cardiac catheterization techniques in pulmonary hypertension

Cardiol Clin 22 (2004) 401–415

Cardiac catheterization techniques in pulmonaryhypertension

Paulo Guillinta, MD, Kirk L. Peterson, MD, Ori Ben-Yehuda, MD*Division of Cardiology, Department of Medicine, University of California, San Diego,

200 West Arbor Drive, San Diego, CA 92110, USA

Once considered dangerous and potentially life

threatening, cardiac catheterization of the patientwith pulmonary hypertension can be performedsafely and provides essential information in thediagnosis and management of pulmonary hyper-

tension. This article summarizes the moderntechniques used for right-heart catheterization,selective pulmonary angiography, and pulmonary

angioscopy in the evaluation of the patient withpulmonary hypertension or with suspected chron-ic thromboembolic disease.

Cardiac catheterization of the patient withsuspected pulmonary hypertension is essential todetermine accurately the cause and extent ofdisease. In patients with suspected chronic throm-

boembolic pulmonary hypertension (CTEPH),pulmonary angiography remains an essentialpart of the diagnostic evaluation and selection

of appropriate patients for surgical pulmonarythrombendarterectomy. Although historically pul-monary angiography has been considered contra-

indicated in the presence of severe pulmonaryhypertension, advances in cardiac and pulmonaryangiographic techniques allow this procedure to be

performed in a safe manner with acceptable risk. Inreviewing the technique of right-heart catheteriza-tion, pulmonary angiography, and angioscopy inthe patient with pulmonary hypertension, the

authors draw on the experience of more than 20years of catheterization of patients with severepulmonary hypertension at the University of

California, San Diego (UCSD) Medical Center,

* Corresponding author.

E-mail address: [email protected]

(O. Ben-Yehuda).

0733-8651/04/$ - see front matter � 2004 Elsevier Inc. All r

doi:10.1016/j.ccl.2004.04.011

where more than 2500 such procedures have beenperformed.

Indications and considerations for catheterization

of the patient with pulmonary hypertension

Catheterization plays an integral part in the

evaluation of the patient with pulmonary hyper-tension. The primary goals of catheterization areto determine right ventricular and pulmonary

artery hemodynamics, to exclude left-to-rightcardiac shunts and any significant left-sided car-diac disorder, to assist in the determination of thecause of pulmonary hypertension, and to test the

response of therapeutic agents. In patients withsuspected CTEPH, pulmonary angiography andangioscopy are used to assess clot location, extent,

and size to determine candidacy for pulmonarythrombendarterectomy.

Safety considerations

Early case reports [1–4] of fatalities associatedwith pulmonary angiography in patients withpulmonary hypertension have led to a lingering

perception that the procedure is associated withconsiderable risk, primarily because of acute rightventricular failure and arrhythmias. Even right-

heart catheterization alone [5] was reported to bepotentially dangerous. Larger series have sincebeen published, both in acute and chronic pulmo-nary embolism and in mild as well as severe

pulmonary hypertension. Mills et al [6] describedthree deaths in 1350 patients (incidence of 0.2%),all of whom had right ventricular end diastolic

pressure of 20 mm Hg or higher. Nicod et al [7]

ights reserved.

mailto:[email protected]

402 P. Guillinta et al / Cardiol Clin 22 (2004) 401–415

reported on the original series of 67 patients fromUCSD undergoing CTEPH evaluation. Meanpulmonary arterial pressures (PAPs) were 47 �13 mm Hg, with a right ventricular end diastolicpressure of 13 � 6 mm Hg and a cardiac index of2.2 � 0.7 L/min. There were no deaths attribut-able to CTEPH. By 1991 this series had expanded

to include more than 300 patients, without a death.Since then right-heart catheterization and pulmo-nary angiography have been performed in ap-

proximately 200 patients with severe pulmonaryhypertension annually at UCSD, without a deathrelated to the procedure (more than 2500 patients

to date). There thus are no absolute contra-indications to pulmonary angiography, and theprocedure can be performed safely, providedcertain precautions and advances in technique

are employed.Nonfatal adverse reactions include transient

hypotension and general catheterization-related

adverse events such as inadvertent arterial punc-ture, oversedation, pneumothorax, and contrastagent–related nephropathy [8]. To minimize these

risks, the authors use the following procedures atUCSD [9]:

1. Before the procedure echocardiography isperformed, detecting potential clots in theright atrium or right ventricle or the presence

of an atrial septal defect/patent foramenovale.

