertension. In the presence of these conditions,

Pulmonary

angiography in pulmonary

Fig. 1, A and B. Normal pulmonary angiogram. A, Arterial phase. Three seconds metrical filling of the entire pulmonary arterial tree. B, Venous phase. Six seconds medium has filled the pulmonary veins, left atrium, and left ventricle.

Table II. Average time to peak arterial phase (seconds after injection)

1i

Groups Total group Angiogram positive embolism No heart disease Clinical evidence heart failure

No. of

Time

studies

(sec.)

310

3.7

71

3.6

113

3.1

127

4.2

M.)

129

3.2

M.)

50

4.9

116

3.1

60

4.1

for

pulmonary

of congestive

Cardiac index normal (>3.0 L./min./sq. Low cardiac index (<2.0 L./min./sq.

Normal pulmonary artery (mean <20 mm. Hg) Pulmonary hypertension (mean >40 mm. Hg)

pressure

timing of films must be adjusted to permit appropriate visualization. The pulmonary veins from each part of the lungs are visualized simultaneously at an average of three seconds after the peak arterial phase (Fig. 1) B) . Indications to pulmonary

and contraindications angiography

The only absolute contraindication to this procedure is known allergy to contrast media. In addition, there are two relative contraindications that must be considered: (1) recent myocardial infarction, and (2)

embolism

after injection after injection

177

there is symthe contrast

ventricular irritability. These two conditions represent relative contraindications because they predispose to the occurrence of ventricular arrhythmias during passage of the catheter to the pulmonary artery. In the presence of these relative contraindications, it is our policy to proceed with pulmonary angiography only if the results of angiography are essential to the determination of the patient’s therapy. For example, in the infrequent circumstance where pulmonary embolectomy is a therapeutic consideration, we proceed with angiography in the presence of relative contraindications even in critically ill, hypoxic, and hypotensive patien.ts. In patients with left bundle branch block, there is the potential that complete heart block will occur when the catheter passes through the right ventricle.rO Therefore, when performing pulmonary angiography in patients with left bundle branch block we use a specially designed ,angiographic catheter that can be used as a unipolar pacemaker. In the absence of these relative contraindications, it is our policy that the suspicion of pulmonary embolism per se is an indication for pulmonary angiography. Complications of pulmonary angiography: Morbidity and mortality r&es

Complications may occur secondary to cardiac catheterization, or as reactions to contrast media. The complications encountered in 367 consecutive patient stud-

178

Dalen et al.

Table III. Com$&cations of pulmonary angiography in 367 consecutive patients

I.

II.

Related to cardiac catheterization Cardiac perforation Pyrogen reaction Arrhythmia Re!ated to angiography Rronchospasm Angioneurotic edema Anaphylaxis Cardiogenic shock Total

2 3 2

0 0 0

3 1 1 1

0 0 0 I

13 (4%)

1 (0.3cj,)

ies over a six-year period in our laboratorv are shown in Table III. There were seven complications related to cardiac catheterization and six related to angiography per se. The total incidence of complications was 4 per cent. Two cardiac perforations occurred in the first 50 patients to be studied by pulmonary angiography in this laboratory. Both perforations occurred during passage of the catheter to the pulmonary artery and were judged to be related to the use of a stiff, nylon core angiographic catheter. With the use of a more pliable woven dacron angiographic catheter* there have been no perforations in more than 300 consecutive angiographic studies. Pyrogen reactions occurred in three patients and were treated with acetylsalicylic acid. Two patients developed rapid atria1 fibrillation when the catheter entered the right atrium. In each case the arrhythmia was controlled with digitalis, and normal sinus rhythm was restored within 24 hours. The most common complication related to contrast media was acute bronchospasm. Each of the three episodes of bronchospasm occurred in patients with a history of bronchial asthma, and each episode was relieved by intravenous epinephrine (1 to 5 ml. of l:lOO,OOO solution). The only death related to the procedure occurred in a 36-year-old woman with ter“Eygendorf, United States Glens Falls, N. Y.

