Acute tricuspid papillary muscle rupture following blunt chest trauma

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of the communication site and the echo-free space displayed the typical flow pattern of a left ventricular pseudoaneurysm (Fig. 2, B). Cardiac catheterization demonstrated severe triple-vessel coronary artery disease and confirmed the presence of an inferior myocardial infarction and a large posterior pseudoaneurysm. At surgery a pseudoaneurysm was found that corresponded in location and size to the transesophageal echocardiographic and cardiac catheterization findings. Repair of the orifice of the pseudoaneurysm, which was located close to the posteromedial papillary muscle, was successfully accomplished without compromising function of the mitral valve, as evidenced by intraoperative transesophageal echocardiography. The patient made an uneventful recovery and remains free of cardiac failure. Left ventricular pseudoaneurysm occurs as a result of rupture of the left ventricular wall, with containment of the resulting hematoma by the pericardium.l Complications include rupture, congestive heart failure, angina, arrhythmias, embolic phenomena, and bacterial endocarditis.‘! z The clinical presentation is often nonspecific. Physical signs, electrocardiogram (ECG), and chest roentgenography are also nonspecific or may mimic the findings of a true left ventricular aneurysm.3 Transthoracic two-dimensional and Doppler echocardiography have been documented to be excellent means of diagnosis.‘, 3 Characteristic features include an extracardiac echo-free space that expands in systole and communicates with the adjacent left ventricular cavity by a narrow opening, in contrast to true aneurysms in which the orifice is wide.“, 3 Doppler echocardiography demonstrates a characteristic blood flow pattern across the communication and within the adjacent left ventricle and pseudoaneurysm. There is bidirectional shunting of blood, with flow entering the pseudoaneurysm during systole and exiting during diastole.3,4 The major limitation of the transthoracic approach is failure to identify the communication between the left ventricle and the extracardiac echo-free space because of a limited acoustic window or because the location of the orifice of the pseudoaneurysm is inaccessible to the ultrasonic beam.2,3 In such instances differentiation between a pseudoaneurysm and other extracardiac echo-free spaces such as a loculated pericardial or pleural effusion or a pericardial cyst may be impossible. Our two cases illustrate that the diagnosis using the transthoracic approach is not always straightforward. Both patients had adequate transthoracic acoustic windows and although extracardiac echo-free spaces were correctly diagnosed, their true sizes were underestimated and they were misinterpreted as loculated pericardial effusions. In neither case was the communication between the extracardisc space and the left ventricle identified, most likely because of its posterior location. In the first patient an additional factor may have been shadowing of the orifice of the pseudoaneurysm by the mechanical aortic valve. Furthermore, pulsed, continuous, and color flow Doppler failed to detect the characteristic flow pattern within the pseudoaneurysms. Presumably, their posterior location resulted in poor alignment of the Doppler beam to the direction of

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flow, resulting in failure to record any flow disturbance. The transesophageal approach, however, provided an unobstructed view of the posterior aspect of the heart and diagnosed the pseudoaneurysms with certainty. In each case it identified echo dropout between the left ventricle and the extracardiac echo-free space, and Doppler interrogation of the suspected orifice confirmed that a communication existed between the two chambers. In the second patient transesophageal echocardiography also proved to be of value intraoperatively. The orifice of the pseudoaneurysm bordered the posteromedial papillary muscle and there was a distinct possibility that adequate repair of the defect would compromise function of the papillary muscle and adversely affect the integrity of the mitral valve. Transesophageal imaging after bypass allowed evaluation of both the adequacy of the repair and competence of the mitral valve before closure of the chest. In conclusion, this report underscores the utility of transesophageal echocardiography in the diagnosis and management of posterior pseudoaneurysms of the left ventricle. REFERENCES

1. Roberts WC, Morrow AG. Pseudoaneurysm of the left ventricle. Am J Med 1967;43:639-44. 2. Catherwood E, Mintz GS, Kotler MN, Parry WR, Segal BL. Two-dimensional echocardiographic recognition of left ventricular pseudoaneurysm. Circulation 1980;62:294-303. 3. Roelandt JRTC, Sutherland GR, Yoshida K, Yoshikawa J. Improved diagnosis and characterization of left ventricular pseudoaneurysm by Doppler color flow imaging. J Am Co11 Cardiol 1988;12:807-11. 4. Tunick PA, Slater W, Kronzon I. The hemodynamics of left ventricular pseudoaneurysm: color Doppler echocardiographic study. AM HEART J 1989;117:1161-5. 5. Sew&d JB, Khandheria BK, Oh JK, Abel MD, Hughes RW, Edwards WD, Nichols BA, Freeman WK, Tajik AJ. Transesophageal echocardiography: technique, anatomic correlations, implementation and clinical applications. Mayo Clin Proc 1988;63:649-80. 6. Donaldson RM, Ross DM. Homograft aortic root replacement for complicated prosthetic valve endocarditis. Circulation 1984;7O(suppl 1):178-81.

