Right ventricular failure after repair of left ventricular aneurysm

J THORAC

CARDIOVASC SURG

80:79-84, 1980

Right ventricular failure after repair of left ventricular aneurysm This report summarizes the experience in two patients who have manifested severe right ventricular (RV) failure after resection of large left ventricular (LV) aneurysms involving the ventricular septum. In the first patient, early postoperative right atrial (RA) mean pressure (14 mm Hg) was similar to the mean pulmonary artery (PA) pressure (16 mm Hg) and exceeded left atrial (LA) pressure (JO mm Hg). A right-to-left shunt through a patent foramen ovale allowed adequate cardiac output at the expense of arterial desaturation. As RV function slowly improved, LA pressure exceeded RA pressure, pulmonary artery pulse pressure increased. and the shunt disappeared as the foramen ovale closed. In the second patient, initial attempts to wean from cardiopulmonary bypass with catecholamines and intra-aortic balloon pump were unsuccessful because of RV failure. RA pressure was 30 mm Hg and LA pressure was 12 mm Hg with a balloon-augmented peak arterial pressure of only 80 mm Hg. A ventricular assist pump (RA to PAY was used to wean the patient from bypass and resulted in adequate LA pressure (17 mm Hg), low RA pressure (6 mm Hg), and adequate cardiac index (1.9 Llminlmi}, On the operative and first postoperative day, there was no pulse pressure generated from RV contraction and all PA pulse pressure (40/15 mm Hg) was due to the assist pump. Beginning on postoperative day 2, the RV generated increasing PA pulse pressures. The patient was weaned from the RV assist device, which was removed on postoperative day 3; then the PA pressure was 36118 mm Hg, RA pressure 16 mm Hg, and LA pressure 18 mm Hg. Both patients remain well. These case histories would indicate that the lack of septal motion may not be a contraindication to repair of LV aneurysm as has previously been suggested; however. in such patients, the possibility of RV failure would make the availability of an assist pump advisable. Recovery of RV function can be expected within a few days.

Grant V. S. Parr, M.D., William S. Pierce, M.D., Gerson Rosenberg, Ph.D., and John A. Waldhausen, M.D., Hershey, Pa.

The incidence of ventricular aneurysm following

myocardial infarction has varied in numerous reports from 3% to 35%.1-5 The incidence of left ventricular aneurysms may be increasing with improvement in survival rates for myocardial infarction." Although the incidence may be uncertain the natural history of left ventricular aneurysms without operation is well known." 5 Approximately 70% of patients with left ventricular aneurysms die within 3 years of their initial infarction. Only 12% survive for 5 years." Complications include congestive heart failure, ventricular arFrom the Division of Cardiovascular and Thoracic Surgery, Department of Surgery, College of Medicine, The Milton S. Hershey Medical Center of The Pennsylvania State University, Hershey, Pa. Received for publication Nov. 15, 1979. Accepted for publication Jan. 11, 1980. Address for reprints: Grant V. S. Parr, M.D., Department of Surgery, The Milton S. Hershey Medical Center, 500 University Drive, Hershey, Pa. 17033.

rhythmias, systemic embolism, and further myocardial infarction.v 7. 8 Thus surgical repair of left ventricular aneurysm is recommended. The risk of surgical resection has been variously reported as between 6.5% and 24% and appears to be decreasing. 8-13 The addition of simultaneous coronary artery bypass grafting does not appear to have altered the operative risk.": 12-14 Nevertheless, the risk of repair exceeds that of most other cardiac procedures and thus various prognostic indices have been used in order to select the appropriate patients for surgical resection. Massively large aneurysms were thought to be an extreme risk," but this has not proved to be the case," nor has a posterior aneurysm been shown to have increased risk. 15 The ejection fraction of the contractile segment has been thought to have prognostic value.!" Others believe that pulmonary artery systolic pressure and preoperative cardiac index are better discriminatory factors.P Recently, Mullen and colleagues" have indicated that lack of septal motion is a contraindication for ventricular aneurysm re-

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Fig. 1. Patient I. Left lateral ventriculogram showing a large diaphragmatic ventricular aneurysm . Left anterior oblique view cine studies showed no septal motion .

section . It is our belief that lack of septal motion may in part give rise to right ventricular failure but, in itself, is not a contraindication to surgical repair . Associated pulmonary artery hypertension may also predispose to right ventricular failure in such patients . The case reports of two patients who developed right ventricular failure after resection of large left ventricular aneurysms and simultaneous single-vessel coronary artery bypass grafting are presented. The succe ssful treatment of right ventricular failure is discus sed .