Catheter

and

Instrummt

Cur>.,

minal primary pulmonary hypertension and recent acute pulmonary embolism. Cardiogenie shock with electromechanical dissociation occurred immediately after injection of 40 ml. of contrast media. Cardiac resuscitation was unsuccessful. One additional death occurred during this six-year period. In this patient, emergency pulmonary angiography was performed thirty minutes after she had been resuscitated from cardiac arrest which was judged to have been due to massive pulmonary embolism. Throughout the angiographic procedure she was ventilated through an endotracheal tube, and marked hypotension persisted despite vasopressors. Pulmonary angiography demonstrated massive central pulmonary embolism. Twenty minutes after the angiogram had been performed, while preparations were being made for pulmonary embolectomy with cardiopulmonary bypass, hypotension became more severe and cardiac arrest recurred. Emergency Trendelenburg embolectomy was performed in the cardiac catheterization laboratory. Although large central pulmonary emboli were removed, the patient could not be resuscitated. Her death was attributed to massive pulmonary embolism; it did not appear to have been precipitated by pulmonary angiography. Seven other patients with massive pulmonary embolism have subsequently undergone emergency pulmonary angiography without untoward reactions despite the presence of hypotension requiring vasopressors throughout the procedure. Wngiographic puimonary

findings embolism

in

The most diagnostic finding in pulmonary embolism is visualization of an intraarterial embolus as a negative intraluminal filling defect, outlined by surrounding radiopaque contrast medium. However, pulmonary embolism may be present without this specific finding; and embolism may cause certain other angiographic abnormalities. These abnormalities have been documented in this laboratorynJ2 using intact, anesthetized dogs. After baseline pulmonary angiograms \vere taken, dogs were embolized with 3 to 10 ml. of autologous blood clot. In some cases the blood

iWrnonary

angiography in pzdrnonary embolism

2. Intraluminal filling defects. Filling defects are well visualized lower lobe. A large nonobstructing filling defect in the left pulmonary in this view, because contrast medium surrounds it. Note that none plete obstruction; therefore, there is minimal oligemia. Fig.

clot was rendered radiopaque by the addition of Dionosil* so that the emboli could be localized by plain chest x-rays taken after embolization. Selective pulmonary angiograms in three projections were taken at intervals after embolization and were compared with the baseline angiograms. These experimental studies demonstrated that the presence of thromboemboli in the pulmonary circulation can cause four different angiographic abnormalities: 1. Intraluminal jilling defects (Fig. 2). This most specific sign of pulmonary embolism was not detected in all cases. A large incompletely obstructing embolus may not be detected becaLuse it is obscured by contrast medium. flowing around it. 2. Cz~toffs of arteries (Fig. 3). As with intraluminal filling defects, this finding was not seen with all emboli. Cutoffs occur only if an embolus causes complete occlusion of an artery. More frequently, the embolus straddles a bifurcation and causes partial occlu*Dim&l Aqueous, gland.

Glaxo

Laboratories

Ltd.,

Greenford,

En-

179

in the right upper lobe and in the right artery (arrow) is difficult to visualize of the filling defects have caused com-

sion of each branch. If an artery is occluded near its origin, a cutoff may be recognized only if the absence of that specific artery is detected. 3. Areas qf oligemia (Fig. 4). Areas of the lung that are distal to a completely obstructed artery are not perfused, and thus will appear oligemic by angiography. However, oligemia may also occur in portions of the vasculature that are distal to incomplete embolic occlusion. In this circumstance, if the embolus itself is not recognized as an intraluminal filling defect, embolism will be evidenced only by the area of oligemia distal to the site of unrecognized incomplete embolic obstruction. Oligemia may also result from embolic occlusion of multiple small peripheral arterial branches in a given area of the lung. In this circumstance the embolized area may appear “pruned,” i.e., the arterial tree in that area may appear as a tree pruned of its small branches. 4. Asymmetry of flow. When contrast medium is injected at or proximal to the pulmonic valve, it flows at the

1so

Amer. Newt I. Febrmry, 1971

Dalen et al.

Fig. 3. Cutoffs of arteries. A large intraluminal filling defect is present in the left the origin of the left upper lobar artery. Although the filling defect is indistinct, point with resultant distal oligemia.

