estimation artery with · interstitial oedema, and left atrial size each contributed independently...

Br HeartJ 1980; 44: 322-9

Estimation of pulmonary artery wedge pressure fromchest radiograph in patients with chronic congestivecardiomyopathy and ischaemic cardiomyopathy*HAROLD DASH,t MARTIN J LIPTON, KANU CHATTERJEE,WILLIAM W PARMLEY

From the Cardiovascular Research Institute and the Cardiovascular Division of the Department of Medicine,University of California, San Francisco, California, USA

suMMARY In order to define the relation between chest x-ray findings and the level of pulmonary arterywedge pressure in patients with chronic congestive cardiomyopathy, 82 patients had chest radiographsbefore undergoing 92 haemodynamic studies. The studies were divided into three groups according tothe level ofpulmonary artery wedge pressure (PAWP) (group 1: < 15 mmHg, group 2: 15 to 24 mmHg,group 3: >25 mmHg.

Venous distribution, interstitial oedema, pleural effusions, left atrial enlargement, and rightventricular enlargement each occurred in less than 10 per cent of group 1 studies. Radiological abnor-malities generally distinguished group 1 from group 2, but none except cardiothoracic ratiodistinguished group 2 from group 3. Cardiothoracic ratio correlated best with pulmonary artery wedgepressure (r=0.70). Alveolar oedema was uncommon whenPAWP >25 mmHg, occurring in 32 per centof group 3 studies.

Stepwise multiple linear regression analysis showed that cardiothoracic ratio, alveolar oedema,interstitial oedema, and left atrial size each contributed independently to the prediction of PAWP.The regression analysis improved the accuracy of the estimation of PAWP from the findings noted onstandard chest radiographs.

A rise in left ventricular diastolic and pulmonaryartery wedge pressures is a characteristic haemo-dynamic finding in patients with chronic congestivecardiomyopathy. However, the magnitude of therise in pulmonary artery wedge pressure may varywidely in such patients; and, in a few, it may evenbe normal. Accurate determination of the level ofpulmonary venous hypertension in these patients isuseful for the choice of appropriate treatment,particularly for the choice of vasodilator agentswhich are now widely used for treatment of chroniccongestive heart failure.1-4 At present, invasivehaemodynamic monitoring is most commonly usedto assess the severity of pulmonary venous hyper-tension in these patients. An accurate noninvasivemethod for the prediction of pulmonary artery* This work was supported in part by a Programme Project.t Present address: Department of Cardiology, Pennsylvania StateSchool of Medicine, Hershey, Pennsylvania, USA.Received for publication 28 January 1980

wedge pressure would thus be extremely useful inclinical practice.The chest radiograph has been used to evaluate

the haemodynamic status of patients with cardiacdisease in the past.5-1' However, much of the dataderives from patients with rheumatic mitral valvulardisease,5-8 2-14 especially mitral stenosis, and itremains to be seen that the established radiologicalcriteria for estimating pulmonary artery wedgepressure are applicable to patients with chronic leftventricular failure. The purpose of this study,therefore, was to assess the value of chest radio-graphic findings for the estimation of pulmonaryartery wedge pressure in patients with chronic leftventricular failure.

Subjects and methods

All patients undergoing haemodynamic monitoringfor symptoms of chronic congestive heart failure at

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Chest x-ray in chronic heart failure

the University of California, San Francisco, betweenJanuary 1975 and January 1979, were evaluated foreligibility in the study. Patients were accepted intothe study if they met the following criteria: (1)symptoms of heart failure of more than one month'sduration; (2) a standard posteroanterior and lateralchest radiograph performed within 72 hours beforehaemodynamic evaluation; (3) a stable clinical statuswithout change in symptomatology or therapeuticregimen during the interval between radiologicaland haemodynamic assessment. Patients withvalvular or congenital heart disease or hypertrophiccardiomyopathy were excluded from the study. Ofa total of 128 patients, 56 met the above criteria.Thirty-eight patients undergoing 46 haemodynamicstudies were evaluated retrospectively. Eighteenpatients undergoing 20 studies were then evaluatedprospectively. An additional 26 patients withoutsymptoms of heart failure who underwent rightheart catheterisation during the course of evaluationfor chest pain syndromes served as a control group.Twenty were evaluated retrospectively and sixprospectively. Thus, the retrospective group con-sisted of 24 patients undergoing 26 haemodynamicstudies.