Case reports CAS E I. A 55-year-old diabetic man had a diaphragmatic myocardial infarction on June 12, 1978. The infarction was complicated by severe congestive heart failure and a systolic murmur appearing on the seventh day after infarction. He continued to have symptoms of shortness of breath and orthopnea and developed bilateral pleural effusions which required thoracentesis on July 31 . He was discharged from the hospital but had one episode of syncope and was readmitted to that hospital on Aug. 22, 1978. A Swan-Ganz catheter was placed and revealed a pulmonary capillary wedge pressure ranging from 37 to 47 mm Hg. No step-up in oxygen saturation was noted in the right side of the heart. He had twopillow orthopnea and was in New York Heart Association Class I V. He was transferred to the Milton S. Hershey Medical Center on March 29, 1978. At the time of transfer, his medications included digoxin 0.125 mg/day, furosemide 80 mg by mouth twice a day, hydralazine 25 mg by mouth three times a day , nitroglycerin paste, insulin , and potassium chloride supplement. On physical examination the blood pressure was 94/60 mm Hg, with a heart rate of 100 beats/min. The carotid pulsations were of low amplitude. There was a 2+ parasternal lift , a soft fourth heart sound, a loud S3 gallop, and a Grade 3/6 systolic murmur at the left sternal border. He underwent card iac catheterization on Aug . 31, 1978, which

showed a massive left ventricular aneurysm (Fig . I). The right coronary artery was completely occluded and was never visualized. There was a complete occlusion of the circumflex coronary artery, but a rather large marginal branch was well visualized . The left anterior descending coronary artery had no significant disease. Operation was performed on Sept. 7, 1978. Prebypa ss central venous pressure was 12 mm Hg, whereas mean left atrial pressure was 36 mm Hg. After minimal dissection , the patient was given heparin and cannulated and cardiopulmonary bypas s was established. Only then was the aneury sm dissected in order to avoid emboli sm of any presumed intraventricular thrombu s . The aorta, was crossclamped for 63 minutes and I ,500 ml of cold potassium cardioplegic solut ion was infused into the aortic root to obtain a myocardial septal temperature of 10° C. 1MThe left ventricular aneurysm was opened longitudinally, a large clot was removed, and a very small ventricular septal defect was identified. The septum was noted to be mostly scar, but the resection did not go into the right ventricle . The ventricular septal defect was closed with a running suture and was then included in the closure of the ventricular aneury sm with Teflon felt strips . An additional 700 ml of cardioplegic solution was infused . A distal anastomosis was constructed between the vein graft and the circumflex marginal coronary artery. Although the perfusate was rewarmed while this anastomosis was performed , the myocardial temperature never exceeded 15° C. A needle vent was placed in the ascending aorta and the aortic cross-clamp was removed. Air was also aspirated with a second needle vent passed through the ventricular suture line . The heart was made to eject to ensure aspiration of all air through the ascending aorta. A side-biting clamp was then placed on the ascending aorta , a circular aortotomy was made , and the proximal anastomosis was constructed to the vein graft. Cardiopulmonary bypass was discontinued after 133 minutes and the initial hemodynamic state was satisfactory; however, it soon deteriorated . Both catecholamines and the insertion of an intra-aortic balloon pump were required . The initial cardiac index was measured at 2.0 Lzrnin/m" on

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RV failure after repair of LV aneurysm

