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DOI:10.2214/AJR.04.0833
AJR 2006; 187:128-134
© American Roentgen Ray Society

Original Research

Hemodynamic Effects of Monomeric Nonionic Contrast Media in Pulmonary Angiography in Chronic Thromboembolic Pulmonary Hypertension

Michael B. Pitton1, Gunter Kemmerich1, Sascha Herber1, Eckhard Mayer2, Manfred Thelen1 and Christoh Düber1

1 Department of Radiology, University Hospital of Mainz, Langenbeckstr. 1, Mainz, Germany 55131.
2 Department of Cardiothoracic Surgery, University Hospital of Mainz, Mainz, Germany.

Received May 27, 2004; accepted after revision April 6, 2005.

 
Address correspondence to M. B. Pitton (pitton{at}radiologie.klinik.uni-mainz.de).


Abstract
Top
 Abstract
Introduction
 Subjects and Methods
 Results
 Discussion
 References
 
OBJECTIVE. The purpose of this study was to investigate the hemodynamic safety of the monomeric nonionic contrast agent iomeprol for selective pulmonary angiography in chronic thromboembolic pulmonary hypertension (CTPH), and to investigate the effect of periinterventional oxygen administration.

SUBJECTS AND METHODS. Selective pulmonary digital subtraction angiography was performed in 94 patients with CTPH using six bolus injections of iomeprol (posteroanterior, oblique, and lateral projections; both pulmonary arteries; iomeprol, 25 mL at 13 mL/s). Hemodynamics were obtained with Swan-Ganz catheters, and systolic pulmonary artery pressure (PAsyst) was classified into one of three groups: 30 mm Hg or less (control group), greater than 30 but less than or equal to 60 mm Hg (group 1, moderate pulmonary hypertension), and greater than 60 mm Hg (group 2, severe pulmonary hypertension).

RESULTS. At baseline, values for PAsyst were 21.4 ± 2.3 (control group, n = 8), 49.8± 8.5 (group 1, n = 18), and 86.5 ± 18.9 (group 2, n = 68) mm Hg (p < 0.001). Pulmonary vascular resistance indexes (PVRI) were 222 ± 105 (control), 703 ± 364 (group 1), and 1,582 ± 562 (group 2) dyne x s x cm-5 x m2 (p < 0.001). The mean cardiac indexes were 3.1 (control), 2.8 (group 1), and 2.3 (group 2) L/min/m2 (p < 0.05). Pulmonary capillary wedge pressure (PCw) indicated healthy left heart function. Periinterventional oxygen inhalation improved oxygen saturation in all groups and slightly reduced pulmonary artery pressure and heart rate. Online measurement of pulmonary artery pressure during contrast bolus injection for angiography showed only a minor increase, predominantly in severe pulmonary hypertension ({triangleup} [difference] PAsyst: 1.3 ± 1.9 [control], 2.9 ± 3.4 [group 1], and 3.8 ± 4.5 [group 2] mm Hg [p < 0.001]). After completion of angiography, right atrial pressure (RAP) and PAsyst were moderately increased: {triangleup} RAP: 1.4 (control), 2.6 (group 1, p < 0.001), and 3.0 (group 2, p < 0.001) mm Hg; {triangleup} PAsyst: 3.2 (control), 7.7 (group 1, p < 0.01), and 8.5 (group 2) mm Hg (p < 0.001). PVRI was significantly higher in group 2 ({triangleup} PVRI: 188 dyne x s x cm-5 x m2, p < 0.001).

CONCLUSION. Selective pulmonary angiography using iomeprol is safe without critical pressure peaks during selective contrast bolus injection or significant hemodynamic derangement in severe CTPH. Periinterventional oxygen inhalation improved pulmonary circulation.

