subacute massive pulmonary embolismpulmonary embolism who died during their initial illness and...

Br Heart J 1981; 45: 681-8

Subacute massive pulmonary embolismRJC HALL,* D McHAFFIE,t C PUSEY,$ GC SUTTON§

From the Cardiac Department, Brompton Hospital, London

SUMMARY Twenty-four patients with subacute massive pulmonary embolism were studied both duringtheir initial illness and up to nine years after it. The most common mode of presentation was progressivedyspnoea over a two to 12 week period, which in some, but not all, patients was accompanied by pleuriticchest pain and haemoptysis. Physical signs at diagnosis usually suggested right heart strain and ventila-tion/perfusion mismatch and in the five patients with the highest pulmonary artery pressures thepulmonary component of the second sound was accentuated. The chest x-ray and electrocardiogramprovided useful diagnostic information in most patients though occasionally they were normal. Earlyresponse to thrombolytic treatment was poor when compared with patients with acute pulmonaryembolism but was occasionally dramatically successful, and heparin alone provided satisfactory treat-ment in the eight patients receiving it. Pulmonary embolectomy provided poor results and four of thefive patients undergoing this form of treatment died. Nine patients died during the initial illness and inseven death was directly related to embolic disease. One patient died from neoplastic disease duringfollow-up. Though the prolonged illness, poor initial response to treatment, and absence of predispos-ing factors suggest that recurrent embolic disease and late pulmonary hypertension might occur therewas no evidence of this during a follow-up period of one to nine years (median five years).

Pulmonary embolic disease can present inmany waysranging from mild pleuritic pain to sudden fatalcollapse. Since the presentation is so varied, classi-fication of these patients into different clinicalsubgroups using the history and pulmonaryangiographic findings is needed before possibledifferences in clinical course, response to treatnent,and late prognosis can be considered.

This study was undertaken to extend our previousobservations of one particular subgroup, subacutemassive pulmonary embolism. We have previouslydefined these patients as having long histories(between two and 12 weeks) without a definiteepisode of cardiovascular collapse and pulmonaryangiograms showing massive pulmonary embolism(>50% obstruction of major pulmonary arteries).This group of patients is of particular interest fortwo reasons.

(1) Since presentation is much less dramatic

*Present address: Royal Victoria Infirmary, Newcastle Upon Tyne.tPresent address: Wellington Hospital, Wellington 2, New Zealand.*Present address: Royal Postgraduate Medical School, London.§Present address: Hillingdon Hospital, Hillingdon, Middlesex.

Received for publication 6 August 1980

than in acute massive pulmonary embolism thediagnosis is often difficult to make. This studyprovides a detailed clinical description of thiscondition so that it can be recognised more readily.

(2) Since these patients have long histories,often lack a well-defined predisposing cause forembolic disease, and frequently show little angio-graphic improvement after initial treatment, theymight be expected to be at particular risk from re-current embolism and the development of thrombo-embolic pulmonary hypertension. This study,therefore, investigated the long-term prognosis ofthese patients with particular reference to thesepoints.

Patients and diagnosis

The series consists of 24 consecutive patients (12male and 12 female, age range 20 to 71 years)referred to the Brompton Hospital with subacutemassive pulmonary embolism. Thirteen of thesepatients have been reported previously'; furtherinformation including up-to-date follow-up wasobtained on these patients and 11 further patientsadded.

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Hall, McHaffie, Pusey, Sutton

DEFINITION OF SUBACUTE MASSIVEPULMONARY EMBOLISMThe criteria used to define the group of patientswere the same as previously reported.1 All patientshad long histories (more than two weeks) without anepisode of cardiovascular collapse, but had massivepulmonary embolism with more than 50 per centobstruction of major pulmonary arteries at angio-graphy or embolectomy. Pulmonary angiogramswere scored2 3 from 0 to 34 depending on theseverity of pulmonary artery obstruction. A scoreof greater than 17 represented massive embolism.

All patients were seen during their initial illnessby either RH or GCS. The diagnosis was confirmedby pulmonary angiography in 22 of the 24 patientsand in the remaining two patients, early in theseries, at pulmonary embolectomy.

