Functional tricuspid regurgitation following replacement of the mitral valve.

In this series, the effect of replacement of the mitral valve was examined in 86/900 (9.6%) patients who had developed moderate functional tricuspid regurgitation, secondary to rheumatic mitral valvar disease. These patients were subdivided according to the severity of pulmonary hypertension and impairment of right ventricular function. Forty-six patients presented with severe pulmonary hypertension and 40 patients had moderate pulmonary hypertension (mean main pulmonary arterial pressure: 78 +/- 14 mmHg vs 41 +/- 6 mmHg; P less than 0.05). The latter had more advanced disease, greater impairment of right ventricular function and dilatation of the right heart chambers. Functional tricuspid regurgitation regressed in 38/42 survivors with severe pulmonary hypertension and persisted or progressed significantly in 22/34 survivors with impaired right ventricular function despite successful replacement of the mitral valve. The latter underwent replacement of the tricuspid valve (n = 16) or tricuspid annuloplasty (n = 6), at a mean interval of 44 +/- 4.4 months after replacement of the mitral valve, which resulted in 8/22 (23.5%) early deaths. Functional tricuspid regurgitation is more likely to persist in patients with advanced right ventricular failure. Tricuspid valvar competence should be restored in these patients at initial replacement of the mitral valve.     

Mitral valve replacement in severe pulmonary hypertension. Long-term results

Between 1972 and 1987, 43 patients underwent isolated mitral valve replacement with mean pulmonary arterial pressures greater than 50 mmHg. The valve disease was stenosis in 13 cases, regurgitation in 15 cases and mixed mitral valve disease in 15 cases. Forty-one patients (95 %) had invalidating cardiac failure (Stages III and IV of the NYHA Classification). The hospital mortality was 2.3%. Thirteen patients died during follow-up, 8 of cardiac failure, 3 of sudden death and 2 died of non-cardiac causes. The 8 year actuarial survival was 82 +/- 7% with an average postoperative follow-up of 96 +/- 41 months. No patients were lost to follow-up. Eighty six per cent of survivors (25/29) are asymptomatic or paucisymptomatic. Doppler studies were performed in 22 patients, showing normal prosthetic function in 18 cases and an obstructive prosthesis in 4 cases. Seventeen patients had tricuspid regurgitation showing normal pulmonary artery systolic pressures in 9 cases and less than 55 mmHg in 5 cases. On average, systolic pulmonary artery pressure fell from 88 +/- 11 mmHg before to 33 +/- 9 mmHg after surgery (p = 0.01). These results show that severe pulmonary hypertension is not prohibitive for mitral valve replacement. The long-term results are good with functional improvement and reduction of pulmonary hypertension.     

Persistent pulmonary hypertension after mitral valve surgery: does surgical procedure affect outcome?

BACKGROUND AND AIM OF THE STUDY: Recently published data suggest that prosthesis-patient mismatch is common after mitral valve replacement (MVR), and manifests as persistent pulmonary hypertension. The study aim was to determine the prevalence and severity of pulmonary hypertension after mitral valve surgery, including mitral valve repair, and to determine whether surgery type affects the prevalence of post-operative pulmonary hypertension. METHODS: Matched preoperative and > or =1 year postoperative Doppler estimates of right ventricular systolic pressure (RVSP) were evaluated in a cohort of 179 patients who underwent MVR or repair (33 after bioprosthetic valve replacement, 20 after mechanical valve replacement, 43 after physiological valve repair (predominantly for myxomatous disease), 78 after undersized annuloplasty for functional regurgitation, and five after repair of rheumatic stenosis). RESULTS: Patients undergoing repair of function mitral regurgitation had a lower left ventricular ejection fraction. The postoperative mean transmitral gradient was slightly higher for patients after bioprosthetic valve replacement (6.9 +/- 2.6 mmHg) compared to mechanical valve replacement (5.2 +/- 2.8 mmHg; p = 0.03), physiological repair (5.2 +/- 2.8 mmHg; p = 0.05), or repair of functional regurgitation (5.5 +/- 2.8 mmHg; p = 0.02). Pulmonary hypertension was common (present in 78% of patients before and 64% after surgery), and there were no significant differences between groups in the prevalence of postoperative pulmonary hypertension. The RVSP tended to decrease in all groups, but reached statistical significance only for patients undergoing bioprosthetic replacement (-9 +/- 24 mmHg; p = 0.04), mechanical replacement (-10 +/- 14 mmHg; p = 0.003) or physiological repair (-6 +/- 16 mmHg; p = 0.01). CONCLUSION: Pulmonary hypertension is common before and after mitral valve surgery. Although there were at least trends toward lower pulmonary artery pressures regardless of surgery type, significant decreases were noted only after MVR and physiological repair. A slightly higher postoperative mean transmitral gradient after bioprosthetic valve replacement may have contributed to postoperative pulmonary hypertension. The physiological repair of organic, non-rheumatic mitral regurgitation appears to offer favorable hemodynamics and a relatively low rate of postoperative pulmonary hypertension.     

