P technique in the treatment of certain types of mitral

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1 Operative Findings After Percutaneous Mitral Dilation Christophe Acar, MD, Alain Deloche, MD, Pierre R. Tibi, MD, Victor Jebara, MD, Juan Carlos Chachques, MD, Jean Noel Fabiani, MD, and Alain Carpentier, MD, PhD Departement de Chirurgie Cardiovasculaire, Hbpital Broussais, Paris, France Ten patients were operated on within one hour to 3 months after percutaneous mitral dilation. Operative analysis of the lesions demonstrated hemopericardium (n = 3, acute mitral insufficiency (n = 71, left atrial thrombus (n = 2), and atrial septa1 defect (n = 3). A conservative treatment of the mitral valve lesion was performed in 6 patients. All patients had uneventful postoperative courses. The complications presented in this series were either due to technical error or occurred in patients with relative contraindications to percutaneous mitral dilation (calcified commissures). (Ann Thorac Surg 1990;49:959-63) ercutaneous mitral dilation (PMD) is an efficacious P technique in the treatment of certain types of mitral stenoses [1-6]. The morbidity and mortality of PMD are very low [7, 81. Aside from perforation of a chamber resulting in hemopericardium, the complications of PMD are usually well tolerated and do not require urgent operative intervention [7, 81. This report examines a series of patients operated on after failed or complicated PMD, most of whom required surgical intervention within 12 hours because of cardiac tamponade or severe acute mitral regurgitation. Material and Methods Since 1986, 10 patients, aged 20 to 54 years, have been operated on after PMD. Urgent surgical intervention (less than 12 hours after PMD) was required in 7 patients. All patients were seen with either pure mitral stenosis or mitral stenosis associated with minimal mitral insufficiency, and 9 of the 10 were in normal sinus rhythm before PMD. Percutaneous mitral dilation was accomplished by a transeptal approach to the mitral orifice after femoral vein catheterization. Two balloons (one conventional and one trefoil) were inflated simultaneously, and the results were evaluated by echocardiography after each inflation. Results Table 1 shows a clinical summary of the results. Hemopericardium (n = 3) Two patients experienced thoracic pain accompanied by hypotension that responded to volume resuscitation during attempts at transeptal puncture. Urgent sternotomy (three to six hours) was performed after echocardiography had shown the existence of increased pericardial fluid. In Accepted for publication Dec 30, Address reprint requests to Dr Acar, Departement de Chirurgie Cardiovasculaire, HGpital Broussais, 96 rue Didot, 75014, Paris, France. both patients, right atrial perforation was found and subsequently repaired, and commissurotomy of the stenosed mitral valve was performed in the same operative procedure. In a separate patient, inflation of the commissurotomy balloon was followed within several minutes by severe hemodynamic collapse with clinical signs of cardiac tamponade. The patient was immediately taken to the operating room. Findings consisted of serious hemopericardium due to a perforation of the left ventricular apex, which was surrounded by a large intramyocardial hematoma. The hemopericardium was evacuated and the ventricular tear was sutured using Teflon strips. The mitral stenosis was surgically treated at a later date. Acute Mitral Insufficiency (n = 5) Five patients were seen with clinically acute mitral insufficiency after PMD (Fig 1). In 2 patients, acute mitral insufficiency produced an unstable hemodynamic state with massive pulmonary edema (V wave of 50 to 70 mm Hg). Surgical intervention followed within two to three hours. The lesions responsible for the mitral regurgitation were diagnosed by transthoracic echocardiography immediately after PMD, and were confirmed by operative analysis of the valve. Rupture of the anterior papillary muscle occurred in 1 patient, who had a complete rupture of the papillary muscle at its zone of insertion on the left ventricular muscular wall. The commissures were otherwise satisfactorily opened and the subvalvular apparatus was moderately diseased (shortened chordae tendineae). A Carpentier-Edwards mitral bioprosthesis was used for valvular replacement. A tear of the interatrial septum at the site of the fossa ovalis (2 cm in length) was closed and a small mural thrombus adherent to the left atrial wall was removed. Tear of the anterior leaflet occurred in another patient, who had asymmetrical mitral stenosis with mild posterior commissural fusion and an extremely involved and calcified anterior commissure (up to the midpoint of the mitral orifice). When the left atrium was opened, a star-shaped by The Society of Thoracic Surgeons /90/$3.50