Keywords: chronic thromboembolic pulmonary hypertension • CTPH • contrast media • digital subtraction angiography • embolism • pulmonary hemodynamics • pulmonary hypertension


Introduction
Top
 Abstract
 Introduction
Subjects and Methods
 Results
 Discussion
 References
 
Selective pulmonary angiography is still the reference method for diagnosing chronic thromboembolic pulmonary hypertension (CTPH). MR angiography and CT angiography are noninvasive alternatives, but the specific changes caused by chronic thromboembolic disease are most reliably confirmed by selective angiography. Typically, angiographic findings of CTPH are webs and bands, unusual stenotic lesions and irregularities of the vessel wall, abrupt diameter reductions, pouchlike endings of arteries, and peripheral perfusion defects [1-3]. On the other hand, thromboembolic findings have to be excluded in cases with primary pulmonary hypertension (PPH). In CTPH cases, pressure measurement and calculation of pulmonary vascular resistance are essential for decision making for pulmonary thromboendarterectomy and are reliably performed with insertion of a Swan-Ganz catheter. Detailed angiographic workup is indicated to identify even subtle thromboembolic deposits for differentiation between CTPH and PPH and for planning the surgical procedure. Furthermore, certain CTPH cases with circumscribed stenoses are eligible for interventional treatment with percutaneous transluminal angioplasty, in cases with segmental and even subsegmental stenoses [4, 5].

However, despite encouraging treatment results with pulmonary thromboendarterectomy, CTPH is still underdiagnosed in many cases [1, 6, 7]. There might be some concerns with respect to angiographic workup because of past reports of deleterious changes of pulmonary circulation in such patients, including considerable deterioration of right heart hemodynamics and fatality during contrast injections [8-12]. However, these older contrast media have been replaced by newer and safer ones. Monomeric contrast agents like iomeprol, with low osmolality and low viscosity, may significantly improve the tolerance of contrast media, and high iodine delivery rates improve image quality. Patients with severe CTPH and reduced vasodilatation capacity should benefit from these physicochemical characteristics. Therefore, the objective of this study is to describe the hemodynamic changes of pulmonary circulation during selective pulmonary angiography with direct pulmonary bolus injection of iomeprol, particularly in cases with severely impaired pulmonary circulation caused by CTPH. Oxygen administration is known to improve pulmonary circulation and is strongly suggested in the literature [8, 13]. Therefore, the effect of oxygen inhalation has been evaluated to identify the residual vasodilating capacity.


Subjects and Methods
Top
 Abstract
 Introduction
 Subjects and Methods
Results
 Discussion
 References
 
Patients with a history of thromboembolic pulmonary disease or evidence of pulmonary hypertension in clinical data, echocardiography, and helical CT were included in this prospective study to evaluate whether they were candidates for surgical pulmonary thromboendarterectomy. After informed consent, the study was performed in 94 patients (53 men and 41 women; mean age, 54 ± 14 years) to evaluate both their hemodynamic and angiographic status. Eligibility for surgery included angiographic determination of the beginning of endoluminal thromboembolic deposits at the level of the main pulmonary artery or first-order segmental arteries to ensure surgical accessibility for the preparation procedure [1, 14]. For hemodynamic assessment, a 7.5-French Swan-Ganz catheter (Baxter) was inserted through a transcubital access. For selective pulmonary angiography, femoral access was used, and angiography was performed using a 6.5-French pigtail catheter selectively in both pulmonary arteries.

Hemodynamic status included measurement of noninvasive systemic blood pressure (systolic, diastolic, and mean), mean right atrial pressure (RAP), pulmonary artery pressure (systolic, diastolic, and mean), pulmonary capillary wedge (PCw) pressure, cardiac index, and arterial oxygen saturation (SaO2). The systemic vascular resistance index (SVRI), pulmonary vascular resistance index (PVRI), total pulmonary resistance index, and right and left ventricular stroke work indexes were computed automatically (Sirecust 1260, Siemens Medical Solutions).

Hemodynamic status was obtained during expiratory breath-hold and was performed three times: at baseline, after 15 minutes of oxygen inhalation, and immediately after completion of the six angiography runs. The baseline data are part of our routine workup for CTPH patients, as well as the hemodynamics after oxygen inhalation, to evaluate whether oxygen has some therapeutic effect—that is, whether residual dilatation capacity of the pulmonary vessels was present. The contrast-enhanced data reflect the hemodynamic effects of the specific contrast medium.