METHOD OF FOLLOW-UPPatients were recalled and examined by two of us(RH and DMcH). Particular notice was taken ofsymptoms and signs that might suggest recurrentpulmonary emboli or pulmonary hypertension. Allpatients had chest x-rays and 12 lead electrocardio-grams. Right heart catheterisation, pulmonaryangiography, and perfusion lung scans (using99mtechnetium labelled albumin macroaggregates)were performed at follow-up in most, but not all,patients.

Clinical presentation

HISTORYAll the patients, by definition, had long historieswithout an episode of cardiovascular collapseprecipitating their presentation. Increasing dysp-noea, either at rest or on exertion, was the mostprominent symptom in all but one patient in whommild dyspnoea was overshadowed by pleuriticpain and haemoptysis. Pleuritic pain occurred atsome stage of the illness in 16 of the 24 patients andwas accompanied by haemoptysis in six. Anothersix patients had haemoptysis without pleuriticpain, and in six patients persistent cough was alsoprominent. Two patients had dyspnoea as theironly complaint.

Although, by definition, no patient presented withan acute episode of collapse three patients had asudden acute exacerbation of symptoms duringthe course of their illness, which suggested that anacute embolic event had occurred at that time.

PREDISPOSING FACTORSEight patients had recognisable factors pre-disposing to thromboembolic disease. These werethe contraceptive pill in four, pregnancy in one,

primary lymphoedema and gross obesity in one,chronic lymphatic leukaemia in one, and systemiclupus erythematosis and a previous splenectomy inone. In seven patients there was a history of deepvein thrombosis; in four this occurred at the sametime as the episode of subacute massive pulmonaryembolism and in three had resolved at least sixmonths beforehand.

PHYSICAL SIGNSDyspnoea at rest or on slight exertion was the mostconstant physical sign and was present in 18 ofthe 24 patients. Clinically detectable centralcyanosis was present in eight patients.Although none of the patients was clinically

shocked and only one had a systolic blood pressure ofless than 100 mmHg, many had physical signs thatsuggested that the cardiac output was compromised.Resting tachycardia was common; of the 24 patients,only eight had a resting heart rate of less than 100,and in six patients the resting heart rate was between120 and 140. Three patients had cool, cyanosedperipheries as well as resting tachycardia and oneof these patients was the only patient with a bloodpressure of less than 100 mmHg (90/60 mmHg).The systolic blood pressure was between 100 and110 mmHg in five patients, between 110 and 120mmHg in four, and above 120 mmHg in theremainder.The jugular venous pressure was raised more than

2 cm above the sternal angle at 450 in 11 patients(range 3 to 10 cm). In two of these patients, therewas a dominant "v" wave to a height of 10 cm abovethe sternal angle accompanied by a pansystolicmurmur at the left sternal border. In both, thejugular venous pressure fell and the murmurdisappeared as the patients recovered. On clinicalgrounds these physical signs were thought to repre-sent functional tricuspid regurgitation; both patientshad high pulmonary artery pressures at theirinitial study (70 mmHg systolic) when these signswere present. The cardiac impulse at the leftsternal border was unusually prominent in fourpatients and 11 patients had a gallop rhythmdetectable at this site. In general a raised jugularvenous pressure, parasternal heave, or galloprhythm did not predict a particularly raised pulmon-ary artery pressure, except in the two patients withtricuspid regurgitation.

In contrast, abnormalities of the second heartsound occurred only in the patients with the highestpulmonary artery pressures. The systolic pulmonaryartery pressure exceeded 55 mmHg in 10 patientsand nine of these patients had abnormalities of thesecond heart sound; in five patients P2 was accentu-ated (systolic pulmonary artery pressures 55, 61, 63,

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Subacute massive pulmonary embolism

Table 1 Chest x-ray and electrocardiogram atpresentation

Abnormality No. of patients

Chest x-ray Oligaemia 18Consolidation orcollapse± pleural fluid 20 Sin 22 patients

Enlarged main Jpulmonary artery 4

Electrocardiogram Sinus tachycardia 16Atrial flutter

(2:1 block) 1SQ5aT3 12T inversion V 1-3 12 Sin 19 patientsPartial right bundle- I

branch block 2 J

75, and 75 mmHg) and in four patients P2 wasof normal intensity but delayed, producing widesplitting of the second sound (systolic pulmonaryartery pressures 55, 70, 70, and 71 mmHg). Anaccentuated P2 was also heard in one of the twopatients who were not catheterised.