Fig. 4. Oligemia due to pulmonary embolism. Multiple obstructed blood flow with resultant oligemia of the entire has occurred secondary to an obstructed segmental artery. the vasculature, the left upper lobe.

filling defects in the right lung. In the left Note the hyperemia

pulmonary the artery

artery, distal to is cut off at this

right pulmonary artery have lower lobe, an area of oligemia of the only normal portion of

Pulmonury

same rate to each part of the lungs. When incomplete embolic occlusion occurs, it may cause a delay in filling of the arterial tree distal to the plaint of incomplete occlusion. There may be associated oligemia of this area of the lung, or perfusion of this area rnay be complete even though delayed. We have shown that each of these four angiographic abnormalities (intraluminal filling defects, cutoffs, oligemia, and asymmetry of flow) occur when healthy dogs are embolized with autologous blood clot. These same four angiographic abnormalities also occur in patients with pulmonary embolism. In patients in whom the diagnosis of pulmonary embolism is certain because of the visualization of intraluminal filling defects and/or cutoffs, areas of oligemia and asymmetry of flow are frequently present. However, in patients who have chronic lung disease or congestive heart failure, these latter two abnormalities, oligemia and asymmetry of flow, may occur in the absence of pulmonary embolism. The angiographic abnormalities associated with embolism in patients with and

Fig. 5. Oligemia without or angiographic evidence and the left upper lobe. roentgenogram.

ungiography

in pulmonnry

embolism

181

without coexistent chronic lung disease or congestive heart failure were assessed in this laboratory by Stein and associates.13 They found that filling defects and cutoffs occur only in patients with pulmonary embolism. These two abnormalities were not present in patients with chronic lung disease or congestive heart failure without pulmonary embolism. However, oligemia and asymmetry of blood flow, although very frequent in documented pulmonary embolism, also occurred in association with chronic lung disease or congestive heart failure in the absence of pulmonary embolism. Oligemia may occur in association with emphysematous blebs in patients with chronic lung disease and may mimic pulmonary embolism as shown in Fig. 5. Asymmetry of flow is often seen in patients with heart disease that has caused increased pulmonary venous pressure (e.g., secondary to left ventricular failure or mitral stenosis). With significant elevation of pulmonary venous pressure, peak flow to both lower lobes may occur one to three seconds after peak visualization of the upper lobar arteries (Fig. 6). The relation-

pulmonary embolism. In this patient of pulmonary embolism. Extensive These areas of oligemia correspond

with chronic lung disease, there was no clinical areas of oligemia are present in the right lung to emphysematous blebs evident on plain chest

182

Daien et al.

Fig. 6, A and B. Asymmetry of flow without pulmonary embolism. A, Two seconds after injection the contrast extends to the periphery of the upper lobes, but has not filled the lower lobes. B, Four seconds after injection contrast has filled the lower lobes indicating that the vasculature in the lower lobes is intact. This patient had mitral stenosis with a left atria1 mean pressure of 20 mm. Hg. There was no clinical or angiographic evidence of pulmonary embolism.

Table IV. Relationship between pulmonary capillary wedge pressftre and jlow patteuf to lower lobes in patients without pulmonary embolism I Puln2onary capillary wedge presswe (mean, mm. Hg)

20

/

Ptrtients Ao._ 0f studies

with lower

bilateral

lobe delay

105

11

15 27

20 48

(7”)

ship of this flow abnormality, bilateral lower lobe delay, to pulmonary venous pressure (as reflected by pulmonary capillary pressure) in patients without pulmonary embolism is shown in Table IV. Whereas delay of flow to the lower lobes was uncommon when pulmonary capillary wedge pressure was less than 20 mm. Hg, bilateral lower lobe delay occurred in 48 per cent of 27 patients with a pulmonary capillary wedge pressure of more than 20 mm. Hg. On the basis of these experimental and clinical observations, we utilize the following criteria in the diagnosis of pulmonary embolism by pulmonary angiography : 1. Definite pulmonary embolism. Intraluminai filling defects and/or cutoffs of arteries. 2. Pyobabk pulmonary embolism. Oligemia and/or asymmetry of blood flow in patients who do not have co-

existent lung disease or heart disease. 3. Equivocal. Plesence of oligemia and/or asymmetry of blood flow in patients with lung disease or heart disease, or presence of uncertain abnormalities, i.e., possible filling defect or possible cutoff.