Angiography was performed during deep inspiratory breath-hold, and three angiography series were obtained for each right and left pulmonary artery, including a posteroanterior view, an oblique view (25°), and a lateral view in all cases. Angiography was performed using the digital subtraction technique. The contrast bolus consisted of 25 mL of Iomeron 300 (iomeprol, Altana Pharma; 300 mg I/mL; osmolality, 521 ± 24 mOsm/kg [37°C]; viscosity, 4.5 ± 0.4 mPa x s [37°C]) at a flow rate of 13 mL/s. This was sufficient to opacify the entire pulmonary artery tree to the level of the fifth- or sixth-order vessel in nearly all patients.

A few patients were unable to sufficiently hold inspiratory arrest for the 10-15 seconds required. In these cases, additional angiography with a bolus injection into the intermediate pulmonary artery helped shorten the angiography time and reduced motion artifacts to ensure an accurate diagnosis. With both catheters in situ, this setup allowed an online registration of pulmonary pressure curves during each sequence for monitoring the pulmonary peak pressure during selective bolus injections. For this purpose, the tip of the Swan-Ganz catheter was positioned in free blood flow to ensure that it would not become mired in the thromboembolic material. Because of the communicating compartments, this position assured that the peak pressure measurements were representative of the pulmonary trunk and both pulmonary arteries.

The registration of the pressure curves started before the onset of the inspiratory breath-hold and was continued during the entire sequence. This procedure allowed discrimination of the inspiration-related pressure increase and the bolus-related pressure peaks during each sequence. Immediately after completion of the angiography, the final hemodynamic status was obtained, again during an expiratory breath-hold, and the respective resistances were calculated and compared with the baseline status. Thus, the complete data set contained a detailed hemodynamic status—during expiratory breath-hold at baseline, after oxygen inhalation, and after completion of the angiography—and six successive pressure curves during inspiratory breath-hold representing the repeated angiography sequences with contrast bolus injections. Three patient groups were defined on the basis of the systolic pulmonary artery (PAsyst) pressure at baseline measurement: No pulmonary hypertension at rest (control group, PAsyst ≤ 30 mm Hg), moderate CTPH (group 1, PAsyst > 30 but ≤ 60 mm Hg), and severe CTPH (group 2, PAsyst > 60 mm Hg).

Statistical Analysis
The Kruskal-Wallis test was used for assessment of differences among the groups. The Friedman test compared intraindividual changes of parameters during the procedure. Values of p < 0.05 were considered statistically significant.


Results
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
Discussion
 References
 
At baseline, eight of 94 patients presented with completely normal hemodynamic parameters at rest and served as the control group, in which the PAsyst was 21.1 ± 2.3 mm Hg (Table 1). Groups 1 and 2 included 18 and 68 patients, respectively, with PAsyst values of 49.8 ± 8.5 mm Hg (group 1) and 86.5 ± 18.9 mm Hg (group 2). The corresponding PVRI was significantly elevated (703 ± 364 dyne x s x cm-5 x m2 in group 1; 1,582 ± 562 dyne x s x cm-5 x m2 in group 2), reflecting the reduced dilation capacity of the pulmonary vessels, which occurs with an increased right ventricular stroke work index (Table 1). In contrast, PCw was within normal range in all groups, indicating a normal function of the left ventricle. However, cardiac index, stroke volume index, and oxygen saturation were reduced as pulmonary hypertension increased. The systemic vascular resistance index (SVRI) increased, which is indicative of decreased circulating volume. In general, the increasing number of affected vessels was associated with an increasing pulmonary artery pressure and elevated pulmonary vascular resistances (Figs. 1, 2A, 2B, 2C, 2D, 3A, 3B, and 3C). Particularly, the numbers of peripheral vessel stenoses and occlusions seemed to affect the vascular resistance and impair the compensation capability of the pulmonary circulation. On the other hand, in individual cases, complete occlusion of one pulmonary artery and preservation of the contralateral side could be associated with only moderate hemodynamic changes, meaning that in these cases the contralateral circulation and vascular resistance were almost unaffected.