In 12 of the 24 patients abnormal chest signssuggesting pleural fluids, pulmonary consolidation,or collapse or pleuritic inflammation were present.Fever occurred in 10 patients.

INITIAL CHEST X-RAY ANDELECTROCARDIOGRAMThese results are summarised in Table 1. In allbut two patients the chest x-ray was obviouslyabnormal. The electrocardiogram was completelynormal in two patients and in three others the onlyabnormality was sinus tachycardia.

PULMONARY ANGIOGRAPHY ANDPULMONARY ARTERY PRESSURERight heart catheterisation and pulmonary angio-graphy were performed in 22 patients.The pulmonary angiographic score was 21 4 ± 3 5

(mean ± SD), the systolic pulmonary artery pressure56&2±15-7 mmHg (mean± SD), and the meanpulmonary artery pressure was 36-7±9 7 mmHg

Table 2 Treatment and outcome in subacute massivepulmonary embolism

Initial treatment No. Deaths Recovered

Embolic Other

Streptokinase 14* 4 (1) 1 9Heparin 8 1 (1) 1 6 (1)Embolectomy 2 2 0 0Total 24 7 2 15

*Streptokinase changed to heparin at 24 hours because of haemo-ptysis in one patient.Numbers in parentheses refer to the number of patients undergoingemergency embolectomy because of deterioration on their initialtreatment.

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(mean ± SD). Both systolic and mean pulmonaryartery pressure were significantly higher (p < 0 05)than in a group of 42 patients with acute massivepulmonary embolism' 3 with a similar degree ofpulmonary artery obstruction. The angiographicscore and pulmonary artery pressure did notdiffer between the patients with subacute massivepulmonary embolism who died during their initialillness and those who survived, nor between thedifferent treatment groups.

Clinical course and treatment duringinitial episode

Treatment was with streptokinase, heparin, embo-lectomy, or a combination of these (Table 2). Thetreatment in the individual case was determined bythe physician under whose care the patient wasadmitted. In general the more severely ill patientsreceived streptokinase in the first instance, but sincepatients were not allocated randomly to differenttreatments it is difficult to compare their efficacy.Nine patients (38 %) died during their initial

illness. Seven of these deaths were directly attribu-table to embolic disease; the other twopatients died of other serious concurrent illnesses(systemic lupus erythematosis and chronic lym-phatic leukaemia) after showing signs of recoveringfrom their embolic episode. Three of the sevenpatients who died of embolic disease did so duringor after a 72 hour course of streptokinase; onedeteriorated and died within 24 hours of startingtreatment and the other two followed prolongeddownhill courses, with a low cardiac output, duringseven and 10 days, respectively, after startingtreatment. The other four patients who died allunderwent pulmonary embolectomy. In two thedeath was unrelated to embolectomy since one wasmoribund, receiving external cardiac massagehaviing deteriorated on streptokinase treatment, andthe other died of a massive recurrent pulmonaryembolus despite adequate heparinisation severaldays after a successful embolectomy. In the othertwo patients, seen early in the series, embolectomywould no longer be considered the correct treat-ment. Neither patient was shocked and both wouldnow be treated medically. One other patientunderwent a successful embolectomy after deterio-rating on heparin, making a total of five patientstreated by embolectomy. Therefore of the sevenpatients, in whom embolic disease caused death,four deteriorated on medical treatment withoutevidence of a further embolus and in one of theseembolectomy was attempted when the patient wasmoribund, one patient died of a further embolusafter a successful embolectomy, and in two death



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Hall, McHaffie, Pusey, Suttcn

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o 20oLUc LU 7-J

o K)\< SMONTHSz 00

DIAGNOSIS 72 HOURS

Fig. 1 The arteriographic response to initial treatmentin subacute massive pulmonary embolism. The patientstreated with streptokinase are represented by circles(a) and with heparin by triangles (A).

was associated with pulmonary embolectomies, thatin the light of present knowledge might have beenavoidable.

