Mitral insufficiency after pericardiectomy for constrictive pericarditis

CASE REPORT BUCKINGHAMET AL MITRALINSUFFICIENCY AND PERICARDIECTOMY

Ann Thorac Surg 1994;58:1171-4

clips in the greater gastric curvature. After excision of the necrotic wall the gastric perforation was closed with interrupted nonabsorbable sutures. The abdominal cavity was washed, cleaned, and closed. Because the clinical signs of diffuse peritonitis persisted and the general condition of the patient detoriated due to septicemia, we did another laparotomy 3 days later. At operation the gastric wall was intact. The intestines were covered with fibrin and again a large volume of peritoneal fluid was removed. The cultures of peritoneal fluid taken at both laparotomies showed high concentrations of Candida albicans, indicating fungal peritonitis. Intravenous antifungal therapy (amphotericin Band flucytosine) was started and continued during 18 days. During the further course we performed 11 reinterventions at 2- or 3-day intervals until the peritoneal cavity was clean and the clinical signs of septicemia had disappeared. Five weeks after the coronary artery bypass procedure the patient finally could be extubated. She was discharged from the hospital in good condition 10 days later. A large incisional hernia resulting from the multiple relaparotomies was successfully corrected 1 month later. We did not do a gastroscopy because of the absence of gastric complaints. Our patient refused the routine angiographic follow-up evaluation of the patency of the GEA graft. Her condition did not yet allow us to perform an exercise test. She presently has no anginal complaints, and her electrocardiogram does not show any signs of ischemia. Furthermore, echocardiography shows a good left ventricular function.

Comment Although the GEA has become increasingly popular as an alternative bypass conduit for coronary revascularization, abdominal complications of harvesting of the GEA are few. We called six other hospitals in the Netherlands and learned that our colleagues used the GEA in a total of 169 patients. They experienced only four incisional hernias and 1 patient with a bleeding in the hilus of the spleen. They reported no postoperative malfunction of the stomach. Therefore, gastric perforation after harvesting the GEA is the first serious gastric complication out of 569 cases operated on in the Netherlands. We hypothesize that the gastric perforation was due to heat injury as a result of overzealous coagulation close to the hemostatic clips on the gastric wall, because during the first laparotomy the walls of the perforation still showed signs of heat injury, whereas no signs of gastritis or ulceration were present. We still believe that a cautious use of coagulation in combination with clips is a satisfactory procedure to harvest the GEA for reason that we used this harvesting technique in 400 other patients without a gastric perforation. However, excessive use of electrocoagulation close to hemostatic clips on the gastric wall should be avoided. © 1994 by The Society of Thoracic Surgeons

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References 1. Suma H, Fukomoto H, Takeuchi A. Coronary artery bypass grafting by utilizing in situ right gastroepiploic artery: basic study and clinical application. Ann Thorac Surg 1987;44:394-7. 2. Buikema H, Grandjean JG, Broek vd S, et al. Differences in vasomotor control between gastroepiploic and left internal mammary artery. Circulation 1992;86(Suppl 2):205-9. 3. Grandjean JG, Boonstra PW, den Heyer P, Ebels T. Arterial revascularization with the right gastroepiploic artery and internal mammary arteries in 300 patients. J Thorac Cardiovasc Surg 1994;107:1309-16. 4. Suma H, Wanibuchi Y, Furuta S, Takeuchi A. Does use of gastroepiploic artery graft increase surgical risk? J Thorac Cardiovasc Surg 1991;101:121-5.

Mitral Insufficiency After Pericardiectomy for Constrictive Pericarditis Richard E. Buckingham, [r, MD, Anthony P. Furnary, MD, Michael T. Weaver, MD, H. Storm Floten, MD, and Richard F. Davis, MD Anesthesiology Service and Cardiac Surgery Section, Surgical Service, Department of Veterans Affairs Medical Center, Portland, Oregon

We report the case of a 24-year-old man in whom a clinical syndrome developed while he was on active military duty in Saudi Arabia that was subsequently diagnosed as constrictive pericarditis. Phrenic nerve to phrenic nerve pericardiectomy and posterior pericardial release successfully relieved the ventricular constriction with a resultant increase in the cardiac index from 1.9 to 3.8 L· min- 1 • m- 2 • Transesophageal echocardiographic monitoring during the operation disclosed trace mitral regurgitation before median sternotomy. The severity of the regurgitation noticeably increased to the moderate level immediately after pericardial resection. This echocardiographic finding had improved 1 week later, but the regurgitation still was greater than baseline. Mitral valve function had returned to baseline by 4 weeks after the operation. Possible mechanisms of this evolving pattern of perioperative mitral valve dysfunction are discussed. (Ann Thorae Surg 1994;58:1171-4)

