1234

Brief Communications

and continuous wave Doppler echocardiography documented systolic turbulent flow in the right ventricle aswell as in the right atrium. A high-velocity systolic jet (3.5 ml set) extended from the tricuspid valve to the posterior wall of right atrium. Since the acceleration time was 90 msec and acceleration time-to-ejection time ratio was0.22, pulmonary hypertension wassuspected.Finally, the existence of a ventricular septal defect wasdocumentedby meansof Doppler color-flow imaging, which revealed turbulent flow of a mosaicpattern reaching the right ventricle below the septal leaflet of the tricuspid valve. Another turbulent jet wasfound in the right atrium above the sameleaflet (Fig. 1). No tricuspid regurgitation was detected. Thus two-dimensionalechocardiographyhad failed to disclosethe discontinuity of the ventricular septum.This wasbecausethe aortic prosthesisovershadowedthe defect. Moreover, continuous and pulsed Doppler echocardiographicrecordings were repeatedly misinterpreted as tricuspid regurgitation. The echocardiographicfindings were confirmed by heart catheterization, which found an oxygenstep-up at the right atria1and right ventricular levelswith a left-to-right shunt reaching 45% of pulmonary blood flow. The subsequent operation (January 1989)verified both septal defects-one (5 mm in diameter) connecting the left ventricle with the right atrium above the root of the septal leaflet of the tricuspid valve and the other (15 mm in diameter) which linked left and right ventricles below the sameleaflet. The patient died due to adult respiratory distresssyndromeon day 6. Autopsy confirmed the operative findings and showedno other pathology. An acquired septal defect with communication between the left ventricle and the right atrium as a consequenceof surgicalintervention is a rare condition reported after mitral valve replacement.4A tight anatomic liaison of the mitral posteromedialcommissurewith the membraneouspart of the interventricular septumabove the attachment of the tricuspid valve can be injured, either becauseof excision of the calcified valve or because of large debridement of fibrous tissue.4We have not encountered any report concerning an acquired communication between the left ventricle and right atrium after aortic valve replacement. A different anatomic relationship of the aortic valve to the interventricular septum probably prevents such a complication. The most likely causeof the acquired defect that appearedin our patient following the aortic valve replacement in 1984seemsto be early postoperative infective endocarditis. A report of a ventricular septal defect connecting the left ventricle with the right atrium asa consequence of Staphylococcus aureus intracardiac infection in a girl with no clinically overt heart diseasewas reported by others5and supports this conclusion. The recognition of left-to-right communications betweenthe left ventricle and right atrium hasbeenmarkedly improved by M-mode and two-dimensional echocardiography and particularly by pulsed Doppler echocardiography.2p6This casereport illustrates the limitation of Mmode, two-dimensional, continuous and pulsed Doppler echocardiography and emphasizesthe utility of Doppler

American

November 1990 Heart Journal

color-flow imaging in accurately depicting the intracardiac shunts. REFERENCES

1.

2.

3I . 4.

GerbodeF,HultgrenH, MelroseD, OsbornJ. Syndromeof left ventricular-rightatria1shunt:successful surgicalrepairof defect in 5 cases with observationof bradycardiaonclosure.Ann Surg 1958;148:433-46. CrossSW, SagarKB, PaulsenWJH. Two-dimensional and pulsedDopplerechocardiographic diagnosisof an acquired left ventricular-right atria1 communication.Am d Cardiol 1984;53:396-7. DunsethW, Ferguson TB. Acquiredcardiacseptal defectdue to thoracictrauma.J Trauma-1965;5:142-9. Seabra-Gomes R. RossDN. Gonzales-Lavin L. Iatroeenicleft ventricular-rightatria1fistulafollowingmitral valve replacement. Thorax 1973;28:235-41.

5.

Aberg T, JohanssonL, MichaelssonM, Rhedin B. Left

ventricular-right atria1 shunt of septic origin. Presentation of a case with surgical closure. J Thorac Cardiovasc Surg 1971;61:212-6. 6. Leung MP, Mok CK, Lo RNS, Lau KC. An echocardiographic

study of perimembraneous ventricularseptaldefectwith left ventricular to right atria1 shunting. Br Heart J 1986;55:45-52.