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9-8-78 0030 LA TO RADIAL

9-8-78 0032

'~ 9-10-78 0700 RA TO RADIAL

Fig. 2. lndocyanine green dye curves on Patient I. A. Left atrial (LA) to radial dye curve (Sept. 8, 1978) showed no shunt. B. Right atrial (RA) to radial dye curve 2 minutes later shows early appearance of dye with a trace characteristic of a right-to-Ieft shunt. C. RA to radial dye curve done 2 days later shows disappearance of the previously seen right-to-Ieft shunt. The recordings begin at the time of injection. Date of study is indicated. the intra-aortic balloon pump with catecholamine support. The atrial pressures were interesting in that the right atrial mean pressure (14 mm Hg) was similar to the pulmonary artery mean pressure of 16 mm Hg, but exceeded the left atrial pressure of 10 mm Hg. A cardiac index, measured from left atrium to radial artery with indocyanine green technique, showed a cardiac index of 2 L'min/m" and no shunt (Fig. 2, A). A right atrium to radial dye curve, however, showed a right-to-Ieft shunt which was presumed to be through a patent foramen ovale (Fig. 2, B). Thus there was severe hypoxia with a P0 2 of 42 mm Hg on a fraction of inspired oxygen (Flo,) of 0.9. The P0 2 was raised to 80 mm Hg with an Flo, of 0.9,5 cm of positive end-expiratory pressure, and by decreasing the intra-aortic balloon pump to I: 2. By postoperative day 3, the patient had been weaned from catecholamines and the intra-aortic balloon pump ratio had been decreased to I : 8. The cardiac index was 2.54 L'min/m" and the left and right atrial pressures had equalized at II mm Hg. Most interestingIy, the right-to-Ieft shunt had entirely resolved (Fig. 2, C) and a good arterial blood-gas analysis was maintained with an arterial P0 2 of 121 mm Hg on an FIo, of 0.4. The intra-aortic balloon pump was removed on that day. The patient was extubated on postoperative day 4, but he had recurrent left lower lobe atelectasis which necessitated eventual tracheostomy. A right-to-Ieft shunt, however, was never again demonstrated. He gradually improved and was discharged from the hospital on Oct. 20, 1978. A routine repeat cardiac catheterization was' obtained Dec. 20, 1978, which showed a cardiac index of 2.7 L'min/m", mild-to-moderate left ventricular dysfunction, a patent coronary artery bypass graft,

Fig. 3. Patient 2. A right anterior oblique ventriculogram shows a massive left ventricular aneurysm. Only the base of the heart was seen to contract. A left anterior oblique view cine showed no septal motion. Lines are shown to clarify aneurysm from the base of the heart in this systolic frame. and no interventricular or interatrial shunts. The right atrial mean pressure was I mm Hg, with a pulmonary artery pressure of 20/9 mm Hg and an arterial pressure of 130175 mm Hg. There was trivial mitral regurgitation. Right ventricular function had returned to normal. Ten months after his initial operation, the patient was in New York Heart Association Class I and was gainfully employed. CASE 2. A 53-year-old man had a severe myocardial infarction in December, 1978, complicated by intermittent complete heart block. A transvenous pacemaker was placed, but he subsequently developed symptoms of congestive heart failure. Cardiac catheterization in February, 1979, at another hospital showed a large left ventricular aneurysm (Fig. 3), complete occlusion of the right coronary artery with poor visualization of the distal posterior descending artery by collaterals, complete occlusion of the left anterior descending coronary artery, and a 70% stenosis of the circumflex coronary artery before a large second marginal coronary. Operation was not offered to the patient at that hospital because of excessive estimated operative risk. The patient was discharged only to be readmitted on May 27, 1979, after a syncopal episode. He was found to have recurrent ventricular tachycardia. Cardioversion led only to further ventricular tachycardia, and treatment with procainamide and propranolol resulted in hypotension and shock. The patient was transferred to The Milton S. Hershey Medical Center on June 4, 1979. Medications at that time included bretyIium 500 mg intravenously every 6 hours, digoxin 0.25 mg/day, furosemide, potassium chloride, heparin, nitroglycerin paste, and isorbide dinitrate 5 mg sublingually every 4 hours. On physical examination, he was seen to be very weak; the blood pressure was 72/44 mm Hg and the heart rate was 150 beats/min. The carotid pulses were weak and rapid; the right neck vein was absent, but the left neck vein was distended to the mandible with the patient sitting upright. There were bibasilar niles and the heart sounds were difficult to hear. In

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Fig. 5. A . Arterial and pulmonary artery (PA) pressure traces on Patient 2 with intra-aortic balloon counterpulsation at 90 beats/min and right ventricular assist pumping at 30 beats/ min. The intra-aortic balloon was not actuated for the fourth and fifth beats. The right ventricular assist pump creates the entire pulmonary artery pressure of 40/18 mm Hg. B. Pulmonary artery (PA ) pressure tracing on postoperative day 3 with the assist pump off. Note the normal pulsatile contour.