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onstrictive pericarditis is the end stage of a chronic inflammatory process that results in a thick, fibrotic constricting pericardium, which impairs systolic and diastolic function of both ventricles. Pericardiectomy often achieves excellent acute and chronic relief of this constriction [1, 2]. Transthoracic and transesophageal echocardiAccepted for publication Jan 28, 1994. The views expressed in this presentation do not necessarily reflect those of the Department of Veterans Affairs or the US Government. Address reprint requests to Dr Davis, Anesthesiology Service, VA Medical Center, 3710 Southwest US Veterans Hospital Rd, Portland, OR 972011034.

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CASE REPORT BUCKINGHAM ET AL MITRAL INSUFFICIENCY AND PERICARDIECTOMY

Ann Thorac Surg 1994;58:1171-4

Fig 1. (A) "Trace" mitral regurgitation before median sternotomy. (B) Moderate mitral regurgitation after sternal closure at the end of the operation. (C) Mild mitral regurgitation 1 week postoperatively. (0) Return to baseline at 4 weeks postoperatively.

ography (TEE) have been used to help make the diagnosis of constrictive pericarditis, and for intraoperative monitoring and evaluation during pericardiotomy [3-7]. We report a case of constrictive pericarditis in which moderate mitral valve regurgitation, diagnosed by TEE, developed after a pericardiectomy. A 24-year-old man while serving in Saudi Arabia in the Marine Corps, noted swelling in his feet and ankles, fatigue, and shortness of breath. These symptoms were progressive and eventually associated with chest pain. He was evaluated at Camp Pendleton Naval Hospital, where the initial diagnosis was cardiomyopathy, and diuretic therapy was instituted. Because of intermittent chest pain and progression of his edema and weakness, he was referred to Portland Veterans Affairs Medical Center in September 1991. Echocardiography then showed pericardial effusion, concentric left ventricular hypertrophy, and diffuse hypokinesis. Trace regurgitation of the mitral valve was noted. Cardiac catheterization revealed a pulmonary capillary wedge pressure of 26 mm Hg, right atrial pressure of 24 mm Hg, a cardiac index of 1.9 L· min- 1 • m- 2 , and an ejection fraction of 0.40. Cardiac biopsy was negative for myocarditis, granuloma, and amyloid. Therapy

with an angiotensin converting enzyme inhibitor and digoxin was initiated together with continuation of his diuretic treatment. In March 1993 he presented with a 6-day history of productive cough and shortness of breath. Physical examination at this time showed a heart rate of 104 beats/min, a respiratory rate of 20 breaths/min, regular cardiac rhythm with an S3' dullness to chest percussion posteriorly, pedal and pretibial edema, and a liver edge palpable 8 em below the costal margin. Chest roentgenogram showed a right pleural effusion, and diagnostic thoracentesis yielded uninfected transudate. Repeat echocardiography and cardiac catheterization were done with findings similar to the previous evaluation (ejection fraction = 0.45). Because the findings were thought to be most compatible with constrictive pericarditis, pericardiectomy was recommended and accepted. A phrenic-to-phrenic pericardiectomy with an inferoposterior pericardial release was performed through a median sternotomy incision after anesthesia with midazolam and sufentanil using radial arterial and pulmonary arterial catheters, electrocardiography, and TEE monitoring. Cardiopulmonary bypass was not used. At the start of the surgical procedure before median sternotomy, TEE

Ann Thorae Surg 1994;58:1171-4

examination revealed trace mitral regurgitation (Fig LA), a bouncing interventricular septum, decreased wall motion, and increased E/A ratio. Arterial pressure at this time was 110/60 mm Hg with a heart rate of 85 beats/min, central venous pressure of 22 mm Hg, pulmonary artery occlusion pressure of 22 mm Hg, and cardiac index of 1.9 L· min-I. m- 2 . After sternal closure (estimated blood loss = 500 mL, fluid replacement of 3,000 ml.), TEE showed improved left ventricular wall motion, decreased central venous pressure to 14 mm Hg, decreased pulmonary artery occlusion pressure to 16 mm Hg, and a cardiac index of 3.8 L· min-I. m- 2 . Transesophageal echocardiographic assessment of left ventricular volume was not appreciably changed; however, mitral regurgitation increased significantly (Fig IB). Repeat TEE 1 week after the operation showed less mitral regurgitation despite similar heart rate and arterial pressure to the intraoperative examinations (Fig lC). A TEE examination performed 4 weeks postoperatively revealed return of mitral valve function to the preoperative baseline, again with similar heart rate and arterial pressure (Fig ID).