Fig. 1 shows the early angiographic responseto treatment in 10 patients. Nine of these patientswere studied 72 hours after the beginning oftreatment; the tenth patient was restudied at fivemonths but was included with the early rcstudies,

34.-

30

20-7Pulmonary patiearterioqraphic 17 - -_ -score

since the distribution of pulmonary angiographicabnormalities was the same as before treatmentand there had been no clinical episode of recurrentembolism during the five month period. Only twopatients showed dramatic clearing of the pulmonaryarteries during the first 72 hours and both of thesepatients were receiving streptokinase. The earlyangiographic response to thrombolytic treatmentwas poor when compared with a group of 24 patientswith acute massive pulmonary embolism receivingstreptokinase (Fig. 2).

Follow-up

PATIENTS AVAILABLE FOR FOLLOW-UPOf the 24 patients, 15 survived the initial illness.Two of these patients were lost to follow-up so thatdata were obtained in only 13 of the 15 survivors.Of these, one died two years after his initial illnessof carcinoma of the pancreas, without clinicalevidence of recurrent pulmonary embolism. Theremaining 12 patients were recalled and seen fivemonths to nine years (median five years) after theirinitial illncss.

INITIAL PREDISPOSING FACTORSOnly four of the 13 patients followed up had well-defined predisposing factors to embolic disease

100% obstruction

6patients

2 patients

Acute massive PE Subacute massive PE(24 patients) (8 patients)

Fig. 2 Comparison of the arteriographic response to treatment with streptokinase in patients with acute andsubacute massive pulmonary embolism.

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(the contraceptive pill-two patients, pregnancy-one patient, severe obesity and primary lymph-oedema-one patient). Three other patients gavelong histories of recurrent phlebitis and had varicoseveins.

ANTICOAGULATION DURING FOLLOW-UPSeven patients received long-term, oral anticoagu-lants (warfarin) during the follow-up period and theremaining six patients were anticoagulated for twoto 18 months after their initial illness. Venousinterruption was not performed in any patient.

CLINICAL FOLLOW-UPNone of the 12 eventual survivors had had symptomsto suggest recurrent embolism and none hadphysical signs suggesting pulmonary hypertension.Ten of the 12 were asymptomatic (NYHA class 1).One grossly obese patient, who also suffered fromprimary lymphoedema, had severe exertionaldyspnoea (NYHA class 3). She had no physicalsigns to suggest pulmonary hypertension orcardiopulmonary disease and repeat right heartcatheterisation showed a normal resting pulmonaryartery pressure (25/12 mmHg) and mild, residualpulmonary angiographic abnormalities (score 8).It was concluded that her symptoms were largelycaused by her gross obesity. The second patientwith symptoms had mild exertional dyspnoea(NYHA class 2), a normal pulmonary arterypressure, and a completely normal pulmonaryangiogram. Clinically he had chronic bronchitiswhich was almost certainly the cause of his symp-toms. Therefore, in neither could non-resolution orrecurrent pulmonary embolism be incriminated asthe cause of disability.

ELECTROCARDIOGRAM, CHEST X -RAY, ANDLUNG SCANElectrocardiograms and chest x-ray films wereobtained in all 12 patients recalled. The electro-cardiogram had returned to normal in 10 patients.Two patients had an abnormal electrocardiogramat follow-up. In one, the S1Q3T3 pattern, partialright bundle-branch block, and T wave inversionin V2 to 6 seen during the initial illness was stillpresent seven years later. This was the patientalready described with severe dyspnoea, obesity,primary lymphoedema, and a normal pulmonaryartery pressure. In the other patient T waveinversion in V2 to 4 was still present one year laterbut the S1Q3T3 pattern, initially present, hadresolved. This patient had a normal pulmonaryartery pressure and only minor pulmonary angio-graphic abnormalities at follow-up. The chestx-ray film was normal in nine patients. In two, there

were some areas of oligaemia and both patientsshowed some residual pulmonary angiographicabnormalities (scores of 7 and 8). One patient whostill had severe residual abnormalities at repeatpulmonary angiography (case 1), had a grosslyabnormal chest x-ray with a raised diaphragm andconsiderable shadowing in the left lung, the onein which nearly all the persistent angiographicabnormalities were seen.