Fig. 4. Patient 2. Operative view of the pulsatile ventricular assist pump as seen from the patient's head. The venous return cannula is seen entering the right atrial appendage . The Dacron graft is sutured to the pulmonary artery (out of the field of the photograph) . The saphenous vein graft passes beneath the Dacron graft, and the aneurysm repair is seen beneath the sternal retractor. The sac-type pulsatile ventricular assist pump is at the top right of the photograph. the cardiac catheterization laboratory an atrial electrogram identified the rhythm as ventricular tachycardia . Rapid ventricular pacing led to return to a ventricularly paced rhythm at 100 beats/min. Nevertheless , the blood pressure did not rise significantly and remained at 84/60 mm Hg. Ventricular tachycardia returned and intravenous bretylium and lidocaine did not control the arrhythmias. The patient was operated upon the morning after admission. A radial artery cannula and a Swan-Ganz catheter were placed under local anesthesia and card iopulmonary bypass was established 15 minutes after the skin incision . Only then were ventricular adhesion s lysed in order to avoid embolization of possible ventricular clot. The aorta was cross-clamped and I ,000 ml of potassium cardioplegic solution was infused until the myocardial septal temperature reached 10° C. The aneurysm was opened; there was no clot. It was clear that the septum had been entirely infarcted; the resection of the aneurysm went well into the right ventricle . By way of destroy ing re-entrant tachyarrhythmias, the infarcted endocardium was cross -hatched where not removed . The aneur ysmectomy was then closed with Teflon strips externally and horizontal mattress sutures including

both the left ventricular wall . the septum, and the right ventricular wall. The closure was reinforced with running polypropylene sutures . This was completed in 25 minutes and an additional 500 ml of potassium cardioplegic solution was infused to return the septal temperature to 10° C . A distal anastomosis was made to the second marginal circumflex coronary artery . We sought the right and posterior descending coronary arteries , but no lumen could be identified in these vessels. The cross-clamp was removed after 53 minutes, air was evacuated from the heart, and the proximal coronary anastomosis was completed . When we initially attempted to discontinue cardiopulmonary bypass, the hemodynamic state was not satisfactory and therefore an intra-aortic balloon pump was inserted and subsequently catecholamines were infused. Again, an attempt to discontinue cardiopulmonary bypa ss resulted in a peak balloon-assisted arterial pressure of only 80 mm Hg, with a left atrial pressure of only 12 mm Hg but a right atrial pressure of 30 mm Hg. Because of this, cardiopulmonary bypass was again established for 27 minutes. A pulsatile ventricular assist device was placed between the right atrial appendage and the pulmonary artery 19 (Fig. 4) . When this was completed , cardiopulmonary bypass was easily discontinued with a peak arterial balloon-assisted pressure of 120 mm Hg, a left atrial pressure of 16 mm Hg, and a right atrial pressure of 7 mm Hg. Interestingly, the relation ship of right and left atrial pressures could be easily controlled by altering the rate of the right ventricular assist pump . All pulmonary artery pulse pressure was initially generated by the right ventricular assist pump , there being no pulse pressure generated by the right ventricular contractions (Fig . 5, A .) . Arteri al and atrial pressures were adequate with no catecholamines and only use of the right ventricular assist and intra-aortic balloon pumps . The initial cardiac index , how-

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ever, was only 1.33 Lzmin/rn" and therefore a dobutamine infusion was added to bring the cardiac index to 1.94 L'min/rn". On postoperative day I, no pulmonary artery pulse pressure was generated by the right ventricle. The patient had been tapered off dobutamine and the rate of right ventricular assist pumping was decreased to a minimal level of 30/min. On the morning of June 8, 1979, with the right ventricular assist pump on, we noted an arterial blood pressure of 100 mm Hg peak balloon assist, pulmonary artery pressures of 48/19 mm Hg, a left atrial pressure of 19 mm Hg, and a right atrial pressure of 16 mm Hg, with a cardiac output of 2.9 L'min/m". With the right ventricular assist pump off, the peak arterial pressure was 95 mm Hg , the pulmonary artery pressure was 40/20 mm Hg (Fig. 5, B), and the right atrial pressure was 17 mm Hg, with a cardiac output of 2.7 L'rnin/rn". Thus, the sternotomy was reopened and the right ventricular assist pump was removed by removing the inflow port from the right atrial appendage, oversewing the right atrial appendage, and simply transecting and oversewing the graft on the pulmonary artery. A brief infusion of dopamine was again necessary, but this was discontinued on June 10, 1979, and the patient was extubated on June II, 1979. The intra-aortic balloon pump was tapered off and removed on June 12, 1979, with the cardiac index remaining 2.2 L'min/rn", The right atrial pressure of 17 mm Hg remained slightly above the pulmonary artery diastolic pressure of 14 mm Hg. Thereafter, the patient did quite well. Occasional ventricular premature contractions could not be well controlled with quinidine but were well controlled with disopyramide. He was discharged from the hospital on July 1, 1979, and remains well 10 months following hospital discharge.