2 960 ACARETAL Ann Thorac Surg 1990;49:95943 Table 1. Operative Findings After Percutaneous Mitral Dilation (n = 10) Patient Timpe Operative No. Lapse Findings Surgical Treatment 1 <1 h Perforation of Repair of bleeding LV site 2 3h Perforation of Repair of bleeding RA site + MC 3 6h Perforation of Repair of bleeding RA site + MC 4 2h AM1 + LAT + MVR + closure of 5 3h AM1 MVR 6 8h AM1 Mitral valve repair 7 12 h AM1 Mitral valve repair 8 13 days AM1 + LAT MVR 9 90 days AM1 + MVR + closure of 10 5 days AM1 + Mitral valve repair + closure of AM1 = acute mitral insufficiency; = atrial septa1 defect; LAT = left atrial thrombus; LV = left ventricle; MC = mitral cornmissurotomy; MVR = mitral valve replacement; RA = right atrium. A papillary muscle rupture N = l tear of the anterior leaflet N = l B Fig 2. Star-shaped tear of the medial portion of the anterior mitral leaflet (AML) (arrow). Note the calcified anterior cornmissure (*) with papillary muscle-commissure fusion. (PML = posterior mitral leaflet.) paracommissural tear anterior posterior N = l N=4 Fig I. Mechanisms of acute mitral insufficiency after percutaneous mitral dilation: papillary muscle rupture (n = l), anterior leaflet tear (n = I), and paracommissural tear (n = 5). tear of the anterior leaflet was found (Fig 2). An attempt at conservative repair was not possible because of the severe involvement of the subvalvular apparatus (fusion of the papillary muscle and anterior commissure), and the valve was replaced with a St. Jude prosthesis. The remaining 3 cases of acute mitral insufficiency, which was initially poorly tolerated (pulmonary edema), were eventually able to be controlled by medical therapy. In 2 of these patients, rapid operative treatment (eight to 12 hours) was necessary in light of massive mitral regurgitation. The responsible lesions were paracommissural valvular tear causing a localized disinsertion of either the anterior (n = 1) or the posterior (n = 1) leaflet (Fig 1). In

3 Ann Thorac Surg 1990;49: ACARETAL 961 both patients, there was no serious involvement of the subvalvular apparatus and the commissures were satisfactorily opened. Surgical reconstruction of the mitral valve was accomplished by reparative suturing of the torn leaflet and Carpentier ring annuloplasty (No. 30). In 1 case, a 43-year-old woman with predominant mitral stenosis was seen with a massively enlarged left atrium (cardiothoracic index = 0.91) (Fig 3A). Transesophageal echocardiography did not show the presence of a left atrial thrombus, and PMD was performed. A satisfactory commissurotomy was accomplished; however, severe mitral insufficiency ensued and was followed by serious pulmonary edema, which resolved rapidly. A left atrial thrombus was found by magnetic resonance imaging (Fig 3B), and the patient was referred to operation 2 weeks later. Operative analysis of the lesion demonstrated a massively enlarged left atrium with an old thrombus (4 cm in diameter) protruding from the floor of the atrium approximately 3 cm from the mitral valve orifice, fibrous involvement of the mitral valve apparatus with a posterior Fig 4. Opening of the right atrium: presence of an atrial septal defect (). paracommissural tear, and tricuspid insufficiency secondary to annular dilatation. These lesions were treated by (1) removal of the thrombus, (2) left atrial plication, (3) Starr-Edwards mitral valve replacement, and (4) Carpentier ring tricuspid annuloplasty. A B Fig 3. (A) Roentgenogram showing cardiomegaly due to massively enlarged left atrium (arrow). (B) Magnetic resonance imaging (transverse cut) showing massive enlargement of the left atrium (LA) with thrombus ( ) seen just to the right of the vertebral column. (RV = right ventricle; LV = left ventricle.) Left-to-Right Shunt Associated With Mitral Insuficiency (n = 2) In a 43-year-old patient with pure mitral stenosis and pulmonary hypertension (mean pulmonary arterial pressure = 30 mm Hg), a transesophageal echocardiography after PMD demonstrated good commissural opening (from 0.8 cm2 to 1.8 cm ), moderate mitral insufficiency of new onset, and the existence of a 2.3:l left-to-right shunt secondary to an intraatrial communication. Because of the progressive worsening of the patient s clinical status over the ensuing 3 months, she was referred to operation. Through a right atriotomy, a 3.5-cm endothelialized vertical tear at the site of the fossa ovalis (Fig 4) was demonstrated. Tricuspid insufficiency due to annular dilatation was also noted. The mitral valve was torn at the posterior commissural area, and there was extensive calcification of the anterior commissure. Surgical treatment was comprised of primary closure of the intraatrial communication, mitral valvular replacement using a St. Jude prosthesis, and tricuspid annuloplasty with a No. 34 Carpentier ring. In a 34-year-old woman, the PMD procedure was followed by severe mitral regurgitation, which was surgically treated five days later. In addition, transesophageal echocardiography revealed the existence of consistent left-to-right shunt (2.2:l). A paracommissural tear of the posterior commissure was repaired by resuturing, and a satisfactory open commissurotomy was realized. Primary closure of a small atrial septal defect (1.5 cm) was simultaneously performed. There was no operative mortality in this series. All patients had uneventful postoperative courses and exhibited good functional results.