All patients had chronic exertional dyspnoea ofover one month's duration. Those who had biplaneleft ventricular angiography had an ejection fraction<0*40. All had, in addition, at least two of thefollowing characteristics: (1) a third heart sound,(2) raised jugular venous pressure, (3) a sustainedlaterally displaced left ventricular impulse, (4)chronic digitalis or diuretic requirements, (5)pulmonary artery wedge pressure >15 mmHg,(6) cardiac index <2-2 1/min per M2. Fifty-three ofthe patients with congestive cardiomyopathy were inNew York Heart Association class III or IV heartfailure at the time of the study; three were inclass II. Two of the patients in class IV hadimproved to class II at the time of their secondstudy.

PATIENT POPULATIONThe mean age of patients with cardiomyopathy was59 ±13 ( ±1 SD) years compared with 55 ± 12 yearsfor the patients in the control group. The differencewas not statistically significant. The mean ages ofthe patients and controls in the retrospective andprospective groups were similar to the groups as awhole.

Both cardiomyopathy and control populationswere predominantly male, with 39 (70%) men in theformer and 21 (81%) men in the latter (NS). Thesex ratios of the cardiomyopathy and controlpatients in the retrospective and prospective groups

were also similar to those of the overall groups andnot statistically different from one anotner.

Thirty-two (57%) of the heart failure patientshad cardiomyopathy secondary to coronary arterydisease, as determined by coronary angiography ora documented history of multiple myocardialinfarctions (ischaemic cardiomyopathy). Three hadalcoholic cardiomyopathy, one was diabetic withnormal coronary arteries, and one was a femalecarrier for the X-linked disorder, Duchenne'smuscular dystrophy. Thirteen (23%) had a conges-tive cardiomyopathy of undetermined aetiology.Because of similar clinical and haemodynamicpresentations in patients with ischaemic cardio-myopathy and in patients with congestivecardiomyopathy, results were analysed together.Of the control population, 21 had coronary artery

disease and five had atypical chest pain with normalcoronary arteries.

HAEMODYNAMIC EVALUATIONRight heart catheterisation with a Swan-Ganzcatheter was performed in the cardiac catheterisa-tion laboratory or the coronary care unit after thepatients gave informed consent. Pulmonary arteryand pulmonary artery wedge pressures weremeasured with the patient lying supine using aStatham P231d or P231a strain gauge. Zeroreference level was at the mid-axillary line.The patients evaluated retrospectively were

divided into three groups according to their meanpulmonary artery wedge pressure: group 1 includedthose with pulmonary artery wedge pressure< 15 mmHg; group 2 included those with pulmon-ary artery wedge pressure 15 to 24 mmHg; andgroup 3 included those with pulmonary arterywedge pressure >25 mmHg.

RADIOLOGICAL INDICESAll chest radiographs were obtained in the RadiologyDepartment. Posteroanterior and lateral projectionswere obtained at end inspiration with an x-raysource-to-film distance of six feet at approximately140 kV.

Cardiac size was evaluated using the cardio-thoracic ratio, which was measured as the maximumtransverse diameter of the heart divided by themaximum thoracic width.15 In addition, the presenceof left and right ventricular and left atrial chamberenlargement was recorded. Definitions of chamberenlargement were based on standard criteria.'5Pulmonary venous flow redistribution was

defined as the presence of a disparity between thecalibre of the upper and lower lobe pulmonaryvessels with distention of the upper vessels.'0 12Interstitial oedema was recognised as perivascular

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Dash, Lipton, Chatterjee, Parmley

or peribronchial cuffing, or Kerley's septal lines.'6Alveolar oedema was diagnosed as a hazy mottlingof small more discrete densities, some confluent,without the linear appearance characteristics ofinterstitial oedema, and with poorly definedborders.7 Pleural effusions were noted. Pulmonaryvenous flow redistribution, interstitial oedema,alveolar oedema, and pleural effusion were termedas "fluid abnormalities".

Finally, the presence or absence of hilar andpulmonary artery enlargement was recorded.6

Chest radiographs were interpreted by oneobserver without knowledge of the clinical orhaemodynamic status of the patients. To assessintraobserver variability, 20 chest radiographs werereinterpreted blindly three months after initialradiological assessment.