Late lung scans were carried out in eight of the12 patients. These were normal in three. Threeothers showed multiple perfusion defects and twohad single defects. All five patients with abnormallung scans showed minor angiographic abnormali-ties but in the three patients with multiple perfusiondefects, the extent of the abnormalities on lungscan greatly exceeded the extent of those onangiography.

CARDIAC CATHETERISATION AND PULMONARYANGIOGRAPHYNine of the 12 patients recalled had a right heartcatheterisation and pulmonary angiography (Table3). Two other patients who had complete angio-graphic and haemodynamic resolution at a restudy72 hours after the onset of initial treatment and nosubsequent symptoms were not restudied but theirresults are included with the late restudy data.One patient who had not had an early restudybut had been completely well for the subsequentthree years refused investigation. One patient had asignificantly raised pulmonary artery pressure butthis was the result of left ventricular dysfunctionwith a pulmonary artery wedge pressure of 20mmHg and the pulmonary angiogram and pul-monary vascular resistance were normal. Threeother patients (cases 1, 8, and 9) had mildlyraised (>30 mmHg) systolic pulmonary arterypressures and in these patients some residualpulmonary angiographic abnormalities were present.Five other patients showed persistent angiographicabnormalities. In four these were minor consistingof mildly reduced perfusion and loss of a few smallperipheral pulmonary arteries. In one patient,restudied at five months, considerable pulmonaryartery obstruction persisted though the systolicpulmonary artery pressure was almost normal(33 mmHg) and the patient was asymptomatic.

Discussion

(A) DIAGNOSIS AND TREATMENT OFINITIAL ILLNESSSubacute massive pulmonary embolism is a well-recognised but rare condition. It is frequentlyreferred to as "recurrent pulmonary embolism"

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Table 3 Systolic pulmonary artery pressure and pulmonary angiographic score at diagnosis and restudy in 12survivors of subacute massive pulmonary embolism

Case Age, sex First study Second studyNo.

Initial Systolic PA Pulmonary Interval Systolic PA Pulmonary Symptoms Commenttreatment pressure angio score from Ist pressure angio score at follow-up

(mmHg) study (mmHg)

1 20 F SK 33 17 5 mth 33 14 02 59 F SK 75 26 (22)* 7 y 25 8 + + Gross obesity3 45 M SK 70 25 (4)* 7 y 28 0 04 45 M Hep 45 22 (16)* 9 y 22 0 05 48 F Hep 60 19 4 y 43 0 0 Normal PVR

LV disease6 31 M Hep 50 18 - - - - Refused study7 38 F SK 60 26 (19)* 5 y 24 0 08 71 M Hep 71 22 3 mth 33 7 09 64 M SK 60 21 1 y 37 6 010 35 F SK 55 25 (23)* 5 mth 30 4 011 55 M Hep+embol 40 18 (0)* 3 d 27 0 + Chronic

bronchitis12 48 F SK 35 18 (3) 3 d 30 3 0

SK, streptokinase; Hep, heparin; embol, embolectomy; PVR, pulmonary vascular resistance.*Pulmonary angio score after three days of treatment.

but this description does not distinguish thosepatients who have repeated pulmonary emboli wellseparated in time from this group of patients inwhom the result is a steadily progressive illness.Though repeated episodes of embolism may berecognised early if typical features such as pleuriticpain and haemoptysis are prominent, these patientsoften present with advanced pulmonary arteryobstruction. There are two main reasons for this.Firstly since recognisable predisposing factorsfor thromboembolic disease are frequently absentthese episodes are often misdiagnosed as chestinfections.4 Secondly, when the history is, as sooften, of increasing dyspnoea alone and the physicalsigns are inconspicuous the illness may not berecognised until at a late stage severe symptomsdemand further assessment and investigation.