Acute tricuspid papillary muscle rupture following blunt chest trauma Andre Linka, MD, Manfred Ritter, MD, Marco Turina, MD,” and Rolf Jenni, MD Zurich, Switzerland Involvement of the tricuspid valve in nonpenetrating cardiac trauma represents a rare condition. To date, only about 100 cases of traumatic tricuspid regurgitation have From the Division of Echocardiography and aDepartment of Cardiovascular Surgery, University Hospital Zurich. Reprint requests: M. Ritter, MD, Division of Echocardiography, University Hospital, Raemistr. 100, 8091 Zurich, Switzerland. 414138732

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Fig. 1. Early systolic stop frame of an angulated apical four-chamber view demonstrating systolic flailing

of the ruptured papillary muscletip of the anterior tricuspid valve leaflet (P) aswell asthe site of rupture of the papillary muscle(X). RA, Right atrium; RV, right ventricle; LV, left ventricle; SC, coronary sinus.

Fig. 2. Pulsed wave Doppler velocity registration with the samplevolume placed within a dilated hepatic vein (top panel). Spectral display of the recorded velocities (bottom panel) showsalmost holosystolic reversal of flow into the hepatic veins as a sign of severetricuspid regurgitation.

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Fig. 3. Diastolic stop frame of a slightly angulated apical four-chamber view. The right atrium and the right ventricle are completely obliterated by the injected contrast (agitated saline). There are numerous isolated microbubbles (B) visible in the left atrium (LA), thus demonstrating the presence of an open foramen ovale with right-to-left shunting.

been reported in the literature.lm3 The pathogenetic mechanism usually consists of an acute deceleration trauma (e.g., car accident) resulting in more or less severe tricuspid regurgitation caused by either rupture of the valve leaflets, chordal rupture, or detachment and rupture of papillary muscles. Clinical symptoms are often very subtle so that the diagnosis is established in most cases only weeks, months, or even years after the initial trauma.4,,5 Isolated papillary muscle rupture of the tricuspid valve is very exceptional (13 cases reported in literature); in this group of patients there is usually an early onset of symptoms because of the severity of tricuspid regurgitation and the often associated right-to-left shunting across a patent foramen ovalee We describe a case of a 24-year-old man with no previous cardiac history who suffered severe blunt chest trauma as a result of hitting against the steering wheel of his car; there was additional trauma including liver rupture, multiple bone fractures, and cerebral contusion. After his admission to the intensive care unit, progressive signs of right heart decompensation and tricuspid regurgitation developed. There were large V waves of about 40 mm Hg and a mean central venous pressure of about 15 mm Hg, creatine phosphokinase values of approximately 1000 U/L with significantly elevated MB fractions, and transaminase values of 100 U/L. Transthoracic Doppler echocardiography as well as transesophageal monoplane Doppler echocardiography for enhanced image quality were performed as di-

agnostic procedures. Two-dimensional imaging revealed rupture of the tips of all papillary muscles of the tricuspid valve, with consecutive systolic flailing into the right atrium (Fig. 1). Severe tricuspid regurgitation was documented by means of color-coded Doppler of the regurgitant flow into the right atrium and by demonstration of pronounced holosystolic reversal of hepatic vein flow using pulsed Doppler with the sample volume placed in one of the dilated hepatic veins (Fig. 2). Additionally, dilation of the right atrium resulted in an open foramen ovale and a consecutive right-to-left shunt that was identified by means of contrast injection (agitated saline) into the central venous catheter and by the passage of air microbubbles from the right atrium into the left atrium and ventricle (Fig. 3). Because of rapidly evolving right heart failure, immediate surgical repair was considered in this situation. An intraoperative examination confirmed the echocardiographic diagnosis. The lateral papillary muscles were reinserted by means of transmural mattress sutures and Teflon felt fixation on the pericardium. The septal papillary muscle was sutured using Teflon felt pledgets that were fixed within the interventricular septum. A second thoracotomy had to be performed the day after the first operation because of a repeat rupture of two of the papillary muscles. This time the surgical repair was successful and the patient’s postoperative course remained uneventful. To our knowledge, this is the first reported case of traumatic tricuspid papillary muscle rupture that features an

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acute simultaneousrupture of all papillary muscles.Doppler echocardiography is able to furnish accurate diagnostic information concerning the precise anatomic localization of the lesionsaswell asthe hemodynamic assessment of this emergency situation, thus greatly facilitating the ensuingsurgical intervention. REFERENCES 1.

2. 3. 4. 5.

6.

Perlroth MG, Hazan E, Lecompte Y, Gougne G. Case report: chronic tricuspid regurgitation and bifascicular block due to blunt chest trauma. Am J Med Sci 1986;2:119-25. Gayet C, Peirre B, Delahaye JP, Champsaur G, Andre-Fouet X, Rueff P. Traumatic tricuspid insufficiency. Chest 1987;92:429-32. Hilton T, Mezei L, Pearson AC. Delayed rupture of tricuspid papillary muscle following blunt chest trauma. AM HEART J 1990;119:1410-12. Richter M, Jenni R. Pulsating tumor of the neck. Schweiz Rundschau Med 1989;78:19-21. Noera G, Sanguinetti M, Pensa P, Biagi B, Cremonesi A, Lodi R, Lessana A, Carbone C. Tricuspid valve incompetence caused by nonpenetrating thoracic trauma. Ann Thorac Surg 1991;51:530-2. Bardy GH, Talano JV, Meyers S, Lesch M. Acquired cyanotic heart disease secondary to traumatic tricuspid regurgitation. Am J Cardiol 1979;44:1401-6.