Balloon dilatation right ventricle

of double-chamber

Yellapragada S. Chandrashekhar, MD, Diplomate NBE, DM, Inder S. Anand, DPhil (Oxon), FRCP (Lond), and Purshottam L. Wahi, MD, FAMS. Chandigarh, India

Double-chamber right ventricle (DCRV) is an uncommon causeof right ventricular outflow obstruction. However, with increasing physician awareness,it is being reported more frequently.’ Although DCRV is usually associated with a ventricular sepia1defect, most seriesalso report a small number of patients with an intact ventricular septum. While many believe DCRV to be a progressivelesion,2 the natural history of this group is unclears3Surgery has beenthe only form of treatment available.4Balloon dilatation of this lesionhasnever before beenreported. Catheter balloon dilatation hasbeenattempted in a large number of congenital and acquired conditions of the cardiovascular system. The best results are seenin patients with valvular pulmonic stenosis.5In this report, wedescribeour attempts at dilating a caseof DCRV with intact ventricular septum. KS, a 21-year-old man, presented with increasingdyspnea on exertion of 7 years’ duration (New York Heart Association functional classIII, at admission).He had signs of severeright ventricular outflow obstruction. Electrocardiogram (ECG) showed right axis deviation and severe From the Department of Cardiology, Postgraduate Institute of Medical Education & Research. Reprint requests: Dr. I. S. Anand, Department of Cardiology, Postgraduate Institute of Medical Education & Research, Chandigarh 160 012, India. 414123683

Volume

120

Number

5

Brief Communications

1235

1. Right ventricular angiogramsin lateral projection before (left) and after (right) balloon dilatation in DCRV.

Fig.

right ventricular hypertrophy. Chest x-ray film revealed a cardiothoracic ratio of 56%) right atria1 enlargement,and normal pulmonary blood flow. Echocardiography showeda largeright ventricle, intact ventricular septum,and normal pulmonary valve. At cardiac catheterization, there wasevidenceof a singleright ventricular outflow obstruction with an intraventricular gradient of 125 mm Hg (Table 1). Angiography confirmed a DCRV with intact ventricular septum (Fig. 1). The patient wastaken for balloon dilatation. Four attempts were madewith a singleballoon (Mansfield 20 mm balloon, 9F catheter, Boston Scientific Corp., Mansfield Division, Mansfield, Mass.). The midcavity gradient fell by 50 mm Hg but the angiographic appearance did not change (Fig 1). There were no complications or ECG changes.He was discharged without any drugs and was followed up at regular intervals. His symptoms improved. Cardiac catheterization repeated 1 year later (Table I) revealed that the reduced gradient wasmaintained. Balloon dilatation was repeated using the double-balloon technique. Two 20 mm balloons were used. Despite the disappearanceof the waist on four occasions,no further fall in gradient occurred. Sincea residual gradient of 70 mm Hg remained, the patient was advised to undergo surgery. Balloon dilatation resulted in partial relief of the intracavitary gradient (- 50 mm Hg), which was sustained for 1 year. The mechanism of this reduction is not clear. Although the residual gradient was still unacceptable, symptomatic improvement was obvious. In comparison with the results of balloon dilatation in pulmonary stenosis,results in this casewere disappointing. The role of balloon dilatation in DCRV therefore remains uncertain. A number of attempts have been made to dilate the right ventricular outflow tract (RVOT) in tetralogy of Fallot with significant benefit. 5,6In such casesthe exact contribution of valvular and infundibular obstruction is difficult

Table I. Hemodynamic data before and after balloon dilatation in DCRV 1st study January

Predilatation Pressures (mm Hg) RV (Proximal)(s) RV (Distal)(s) PA LV (4

RV (4 IV gradient Cardiac index (L/min) IV, Intraventricular; LV, Left ventricle.

14,

1987

Postdilatation

150 25 21 112 152 125 3.0

RV, right ventricle;

100 25 18 110 82 75 2.8

2nd study January 6,1988 Predilatation

Postdilatation

95 22 25 143 102 73 3.1

a, systolic; PA, pulmonary

90 20 20 143 90 IO 3.3

artery;

to quantitate preoperatively,6B7and it is likely that benefit of balloon dilatation may be partially due to dilatation of the RVOT. Rao and Brais, however, did not find any reduction in infundibular gradient in their patients with combined valvular and subvalvular RVOT obstruction. There appearsto be no theoretical ground for balloon dilatation in “muscular” DCRV. However, nonmuscular subvalvular obstructions of the left ventricular outflow tract canbe partially relieved8and DCRV can occasionally be due to a fibromuscular diaphragm.g With a VSD (appearing in the majority of casesof DCRV), dilatation alone will not help, sincesurgery would be indicated if the VSD were large. Natural history studiessuggesta progressive increasein obstruction in thesepatients2 Thus the relief at dilatation may not be maintained. In our patient,

1236

Brief Communications

American

November 1990 Heart Journal

however, the reduced gradient persistedfor at least 1 year. Whether drugslike propranolol would have further benefit, as they probably do in reactive hypertrophy associated with severevalvular pulmonary stenosisfollowing balloon dilatation, is not known. While surgery has a good result, the experience is small. Apart from the risk of surgery itself, accidentslike closureof the outlet between the muscle bundlesof the ventricle (mistakenfor a VSD) have been reported. lo Although our casesuggestslittle opportunity for balloon dilatation in DCRV, further experiencewould clarify this issue. REFERENCES 1.