4 962 ACARETAL Ann Thorac Surg 1990;49: Comment Since the first reports by Inoue and associates [l] in 1984, indications for PMD have had a tendency to be liberalized [2-61. According to the cardiology literature, complications from this technique are rare, and the mortality is minimal [7, 81. However, there are two post-pmd situations that require urgent surgical intervention: cardiac tamponade and severe acute mitral insufficiency. Tamponade can be secondary to a puncture of the right atrium during attempts at transseptal catheterization (2 patients in this series). These events are of variable gravity, but can be well tolerated. Echocardiography will confirm the existence of pericardial fluid that had been absent before PMD. In these circumstances, it is logical to simultaneously treat the hemopericardium as well as the mitral valve pathology. Hemopericardium secondary to perforation of the left ventricle with severe hemodynamic compromise occurred in 1 patient. This was probably secondary to balloon slippage at the time of inflation, causing left ventricular apical injury and an intramural hematoma that subsequently exteriorized into the free pericardium. This complication necessitated immediate control of the ventricular tear. Acute mitral insufficiency secondary to PMD can have very different clinical presentations, depending on the mechanical lesion incurred. The onset of massive pulmonary edema associated with serious hemodynamic instability refractory to medical therapy frequently signifies severe trauma to the mitral apparatus. Transthoracic echocardiography allows precise identification of the lesion. This complication was observed in 2 patients, who required surgical intervention within two to four hours. In 1 patient, papillary muscle rupture at its ventricular insertion was probably the consequence of balloon inflation between the subvalvular apparatus and the ventricular wall [9]. Routine use of a floating balloon catheter before insertion of the PMD balloon, to assure correct positioning of it within the mitral orifice, should prevent this complication. In the second patient, an extensive tear of the anterior leaflet was present. The leaflet injury was located at its midportion because of substantial asymmetry of the mitral stenosis (anterior commissural calcification and fusion to the midportion of the mitral orifice with a normal posterior commissure). In retrospect, this may have been a contraindication to PMD. Acute mitral insufficiency after PMD can also manifest itself by initial pulmonary edema, which favorably responds to medical treatment. In 2 patients, rapid operative intervention was carried out because of massive mitral insufficiency. Each time, a disinsertion of a mitral leaflet secondary to a paraannular tear at the site of a commissure was found. These lesions were treated by simple resuturing of the leaflet and Carpentier ring annuloplasty. Interestingly, in both cases the diameter of the mitral annulus was relatively small (No. 30 Carpentier ring). Radial twisting of the balloon during inflation while in the mitral orifice was the probable mode of injury. The possibility of a conservative reconstructive repair of the mitral valve after PMD does not seem to be related to the extent of the valvular tear, which is usually easily suturable, but is related more importantly to the degree of pathological involvement of the valvular and subvalvular apparatus (ie, calcification of the commissures), which may necessitate valve replacement. In spite of the usefulness of transesophageal echocardiography in the diagnosis of intraatrial thrombi [lo], this technique was inaccurate in 2 cases in this series (1 case involved a small adherent thrombus, and the other, a large thrombus protruding into a massively enlarged left atrium). Fortunately, no embolic complications occurred after PMD. The existence of associated lesions that are primarily