2. Heart rate, rhythm, oxygen saturation, and

systemic and PAP should be continuouslymonitored. Supplemental oxygen is providedto maintain oxygen saturation over 90%.

3. Access to the pulmonary vessels through theneck is preferred to avoid potential dislodge-ment of unsuspected venous thrombi involv-

ing the femoral vein, iliac vein, or inferiorvena cava and to facilitate angioscopy. Theauthors prefer the internal jugular vein to thesubclavian vein to reduce the risk of pneu-

mothorax, which is likely to be poorlytolerated in these patients who are oftenhypoxemic.

4. Hemodynamics are assessed using a balloonflotation catheter (Swan-Ganz catheter), attimes stiffened with a 0.025-cm guide wire.

This stiffening greatly facilitates the catheter-ization in these patients, who frequentlyhave enlarged right ventricles, significanttricuspid regurgitation, severely elevated

PAPs, and low cardiac output. CO2 is usedfor balloon inflation to minimize the possi-

bility of paradoxical embolism in case ofballoon rupture.

5. A stiff, side-hole catheter such as a 7-F or 8-F

NIH or Berman catheter is most commonlyused to inject the pulmonary arteries. Theinjection through the side holes allows goodopacification with reduced injection velocity

and pressure. Catheter retraction and whip-ping during injection are also minimized.

6. Unilateral, sequential injection of the contrast

agent in to each main pulmonary artery ispreferred. Injection into the right atrium orright ventricle is avoided, thereby eliminating

the possibility of intramyocardial injection.The catheter is positioned near the origin ofthe lower lobe vessels, and the contrast agentis allowed to fill the upper lobes in retrograde

fashion.7. Non-ionic contrast is preferred because fewer

adverse reactions and minimal hemodynamic

compromise are experienced [10,11].8. Cardiac output and speed of run-off during

small hand injection are used to determine the

amount of contrast agent needed for assess-ment of the pulmonary vasculature anatomy.A smaller amount of contrast material is

needed in patients with slow run-off or lowcardiac output. At UCSD, the total amount ofcontrast medium used ranges from 20 to 65mL. The usual injection is of 55 mL at a rate of

22 mL/second, with adjustments based on thepatient’s cardiac output, assessment of thepulmonary vasculature during the hand in-

jection, and pulmonary pressures. For exam-ple, the total occlusion of the main descendingpulmonary artery after the takeoff of the

upper lobe branch would necessitate a reduc-tion of the total contrast to approximately 20mL. Conversely, the presence of a brisk runoffduring the hand injection coupled with a high

cardiac output would lead to injection of morethan the standard 55 mL.

Right-heart catheterization

Evaluation of hemodynamics by right-heartcatheterization plays an integral part of theevaluation of patients with pulmonary hyperten-

sion. The goals of right-sided catheterization are(1) to measure PAP directly and estimate pulmo-nary vascular resistance, (2) to evaluate for left-to-

right shunts, and (3) to test the response totherapeutic agents.

403P. Guillinta et al / Cardiol Clin 22 (2004) 401–415

During right-heart catheterization by balloonflotation catheter, rapid determination and contin-uous monitoring of pressures in the right ventricle,right atrium, and pulmonary artery and of post-

capillary wedge pressure are possible. Understand-ing of normal and pathologic pressure waveformsis important to recognize certain cardiac disorders

such as valvular and pericardial disease. In patientswith primary pulmonary hypertension (PPH),particular attention should be paid to the right

atrial pressure and right ventricle end-diastolicpressure. In the National Heart Lung and BloodInstitute registry, mean right atrial pressure and

decreased cardiac index were the most importantpredictive variables for survival in patients withPPH [12]. The patient with PPH commonly haselevated right atrial pressure, elevated mean PAP,

reduced cardiac index, and low or normal post-capillary wedge pressure [8].