Effect of Inoue balloon mitral valvotomy on severe pulmonary arterial hypertension in 315 patients with rheumatic mitral stenosis: immediate and long-term results

BACKGROUND AND AIMS OF THE STUDY: Despite advances in surgical techniques, mitral valve surgery in patients with severe pulmonary arterial hypertension (PAH) causes considerable mortality and morbidity. Balloon mitral valvotomy (BMV) is an established alternative to treat high-risk surgical patients with mitral stenosis (MS). The study aims were to evaluate immediate and long-term efficacy of BMV in patients with MS and severe PAH, compared to those with mild/moderate PAH. METHODS: Among 1,125 patients who underwent Inoue BMV, 315 had severe PAH (mean pulmonary artery (PA) pressure > or = 50 mmHg (group I; 79 of these patients had suprasystemic PAH). Results from this group were compared with those of patients with mild/moderate PAH (group II). RESULTS: Group I patients were younger and more symptomatic (mean PA pressure 62 +/- 10.6 mmHg versus 32.6 +/- 8.2 mmHg in group II). Before BMV, mean transmitral gradient (17.8 +/- 6.5 versus 14.4 +/- 5.4 mmHg) and pulmonary capillary wedge pressure (PCWP) (31.6 +/- 6.1 versus 22.8 +/- 6.2 mmHg) were significantly higher, while mitral valve area (MVA) (0.66 +/- 0.2 versus 0.85 +/- 0.2 cm2) was significantly lower in group I. After BMV, PA mean pressure was significantly reduced (34.8 +/- 11.2 and 21.1 +/- 8.4 mmHg), transmitral gradient (8.0 +/- 3.9 and 6.9 +/- 3.2 mmHg) and mean PCWP (12.8 +/- 5.8 and 11.0 +/- 5.1 mmHg) in groups I and II, respectively, with a comparable increase in MVA (1.77 +/- 0.4 and 1.84 +/- 0.5 cm2). Group I patients had worse baseline hemodynamic parameters than group II, but the former had a higher absolute gain in hemodynamic parameters. Residual severe PAH after BMV was seen in 9.8% of patients, with PA pressures normalized in 9.5%. Among 79 patients with suprasystemic PA pressure (mean PA systolic pressure 116.6 +/- 28.2 mmHg), 16.5% normalized their PA pressures and 25.3% had residual severe PAH. At mean follow up of 33 months, 80.4% were in NYHA class I. Mean PA systolic pressure in 161 patients was 39.0 +/- 14.2 mmHg compared with a post-BMV value of 55.0 +/- 16.9 mmHg; thus, a sustained fall in pressure was demonstrated at follow up. CONCLUSION: Inoue BMV is safe and effective in patients with MS and severe PAH. Although these patients have worse clinical and hemodynamic parameters before BMV, they achieve a greater absolute gain in terms of improvement in all hemodynamic parameters.     

