Pulmonary thrombosis and vascular disease after mustard operation for transposition of great arteries

LETTERS

have occurred before coronary arteriography or spasm could have occurred at the time of arteriography In their Case 2 the left circumflex artery appeared on aortograms, but was occluded at the time of left coronary arterial mlection with the Judkms techmque As with Case 3 of Cheng et a1.,3 selective mlection of the left anterior descending artery wrth this technique can lead to spasm of the left cucumflex artery The lack of tapermg at the site of occlusion m these two cases is a pomt agamst spasm, but previous reports have emphasized lumen irregularity after recanahzation of thromboembohsm Finally, a few mmor editorial changes m our report may have given the impression that we definitely ruled out thromboembolism, which was not our origmal intention Lewis Sasse, MD, FACC Department of Internal MedIcme So&her6 Callfornla Permanente Medical Group Los Angeles, Caltfornla

2

3

S D Moulopoulos, MD Department of Cltnical Therapeutics University of Athens Athens, Greece

References

1 2

References 1

aortic pressure He concludes that afterload IS not reduced except when blood IS withdrawn from the aorta during cardiac systole With respect to the mtraaortic balloon,l there IS much evidence that end-diastohc pressure is sigmftcantly reduced after balloon deflation Thus, when the aortlc valve opens, the left ventricle 1s indeed facing a reduced central aortic pressure and hence a reduced afterload When the systohc aortlc pressure IS not appreciably reduced, it is because of changes m volume of cardiac output I see no difference m this respect between mtraaortlc balloon pumpmg and counterpulsation by drawing and remlectmg blood mto the aorta

Bruochke AVG, Btuyneel KJ, Bloch A, d al Acute myocardlal anfarctlon wthout obstructwe coronary arlely dwease demonstrated by selectwe cwwtenography Br Heart J 33 565-594. 1971 Lynch RP, Edwards JE Pathology of coronary atherosclerosis and Its compl#cabons 1970, In. The Heart. second e&bon (Hurst JW. Logue RB. ed) New York, McGraw-titll D 914 ‘Chmg TO. Beehour T. Slngh BK, et at Myocardaal ,nfarcbon I” the absence of coronary arter~~~cler~~~s Result of coronary spasm(7) Am J Card01 30 660-662 1972

INTRAAORTlC BALLOON PUMPING AND COUNTERPULSATION In a recent letter Cokkmosl states that neither of these techniques [sequenced external counterpulsation and mtraaortlc balloon pumpmg] should cause a reduction of systohc central

Cokklnos DV External counterpulsabon and ao,t,c balloon pwnpng Am J Cerdlol35 59 1 1975 MOulopoulos SD, Topaz SR, Kolll WJ Dlastokc balloon pump#“g (wtth carbon dloxlds) 10 the awta--a mechanical ass,stanoe to the falltng cwculabon Am Heert J 63 669-675. 1962

PULMONARY THROMBOSIS AND VASCULAR DISEASE AFTER MUSTARD OPERATION FOR TRANSPOSITION OF GREAT ARTERIES We read with interest the report by Rosengart et al 1of progressive pulmonary vascular disease after the Mustard operation for transposition of the great arteries smce we described’ a similar occurrence m a patient with transposition, intact ventricular septum and subpulmonary stenosrs In our case preoperative cardiac catheterization at age 1 year revealed

FIGURE 1 Lung btopsy spec,mens A, at Mustard opera&on Arrow ponnts to cushton leenon of patchy nnhmel flbrosls B to D, 16 months afte, operebon, showng a plexlfwm lesson arwng from an ertery wth medial hypertrophy (B and enlarged In D) and an arteriole wth marked medal hypertrophy and eccentrvz Mmal fIbross resulbng from an orQa”,z,“g thrombus (C)

June

1976

The American

Journal

of CARDIOLOGY

Volume 37

1115

LETTERS

normal pulmonary arterial pressure (20/l& mean 15 mm Hg) A lung biopsy specimen obtained during the Mustard operation at age 13 months revealed normal thu-walled pulmonary arteries, but several vessels had evidence of organizing thrombl (Fig 1A) Eighteen months postoperatively, repeat cardiac catheterization revealed pulmonary hypertension (blood pressure 60/35, mean 40 mm Hg) and elevated pulmonary vascular resistance An open lung biopsy revealed grade IV pulmonary vascular disease (Heath-Edwards classlflcatlon).d but there were also pulmonary arterial thrombotlc lesions In various stages of orgamzatlon (Fig 1. B to D) We have continued to obtain lung biopsy specimens from patients undergoing cardiac surgery for transposltlon and have freque:ltly found hlstologlc evidence for pulmonary thrombosis These observations suggest that pulmonary arterial thrombosis may play a major role m the occurrence of pulmonary vascular disease m patients with transposltlon with intact ventricular septum In the report of Rosengart et al ,I cardiac catheterization at age 11 months revealed an elevated pulmonary arterial mean pressure of 30 mm Hg, and the patient might have had elevated pulmonary vascular resistance preoperatlvely It would be of mterest to know whether evidence of small vessel pulmonary thrombosis was found m the autopsy study on this patient Edgar A