A postcapillary wedge pressure is obtained with

an end-hole catheter positioned in a side branch ofthe pulmonary artery facing a pulmonary capillarybed. One pitfall to avoid is wedging the balloon too

proximally, creating a hybrid tracing of pressuresbetween actual PAP and postcapillary wedgepressure, resulting in an overestimation of the

postcapillary wedge pressure (Fig. 1). Deflatingthe balloon to decrease its size will allow thecatheter to be wedged in a smaller, more distalbranch of the pulmonary artery. Caution should be

taken to avoid overwedging and possible pulmo-nary artery rupture, a potentially lethal event.Fortunately in pulmonary hypertension the thick-

ened, hypertrophied arterial wall provides someprotection against rupture. When it is not clearwhether awedge tracing has been obtained, a blood

sample is obtained through the distal port. In thewedge position arterial saturation should be pres-ent as blood from the capillary bed is aspirated.The authors have also found that typically the

more narrow, tapering anatomy of the left pulmo-nary artery allows more reliable wedge determi-nations. The use of a J-tipped 0.25 wire to guide the

Swan-Ganz catheter to the left pulmonary artery isessential. Typically patients with either PPH orCTEPH have low to normal wedge pressures.

In the presence of substantially elevated postcap-illary wedge pressure, left-heart catheterizationshould be performed to exclude pulmonary veno-

occlusive disease, mitral stenosis, or left ventriculardysfunction.

Cardiac output is best determined by the Fickmethod in the setting of low cardiac output states

or when there is significant tricuspid regurgita-

tion. This method requires measuring oxygenconsumption directly, because estimations ofoxygen consumption may not apply to seriouslyill patients with pulmonary hypertension and may

introduce significant calculation errors. In experi-enced hands, however, determination of cardiacoutput by thermodilution techniques is usually

satisfactory for the adjustment of therapy in thesepatients [13].

Response of vasodilator challenge in the cardiac

catheterization laboratory

Vasoconstriction of the pulmonary vessels is

one of the prominent pathologic features seen inpatients with pulmonary hypertension of anycause, particularly in those with PPH [14]. Un-fortunately, no hemodynamic or demographic

characteristics exist to predict which patients arelikely to benefit from long-term vasodilator ther-apy [15,16]. In more recent studies, Groves et al

[17] illustrated that the initial response to vaso-dilatory therapy accurately predicts the patientwith PPH who is likely to benefit from long-term

oral therapy. In addition, patients who demon-strate a reduction in total pulmonary resistanceindex of more than 50% in response to short-termepoprostenol (prostacyclin, PGI2) challenge at the

time of diagnosis had longer disease evolutionsand better prognoses than patients with a lowervasodilator response [18,19]. For these reasons [3],

it is important to assess the response to vasodila-tor therapy in patients with PPH in the cardiaccatheterization laboratory.

Nitric oxide and PGI2 are useful drugs to testpulmonary vasoreactivity because they are potent,short acting, and can be titrated. The acute effects

of inhaled nitric oxide and PGI2 on pulmonaryartery pressure are similar [20,21]. Inhaled nitricoxide more consistently reflects the changes inpulmonary vascular tone and seems to be the

better predictor of the long-term response to oralvasodilator treatment, making it the preferredagent for assessing pulmonary vasoreactivity [22].

Nitroprusside has fallen out of favor forassessing pulmonary vasoreactivity in patientswith chronic pulmonary hypertension because this

drug causes systemic hypotension compared withnitric oxide, at doses that cause similar degrees ofpulmonary vasodilation [23].

Pulmonary arterial pressures, right ventricularpressures, cardiac output, and postcapillary wedgepressure are recorded during infusions of inhaled


Fig. 1. (A) Hybrid tracing of pulmonary artery pressure and wedge tracing overestimating wedge pressure. (B) Actual

pulmonary capillary wedge pressure tracing once the balloon is deflated and allowed to wedge in a smaller, more distal

branch of the pulmonary artery.


nitric oxide. Administration of inhaled nitricoxide with oxygen seems to be safe and providesadditional pulmonary vasodilation in this patientpopulation [24]. Pulmonary pressure are recorded

during administration of 100% oxygen and in-haled nitric oxide dosed at 20 to 80 parts permillion. The authors typically administer nitric

oxide for 10 minutes, with repeat recordingsobtained during the final 5 minutes of the in-halation. Although a mild reduction in pulmonary

vascular resistance (<20%) can be seen in mostpatients, even those with CTEPH, significantreductions of more than 20% are seen in only

one fourth of patients [25].

