Asian Cardiovasc Thorac Ann 2006;14:26-29
© 2006 Asia Publishing EXchange Ltd
Left Ventricular Rupture after Mitral Valve Replacement: A Report of 13 Cases
Huai-Jun Zhang, MD,
Wei-Guo Ma, MD,
Jian-Ping Xu, MD,
Sheng-Shou Hu, MD,
Xiao-Dong Zhu, MD
Department of Adult Cardiac Surgery, Fu Wai Hospital, Chinese Academy of Medical Sciences, Beijing, China
For reprint information contact: Wei-Guo Ma, MD Tel: 86 10 8839 8652 Fax: 86 10 6831 3012 Email: wgma{at}yahoo.com, Department of Adult Cardiac Surgery, Fu Wai Hospital, 167 Northern Lishi Road, Beijing 100037, China.
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ABSTRACT
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Left ventricular rupture after mitral valve replacement is a rare but lethal complication. Between 1995 and 2003, left ventricular rupture occurred in 13 of 5,449 patients who underwent mitral valve replacement, with an incidence of 0.24%. There were 4 immediate ruptures and 9 delayed ruptures. Urgent repair of the rupture was performed under cardiopulmonary bypass in 11 cases. All mitral prostheses were explanted. External repair alone was performed in one patient. External repair combined with internal repair was performed in 10 patients. Two patients died of cardiac tamponade and failure of cardiac resuscitation. Of the 11 patients who had a re-operation, 6 died in hospital and 5 survived. The mortality was 61.5% (8/13). At a mean follow-up of 4 years, 2 patients were in New York Heart Association functional class II and 3 were in class III. Proper diseased valve removal, decalcification, and prosthesis selection could minimize the incidence of left ventricular rupture. Immediate diagnosis and urgent surgical intervention are crucial for successful repair.
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INTRODUCTION
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Rupture of the left ventricle (LV) is a lethal complication following mitral valve replacement (MVR). The reported incidence is 0.52% to 14.3%, with a high mortality rate of 65% to 100%.1–5 A critical analysis of the experience of this catastrophe is essential for understanding the nature of this problem and implementing effective prevention and treatment. We retrospectively reviewed all cases of LV rupture following MVR in our hospital between 1995 and 2003 to elucidate the risk factors and surgical strategy.
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PATIENTS AND METHODS
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In the 5,449 MVR operations performed in our hospital between 1995 and 2003, there were 13 cases of postoperative LV rupture, with an incidence of 0.24%. There were 5 male and 8 female patients. Eleven (84.6%) patients had a history of rheumatic fever. The clinical profile is shown in Table 1
. At surgery, the mitral valves were found to have severe calcification and thickening and fusion of the chordae. The anterior leaflets and relevant chordae were completely excised in all cases; the posterior leaflets were preserved in 2 patients and resected in the other 11. Mechanical valves were inserted in 11 patients with a running suture; bioprostheses were inserted in 2, with interrupted sutures. Associated procedures included aortic valve replacement (3 cases), tricuspid valvuloplasty (6 cases), left atrial plication (2 cases), and coronary artery bypass grafting (1 case).
The main clinical signs before LV rupture included unstable blood pressure on weaning from cardiopulmonary bypass (CPB), ventricular arrhythmia or ST-T segment elevation on the electrocardiogram, or massive bleeding into the pericardium or chest drainage tubes. Four cases occurred in the operating room (immediate rupture) and the others in the intensive care unit (delayed rupture). According to the rupture site, 2 cases could be classified as Type I, 4 cases as Type II, and 2 cases as type III, while the other 5 cases could not be assigned to a particular type. Two patients died of cardiac tamponade with failure of resuscitation before surgical intervention could be undertaken. The other 11 ruptures were repaired under CPB. The mitral valve prosthesis was removed first and the interior of the LV was inspected to determine the site of rupture. One case was repaired using isolated external sutures and the other 10 were repaired with both external and internal sutures. External repair was undertaken with deeply placed interrupted 2/0 polypropylene sutures extending well into the normal myocardium. Interrupted buttressed sutures were used in 3 cases of internal repair. Covering the rupture site with a pericardial or Dacron patch was employed in 8 cases.
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RESULTS
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Of the 11 patients repaired under CPB, 5 survived (3 with immediate ruptures, 2 with delayed ruptures) and 6 died in hospital. The mortality of LV rupture was 61.5% (8/13 cases). The causes of death were cardiogenic shock in 3 patients, irreparable rupture in 2, and ventricular fibrillation in 1. Of the 9 patients with a delayed rupture, occurring 30 min to 21 hours postoperatively in the intensive care unit, 7 died. Three of the 4 patients with immediate rupture survived, whereas only 2 of 9 patients survived a delayed rupture (Table 2).
The survivors were free from myocardial ischemia on the electrocardiogram at discharge. There was a decrease of ventricular function on echocardiographic evaluation. The 5 survivors were still doing well after a mean follow-up of 4 years. At the latest follow-up, two were in New York Heart Association functional class II and 3 were in class III. They needed oral hydrochlorothiazide and digoxin intermittently. The end-diastolic LV diameters in 2 survivors were 54 and 52 mm, vs. 42 and 39 mm prior to MVR, but without signs of ventricular aneurysm formation.