STATISTICAL ANALYSISThe data were processed using the statisticalpackages provided by the BMDP BiomedicalComputer Programs P-series.'8 Comparisons ofgroups of data consisting of continuous variables(as in Table 1 and Fig. 1) were done with t tests oranalysis of variance followed by a Student-Newman-Keuls multiple comparison test. Groups of discretevariable (see Fig. 2 and 3) were evaluated with non-parametric statistics, including the Mann-Whitneyand Kruskal-Wallis tests.

Table Haemodynamic results

Group PAWP (mmHg) PAP (mmHg)

1 (N=25) 9 4±2-6* }p<0-001 15-6 +2-6 l<0002 (2 (N= 13) 19-7 ±3-2 1 30 0 ±6.0 <

3 (N =28) 30-8 ±4-5 }p<0-001 40 4 ±6-0 p< 0-001

*Mean + 1 SD.Abbreviations: PAWP = pulmonary artery wedge pressure;PAP = pulmonary artery pressure; N = number of studies;1 = studies with PAWP < 15; 2 = studies with PAWP 15 to 24;3 = studies with PAWP >25.

Bivariate linear regression and stepwise multiplelinear regression analysis were also used to relatethe radiological data to the haemodynamics (Fig. 4).The stepwise regression program evaluated all thevariables presented to it and selected only thoseradiological variables which contributed independ-ently to a significant degree to the prediction ofpulmonary artery wedge pressure. Multiple cor-relation coefficients (r), fraction of variance ex-plained (R2), levels of significance for each variableand the overall regression, and standardisedregression coefficients were obtained at each step.The latter are normalised values which take intoaccount the different units and variances of thevariables.

Results

INTRAOBSERVER VARIABILITYAnalysis of intraobserver variability showed thatinterpretation of the chest radiographs was highlyconsistent, except for the assessment of hilar andpulmonary artery size. The initial mean cardio-thoracic ratio of the 20 radiographs read twice was0-58 ±0-11 (± 1SD) and the subsequent value0-58±0 10. All paired cardiothoracic ratios wereconsistent to 2 per cent except two pairs which wereaccurate to 6 and 5 per cent of one another. Paired

0 80

0-70

0-60

0*50-

0 40

0 30

0.20

0 10

P< 0-001

.0

p 0 025 :.

M * i {

4 5:*{ I

M = Mean

I = +SEMI =PAW<1511 = PAW15-24III= PAW,25

1i I1I IIIGroup

Fig. 1 Plotted are the means and individual values forthe cardiothoracic ratios in each group of patients. Themean value of group 2 was significantly higher (p < 0 001)than group 1, and that of group 3 significantly higherthan group 2 (p < 0 025).

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* p<001 I=PAW <15* pcO05 11 =PAW 15-24

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II III 1l III II IIILV LA RV

Fig. 2 Presented are histograms showing the percentageoffindings with left ventricular (LV) enlargement, leftatrial (LA) enlargement, and right ventricular (R V)enlargement in each group.

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estimates of the pulmonary venous pattern, presenceof interstitial and alveolar oedema, pleural effusions,left and right ventricular size, and left atrial sizewere all consistent in at least 90 per cent of cases. Onthe other hand, 20 per cent ofestimates ofpulmonaryartery size and 40 per cent of estimates of hilarsize were inconsistent. Given the high variability

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in the assessment ofpulmonary artery and hilar size,these two radiological variables were excluded fromthe analysis relating the chest radiographic findingsto pulmonary artery wedge pressure. All the otherchest x-ray indices described above form the basesfor the subsequent results.

Retrospective results

HAEMODYNAMIC FINDINGS* pc0001 Of the 66 studies done retrospectively, the mean

** pcO05 pulmonary artery wedge pressure was 260 ±8-2+ p:OO-1I PAW<15 (±1 SD) mmHg for the cardiomyopathy group

* 11 = PAW 15-24 and 91 ±2-5 mmHg for the control populationIII = PAW->25

(p <0001). The Table lists the resultant mean

k\** pulmonary artery wedge and pulmonary arterya2+ X pressures after the patients and controls were

divided into three groups according to their* 0 ** f + m * 0 pulmonary artery wedge pressure. It is, therefore,

E77-7 XLnot surprising that the haemodynamics of each

VR I IOe A0Oe EFFI group were highly statistically different (p <0-001)arouD 1 vs. 2. and 2 vs. 3 for nulmonarv arterv

Fig. 3 Presented are histograms showing the percentageoffindings with venous redistribution (VR), interstitialoedema (IOe), alveolar oedema (AOe), and pleuraleffusions (EFF) in each group.