Pulmonary angiography: anatomy

Accurate evaluation of the pulmonary angio-

gram requires knowledge of the pulmonary vas-

culature anatomy (Figs. 2 and 3). The mainpulmonary artery arises from the pulmonaryconus of the right ventricle, anterior and to theleft of the aorta. It takes a posteromedial direction

until its bifurcation into the right and left pulmo-nary arteries. The right pulmonary artery coursesanterior to the right mainstem bronchus. It gives

rise to the right upper lobe branch within themediastinum. The left pulmonary artery passesover the left mainstem bronchus and descends

posterior to the bronchus before the origin of theleft upper lobe branch. The vessels then branchand are closely related to bronchial branching

within the lung. Angiographic films are takenusing anteroposterior and lateral projections. Thelateral projection is particularly helpful in sepa-rating the overlapping tributaries of the right

middle and right lower lobe and left lingual andleft lower lobe. It also allows a clear separation

Fig. 2. (A) Anteroposterior view of the anatomy of the right pulmonary artery. (B) Lateral view. (Reproduced from

Peterson KL, Nicod P. Catheterization and angiography in pulmonary hypertension. In: Shure D, Auger W, Moser K,

et al, editors. Cardiac catheterization: methods, diagnosis, and therapy. Philadelphia: W.B. Saunders; 1977. p. 404;

with permission.)


Fig. 3. Anatomy of the left pulmonary artery in (A) anteroposterior and (B) lateral views. (Reproduced from Peterson

KL, Nicod P. Catheterization and angiography in pulmonary hypertension. In: Shure D, Auger W, Moser K, et al,

editors. Cardiac catheterization: methods, diagnosis, and therapy. Philadelphia: W.B. Saunders; 1977. p. 405; with

permission).

between the superior segmental artery and the

artery to the middle lobe.

Pulmonary angiography: interpretation in the

patient with pulmonary hypertension

Pulmonary angiography of the patient withpulmonary hypertension plays a central role in

delineating the precapillary cause of elevatedpulmonary pressures. Distinguishing major-vesselfrom small-vessel disease allows the correct ther-

apeutic approach to be determined.Auger et al [26] described the angiographic

patterns seen in patients with chronic thrombo-

embolic disease. These patterns include pouchingabnormalities, vascular webs or bandlike constric-tions, intimal irregularities, abrupt narrowing of

major pulmonary vessels, and obstruction of

major pulmonary vessels, most commonly atpoints of origin (Figs. 4–8).

Although pulmonary arterial webs are typical-

ly seen in patients with chronic thromboemboli,they are also seen in congenital stenotic lesions ofthe pulmonary vessels and with vasculitides such

as Takayasu’s arteritis [27,28]. Patients withcongenital stenotic lesions of the pulmonaryvasculature present at an early age and typicallyhave coexisting cardiac abnormalities. Most

Takayasu patients with pulmonary vessel involve-ment demonstrate systemic manifestations.

Total obstruction or abrupt narrowing of the

pulmonary vessel, typically seen in chronic throm-boemboli, can also be seen in extrinsic compressionfrom extensive mediastinal or hilar lympha-

denopathy, fibrosing mediastinitis, and pulmonary


Fig. 4. (A) The anteroposterior view of the right pulmonary artery in a patient with CTEPH. Note the marked

hypovascularity, irregularity of the main descending pulmonary artery, and complete occlusion of most segmental

branches. (B) The lateral view of the artery shown in 4A. Note the separation of the right middle lobe branches from the

right lower lobe segments. In this view the middle lobe is perfused, as is the superior segment.

vascular or primary lung malignancies [29–32].Chest CT aids in making the distinguishing theseentities from chronic thromboembolic disease.

Occasionally, several vascular abnormalities

occur in the same patient. In this scenario, thepulmonary angiogram may aid in identifying the

Fig. 5. Right pulmonary angiogram shows central

pulmonary artery enlargement and pouching abnormal-

ity in the right lower lobe vessel seen in chronic thrombo-

embolic disease.

patient with acute on chronic thromboem-bolic disease (Fig. 9). Sharply defined luminaldefects are seen in small, acute emboli. Proximalpulmonary artery enlargement and bandlike

abnormalities are typically seen in chronic throm-boembolic disease but not in acute embolicdisease.

The hemodynamic data can also assist indistinguishing chronic from acute embolism. Pul-monary hypertension with mean PAPs above 35

mm Hg suggest chronicity, because the rightventricle in acute pulmonary embolism withoutprevious pulmonary hypertension is incapable ofgenerating such high pulmonary pressures [33].