2. 3.

4. 5. 6. 7.

Joseph Joy MV, Subramanium R, Balkrishnan KG. DCRV: a clinical, haemodynamic and angiographic profile. Ind Heart J 1988;40:203-9. Hartman AF Jr, Goldring D, Fergusson TB, et al. The course of children with two chamber right ventricle. J Thorac Cardiovasc Surg 19’70;60:72-5. Emmanoulides GC. Bavlen BG. Pulmonarv stenosis. In: Ad” ams FH, Emmanoulides GC, eds. Moss’ Heart disease in infants, children and adolescents. Baltimore: William & Wilkins Co, 1982:234-62. Kirklin JW, Baratt-Boyes BG, eds. Cardiac surgery. 1st ed. New York: John Wiley & Sons, 1985:804-15. Rao I’S, Brais M. Balloon pulmonary valvuloplasty for congenital cynotic heart defects. AM HEART J 1988;115:1105-10. Boucek MM, Webster HE, Orsmond GS, Ruttenberg HD. Balloon pulmonary valvotomy: palliation for cynotic heart disease. .&M HEART J 1988;115:3k22. Kirklin JW. The tetroloev of Fallot. Am J Roenteenol VI

1968;102:253-60.

8. Suarez J, Pan M, Sancho M, Herrera N, Arizon J, Frnaco M, Concha M, Valles F, Romanos A. Percutaneous transluminal balloon dilatation for discrete subaortic stenosis. Am J Cardiol 1986;58:619-21. 9. Bashour TT, Kabbaini S, Sandok KA, Cheng TO. DCRV due to fihromuscular diaphragm. AM HEART J 1984;107:792-4. 10. Lucas RB Jr. Varco RL. Lallehei CW. Adams P Jr. Anderson RC, Edward’JE. Anomalous muscle bundles of the’ right ventricle. Hemodynamic consequences and surgical consideration. Circulation 1962;25:443-7.

Echocardiographic embolus

diagnosis

of pulmonary

Bradley H. Evans, MD, and Gerald Maurer, MD. Los Angeles,

Calif.

Several recent reports have described the use of twodimensionalechocardiography (2D-Echo) in the setting of pulmonary embolism. Thromboemboli have been visualized in the right atrium,rm6the right ventricle,‘, 3*6 and the pulmonary artery.3 We describea caseof a thromboembolus extending from the tricuspid valve to the left pulmonary artery. From

Cedars-Sinai

Reprint Room

requests: 5311, 8700

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Medical Bradley Beverly

Fig. 1. Orthogonal parasternalplanes.The thrombus can be seenin the right ventricle in both the long-axis (A) and short-axis (13)views. RV, Right ventricle; Thr, thrombus; Ao, aorta; Lb’, left ventricle; LA, left atrium.

Center. H. Evans, MD, Cedars-Sinai Blvd., Los Angeles, CA 90048.

Medical

Center,

The patient wasa 58-year-old fireman admitted with increasing shortnessof breath and fatigue. Three months prior to admission,he noted the onset of dyspnea at rest and a 23-pound weight loss.BD-Echo at the time wasnotable for increasedleft atria1 size, concentric left ventricular hypertrophy, and normal left and right ventricular wall motion. On admission,the patient appeared comfortable and was afebrile with a blood pressureof 110/80 mm Hg and a pulse of 88/min. The lungs were clear. With the patient elevated to 45 degrees,the jugular venous pressure waselevated to the angle of the jaw. The first and second heart soundswere normal and there wasan audible rightsided third heart sound. The electrocardiogram (ECG) demonstrated normal sinus rhythm with a right bundle branch block that was unchangedfrom baseline.An arterial blood gasmeasurementwith pH 7.47,PCOZ 34, and POZ 160 wasobtained with the patient receiving 4 L of oxygen by nasal cannula. The chest x-ray film disclosedmarked

Balloon dilatation of double-chamber right ventricle.

1234 Brief Communications and continuous wave Doppler echocardiography documented systolic turbulent flow in the right ventricle aswell as in the ri...
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