50 00PAWP predicted from CXR data

45*00 Slope=0-788 Intercept= 4074 r=0-824 n-26

40 00 /

35*00

E313000 - /

<2500-

20-00 -

.0o 15-00.

10.00

5-00-

0*00000 500 1000 15:00 2000 2500 3000 3500 4000Predicted PAWP (mmHg)

Fig. 4 Plotted is the predicted versus the observedpulmonary artery wedge pressures in the prospective groupof studies, the resultant linear regression formula(slope = 0 79, r = 0.82), and the 95 per cent confidencelimits.

edgeO and pulmnAr a y -- r r s.-_- j

wedge and pulmonary artery pressures.

RADIOLOGICAL ASSESSMENT OF CARDIACENLARGEMENT AND CHAMBER SIZEHeart size alone, as estimated by cardiothoracicratio, correlated well with pulmonary artery wedgepressure (r=0-70). However, the 95 per centconfidence limits were wide, making the predictionof an individual patient's pulmonary artery wedgepressure somewhat uncertain. This difficulty isillustrated in Fig. 1, in which the cardiothoracicratios for all the retrospective studies are plottedaccording to group. Mean cardiothoracic ratio forthe group 1 patients was 0-45 ±0-06; for the group 2patients, 0 57 ±0-08; and for the group 3 patients,062 ±008 (p <0-001 1 vs. 2, p <0-025 2 vs. 3). Itcan be seen, however, that the overlap among thegroups is great enough to make the classification ofindividual patients difficult. Generally, a cardio-thoracic ratio >0-60 was predictive of pulmonaryartery wedge pressure >25 mmHg; 77 per cent ofstudies with a cardiothoracic ratio >0-60 occurredwhen pulmonary artery wedge pressure was>25 mmHg. On the other hand, the sensitivity ofsuch an abnormal cardiothoracic ratio for a pulmon-ary artery wedge pressure >25 mmHg was low,occurring in 58 per cent of the group 3 patients.Normal cardiothoracic ratio ( <0-50) suggestednormal pulmonary venous pressure; 88 per cent ofstudies with cardiothoracic ratio <0-50 had pul-monary artery wedge pressure < 15 mmHg. Only68 per cent of all studies, however, with pulmonaryartery wedge pressure < 15 mmHg had a normalcardiothoracic ratio.

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Fig. 2 depicts the presence of chamber enlarge-ment in the three groups. Left ventricular enlarge-ment occurred in 27 per cent of group 1 patients,whereas left atrial or right ventricular enlargementoccurred in less than 10 per cent of group 1 patients.Though left ventricular and left atrial enlargementwere statistically more frequent when pulmonaryartery wedge pressure was raised (p < 0 01), nochamber assessment discriminated those with mildto moderate (group 2) from those with severe(group 3) rises in pulmonary artery wedge pressure.

Fig. 3 shows the presence of "fluid abnormalities"in the three groups. Fluid abnormalities wereuncommon when pulmonary artery wedge pressurewas 15 mmHg. Venous redistribution, interstitialoedema, and pleural effusions occurred in less than10 per cent of group 1 patients, while alveolaroedema occurred in none. Venous abnormalities(p <0-001), interstitial oedema (p <0-05), andpleural effusions (p < 005) all distinguished group 1from group 2. None of the radiological types offluid abnormalities, however, were statisticallymore frequent when the group 3 studies werecompared with those in group 2. Alveolar oedemawas present rarely even when pulmonary capillarywedge pressure was > 25 mmHg, when it waspresent in 32 per cent of studies.

Multiple linear regression analysis showed thatradiological assessment of cardiothoracic ratio,alveolar oedema, interstitial oedema, and left atrialsize (in that order of importance) all independentlycontributed to the estimation of pulmonary arterywedge pressure r=0-82). Cardiothoracic ratioaccounted for 48 per cent of the variance explained(R2); alveolar oedema 11 per cent, and inter-stitial oedema and left atrial size, each 4 per cent.The standardised regression coefficients of eachvariable were similar, however, indicating that allfour variables were important for the estimation ofpulmonary artery wedge pressure from the chestradiograph. The regression formula was:

PAWP = -26±21 1 (CTR) + 5.5 (AOe)+ 5.4 (IOe) + 6-3 (LA)

where PAWP = pulmonary artery wedge pressureand is measured in mmHg, CTR = cardiothoracicratio, AOe = alveolar oedema, IOe = interstitialoedema, and LA = left atrial enlargement. AOe,IOe, or LA were given a value of "1" if the particu-lar abnormality was present and "0" if absent.