Comment Echocardiography has been used for some time to help make the diagnosis of constrictive pericarditis [4]. An echo-dense (bright) and thickened pericardium commonly is noted in constrictive pericarditis during TEE [3]. A second echocardiographic finding is a brisk early diastolic bouncing motion of the interventricular septum most evident during inspiration [3]. This "quivering" or "stuttering" of the interventricular septum is thought to be due to high right ventricular pressures and competition between the ventricles for the available volume within the nondistensible pericardiaI sack. A less specific finding in constrictive pericarditis is an increased early diastolic filling velocity (E velocity) with a rapid deceleration and a decreased late diastolic filling velocity after atrial contraction (A velocity), resulting in an increase in the E/ A ratio. This increase of the normal E/ A ratio also can be seen in

anteriorleaflet

antero-lateral papillary muscle

Fig 2. Before and after representation of hypothesis one, whereby the anterolateral papillary muscle becomes relatively too long after the lateral wall of the left ventricle is freed from the constricting pericardium.

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Fig 3. Before and after representation of hypothesis two, whereby the posteromedial papillary muscle becomes relatively too short after the pericardiectomy has relieved the high right ventricular pressures allowing the interventricular septum to move outward to a more normal position.

restrictive cardiomyopathy and in severe mitral regurgitation [3]. In each of the four TEE examinations done in this case, the mitral regurgitant jet was interrogated to obtain and photograph the image with the largest length and crosssectional area. The color-flow two-dimensional TEE image obtained before the median sternotomy shows only trace mitral insufficiency located centrally within the valve (see Fig I A). The same view obtained after the sternum was reapproximated showed relatively unchanged left ventricular volume, but significantly increased mitral regurgitation (2+) (see Fig LB). An awake TEE examination was done 6 days later (with a similar heart rate and arterial pressure, and using the same machine and settings as previously), which showed a 1 + mitral insufficiency jet (see Fig lC) that was neither as persistent nor as large as in the image of the end of the operation. The patient was studied again with TEE at 4 weeks postoperatively (see Fig ID), at which time the mitral insufficiency had returned to the baseline "trace" amount. Because changes in left ventricular (long axis and short axis two-dimensional TEE) dimensions and mitral valve orifice diameter were not apparent, we propose two alternative hypotheses for this evolving pattern of mitral valve dysfunction following pericardiectomy. The increased mobility of the lateral wall of the left ventricle and the anterolateral papillary muscle after pericardiectomy allows an increased inward movement of the wall during systole that shortens the distance between the papillary muscle and the attachment points of its chordae on the mitral valve. This decreased distance makes the anterolateral papillary apparatus too long functionally to coapt the valve leaflets optimally during systole (Fig 2). Alternatively, the return of the interventricular septum and posterior left ventricular wall to a more normal resting position (less displaced into the left ventricular cavity) after pericardiectomy effectively increases the distance from the posteromedial papillary muscle to the attachment points of

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CASE REPORT PARRY ET AL HEART-LUNG TRANSPLANTATION IN CHEST DEFORMITY

its chordae on the mitral valve. The subvalvar apparatus then is too short functionally to produce normal coaptation of the mitral valve leaflets (Fig 3). These two hypotheses are not mutually exclusive, and either mechanism, or both, especially in combination with a significant increase in left ventricular volume (which we did not observe) would disturb the normal coaptation of the two mitral leaflets to allow mitral insufficiency. It also is likely that compensation for the altered ventricular geometry brought about by the removal of the constrictive pericardium would occur over time, which could account for subsequent decreases in the regurgitant jet as was seen in this case. References 1. Bashi VV, John S, Ravikumar E, [airaj PS, Shyamsunder K, Krishnaswami S. Early and late results of pericardiectomy in 118 cases of constrictive pericarditis. Thorax 1988;43:637-41. 2. McCaughan BC, Schaff HV, Piehler JM, et al. Early and late results of pericardiectomy for constrictive pericarditis. J Cardiovasc Surg 1985;89:340-50. 3. Brockington PM, Schwartz SL, Pandian NG. Echocardiography in pericardial diseases. In: Marcus ML, Schelbert HR, Skorton DJ, Wolf GL, eds. Cardiac imaging. Philadelphia: Saunders, 1991:470-5. 4. Hinds SW, Reisner SA, Amico AF, Meltzer RS. Diagnosis of pericardial abnormalities by 2D-echo: a pathology echocardiography correlation in 85 patients. Am Heart J 1992;123:143-50. 5. Kyo S, Takamoto S, Matsumura M, et al. Immediate and early postoperative evaluation of results of cardiac surgery by transesophageal two-dimensional doppler echocardiography. Circulation 1987;76(Suppl 5):113-21. 6. Reynertson SI, Konstadt SN, Louie EK, Segil L, Rao TL, Scanlon PJ. Alterations in transesophageal pulsed Doppler indexes of filling of the left ventricle after pericardiotomy. J Am Coli Cardiol 1991;18:1655-60. 7. Hogue CW, Platin M, Barzilai B, Kaiser LR. Intraoperative use of transesophageal echocardiography with pulsed-wave Doppler evaluation of ventricular filling dynamics during pericardiotomy. Anesthesiology 1991;75:701-4.