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  		TABLE 1: Characterization of Patient Groups

 

Figure 1
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  		Fig. 1 —22-year-old woman with primary pulmonary hypertension. Pulmonary angiography with digital subtraction angiography technique; complete digital subtraction without anatomic background, posteroanterior projection. No evidence for chronic thromboembolic deposits is seen.

 

Figure 2
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  		Fig. 2A —36-year-old man with angiographic findings of moderate thromboembolic deposits in chronic thromboembolic pulmonary hypertension. Right anterior oblique (20°) and lateral projections of right pulmonary artery. Thromboembolic deposits are shown by irregularities in main artery and in segmental arteries (arrows), abrupt diameter reduction (arrowhead, A), and pouching (asterisk, B).

 

Figure 3
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  		Fig. 2B —36-year-old man with angiographic findings of moderate thromboembolic deposits in chronic thromboembolic pulmonary hypertension. Right anterior oblique (20°) and lateral projections of right pulmonary artery. Thromboembolic deposits are shown by irregularities in main artery and in segmental arteries (arrows), abrupt diameter reduction (arrowhead, A), and pouching (asterisk, B).

 

Figure 4
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  		Fig. 2C —36-year-old man with angiographic findings of moderate thromboembolic deposits in chronic thromboembolic pulmonary hypertension. Posteroanterior projection of right pulmonary artery shows bands (arrow), abrupt diameter reductions (arrowhead), and webs (asterisk).

 

Figure 5
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  		Fig. 2D —36-year-old man with angiographic findings of moderate thromboembolic deposits in chronic thromboembolic pulmonary hypertension. Posteroanterior projection of left pulmonary artery, complete subtraction without anatomic background, late phase. All segmental arteries have no parenchymal staining with one exception (arrow). Occlusion is seen in all basal segmental arteries with one exception.

 

Figure 6
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  		Fig. 3A —69-year-old woman with angiographic findings of severe thromboembolic deposits in chronic thromboembolic pulmonary hypertension. Posteroanterior and lateral projections of right pulmonary artery show peripheral thromboembolic occlusion of subsegmental arteries of various sizes, particularly in lower lobe arteries (arrows).

 

Figure 7
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  		Fig. 3B —69-year-old woman with angiographic findings of severe thromboembolic deposits in chronic thromboembolic pulmonary hypertension. Posteroanterior and lateral projections of right pulmonary artery show peripheral thromboembolic occlusion of subsegmental arteries of various sizes, particularly in lower lobe arteries (arrows).

 

Figure 8
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  		Fig. 3C —69-year-old woman with angiographic findings of severe thromboembolic deposits in chronic thromboembolic pulmonary hypertension. Lateral projection of left pulmonary artery shows complete occlusion of lower lobe artery (arrow). Perfusion is preserved in upper lobe and lingula arteries.

 

Inhalation of oxygen significantly improved oxygen saturation in all groups. The heart rate decreased because of the improving systemic oxygen supply. Pulmonary artery pressure slightly decreased in both groups. However, PVRI was slightly reduced in moderate pulmonary hypertension (group 1) but showed a loss of vasodilatation capacity in severe cases (group 2) (Table 2).


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  		TABLE 2: Changes of Hemodynamic Parameters After Oxygen Inhalation

 

Selective angiography was performed during inspiratory breath-hold. Inspiration in itself caused a significant increase of RAP ({triangleup} mean RAP, 4.5 ± 3.3 mm Hg in group 1 [p < 0.001]) and 3.8 ± 3.8 mm Hg in group 2 [p < 0.001]), and diastolic pulmonary artery pressure (PAdiast) ({triangleup} PAdiast, 6.4 ± 6.5 mm Hg in group 1 [p < 0.01] and 5.3 ± 7.9 mm Hg in group 2 [p < 0.001]), whereas inspiratory systolic pressure changes were less (Table 3). The contrast medium bolus injection started shortly after equilibrium of the elevated inspiratory pressure level and was well defined on the online pressure curves. However, compared with the inspiratory pressure level, the contrast medium bolus injection by itself resulted in a statistically significant but clinically marginal additional pressure peak that increased as pulmonary hypertension rose ({triangleup} PAsyst: 1.3 ± 1.9 mm Hg in the control group, 2.9 ± 3.4 mm Hg in group 1, and 3.8 ± 4.5 mm Hg in group 2 [p < 0.001]). The diastolic pressure peak was less pronounced (Table 4).