Prospective results

In order to test the validity of the derived stepwiselinear regression formula, the formula was then

applied to the radiological data of the studiesobtained prospectively. The formula was used toderive predicted pulmonary artery wedge pressuresfrom the prospective radiological data. Thepredicted pressures were then correlated withactual pressures. The results are plotted in Fig. 4.The correlation is excellent, with r=0-82, a valuesimilar to that obtained from the retrospective data.

Discussion

Previous investigations documented the value ofthe chest radiographic findings ofpulmonary venousflow redistribution, interstitial oedema, alveolaroedema, and pulmonary arterial enlargement in thenoninvasive estimation of the haemodynamics inpatients with rheumatic mitral valvular dis-ease. 5 7 8 12-14 19 20 Indeed, Milne"3 synthesisedthe available data and presented specific radiologicalcriteria for the estimation of both mean pulmonaryartery and pulmonary artery wedge pressures inpatients with mitral stenosis.

In the present study an attempt was made toevaluate the predictive value of various radiologicalfindings for the estimation of pulmonary venouspressure in patients with chronic congestive heartfailure who did not have valvular heart disease. Ourfindings document that the presence of most chestradiographic abnormalities in patients with chroniccongestive cardiomyopathy and ischaemic cardio-myopathy indicates raised pulmonary artery wedgepressure (Fig. 1 to 3). Alveolar oedema wasconspicuously absent in patients with normalpulmonary artery wedge pressure. Left atrial andright ventricular enlargement also occurred rarely(< 10%) when pulmonary venous pressure wasnormal. The only radiological abnormality commondespite a normal pulmonary artery wedge pressurewas left ventricular enlargement (27% of group 1studies). This finding may reflect the nature of ourcontrol patients: many had prior myocardialinfarction and/or hypertension.Our observations in patients with chronic

congestive cardiomyopathy are at variance withthose in patients with acute heart failure secondary tomyocardial infarction as reported by Kostuk et al.2'who showed that in the setting of acute myocardialinfarction, the chest radiograph predicted accuratelythe pulmonary artery wedge pressure in only 43 percent of patients, underestimated it in 24 per cent,and overestimated it in 33 per cent. We found thatradiographic analysis in chronic heart failure rarelyoverestimated pulmonary artery wedge pressure.Rapidly changing haemodynamics in patients withacute myocardial infarction may account for thisdiscrepant result.

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Although the presence of "fluid abnormalities"in patients with chronic congestive heart failure inour study was useful to separate patients withnormal pulmonary artery wedge pressure fromthose with raised pulmonary artery wedge pressure,the findings did not help in distinguishing patientswith moderate increases in pulmonary artery wedgepressure (group 2) from those with severe increases(group 3) (Fig. 2). Our findings differ from thoseof Turner et al.11 who estimated pulmonaryhaemodynamics from the chest radiographic analysisof fluid abnormalities and pulmonary arterial size.However, in their study haemodynamic and radio-logical correlations are not presented other thanseveral individual cases, and the patient populationis not identified. Moreover, in our study we haveshown, as have others previously,9 that the radiologi-cal estimation of pulmonary size may be in error.Of the fluid abnormalities, alveolar oedema was

the most specific predictor of a raised pulmonaryartery wedge pressure in our study. No group 1patient had alveolar oedema. Yet alveolar oedemawas also uncommon, despite severe increasesin pulmonary artery wedge pressure.'8 Someauthors" 15 have suggested that transudation ofoedema into the alveoli does not occur until thepulmonary artery wedge pressure reaches 30 to35 mmHg. Of our studies in which pulmonaryartery wedge pressure was at least 30 mmHg,alveolar oedema was present in 30 per cent. Onepossible explanation for infrequent pulmonaryoedema despite severe rises in pulmonary venouspressure is that, during chronic heart failure,lymphatic hypertrophy and hyperplasia and changesin the pulmonary interstitium allow for a moreefficient removal of oedema from the lungs than inacute heart failure.22