4. Negative. No angiographic abnormalities consistent with pulmonary embolism. Angiographic suspected embolism

of

findings in patients acute pulmonary

The angiographic diagnosis (using the above criteria) in 247 consecutive patients suspected of acute pulmonary embolism (symptoms within four weeks of the study) are shown in Chart I. As can be seen, a definitive angiographic diagnosis, i.e., definite pulmonary embolism or negative for pulmonary embolism (normal angiogram) was made in 74 per cent of the 247 patients. The current limitation of this technique is reflected by the large number of studies (17 per cent) which were interpreted as equivocal. In these latter cases pulmonary embolism was neither established nor excluded by the angiographic study. Definite pulmonary embolism. The angiographic abnormalities present in the 89 patients with angiographic abnormalities interpreted as demonstrating definite pulmonary embolism are shown in Chart II. As a result of our criteria for an angio-

Voluma Number

81 2

Pukmonary angiography in pulmonary

Chart I. No. D+pOSiS

Definite Probable Equivocal Negative

pulmonary pulmonary

I embolism embolism

of

pntients

1

89 22 42 94

% 36 9 17 38

Chart II. Divisions

No. I

Intraluminal cutoffs Oligemia Asymmetry

filling

of flow

defects

I 71 55 67 62

% 80 ;: 70

graphic diagnosis of definite pulmonary embolism, all 89 patients had intraluminal filling defects and/or cutoffs. The high incidence of the less diagnostic findings, oligemia (7.5 per cent) and asymmetry of flow (70 per cent), is evident. In these 89 patients, evidence of embolism was rarely limited to one artery or one lobe. In 47 per cent of these cases, filling defects were present in both lungs. This is consistent with observations made at post mortem by Smith, Dexter, and Dammin.14 Utilizing postmortem arteriography in 54 patients with pulmonary embolism, they found that in each case multiple emboli were widely scattered through all segments of the lungs. Probable puknonary embolism. Each of the 22 patients whose angiogram was interpreted as probable pulmonary embolism had asymmetry of flow (86 per cent) and/or oligemia (50 per cent) in the absence of lung disease or congestive heart failure. In addition, 50 per cent had possible intraluminal filling defects and 41 per cent had possible cutoffs. Each of these patients was treated for acute pulmonary embolism. Equivocal. The 42 patients in whom pulmonary embolism was neither excluded nor established by the angiographic study highlight the shortcoming of this technique. In these patients, the decision regarding ther-

embolism

183

apy was of necessity based on the clinical findings. In 10 patients the diagnosis was equivocal due to the fact that the angiographic study was of suboptimal technical quality. Suboptimal studies were most common in patients with congestive failure, chronic lung disease, or obesity. As noted, technically poor studies were especially common when injection was made in the right atrium rather than the right ventricle or pulmonary artery (Table I). In the remaining 32 patients, the study was equivocal because of the presence of nondiagnostic abnormalities, i.e., possible filling defects or cutoffs, or oligemia and/or asymmetrical flaw in patients with preexistent heart disease or lung disease. Heart disease with congestive failure presents a particular problem in the interpretation of pulmonary angiograms. Of 117 patients without previous heart disease, the angiographic study was equivocal for pulmonary embolism in only 11 per cent; whereas, in 125 patients with coexistent congestive heart failure, equivocal studies were obtained in 21 per cent. There was no increase in the per cent of equivocal studies in 60 patients studied more than four weeks after the onset of symptoms (19 per cent) than in the 247 patients studied within four weeks of the onset of symptoms (17 per cent). Negative angiographic studies. Ninetyfour (38 per cent) of the 247 patients clinically suspected of acute pulmonary embolism had no evidence of pulmonary embolism at angiography. We believe that this high percentage of negative studies can be attributed to two factors. It has been our philosophy that in patients without relative contraindications, the risks of pulmonary angiography are less than the risks of inappropriate surgical or medical therapy of presumed pulmonary embolism. Therefore, the primary indication for angiography in this group of patients was suspicion of pulmonary embolism. Rigorous criteria for the clinical diagnosis were not employed in selecting patients for angiography. Thus, the high percentage of negative studies in this series may be a reflection of the difficulties of the clinical diagnosis of pulmonary embolism.

Dalen at al.