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  		TABLE 3: Pressure Changes Caused by Inspiratory Breath-Hold

 

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  		TABLE 4: Pressure Changes Caused by Contrast Bolus Injection

 

The final hemodynamic status in expiratory breath-hold after completion of angiography showed a significantly increased cardiac index and stroke volume index compared with baseline hemodynamics, predominantly in the control group and in moderate pulmonary hypertension (group 1). Conversely, the SVRI was reduced ({triangleup} SVRI: -372 ± 525 dyne x s x cm-5 x m2 in the control group, -281 ± 453 dyne x s x cm-5 x m2 in group 1 [p < 0.05], and -146 ± 543 dyne x s x cm-5 x m2 in group 2) because of the increased circulating blood volume (Table 5). Thereby, the slightly increased PCw indicated improved filling volume of the left ventricle. The increase of PAsyst was moderate in all groups but was accentuated in severe cases ({triangleup} PAsyst: 3.2 ± 4.6 mm Hg in the control group, 7.7 ± 8.6 mm Hg in group 1 [p < 0.01], and 8.5 ± 8.8 mm Hg in group 2 [p < 0.001]). Compared with baseline status, pulmonary vascular resistance was not significantly changed in the control group and group 1 but was significantly increased in severe cases ({triangleup} PVRI: 188 ± 337 dyne x s x cm-5 x m2 [p < 0.001]), indicating the loss of vasodilatation capacity.


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  		TABLE 5: Changes of Hemodynamic Parameters After Angiography

 


Discussion
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
 Discussion
References
 
CTPH remains undiagnosed in many cases. The prognosis is poor if left untreated. Compared with PPH, which has a mean survival of 3.6 years, the prognosis for CTPH is somewhat better, with a mean survival of 6.8 years [6]. In contrast to PPH, a surgical option, pulmonary thromboendarterectomy, is available for treating CTPH with encouraging long-term results [1]. The distribution of thromboembolic deposits is crucial for the surgical outcome [15]. Therefore, a detailed diagnostic workup is required to confirm the diagnosis and to identify the distribution and location of specific findings, such as irregularities and stenotic lesions, webs and bands, abrupt diameter reductions, and pouchlike endings of arteries [1-3].

The modern cross-sectional imaging techniques MDCT angiography and MR angiography have had significant improvement in their diagnostic sensitivity and have been discussed as noninvasive alternatives to selective angiography [2, 16]. These techniques directly visualize thromboembolic deposits at the endoluminal surface and provide excellent diagnostic images, particularly in central and segmental arteries up to the second-order pulmonary vessels [2, 16]. However, selective angiography is still superior in terms of correct detection of the numbers of affected vessels and for showing specific findings in smaller vessels. In a considerable number of cases, typical findings are shown only in peripheral vessels. However, discrimination from PPH requires exclusion of thromboembolic findings at all levels to stratify these patients for appropriate medical treatment regimes. Also, detailed knowledge of the distribution of thromboembolic deposits is necessary for correct decision making and for planning the thromboendarterectomy [1, 7, 14, 15, 17].