The classic angiographic findings in patientswith PPH include normal or dilated centralarteries with pruning of the small, more distal,

nonelastic arteries [8]. Pruning of the pulmonaryvessels may also be seen with chronic thrombo-embolic disease, but in this scenario pruning is

regional and more proximal [34].A key question that the pulmonary angiogram

addresses in patients with suspected CTEPH is the

extent and surgical accessibility of chronic clot.The presence of bilateral disease and proximalinvolvement (main pulmonary trunks, lobar ar-teries, and segmental arteries) predicts surgical

accessibility. Correlation with findings on theperfusion scan is essential, because the presence


Fig. 6. (A) Anteroposterior view of the right pulmonary artery demonstrating hypoperfusion of the lower lobe. (B) Only

on the lateral film does the extent of occlusion of the posterior basal segment and narrowing of the middle lobe branch

become evident. The superior segment is also subtotally occluded.

of segmental defects is predictive of surgical

success (see articles in this issue by Auger et aland Thistlethwaite et al).

Pulmonary angioscopy

When there is significant proximal disease (eg,

complete occlusions of lobar vessels), the inter-

Fig. 7. Abrupt narrowing of the pulmonary vessel seen

in chronic thromboembolic disease.

pretation of pulmonary angiograms is straightfor-

ward. In the UCSD experience the pulmonaryangiogram is suggestive but not definitive in about20% to 25% of cases. The recanalization of

chronic clot allows contrast to permeate throughthe lesions, and the pulmonary angiogram canunderestimate disease just as the perfusion scancan. In addition, the presence of defects at the

Fig. 8. Anteroposterior projection shows complete ob-

struction of the right main pulmonary artery.


transition between segmental and subsegmental

vessels may raise doubt regarding the surgicalaccessibility. In the patient with markedly elevatedpulmonary hypertension (pulmonary vascular re-

sistance >800 dynes/second/cm�5) surgical risksrise significantly if insignificant clot is removedduring surgery, leaving the patient with severepulmonary hypertension.

Fiberoptic angioscopy, developed to allow di-rect visualization of the interior of the centralpulmonary vessels up to the segmental and sub-

Fig. 9. Anteroposterior view demonstrates acute on

chronic thromboemboli. Note the distinct numerous

luminal filling defects (solid arrow) in a bandlike or web

abnormality.

segmental levels, is used to define surgical acces-sibility better in borderline cases [35,36]. Thechallenges entailed in performing pulmonary an-gioscopy include the need to maneuver through an

often hypertrophied right ventricle, the widevariation in pulmonary vessel size with varyinganatomic branching, the large number of

branches that require visualization, and the robustcollateral circulation from the bronchial circula-tion. At UCSD pulmonary angioscopy has pro-

gressed through several stages of developmentover the past 20 years. The approach has beento use a balloon system to occlude blood flow

completely in the vessel that is being visualized,rather than a flushing (hemodilution) approach ashas been used in the coronary circulation. Hemo-dilution is not practicable in the large pulmonary

arteries and would entail dangerous fluid overloadin these patients with right-heart failure.

The angioscope presently used is a 120-cm

fiberoptic device, 3 mm in diameter (Figs. 10 and11). It can be flexed 90( at the tip allowing navi-gation through the pulmonary tree. The occluding

balloon is attached at a modified spool-like stain-less steel lip, which allows secure tying of thedisposable balloons. The balloon at the distal end

is inflated with carbon dioxide to protect from airembolism in case of balloon rupture, a precautionof particular importance given the elevated right-sided pressures with potential for right- to-left

embolism in patients with patent foramen ovale.The balloon is connected to a syringe by a tube inthe angioscope, allowing deflation during the

advancement of the catheter and inflation toocclude the vessel as well as allow flotation furtherdownstream.

Fig. 10. The pulmonary angioscope. (Courtesy of Olympus Corporation, Lake Success, NY.)


Because of the size of the angioscope (3 mm) an11-F sheath is used. Although angioscopy can beaccomplished from the femoral approach, it is

much easier to navigate the instrument through theright ventricle using the internal jugular veinapproach, particularly from the right. Two oper-

ators are needed to guide the angioscope, with oneadvancing and torquing the instrument and theother flexing and extending it using the built-in

deflectors. Angioscopy is most helpful in definingthe starting point of chronic thrombi and establish-ing whether they are within surgical reach. Thisprocedure enables the examiner to determine

operability of patients with chronic pulmonarythromboemboli in approximately 75% of the caseswhen the findings on the pulmonary angiogram are

questionable [34]. A detailed map of the majorpulmonary vessels can be performed safely within20 minutes, without significant morbidity, in this

patient population. The main complications en-countered have been transient ventricular ectopyduring transit in the ventricle and minor local

bleeding from the 11-F sheath site in the neck.During the procedure the fluoroscopy images

are recorded to localize the lesions seen onangioscopy and are correlated with the anatomy

as defined in the pulmonary angiogram. Normalpulmonary findings are of smooth, pale white,glistening intima (Fig. 12). Bifurcations are typi-

cally round and regular in appearance. In patientswith pulmonary hypertension, either primaryarterial hypertension or secondary to CTEPH,

the arterial walls may demonstrate small, yellow-ish atheroscleroticlike plaques as well as morediffuse yellowish colorations (Figs. 13 and 14).