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cardiac tamponade, or constrictive pericarditis.” Roent genologicfindings are nonspecific, and cytologic diagnosis from pericardial fluid is difficult.” A combination of cvtologic and immunohistochemicaltechniques,the finding of high pericardial fluid hyaluronic acid content,” and extensive pericardial uptake of gallium 67 by scintigraphy” are helpful in diagnosis. Echocardiography as a screening method has certain limitations, and magnetic resonance imaging is preferred.’ The survival period is short: the median period of survival is only a little more than 6 mont,hs” in spite of current surgical and radiotherapeutic efforts.

M. H., a 12-year-old boy, was admitted to Salmaniya Medical

Center in Bahrain,

on October

8, 1990 with a his-

tory of progressivedyspnea, abdominal discomfort, and a cough of 20 days’ duration. He had experiencedorthopnea for the last few days. He had no history of fever, joint pains, or any other symptoms. There was no history of asbestos exposure. Physical examination showedevidence of massive pericardial effusion with tamponade, which was confirmed

by chest x-ray films and two-dimensional

echocar-

diography. No masswas detected. An ECG showedlowvoltage complexes with nonspecific precordial T-wave inversion. Laboratory investigation resultswereall normal, and results of viral antibody screen,antistreptolysin (ASO) titer, and purified protein derivative (tuberculin) tests were negative. Emergency pericardial aspiration yielded

hemorrhagic fluid. Results of cytologic studies were nega-

Primary pericardial mesothelioma: One-year event-free survival C. A. Nambiar, MD, DM (Card), Habib E. Tareif, FRCSI, K. U. Kishore, MD, J. Ravindran, MD, MRCP (UK), and Ashru K. Banerjee, MD, FAMS, FRCPath Bahrain,

Arabian

Gulf

tive for malignant

cells.

After

the diagnostic

tap, the

patient underwent open pericardial drainage.After 800ml of hemorrhagic fluid was aspirated from the pericardial cavity, a mass of about 5 cm x 3 cm lying in the diaphragmatic wall of parietal pericardium was removed; 1300 ml of

straw-colored fluid in the right pleural cavity wasalso aspirated. Histopathologic examination revealed a spindle cell malignant tumor, which had infiltrated the pericardium and adjacent soft tissues of the chest wall. This was

interpreted asa malignant localized fibrous mesothelioma Malignant pericardial involvement has been reported in 0.15% to 6.5% of all deathsand in 1.5% to 21% of patients who die of underlying malignancies.1Primary tumors of the pericardium are exceedingly rare and include mesothelioma, fibrosarcoma,angiosarcoma,and malignant teratoma.’ Primary pericardial mesotheliomais a rarity, the incidence of which was below 0.0022% among500,000cases in a large autopsy study.2 Three histologic types of pericardial mesotheliomahave been described: (1) pure epithelial, (2) spindle cell, and (3) mixed.3Within the pericardial sac,the tumor may be either a localized massor a diffuse mass that encasesthe heart and obliterates the pericardial spaces.3 The antemortem diagnosisisextremely difficult. Of the 120casesreported before 1985, 75% were postmortem diagnoses4The clinical signsand symptoms may be nonspecific3or may resembleeffusive pericarditis, From Salmaniya Medical Center, Bahrain, Arabian Gulf. Reprint requests: C. A. Nambiar, MD, DM (Card), Salmaniya Medical Center, P.O. Box 12, Bahrain, Arabian Gulf. 4/4/38121

(Figs. 1 and 2). A postoperative computed tomographic scan of the thorax showedsegmentalcollapseof the left

lower lobe, no massin the pericardium or lungs, and no mediastinal lymph nodes. A repeat echocardiographic evaluation showed an increase in cardiac chamber size and a left ventricular ejection fraction of 36”; The patient received combination chemotherapy of doxorubicin, (1.4 mg/kg), vincristine (0.06 mg/kg), and cyclophosphamide (17 mg/kg) every 3 weeks for a total period

of 18 weeks.Treatment wascompleted with no side effects in April 1991, and at that time there was no clinical or echocardiographic evidence of pericardial or systemic disease. The patient was followed up every 8 weeks, and on the last visit on October 21,1991, he was free of symptoms and had no objective evidence of any disease or recurrence as determined by detailed clinical and echocardiographic evaluation. Pericardial mesothelioma remains a diagnostic and therapeutic challenge.3 Patients with hemorrhagic pericardial effusions should undergo open exploration, in spite of negative noninvasive or cytologic test results. We believe that this boy is one of the rare patients with primary pericardial