Pulmonary digital subtraction angiography using selective contrast medium bolus injection in both pulmonary arteries is still the diagnostic gold standard. Iomeprol is a monomeric contrast medium that features low osmolality and viscosity and a high iodine delivery rate that contributes to tolerance and improves opacification for IV and intraarterial bolus application [18-22]. We investigated the hemodynamic safety of selective pulmonary artery bolus injection of iomeprol in normal hemodynamics (control), moderately severe pulmonary hypertension (group 1), and severe thromboembolic pulmonary hypertension (group 2). Patients in the control group were not healthy volunteers, but patients with a history of pulmonary embolism. Therefore, despite completely normal hemodynamics at rest, their vasodilatation capacity was likely to be somewhat reduced. However, the three groups represented distinct hemodynamic conditions to evaluate the tolerance to iomeprol in thromboembolic disease of different severity. At baseline, groups 1 and 2 were characterized by increased pulmonary artery pressure and pulmonary vascular resistance. The reduced cardiac and stroke volume indexes reflected the restricted circulating volume caused by increased pulmonary vascular resistance. The slightly increased PCw in groups 1 and 2 might be explained by a paradoxical movement of the ventricular septum [23]. The effect is an impaired filling of the left ventricle resulting in a reduced stroke volume. No evidence was found for left ventricular disease, meaning that the hemodynamic effects were a consequence of the severity of the CTPH.

Oxygen inhalation resulted in a reduced heart rate and a significant reduction of the pulmonary artery pressure, particularly in severe cases. The reduced heart rate represents the improved systemic oxygen supply and indicates the benefit of oxygen in both moderate and severe thromboembolic disease. However, a somewhat preserved dilation capacity of the pulmonary arteries was seen only in moderate cases with a slightly reduced PVRI. Apparently, in severe cases the vasodilatation capacity was completely lost, which might be explained by hypertensive plexogenic lesions of the small pulmonary arteries [7]. Nonetheless, oxygen may activate the residual dilation capacity of some unaffected vessels in individual cases and may thereby balance pulmonary hemodynamics. Oxygen can be easily administered and during the procedure it improves oxygen saturation and reduces heart rate; it is therefore recommended, particularly in severe cases.

Our data showed no major pressure peaks during angiography. The inspiratory breath-holds before the contrast medium bolus injections caused a significant elevation of RAP and pulmonary artery pressure. Compared with these inspiration-related effects, the subsequent contrast medium bolus injections caused only moderate pressure peaks. The maximum bolus-related pressure changes varied between -2.7 and + 17.8 mm Hg systolic in patients with severe thromboembolic disease and can be explained by the abrupt volume loading. Therefore, a continuous monitoring of RAP and pulmonary artery pressure might improve safety during the procedure to avoid critical pressure levels. After angiography, the slightly increased RAP and PCw and the decreased SVRI reflected the increased circulating volume (cardiac index). In the control group, this was accompanied by a slight reduction of pulmonary vascular resistance, meaning that some vasodilatation capacity was preserved in these patients. In contrast, patients with severe pulmonary hypertension showed an increased pulmonary vascular resistance, reflecting the loss of vasodilatation capacity with a respective pulmonary pressure increase. One patient suffered from dyspnea 6 hours after angiography. In this case, the baseline hemodynamics showed PAsyst higher than systolic arterial pressure, indicating very poorly compensated hemodynamics. Hemodynamics were not performed at the time of the dyspnea; however, most probably the increased volume load had changed the right ventricular function. The patient was monitored overnight and underwent surgery the next day. Therefore, patients with near systemic or suprasystemic pulmonary artery pressure need particular attention and right heart monitoring. We recommend inserting a Swan-Ganz catheter with online monitoring of RAP and pulmonary artery pressure to realize significant peak pressure increase during pulmonary bolus injection. This might influence the procedure in terms of total number of contrast medium bolus injections, the time interval between repetitive bolus injections, and the flow rate of contrast medium bolus injections.

The relationship between osmolality and cardiovascular effects has been shown experimentally for contrast media and for hypertonic glucose and mannitol solutions. The duration of these effects has also been related to osmolality [10, 12, 24]. Therefore, monomeric contrast agents reduce these adverse effects, which the data in our study confirm. The study gives insight into the hemodynamic effects of the monomeric agent iomeprol for selective pulmonary digital subtraction angiography in severe CTPH. This is consistent with analogous reports on iohexol [25], which also shows tolerance in severe CTPH.

In conclusion, as a general rule we do not expect major hemodynamic changes during selective pulmonary angiography with iomeprol, even in severe thromboembolic pulmonary hypertension. However, continuous monitoring of the hemodynamic parameters is recommended during angiography, and oxygen may contribute to safety during the procedure.


References
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
 Discussion
 References
 

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