amenable to surgical therapy (left atrial ectasia, severe tricuspid insufficiency, thrombus of the left atrium) should provoke consideration of offering surgical treatment of mitral stenosis without first attempting PMD. The onset of a left-to-right shunt after PMD is not rare [ll], although it is usually a modest shunt without clinical consequence (shunt fraction 1.3:l to 1.8:l) [12]. The intraatrial communications after PMD reported in this series are exceptionally large (2.3:l). This shunt was probably poorly tolerated because of the onset of mitral insufficiency secondary to PMD, as well as the preexistence of pulmonary arterial hypertension and tricuspid insufficiency. As in other reports in the literature [12, 131, these complications may be the consequence of premature PMD catheter withdrawal before complete balloon deflation. The patients operated on in this series were referred from different cardiology departments who do not refer all their complications to us; consequently, it seems difficult to establish the exact incidence of complicated PMD. However, the complications of PMD reported here are rare according to the cardiology literature [7, 81, and no mortality or eventual serious sequelae related to PMD were observed in our series. The complications were either due to technical error or to PMD in patients with relative contraindications (ie, calcified commissures). We do not believe that a permanent surgical standby is mandatory for PMD procedures performed by experienced cardiology centers; when complications do occur, there is usually ample time to allow mobilization of the cardiac surgical team. In rare instances, readily available on-site circulatory support equipment in the catheterization laboratory could be advantageously used to assure transfer of the patient to the operating room in a satisfactory hemodynamic condition. References 1. Inoue K, Owaki T, Nakamura T, Kitamura F, Miyamoto N. Clinical application of transvenous mitral commissurotomy by a new balloon catheter. J Thorac Cardiovasc Surg 1984; Lock JE, Khalilullah M, Shrivatava S, Bahl V, Keane JF. Percutaneous catheter commissurotomy in rheumatic mitral stenosis. N Engl J Med 1985;313: A1 Zaibag M, Ribeiro PA, A1 Kasab S, A1 Fagih MR. Percutaneous double balloon mitral valvotomy for rheumatic mitral valve stenosis. Lancet 1986;1: Vahanian A, Slama M, Cormier 8, Michel PL, Savier C, Acar

5 Ann Thorac Surg 1990;4995!&63 ACARETAL 963 J. Valvuloplastie mitrale percutanke chez l'adulte. Arch Ma1 Coeur 1986;79: Palacios I, Block PC, Brandi S, et al. Percutaneous balloon valvotomy for patients with severe mitral stenosis. Circulation 1987;75: McKay RG, Lock JE, Safian RD, et al. Balloon dilatation of mitral stenosis in adult patients: postmortem and percutaneous mitral valvuloplasty studies. J Am Coll Cardiol 1987; 9: Vahanian A, Michel PL, Cormier 8, et al. Results of percutaneous mitral commissurotomy in 200 patients. Am J Cardiol 1989;63: Inoue K. Efficacy of percutaneous transvenous mitral commissurotomy by Inoue-balloon. Eur Heart J 1989;10: Acar C, Vahanian A, Deloche A, Acar J, Carpentier A. Traumatic rupture of papillary muscle following percutane- ous mitral commissurotomy [Letter]. J Thorac Cardiovasc Surg (in press). 10. Aschenberg W, Schulter M, Kremer P, et al. Transoesophageal two-dimensional echocardiography for detection of the left atrial appendage thrombus. J Am Coll Cardiol 1986; Bernard Y, Schiele F, Bassand JP, Anguenot T, Jacoulet P, Maurat JP. Characteristics of flow through the atrial septa1 defect following percutaneous mitral valvuloplasty. Eur Heart J 1989;10: Goldberg N, Roman CF, Do Cha S, et al. Right to left interatrial shunting following balloon mitral valvuloplasty. Cather Cardiovasc Diagn 1989;16: L'Epine G, Drobinski Y, Sotirov N, et al. Right heart failure due to an inter-atrial shunt after percutaneous mitral balloon dilatation. Eur Heart J 1989;10:285-7.