Discussion

The clinical syndrome of right ventricular failure is most commonly seen after surgical repair of congenital heart disease, although it may also be seen after right ventricular infarction. 20. 21 In these cases, the right ventricle is unable to generate adequate pulmonary artery and thus left atrial pressures. Volume loading of the patient in order to obtain an adequate left atrial pressure results in an excessively high right atrial pressure. If a patent foramen ovale is present, as in the first case, right-to-Ieft shunting will then occur. Filling of the left side of the heart and cardiac output are then maintained at the expense of arterial oxygen desaturation. If the foramen ovale is not patent, another means of supporting right-sided cardiac output must be achieved. Bernhard and colleagues" have recommended massive doses of isoproterenol. We have found that this gives rise to severe tachyarrhythmias and have thus preferred to use a right ventricular assist pump." Weare uncertain why recovery of right ventricular function is relatively rapid and complete. However, this rapid recovery of right ventricular function has been noted by Turina, Bosio, and Senning.t" Several groups have demonstrated the dependence of ventricu-

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lar distensibility on filling of the opposite ventricle. 25-28 This dependence appears to be more important with the pericardium open, as in patients after cardiac operaticn.P">" It may well be that the infarcted, scarred ventricular septum makes the interdependence of ventricular function more pronounced. It may also be hypothesized that recovery of right ventricular function in these two patients was a result of recovery from an ischemic injury during aortic cross-clamping due to inadequate distribution of cold potassium cardioplegia. Occlusions of the right coronary arteries of both patients may have given rise to poor distribution of cardioplegic solution to the right ventricle. However, myocardial protection was good in all respects by our usual criteria. There was not a significant rise in creatine phosphokinase isoenzyme (CPK-MB) in either patient. Both patients had proximal occlusions of the right coronary artery which prevented any air embolus to the right ventricular myocardium and thus transient depression of its function. Finally, right ventricular recovery was not due to revascularization, as only a circumflex marginal artery was revascularized in each case. We do not believe, however, that recovery is the result of decreasing pulmonary vascular resistance in the postoperative period with passive flow of the blood through the lungs. Postoperative cardiac catheterization in the first patient demonstrated adequate right ventricular function with a pulmonary artery pressure of 20/9 mm Hg and a right atrial mean pressure of only I. Recovery of right ventricular function in the second patient is demonstrated by the presence of pulmonary arterial pressure pulses after postoperative day 2 where there had been pressure pulses only from the assist pump on the operative and first postoperative days. Treatment of early postoperative right ventricular failure with an assist pump presented few, if any, problems when used in the second case presented. Reopening of the sternotomy was necessary for pump removal, and this may have delayed endotracheal extubation for 24 to 36 hours. Otherwise, we are not aware of any problem with its use. Postoperative bleeding was not a problem in this patient as it has been when left ventricular assist pumps or biventricular assist pumping have been employed;" Filling of the assist pump from the right atrium was excellent. We have had no previous or subsequent experience, nor are we aware of any previous use of a right ventricular assist pump in the absence of a left ventricular assist pump. Our favorable experience with the second patient presented would indicate that an assist pump may be the treatment of choice of severe postoperative right ventricular failure.