Patients with chronic thrombi have irregularpulmonary arterial walls with transluminal bands

Fig. 11. Inflated balloon attached to the distal tip of the

angioscope.

and obstructive lesions and irregular vessel ostia.Thin membranes can also be visualized. At times

reddish-purplish subacute thrombi can be seen,which are distinct from the white fibrotic lesionsof chronic organized and recanalized clot.

Small-vessel arteriopathy in patients with chronicthromboembolic pulmonary hypertension

Although the main site of vasculopathy and

increased resistance in CTEPH is in the large,elastic pulmonary arteries, a significant number ofpatients have concomitant small-vessel arterio-

pathy that may persist despite the removal ofproximal clot. These patients are at increased riskof persistent pulmonary hypertension after pul-monary thrombendarterectomy. Severe persistent

pulmonary hypertension after surgery accountsfor more than one third of perioperative mortalityand up to 50% of long-term deaths. Recently the

pulmonary artery occlusion technique [37] hasbeen used to attempt to partition the pulmonaryresistance into an upstream component (Rup) and

downstream (small arterial plus venous) compo-nent. Using a standard Swan-Ganz catheter (Ed-wards Lifesciences Corporation, Irvine, CA) thepulmonary pressure signal is filtered using a two-

pole digital low-pass filter with a cutoff at 18 Hz.A biexponential fitting of the pressure decay curveis then performed, which allows estimation of the

derived occlusion pressure (Poccl). Rup is thencalculated as follows:

Rup

ð%Þ ¼ mean pulmonary artery pressure� Poccl

mean pulmonary artery pressure� Ppao

where Ppao is the final pulmonary artery oc-cluded pressure (wedge pressure). In patients with

Fig. 12. Normal bifurcation of a pulmonary artery.


Fig. 14. Angioscopic findings in CTEPH. Note the yellow plaque prominent in B, G, and K. Membranes, webs, and

masslike fibrotic tissue can be seen.

Fig. 13. Angioscopic findings in CTEPH. Note the fibrotic white material with membranes, webs, and pitting.


Fig. 15. Pulmonary artery pressure occlusion waveforms from two patients with (A) mainly upstream resistance and (B)

mainly downstream resistance. In A the pressure drops more rapidly with balloon occlusion, resulting in lower Poccl and

higher Rup%.

small-vessel arteriopathy the Poccl pressure ishigher (a longer time is required for the pressure

to reach Ppao), and therefore the Rup % is lower(Fig. 15). In a study [37] of 26 patients withsuspected CTEPH, there was an excellent corre-

lation between Rup % before pulmonary throm-bendarterectomy and hemodynamic response tosurgery. Moreover, all four patients with Rup %

below 60 did not survive surgery (Fig. 16).

Coronary arteriography

Before pulmonary thrombendarterectomy the

authors routinely perform coronary arteriographyon all male patients above the age of 40 andfemale patients above the age of 45 and do so for

younger patients if findings are suggestive ofcoronary disease. In the presence of markedly

enlarged proximal pulmonary arteries, the leftmain pulmonary artery may become compressedand give the appearance of ostial left main

stenosis [38]. Best visualized in the let anterioroblique cranial view (Fig. 17), this finding isusually devoid of other evidence of atherosclerosis

and is not in itself an indication for bypasssurgery, especially if the patient’s pulmonarypressures decrease after surgery.

Summary

Cardiac catheterization of the patient withpulmonary hypertension plays an integral part in


Fig. 16. Correlation between preoperative Rup % and postoperative outcomes. (A) Postoperative pulmonary resistance

(B) Mean postoperative pulmonary pressure. (Reproduced from Kim NH, Fesler P, Channick RN, et al. Preoperative

pulmonary partitioning of pulmonary vascular resistance correlates with early outcome after thromboendarterectomy

for chronic thromboembolic pulmonary hypertension circulation. 2004;109:19; with permission.)


the diagnostic evaluation. Right-heart hemody-namics, pulmonary angiography, and pulmonaryangioscopy offer a way to determine the cause of

disease safely and accurately and to offer poten-tially life-saving therapies.