184

Table V. Comparison of firemortem angiography with postmortem jindings Postmortem

Premorfem angiographic diagnosis

Pulmonary embolism

Definite pulmonary embolism Probable pulmonary

diagnosis No pulmonnvy euzboliswa

7

0

embolism

1

0

Equivocal Negative

1 0

2 6

The second factor to be considered is that a negative angiographic study may not per se exclude embolism that is limited to arteries that are too small to be visualized by conventional angiography. It is difficult to determine how often embolism may be limited to third order or lobular arteries and still present symptoms. At postmortem, embolic obstruction of these small arteries is very common.14 Of the 94 patients with normal pulmonary angiograms, 53 had lung scans. Fortythree of these 53 lung scans were abnormal. However, 21 of these 43 patients had an infiltrate and/or pleural effusion by chest x-ray at the time of lung scan. Thus, the perfusion defects noted by lung scan may have been due to abnormalities other than pulmonary embolism.r5,r6 It is also possible that some of these patients with an abnormal lung scan but normal pulmonary angiogram had embolism limited to the smallest branches of the pulmonary vasculature. Validity diagnosis

of of

the angiographic pulmonary embsiism

The ultimate criterion for the accuracy of interpretation of pulmonary angiograms is postmortem examination of the lungs. However, comparison of angiographic and postmortem findings is pertinent only if the postmortem examination is performed in close proximity to the premortem angiographic study. Significant resolution of pulmonary embolism may occur in periods longer than two weeks.rr During this five-year period, 17 of our patients who had been studied by pulmo-

nary angiography died and had postmortem_ examination within two weeks of the angiographic study. Of seven patients with an angiographic diagnosis of definite pulmonary embolism and one with probable pulmonary emboilsm, all eight had embolism at postmortem. Thus there were no false positive angiographic diagnoses. Of six patients with a negative pulmonary angiogram studied at postmortem, none had pulmonary emboli. However, of the three patients with a diagnosis of equivocal, one had emboli at postmortem examination and two did not. It is our conclusion that using the angiographic criteria that we have outlined, false positive angiographic diagnoses of pulmonary embolism are rare. False negative diagnoses present a potential problem. Since pulmonary embolism may be present without demonstrable filling defects or cutoffs, reliance upon these two criteria for a definitive diagnosis allows the potential of a false negative diagnosis. Iiowever, since embolism rarely occurs without at least a nonspecific angiographic abnormality, most false negative interpretations would be categorized in the equivocal or probable group by our criteria. It is our policy to treat for pulmonary embolism when the angiogram is definite or probable and to treat most patients whose angiograms are read as equivocal. We believe that it is sufficiently important to avoid false positive angiographic diagnosis, that we tolerate a sizeable percentage of equivocal interpretations. We anticipate that the use of magnification angiographic technique@ and the use of selective cineangiographyrg as an adjunct to conventional pulmonary angiography will permit the more accurate recognition of embolism in studies currently interpreted as equivocal. Summary

Pulmonary angiography is the most specific test available for the diagnosis of acute pulmonary embolism. This technique can safely be performed in critically ill patients. In 367’ consecutive studies our incidence of complications has been 4 per cent, and there has been only one death. Hemodynamic studies done as part of

Volume 81

Nwnber

2

Pulmonary

the procedure permit evaluation of the severity and the pathophysiology of acute pulmonary embolism. The two diagnostic angiographic findings of pulmonary embolism. are intraluminal filling defects and cutoff arteries. Oligemia and asymmetry of blood flow are frequently seen in pulmonary embolism, but are not specific. These latter two abnormalities may occur in chronic lung disease or congestive heart failure without pulmonary embolism. Using these diagnostic criteria in 247 patients studied because of a clinical diagnosis of acute pulmonary embolism, a definitive diagnosis (either definite pulmonary embolism or negative) was established by angiography in 74 per cent. In 9 per cent the diagnosis was probable pulmonary embolism, and in 17 per cent the findings were equivocal for pulmonary embolism. Application of these diagnostic criteria results in minimal false positive iangiographic diagnoses. False negative diagnoses may occur if embolism is limited to peripheral branches of the pulmonary vasculature that are not visualized by current angiographic techniques. The incidence of symptomatic pulmonary embolism limited to these small arteries is uncertain. The primary limitation of this technique is, that in patients with underlying heart disease or chronic lung disease, the results of angiography may be equivocal. The application of new techniques of magnification angiography and/or selective cineangiography offer promise in enhancing the recognition of embolism in this group of patients. REFERENCES Carvalho, L., and Moniz, E.: Visibility of the pulmonary vessels (angiopneumography), Acta Radiol. Lisbon 14:433, 1933. 2. Robb, G. P., and Steinberg, I.: Visualization of the chambers of the heart, the pulmonar:y circulation, and the great blood vessels in man, Amer. J. Roentgen. Pl:l, 1939. 3. Carroll, D.: Chronic obstruction of major pulmonary arteries, Amer. T. Med. 9:175, 1950. 4. Davison, P. H., ‘Armitage, G. H., and McIlveen, D. J. S.: Chronic car pulmonale due to silent pulmonary embolism, Lancet 2:224, 19!56. .5 . Ehrner, L., Garlind, T., and Linderholm, H.: Chronic car pulmonale following thromboembolism, Acta Med. Stand. 164:279, 1959. 1.