Occasionally the patient presents with very fewhelpful physical signs and with a normal chest x-rayfilm and electrocardiogram. In this unusualsituation the most helpful clue to the true diagnosisis the history of progressive dyspnoea over a periodof a few weeks. In the majority of patients, however,the physical signs combined with the chest x-rayand electrocardiographic findings point towardsthe true diagnosis. Dyspnoea at rest or on slightexertion, without evidence of obvious left heartfailure, airways obstruction, or chronic lungdisease, is the most prominent feature. A history ofepisodes that could represent pulmonary infarction,and a pronounced sudden increase in symptomson the background of steady deterioration is alsohelpful though often not present.Many patients also have sinus tachycardia,

cyanosis at rest or on mild exertion, a raisedjugular venous pressure, or a gallop rhythm at the

left sternal border to help in diagnosis. Morerarely, evidence of pulmonary hypertension in theform of an accentuated pulmonary component ofthe second heart sound may occur. This was foundin the five of our patients with the highest pulmonaryartery pressures. Even more infrequently there maybe tricuspid regurgitation that resolves withsuccessful treatment. Neither of these physicalsigns is a feature of acute massive pulmonaryembolism.

Since these patients usually present late, andare often not under medical observation during theearly stages of the illness, angiographic evidencefor the way that the pulmonary artery obstructionoccurs is not available, nor is there any explanationin many patients why embolic disease should occur.Despite this, it is a reasonable assumption that it iscaused by the accumulation of multiple small andmedium sized emboli in the pulmonary vascularbed over a period of weeks. The occurrence ofdiscrete episodes of pleuritic pain and haemoptysisin some patients, the progressive increase insymptoms, the occasional sudden exacerbation ofsymptoms possibly caused by a larger embolus,and the finding of clot of different ages at embolec-tomy or necropsy all suggest that this is the mechan-ism. Such a progression would explain the observeddifferences in pulmonary artery pressure in patientswith subacute and acute massive pulmonaryembolism with the same degree of pulmonaryartery obstruction. In acute massive pulmonaryembolism the pulmonary vascular bed is suddenlyobstructed and the acutely stressed, thin-walledright ventricle is unable to generate a systolicpulmonary artery pressure much in excess of 50mmHg. In contrast, in subacute massive pulmonary

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embolism, the right ventricle has had time toadapt and hypertrophy as the pulmonary vascularresistance slowly increases and therefore cangenerate much higher pulmonary artery pressures.The clinical consequence of this haemodynamicdifference is that, on occasion, signs of pulmonaryhypertension are a feature of subacute massivepulmonary embolism but they never occur inacute massive pulmonary embolism.The electrocardiogram and chest x-ray film were

useful clues to the correct diagnosis. Nearly 80per cent (19 of 24 patients) had electrocardiographicchanges suggesting right heart strain. None hadevidence of right ventricular hypertrophy, but thisdoes not mean that this did not develop during thecourse of the illness since the electrocardiogramis notoriously insensitive to mild degrees of rightventricular hypertrophy.5 Similarly, the chestx-ray film was extremely helpful. Twenty-two ofthe 24 patients had either obvious oligaemic zonesor, more frequently, x-ray changes consistent withpulmonary infarction. We do not have lung scansduring the initial illness in these patients, butperfusion lung scans are likely to be grossly abnor-mal in most patients with this condition and anormal perfusion scan should rule out the diagnosis.

Analysis of the results of treatment is difficultsince individual patients were treated according tothe wishes of the physician under whom they wereadmitted. In general the more severely ill patientsreceived streptokinase and this probably accountsfor the larger number of failures with this treatmentwhen compared with heparin. Comparison of theeffect of streptokinase in subacute and acutemassive pulmonary embolism suggests that therapid clearing of the pulmonary circulation thatoccurs so frequently in the latter is uncommon inthe former. This is not surprising since much ofthe pulmonary artery obstruction may be caused byclot that is too old to be lysed by streptokinase.This explanation is borne out by our limitedexperience of pulmonary embolectomy in thesepatients, when despite angiographically demon-strated massive proximal pulmonary artery obstruc-tion all that could be obtained at operation weresmall amounts of the more proximal thrombus,friable and often adherent to the pulmonaryarteries. This contrasts with the situation in acutemassive pulmonary embolism when the surgeonis usually able to pull out several hundred gramsof clot. These differences in the surgical findings alsoexplain the generally dismal results of embolectomy.

Since heparin appeared as effective as strepto-kinase in the majority of patients we suggest thatall patients with subacute massive pulmonaryembolism should receive intravenous heparin

as initial treatment. If deterioration continuesdespite heparin thrombolytic treatment should beused since it is spectacularly successful in a fewpatients. If this fails embolectomy should beundertaken as a last resort. All patients shouldreceive full intravenous heparinisation until theyare fully mobile and only then be transferred tooral anticoagulants.