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DISCUSSION
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In 1974, Treasure and colleagues6 proposed classification of LV rupture after MVR into 2 types according to the location of the epicardial tear. A type I lesion is defined as a defect along the posterior atrioventricular sulcus. This type usually results from any injury of the mitral valve annulus, such as excessive decalcification, insertion of an oversize prosthesis, deep sutures entering the myocardium, and manual cardiac compression. A type II tear refers to rupture of the LV posterior wall at the base of the papillary muscle. This can occur with avulsion or excessive debridement of the intravalvular structures, secondary myocardial hematoma, and mechanical injury from suckers or bioprosthetic struts. Later, Miller and colleagues7 suggested the addition of a third category (type III) to denote rupture of the LV posterior wall between the base of the papillary muscle and the atrioventricular groove. Mechanical injury to the ventricular endocardium is believed to be the most common reason. However, distinction of the 3 types is sometimes difficult. Because the ventricular tear expands as the rupture progresses, some cases become a mixed type. There were 5 such cases in our series. Each type of LV rupture can be further categorized as immediate, delayed, and chronic. Immediate tears occur in the operating room before or after weaning from CPB; these patients have a higher survival rate because resuscitation is always on time. Delayed tears present hours to days after leaving the operating room. The clinical signs are hypotension and massive bleeding into the drainage tubes. Chronic tears appear days to years after MVR and present as LV pseudoaneurysm. In a review of 104 cases, 55% of the tears were immediate with a survival rate of 40%, and 34% were delayed tears with a survival rate of 11%.1 In our series, 3 of the 4 cases of immediate rupture survived while only 2 of 9 patients survived a delayed rupture.
The basic requirements for successful repair of this lethal defect comprise removal of the mitral valve prosthesis with accurate identification of the internal tear site, closure of the full extent of the wound, and placement of sutures into healthy myocardium. All repairs should be carried out under CPB with the ventricle decompressed, which should be instituted as quickly as possible once the tear has been recognized. Often, the tear in the myocardial surface is small and the inner tear extends beyond the outer margins; after blood enters the myocardium and forms a hematoma, the frigidity of tissues in the vicinity of the wound increases, making repair difficult. The 3 types of rupture have similar surgical treatment, and ideally a combination of external and internal repair should be adopted. The mitral valve prosthesis should be removed to identify the site and range of the tear. A type I tear should be repaired with felt strip buttressed sutures. The sutures are best fixed on the annulus. Type II and III tears should be fully covered with patches sutured to good myocardium. This is very difficult because of the intracardiac structures. External repair can be approached with deeply placed 2/0 polypropylene sutures extending beyond the limits of the external tear. Care should be taken to avoid injury to the circumflex coronary artery and its major branches.
As it is easier to prevent LV rupture than to repair it once it has occurred, avoidance of rupture should be the primary goal. Most of the patients in our series had a history of chronic rheumatic disease, and mitral stenosis was the chief pathological feature. The LV was relatively small, and the mural leaflet was excised in 11 of the 13 cases. In addition, 73% were female. All of these factors have been suggested to predispose to LV rupture after MVR.1,4 Given the possible etiology and predisposing factors, measures need to be taken in several respects. First, part or whole of the posterior leaflet should be preserved in high-risk patients. The calcified annulus should be properly debrided to sustain the integrity of mitral valve annulus, maintaining the support and suspension of the mitral valve on the LV posterior wall. Second, mechanical injury should be avoided. Proper sizing of the mitral valve prosthesis is important: a small prosthesis should be used in a small left ventricle with a severely stenosed mitral valve. Excessive traction should never be applied on the ventricle during resection of the valve, to avoid injury to the root of the papillary muscle. Third, stable hemodynamics should be maintained during and after MVR. A myocardial tear should be suspected in cases of abrupt postoperative hypotension and inexplicable frequent ventricular rhythms. This is often suggestive of endomyocardial injury and hematoma formation due to blood infiltration of the myocardium. Measures to reduce LV pressure-volume work and distention should be utilized. Systemic hypertension should be prevented by vasodilator therapy. A pacemaker should be installed in high-risk patients to increase postoperative heart rate, shorten the time of diastole and avoid ventricular over-dilation.
The long-term survival of patients after repair of LV rupture varies in different reports.4–5 In this series, the 5 survivors suffered mild to severe cardiac insufficiency during long-term follow-up, and needed chronic inotropic support. The hearts of 2 patients tended to dilate without definite signs of ventricular aneurysm formation, which may have been caused by local myocardial infarction resulting from injury to coronary artery branches during repair of the LV rupture.
This experience confirms that LV rupture after MVR is a rare but lethal complication. Careful removal of the diseased valve, decalcification, and prosthesis selection could minimize its incidence. Immediate diagnosis, rapid institution of CPB, and urgent surgical intervention are crucial to saving the patient’s life.
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REFERENCES
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- Spencer FC, Galloway AC, Colvin SB. Clinical evaluation of the hypothesis that rupture of the left ventricle following mitral valve replacement can be prevented by preservation of the chordae of the mural leaflet. Ann Surg 1985;202:673–80.[Medline]
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- Miller DW Jr, Johnson DD, Ivey TD. Does preservation of the posterior chordae tendineae enhance survival during mitral valve replacement? Ann Thorac Surg 1979;28:22–7.[Abstract]
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ABSTRACT
INTRODUCTION