Newfeld,

MD

Dlvlslon of Cardiology WIIIIS J Potts Children’s

Heart Center

The Children’s

Hospital

Chicago,

Memorlal

Illinois

creased blood flow Careful follow-up studies of their patlent would be of great mtere\t Ronald Rosengart, Michael

Flshbein,

MD MD

George C Emmanoullldes, Departments

of Pedlatrlcs

Harbor General University

MD, FACC and Pathology

Hospital

of California

Los Angeles

School of Medlclne Torrance,

Callfornla

References 1 2

Best PV, Heath D Pulmonary thrombws in cyan&c congenital heart disease wthout pulmonary hypertension J Pathol Bacternl 75 281-291 1958 Ferencz C The pulmonary vascular bed I” tetralogy of Fallot Changes associated wth pulmon~c stern% Bull Johns Hopklns Hosp 106 81-99 1960

I

PSYCHOLOGIC

STRESS

IN ANIMAL

STUDIES

The small amount of information gamed by the experiment of Corbalan et al ’ 1sovershadowed by the detriment to the medical profession m general and to animal experlmentatlon m particular The design of then experiment 15 not m compliance with the guldelmes pubhrhed m the Code of Federal Regulations, Title 9, Chapter 1, Part 3. Section 3 0, Paragraph c (3) stating that the use of three classes of drugs (anesthetics, analge\lcs and tranqulhzers) shall effectively mmlmlze the pam and discomfort of the animals while under experlmentatlon Pubhshmg such an article can only add fuel to the fires of the antn lvlqectlomsts who would stop all animal experlmentatlon Future reports of similar experiments should be reJected by every reputable medical Journal Richard S White, MD, FACC

1

Rosengarl

R Fisbbeln

GC Proaressw? pulmonary vascular disease of tran-sposk of great artenes with Mad ventricular septum Am J Cardlol 35 107-I 11 1975 Newfeld EA,‘Paul Mfi, Muster AJ, et al Pulmonary vascular drsease !n complete transposlbon of the great arteries a study of 200 pabents Am J Cardlol 34 75-82 1974 1973 Waaenvoorf CA Classlfwna pulmonary vascular disease Chest 64 503-504 Heath D, Edwards JE The pathology of hypertenwe pulmonary vascular dwease a descrlptmn of SIX grades of structural changes !n the pulmonary artenes with special reference la congenital cardiac septal defects Cwculat!on 18 533-547 1958

Cardiopulmonary

M, EmmanoullfUes

McKay-Dee

after sirglcal ccxrectlon(Mustard procedurel

2 3 4

_.

Dlvlslon

Hospital

Ogden, Utah Reference 1

Corbalan R, Verrier R, Low B Psychological stress and ventncular arrhylhmlas myocardlal mfarctlon I” the consc!au~ dog Am J Cardnl 34 692-703. 1974

dwng

REPLY REPLY

The important chmcal-pathologic study by Newfeld and his associates (his Reference 2) appeared when our manuscript was m press Then patient had slgmflcant subpulmonary stenosis, thus the small vessel thromboses seen at operation m their case can be explained only on the basis of reduced pulmonary blood flow, polycythemla and stasis l,” The postoperative development of moderate pulmonary hypertension with orgamzmg thrombl m small pulmonary arteries and grade III to IV pulmonary vascular changes 1s difficult to explain on the same basis In our patient there was no left ventricular outflow tract obstruction and, as we mdlcated, there was moderate pulmonary hypertension suggestive of increased pulmonary vascular resistance at the time of operation Wlthm a year after operation severe pulmonary hypertension (left ventricular pressure 125/4-18 mm Hg) and severe congestlbe heart failure developed and led to death At autopsy, grade III to IV changes m the small pulmonary arteries were present, there was no evidence of small vessel pulmonary thrombosis It 1s possible that the small vessel dlsea5e seen by Newfeld et al m the postoperative lung biopsy specimen of their pat lent represents a patchy rather than a generalized phenomenon and that the moderate increase m pulmonary arterial pressure that they observed postoperatively was m part due to In-

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June 1976

The American

Journal

of CARDIOLOGY

Volume

We have reached a stage m our work where it 1s imperative to deal with the intact, alert, unsedated animal Otherwise, we shall not be able to define the role of psychologlc factors on the heart and speclflcallq upon cardiac kulnerabllity to ventricular flbrlllatlon In the highly pressing chmcal problem of sudden death we believe psvchologlc factors are of paramount importance How 1s one to model this problem m the animal laboratory? I am open to White’s suggestions The moment the animal 1s treated with analgesic<, \edatlves or tranqulllzers, the psychologlc stressful effects on the heart are altered or annulled Let us examme some of the details of the animal experiment that has provoked White’s anger The stressful environment was a qlmg-used qmce the day of Pavlo\ for animal restraint The dog was retained m the sling for 1 hour during which time nonaverslve electrophyslologlc studies were conducted At the end of this period a single low energy transthoraclc discharge was delivered The procedure was repeated on 5 successive days This waq the hmlt of the mJur> mfhcted on the animal “The small amount of mformatlon gamed” was that eben this minor stress was sufflclent to provoke ventricular tachycardla m the ammal with prior myocardlal mfarctlon as well as to suhstantlally reduce cardiac vulnerablhty for ventricular flbrlllatlon Our fmdmgs provided a new and unique model for

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