References

[1] Dotter CT, Jackson FS. Death following angiocar-

diography. Radiology 1950;54:527–33.

[2] Diamond EG, Gonlubol F. Death following

angiocardiography: report of two cases after admin-

istration of diodrast and neo-iopax, respectively.

N Engl J Med 1953;249:1029–31.

[3] Alexander JK, Gonzales DA, Fred HL. Angio-

graphic studies in cardiorespiratory diseases: special

reference to thromboembolism. JAMA 1966;198:

575–8.

[4] Snider GL, Ferris E, Gaensler EA, et al. Primary

pulmonary hypertension: a fatality during pulmo-

nary angiography. Chest 1973;64:628–35.

[5] Caldini P, Gensini GG, Hoffman MS. Primary

pulmonary hypertension with death during right

heart catheterization. Am J Cardiol 1959;519–27.

[6] Mills SR, Jackson DC, Older RA, et al. The

incidence, etiologies, and avoidance of complica-

tions of pulmonary angiography in a large series.

Radiology 1980;136:295–9.

[7] Nicod P, Peterson KL, Levine M, et al. Pulmonary

angiography in severe chronic pulmonary hyper-

tension. Ann Intern Med 1987;107:565–8.

[8] Rich S, Dantzker DR, Ayres SM, et al. Primary

pulmonary hypertension: a national prospective

study. Ann Intern Med 1987;107:216–23.

Fig. 17. Left main ostial compression from an enlarged

pulmonary artery. (Reproduced from Bonderman D,

Fleischmann D, Prokop M, et al. Imges in cardiovascu-

lar medicine. Left main coronary artery compression by

the pulmonary trunk in pulmonary hypertension.

Circulation 2002;105:265; with permission.)

[9] Peterson KL, Nicod P. Catheterization and

angiography in pulmonary hypertension. In:

Shure D, Auger W, Moser K, et al, editors.

Cardiac catheterization: methods, diagnosis, and

therapy. Philadelphia: W.B. Saunders; 1977.

p. 401–14.

[10] Kumazaki T. Ioxaglate versus diatrizoate in selec-

tive pulmonary angiography. Part II: cardiovascu-

lar responses. Acta Radiol 1985;26:635.

[11] Smith DC, Lois JF, Gomes AS, et al. Pulmonary

angiography: comparison of cough stimulation

effects of diatrizoate and ioxaglate. Radiology 1987;

162:617–8.

[12] D’Alonzo GE, Barst RJ, Ayres SM, et al. Survival

in patients with primary pulmonary hypertension:

result from a national prospective registry. Ann

Intern Med 1991;115:343–9.

[13] Rubin LW, Rich S. Primary pulmonary hyperten-

sion. In: Georgiou D, Cao T, Shapiro S, et al,

editors. Hemodynamic evaluation in primary pul-

monary hypertension. New York: Marcel Dekker;

1997. p. 253–86.

[14] Wagenvoort CA. Vasoconstriction and medial

hypertrophy in pulmonary hypertension. Circula-

tion 1960;22:535–46.

[15] Weir EK, Rubin LJ, Ayres SM, et al. The acute

administration of vasodilator therapy in primary

pulmonary hypertension: experience from the Na-

tional Institute of Health Registry on Primary

Pulmonary Hypertension. Am Rev Resp Dis 1989;

140:1623–40.

[16] Weir EK. Acute vasodilator testing and pharmaco-

logical treatment of primary pulmonary hyperten-

sion. In: Fishman AP, editor. The pulmonary

circulation: normal and abnormal: mechanisms,

management and the national registry. Phila-

delphia: University of Pennsylvania Press; 1990.

p. 485–99.

[17] Groves BM, Badesch DB, Turkevich D, et al.

Correlation of acute prostacyclin response in

primary (unexplained) pulmonary hypertension

with efficacy of treatment with calcium channel

blockers and survival. In: Hummes JR, Reeves JT,

Weir EK, editors. Ion flux in pulmonary vascular

control. New York: Plenum Press; 1993. p. 317–30.