Cardiomegaly as assessed by cardiothoracic ratioproved to be the single most important predictorof pulmonary artery wedge pressure in our study(Fig. 1). This finding, however, is contrary to thedata reported in the setting of acute myocardialinfarction by McHugh et al.23 and Kostuk et al.21The different findings may relate to cardiovascularadaptation to heart failure. Gradual left ventriculardilatation is the usual pathophysiological responseto an increase in left ventricular filling pressureand a reduction in myocardial contractility.24Consequently, cardiomegaly is more likely to bepresent in chronic rather than acute left ventricularfailure. In fact, Kostuk et al.2' noted that thosepatients with radiographic cardiomegaly nearlyalways had raised pulmonary capillary wedgepressure.Our data are in agreement with those of Harlan

et ai.25 who found that radiological estimate of

heart volume was the most important clinicaldescriptor of a group of patients with ischaemiccardiomyopathy. Though Yatteau et al.26 foundnormal heart size in 27 per cent of their patientswith ischaemic cardiomyopathy, 60 per cent oftheir patients were in New York Heart Associationclass I or II heart failure, whereas only 6 per centof our patients were in class I or II.Although in the present study cardiothoracic

ratio correlated best with pulmonary artery wedgepressure (r=0-70), the accuracy of the ratio inpredicting the level of increase in pulmonary arterywedge pressure in individual patients was low. Inmany patients the cardiothoracic ratio could not beused to estimate the pulmonary artery wedgepressure with enough precision to be clinicallyuseful.The present study indicates that a combination

of radiological variables might more accuratelypredict the level of pulmonary artery wedgepressure. The stepwise multiple linear regressionformula, using the variables cardiothoracic ratio,alveolar oedema, interstitial oedema, and leftatrial size, predicted pulmonary capillary wedgepressure fairly accurately in patients with ischaemicas well as congestive cardiomyopathy (r-=082).The regression equation derived from the retro-spective data was used prospectively to estimatepulmonary artery wedge pressure in 26 studies,and a close estimation of pulmonary artery wedgepressure was possible in most patients (r=0-82).It needs to be emphasised, however, that the slopeof the regression line in the prospective evaluationwas 0 79, indicating that the radiological findingstended to underestimate the pulmonary arterywedge pressure to some extent (Fig. 4). This isnot surprising given that alveolar oedema occurredinfrequently, yet was the second most importantpredictor for raised pulmonary artery wedgepressure in our study. Fig. 5 illustrates the difficultythat exists in the radiological estimation of thepulmonary haemodynamics in patients with chroniccongestive cardiomyopathy. The two patients whosex-rays are shown in Fig. 5 both had identicalhaemodynamic findings with cardiac indices of1-5 1/min per m2 and pulmonary artery wedgepressure of 32 mmHg. Both patients had grosscardiomegaly and left ventricular and atrialenlargement, yet only the patient in Fig. 5A hadpulmonary venous flow redistribution, interstitialoedema, and alveolar oedema. Using traditionalcriteria, a radiologist might estimate that the patientin Fig. 5B had normal or minimally raised leftventricular filling pressures; using the stepwiselinear regression formula, the estimated pulmonaryartery wedge pressure is 23 mmHg, and slightly

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PT060 PCW:32mmHg ClI:1 41/minperm2A

069 PCW:32mmHg CI:1 51/minperm2B

Fig. 5 Shown are chest radiographs from two patients with identical haemodynamics (pulmonary artery wedgepressure = 32 mmHg and cardiac index = 1-5 l/min per mi) and different radiographic findings.

underestimates the true pulmonary artery wedgepressure, though it is still grossly abnornal.

In conclusion, our study has shown that, thoughchest radiographic abnormalities are helpful toidentify the presence of raised pulmonary venouspressure in patients with ischaemic and congestivecardiomyopathy, the prediction of the level ofpulmonary venous pressure from any singleradiological variable is not possible. Multiplestepwise linear regression analysis improves thepredictive value of the radiological variables for theestimation of pulmonary artery wedge pressure. Aprospective study involving a much larger group ofpatients will be needed to evaluate further the valueof the regression analysis for the estimation ofpulmonary artery wedge pressure in these patients.

The authors thank Drs James Ostlund and StantonGlantz for their assistance with the statisticalanalysis.

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estimation artery with · interstitial oedema, and left atrial size each contributed independently...

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