angiography in pulmonary

6.

embolism

185

Chrispin, A. R., Goodwin, J. F., and Steiner, R. E.: The radiology of obliterative pulmonary hypertension and thromboembolism, Brit. J. Radiol. 36:705, 1963. 7. Williams, J. R., and Wilcox, W. C.: Pulmonary embolism: roentgenographic and angiographic considerations, Amer. J. Roentgen., Rad. Therapy and Nuclear Med. 89:333, 1963. 8. Sasahara, A. A., Stein, M., Simon, M., and Littmann, D.: Pulmonary angiography in the diagnosis of thromboembolic disease, New Eng. J. Med. 270:1075, 1964. 9. Alexander, J. K., Lewis, J. M., Axelrad, M. A., Lockhart, R. W.. and Fred. H. L.: Cardiorespiratory function in patients with acute pulmonary thromboembolism demonstrated angiographically, Clin. Res. 13:346, 1965. 10. Stein. P. D.. Mathur. V. S.. Herman. M. V.. and Levine, H. D.: Complete heart block induced during cardiac catheterization of patients with preexistent bundle branch block, Circulation 34:783, 1966. 11. Dalen, J. E., Mathur, V. S., Evans, H., Haynes, F. W., Pur-Shahriari, A. A., Stein, P. D., and Dexter, L.: Pulmonary angiography in experimental pulmonary embolism, AMER. HEART J. 72:509, 1966. 12. Mathur, V. S., Dalen, J. E., Evans, H., Haynes, F. W., Pur-Shahriari, A. A., Stein, P. D., and Dexter, L.: Pulmonary angiography one to seven days after experimental pulmonary embolism, Invest. Radiol. 2:304, 1967. 13. Stein, P. D., O’Connor, J. F., Dalen, J. E., PurShahriari, A. A., Hoppin, F. G., Jr., Hammond, D. T., Haynes, F. W., Fleischner, F. G., and Dexter, L.: The angiographic diagnosis of acute pulmonary embolism: evaluation of criteria, AMER. HEART J. 73:730, 1967. 14. Smith, G. T., Dexter, L., and Dammin, G. J.: Postmortem quantitative studies in pulmonary embolism, in Sasahara, A. A.. and Stein. M.. editors: Pulmonary embolic disease, New York; 1965, Grune & Stratton, Inc., p. 120. 15. Poulose, K., Reba, R. C., and Wagner, H. N., Jr.: Characterization of the shape and location of perfusion defects in certain pulmonary diseases, New Eng. J. Med. 279:1020, 1968. 16. Quinn, J. L., III: The lung: the challenge of nuclear medicine, Amer. J. Roentgen. 105:251, 1969. 17. Dalen, J. E., Banas, J. S., Jr., Brooks, H. L., Evans, G. L., Paraskos, J. A., and Dexter, L.: Resolution rate of acute pulmonary embolism in man, New Eng. J. Med. 280:1194, 1969. 18. Greenspan, R. H., Simon, A. L., Ricketts, H. J,, Rojas, R. H., and Watson, J. C.: In vivo magnification angiography, Invest. Radiol. 2:419, 1967. 19. Brooks, H., Meister, S., Szucs, M., Jr., Banas, J., Jr., Dexter, L., and Dalen, J.: Selective cineangiography in the diagnosis of pulmonary embolism, Circulation 4O:III-51, 1969. (Suppl. III).