Heart-Lung Transplantation in Situs Inversus and Chest Wall Deformity Andrew J. Parry, FRCS, John O'Fiesh, FRCS, John Wallwork, PRCS, and Stephen R. Large, PRCS Transplant Unit, Papworth Hospital, Cambridge, England

Heart-lung transplantation in the presence of complex congenital heart disease including situs inversus and significant chest wall deformity can be accomplished successfully. However, the postoperative course is apt to be prolonged because of mechanical respiratory problems, which will respond to a protocol of weaning and nutritional supplementation. (Ann Thorae Surg 1994;58:1174-6) Accepted for publication Feb 4, 1994. Address reprint requests to Mr Parry, Transplant Unit, Papworth Hospital, Papworth Everard, Cambridge, CB3 8RE, England.

© 1994 by The Society of Thoracic Surgeons

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36-year-old woman with a history of complex congenital heart disease presented for heart-lung transplantation. Preoperative assessment revealed situs inversus with dextrocardia, a large subarterial ventricular septal defect, and pulmonary hypertension (Eisenmenger's complex). In addition she had a severe chest wall deformity due to Klippel-Feil syndrome and scoliosis. Although there was a significant restrictive element to her ventilatory mechanics from chest wall causes, it was considered that they did not contribute significantly to her gas exchange problem. At operation she was found to have a large innominate vein with left-sided superior vena cava and a left-sided inferior vena cava with the hepatic vein entering the morphologic right atrium independently. She had both atrioventricular and ventriculoarterial discordance with a right-sided aortic arch. The presence of a ventricular septal defect was confirmed. The trachea lay posteromedially to the right aortic arch with the right main bronchus passing through the concavity of the arch. The anatomy of the lungs was conventional with the trilobed lung lying on the right and the bilobed lung on the left. Through a median sternotomy cardiopulmonary bypass was instituted using standard aortic cannulation. Venous drainage was via three cannulas placed separately in the innominate vein, the hepatic vein, and the inferior vena cava, the latter two via the right atrium. The heart was excised leaving the right atrium behind. This then was divided transversely, and the upper portion was oversewn at the inflow of the superior vena cava. The remaining lower portion then was fashioned into a common conduit to drain both the hepatic vein and inferior vena cava (Fig lA). Removal of the lungs was performed in the standard way ensuring that the phrenic nerves were not damaged. The pericardial windows extended from the insertion of the bronchus superiorly to the lower margin of the pulmonary ligament inferiorly, and from the phrenic nerve anteriorly to the vagus posteriorly. The donor heart-lung block was inserted passing through the pericardial windows posterior to the phrenic nerve pedicles. The tracheal anastomosis was performed in the normal way. The donor inferior vena cava was anastomosed to the reconstituted recipient right atrial conduit/ inferior vena cava without problem. Despite harvesting of excess superior vena cava and innominate vein, the donor superior vena cava still was too short to reach the recipient innominate vein arching anteriorly around the donor aorta; therefore, a length of donor aorta was interposed. This, however, was inadequate for venous drainage of the upper body, and an additional connection between the innominate vein and the right atrial appendage was fashioned using a length of recipient great saphenous vein as a spiral graft (Fig 18). During weaning from bypass it was evident that the left phrenic nerve was under considerable tension due to the relocation of the heart into the left chest. This tension could be relieved by deflecting the phrenic nerve anteriorly relative to the heart, but this put considerable pressure on the atrioventricular groove as the heart herniated through the pericardial opening into the left chest. Deflecting the phrenic posteriorly did not relieve the 0003-4975/94/$7.00