[18] Rich S, Brundage BH. High-dose calcium channel-

blocking therapy for primary pulmonary hyperten-

sion: evidence of long-term reduction in pulmonary

arterial hypertension and regression of right ven-

tricular hypertrophy. Circulation 1987;76:135–41.

[19] Olivier R, Reza A, Francois B, et al. Clinical

significance of the pulmonary vasodilator response

during short-term infusion of prostacyclin in

primary pulmonary hypertension. Circulation 1996;

93:484–8.

[20] Rich S, Kaufmann E, Levy PS. The effects of high

doses of calcium-channel blocker on survival in

primary pulmonary hypertension. N Engl J Med

1992;327:76–81.


[21] Sitbon O, Brenot F, Denjean A, et al. Inhaled nitric

oxide as a screening vasodilator agent in primary

pulmonary hypertension. Am J Respir Crit Care

Med 1995;151:384–9.

[22] Morales-Blanhir J, Santos S, de Jover L, et al.

Clinical value of vasodilator test with inhaled nitric

oxide for predicting long-term response to oral

vasodilators in pulmonary hypertension. Respir

Med 2004;98:225–34.

[23] Cockrill BA, Kacmarek RM, Fifer MA, et al.

Comparison of effects of nitric oxide, nitro-

prusside, and nifedipine on hemodynamics and

right ventricular contractility in patient with

chronic pulmonary hypertension. Chest 2001;119:

128–36.

[24] Atz AM, Adatia I, Lock JE, et al. Combined effects

of nitric oxide and oxygen during acute pulmonary

vasodilator testing. J Am Coll Cardiol 1999;33:

813–9.

[25] Rich S, Kaufmann E, Levy PS. The effect of high

doses of calcium-channel blockers on survival in

primary pulmonary hypertension. N Engl J Med

1992;327:76.

[26] Auger WR, Fedullo PF, Moser KM, et al. Chronic

major-vessel thromboembolic pulmonary artery

obstruction: appearance at angiography. Radiology

1992;182:393–8.

[27] Peterson KL, Fred HL, Alexander JK. Pulmonary

arterial webs: a new angiographic sign of previous

thromboembolism. N Engl J Med 1967;277:33.

[28] Haas A, Stiehm R. Takayasu’s arteritis presenting

as pulmonary hypertension. Am J Dis Child 1986;

140:372–4.

[29] Cho SR, Tisnado J, Cockrell CH, et al. Angio-

graphic evaluation of patients with unilateral

massive perfusion defects in the lung scan. Radio-

graphics 1987;7:729–45.

[30] Arnett EN, Bacos JM, Macher AM, et al. Fibrosing

mediastinitis causing pulmonary arterial hyperten-

sion without pulmonary venous hypertension. Am J

Med 1977;63:634–43.

[31] Carlin BW, Moser KM. Pulmonary artery obstruc-

tion due to malignant fibrous histiocytoma. Chest

1987;92:173–5.

[32] Schermoly M, Overman J, Pingleton SK. Pulmo-

nary artery sarcoma—unusual pulmonary angio-

graphic findings—a case report. Angiology 1987;38:

617–21.

[33] Dalen JE, Banas JS, Brooks HL, et al. Resolution

rate of acute pulmonary embolism in man. N Engl J

Med 1969;280:1194–9.

[34] Peterson KL, Nicod P. Cardiac catheterization:

methods, diagnosis, and therapy. In: Shure D,

Auger W, Moser K, et al, editors. Pulmonary

angioscopy. Philadelphia: W.B. Saunders; 1997.

p. 257–65.

[35] Shure D, Gregoratos G, Moser KM. Fiberoptic

angioscopy: role in the diagnosis of chronic

pulmonary arterial obstruction. Ann Intern Med

1985;103:844–50.

[36] Ricou F, Nicod PH, Moser KM, et al. Catheter-

based intravascular ultrasound imaging of chronic

thromboembolic pulmonary disease. Am J Cardiol

1991;67:749–52.

[37] Kim NHS, Fesler P, Channick RN, et al. Pre-

operative partitioning of pulmonary vascular

resistance correlates with early outcome after

thromboendarterectomy for chronic thromboem-

bolic pulmonary hypertension. Circulation 2004;

109:18–22.

[38] Bonderman D, Fleischmann D, Mathias P, et al.

Left main coronary artery compression by the

pulmonary trunk in pulmonary hypertension. Cir-

culation 2002;105:265.

cardiac catheterization techniques in pulmonary hypertension

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