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REFERENCES Abrams DL, Edlist A, Lurai MH, et al: Ventricular aneurysm. A reappraisal based on a study of sixty-five consecutive autopsy cases. Circulation 27:164-169, 1963 Cheng TO: Incidence of ventricular aneurysm in coronary artery disease. An angiographic appraisal. Am 1 Med 50: 340-355, 1971 Dubnow MH, Burchell HB, Titus Jl., et al: Postinfarction ventricular aneurysm. A clinicomorphologic and electrocardiographic study of 80 cases. Am Heart 1 70:753-760, 1965 Sandiford FM, Dawson J'I', Reul Al Jr, et al: Resection of left ventricular aneurysm: Report of 275 patients, Coronary Artery Medicine and Surgery. Concepts and Controversies, lC Norman, ed., New York, 1975, Appleton-Century-Crofts Schlichter 1, Hellerstein HK, Katz LN: Aneurysm of the heart. Medicine 33:43-86, 1954 Ebert PA: Ventricular aneurysm. Hosp Med Feb: 36-53, 1978 Gorlin R, Klein MD, Sullivan 1M: Prospective correlative study of ventricular aneurysm. Am 1 Med 42:512-531, 1967 Loop FD, Effler DB, Navia lA, et al: Aneurysms of the left ventricle. Survival and results of a ten-year surgical experience. Ann Surg 178:399-405, 1973 Cooperman M, Stinson EB, Griepp RB, et al: Survival and function after left ventricular aneurysmectomy. 1 THORAC CARDIOVASC SURG 69:321-328, 1975 Cullhed I, DeIium W, Bjork L, et al: Resection of left ventricular aneurysm-Late results. Acta Med Scand 197:141-148, 1975 Effler DB: Post infarction ventricular aneurysm. Isr 1 Med Sci 11:239-244, 1975 Moran 1M, Scanlon Pl. Nemickas R, et al: Surgical treatment of postinfarction ventricular aneurysm. Ann Thorac Surg 21:107-113, 1976 Rogers Wl, Oberman A, Kouchoukos NT: Left ventricular aneurysmectomy in patients with single vs. multivessel coronary artery disease. Circulation 58:Suppl 1:50-56, 1978 Najafi H, Dye WS, Javid H, et al: Current surgical management of left ventricular aneurysm. Arch Surg 110: 1027-1030, 1975 Loop FD, Effler DB, Webster lS, et al: Posterior ventricular aneurysms. N Engl 1 Med 288:237-239, 1973 Watson LE, Dickhaus DW, Martin RH: Left ventricular aneurysm. Preoperative hemodynamics, chamber volume and results of aneurysmectomy. Circulation 62:868-873, 1975

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17 Mullen DC, Posey L, Gabriel R, et al: Prognostic considerations in the management of left ventricular aneurysms. Ann Thorac Surg 23:455-460, 1977 18 Tyers GFO, Manley Nl, Williams DR, et al: Preliminary experience with isotonic hypothermic potassium arrest. 1 THoRAc CARDIOVASC SURG 74:674-681, 1977 19 Pierce WS, Donachy JH, Landis DL, et al: Prolonged mechanical support of the left ventricle. Circulation 58:Suppl I: 133-146, 1978 20 Cohn HN, Guiha NH, Broder MI, et al: Right ventricular infarction. Clinical and hemodynamic features. Am J Cardiol 33:209-324, 1974 21 Guiha NH, Limas Cl. Cohn IN: Predominant right ventricular dysfunction after right ventricular destruction in the dog. Am 1 Cardiol 33:254-258, 1974 22 Bernhard WF, Fishbein MC, Khuri SF, et al: Myocardial recovery following intractable cardiogenic shock. Circulation (Suppl , in press) 23 Pierce WS: Clinical left ventricular bypass: Problems of pump inflow obstruction and right ventricular failure. Am Soc Artif Intern Organs 1 2: 1-9, 1979 24 Turina M, Bosio R, Senning A: Clinical application of paracorporeal uni- and biventricular artificial heart. Trans Am Soc Artif Intern Organs 24:625-631, 1978 25 Kelly DT, Spotnitz HM, Beiser GD, et al: Effects of chronic right ventricular volume and pressure loading on left ventricular performance. Circulation 44:403-412, 1971 26 Ludbrook PA, Bryne lD, McKnight RB: Influence of right ventricular hemodynamics on left ventricular diastolic pressure-volume relations in man. Circulation 59:21-31, 1979 27 Taylor RR, Covell lW, Sonnenblick EH, et al: Dependence of ventricular distensibility on filling of the opposite ventricle. Am J Physiol 213:711-718, 1967 28 Weiss Jl., Brinker lA, Lappe DL, et al: Leftward displacement during right ventricular loading in man. Demonstration by two dimensional echo (abstr.) Am 1 Cardiol 41:362, 1978 29 Bemis CE, Serur lR, Borkenhagen D, et al: Influence of right ventricular filling pressure on left ventricular pressure and dimension. Circ Res 34:498-504, 1974 30 Holt lP: The normal pericardium. Am J Cardiol 26:455465, 1970 31 Ross 1 Jr: Editorial: Acute displacement of the diastolic pressure-volume curve of the left ventricle. Role of the pericardium and the right ventricle. Circulation 59:32-37, 1979