(B) LATE PROGNOSISTreated acute massive pulmonary embolism has agood long-term prognosis, and recurrent pulmonaryembolism, poor resolution of pulmonary arteryobstruction, and the development of pulmonaryhypertension are extremely rare.) 6 This is notsurprising since most of these patients have well-defined and often temporary factors predisposingto embolism, the embolus is of recent formation,and it is susceptible to both therapeutic andnatural lysis. In contrast, in subacute massivepulmonary embolism the predisposing factor isoften unknown and potentially might continue tooperate after initial treatment, causing recurrenceof emboli. Furthermore, older clot, accumulated inthe pulmonary circulation over a period of weeks,might be expected to lyse less easily. If so, thrombo-embolic pulmonary hypertension ought to bemore likely to develop in subacute rather than inacute massive pulmonary embolism. This, however,was not our experience. Recurrent pulmonaryembolism did not occur. Since several patientsreceived long-term anticoagulants these could havebeen important but there is insufficient informationto assess this. The lack of recurrence cannot beattributed to surgical interruption of venousdrainage since no such operations were performed,and our results suggest that such treatment is notindicated in patients with a single episode ofsubacute massive pulmonary embolism. Resolutionof pulmonary artery obstruction assessed angio-graphically was generally good though minorabnormalities persisted in some patients and onepatient showed significant abnormalities withoutpulmonary hypertension or symptoms when re-studied only five months after the initial episode.The rather more frequent and widespread perfusionabnormalities, seen on perfusion lung scans, aresimilar to the findings in acute massive pulmonaryembolism2 and suggest that long-term damage tovessels smaller than those seen angiographicallyis common. The patients we describe must bedistinguished from those with repeated, discreteepisodes of embolism, well separated in time, whoare even less commonly seen than patients withsubacute massive pulmonary embolism, and appearto have a poor prognosis.7 Though there is no

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controlled evidence for the benefits of long-termanticoagulants in subacute massive pulmonaryembolism, our policy in this group of patientshas been to give oral anticoagulants indefinitelyunless a well-defined, temporary predisposingfactor for the episode was identified or there was a

strong contraindication to this treatment.Therefore, patients surviving an episode of

subacute massive pulmonary embolism have agood long-term prognosis and recurrent embolismis rare. Resolution of pulmonary artery obstructionis usually good though minor abnormalities of thepulmonary vasculature may persist which are notassociated with significant pulmonary hyper-tension of clinical disability.

References

1 Sutton GC, Hall RJC, Kerr IH. Clinical course andlate prognosis of treated subacute massive, acuteminor, and chronic pulmonary thromboembolism.Br Heart 1977; 39: 1135-42.

2 Hall RJC, Sutton GC, Kerr IH. Long-term prognosis

Hall, McHaffie, Pusey, Sutton

of treated acute massive pulmonary embolism.Br HeartJf 1977; 39: 1128-34.

3 Miller GAH, Sutton GC, Kerr IH, Gibson RV,Honey M. Comparison of streptokinase and heparinin treatment of isolated acute massive pulmonaryembolism. Br Med J 1971; ii: 681-4.

4 Fleischner FG. Recurrent pulmonary embolism andcor pulmonale. N Engl J Med 1967; 276: 1213-20.

5 Flowers NC, Horan LG. Subtle signs of rightventricular enlargement and their relative importance.In: Schlant RC, Hurst JW, eds. Advances in electro-cardiography. New York: Grune & Stratton, 1972:297-308.

6 Paraskos JA, Adelstein SJ, Smith RE, et al. Lateprognosis of acute pulmonary embolism. N EnglJf Med 1973; 289: 55-8.

7 Riedel M, Prerovsky I, Stanek V, Ressl J, StadlerovaV, Widimsky J. Chronic thromboembolic disease.Long-term follow-up. Prog Respir Res; 13: 134-40.

Requests for reprints to Dr R J C Hall, The RoyalVictoria Infirmary, Queen Victoria Road, NewcastleUpon Tyne NEl 4LP.



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