Role of closed mitral commissurotomy in mitral stenosis with severe pulmonary hypertension

BACKGROUND AND AIMS OF THE STUDY: Closed mitral commissurotomy (CMC) is a well-established method for treatment of rheumatic mitral stenosis, but outcome in patients with severe pulmonary arterial hypertension (PAH) has not been clearly documented. METHODS: Between April 1996 and October 1999, among 61 patients who underwent CMC, 27 had severe PAH (systolic pressure > 100 mmHg). Of these patients, 11 were in NYHA class III, and 16 were in class IV. Preoperatively, the mean pulmonary artery (PA) pressure was 107.85 +/- 5.74 mmHg (range: 100-118 mmHg), mitral valve area (MVA) 0.704 +/- 0.106 cm2 (range: 0.5-0.91 cm2), and transmitral gradient 11.93 +/- 1.54 mmHg (range: 10-15 mmHg). The echocardiographic mitral valve score was 6.37 +/- 1.11 (range: 6-10). RESULTS: There was no operative mortality or incidence of significant (> or = 2+) post-CMC mitral regurgitation or cerebrovascular accident. The MVA increased to 2.385 +/- 0.248 cm2 (range: 1.9-2.8 cm2), the transmitral gradient fell to 2.44 +/- 0.51 mmHg (range: 2-3 mmHg), and postoperative PA systolic pressure fell to 33.33 +/- 8.20 mmHg (range: 30-60 mmHg). During a mean follow up of 26.9 months (range: 11-51 months), 23 patients were in NYHA class I and four were in class II. There were no significant differences in parameters between sexes, but mean male age was five years less than mean female age. CONCLUSION: In the subset of patients with severe PAH, surgical CMC is a safe and effective procedure that results in greater MVA and a more significant and sustained fall in PA pressure compared with reported series of percutaneous balloon mitral valvuloplasty.     

Long-term surgical prognosis of aortic valve diseases with pulmonary hypertension. Apropos of 34 cases]

Thirty-four patients underwent isolated aortic valve replacement with mean pulmonary artery pressures greater than 40 mmHg between 1972 and 1988. The aortic valve disease was stenotic in 10 cases, regurgitant in 14 cases and mixed in 10 cases. Thirty patients (88%) had invalidating cardiac failure (NYHA Classes III and IV). The mean preoperative ejection fraction was 44 +/- 15%. The hospital mortality was 17.6%. Ten patients died secondarily, five with terminal cardiac failure. The 5 year actuarial survival was 70 +/- 16%; the 10 year survival was 60 +/- 18% with an average follow-up of 115 +/- 61 months. None of the patients was lost to follow-up. Fifteen of the 18 survivors (83%) are asymptomatic or pauci-symptomatic after a follow-up of 126 +/- 62 months. Doppler echocardiography (n = 12) showed normal prosthetic valve function in 11 cases and aortic regurgitation in 1 case. Eight patients had tricuspid regurgitation with pulmonary artery systolic pressures less than 30 mmHg in 6 cases and between 30 and 40 mmHg in 2 cases. Severe pulmonary hypertension is therefore a poor early postoperative prognostic factor in aortic valve replacement surgery due to the associated left ventricular dysfunction. However, the long-term results are satisfactory: clinical improvement is usually related to a reduction of pulmonary hypertension.     

Emergency mitral valve replacement for traumatic mitral insufficiency following balloon mitral valvotomy: an early haemodynamic study

Acute severe mitral insufficiency may occur during percutaneous transvenous balloon mitarl valvotomy. Urgent surgical intervention in the form of mitral valve repair or replacement may be necessary in these patients. The haemodynamic measurements at various stages in these patients were obtained and compared with those of patients undergoing elective mitral valve replacement for chronic mitral regurgitation. Between September 1995 and December 1947, urgent mitral valve replacement was performed in 14 patients out of a total of 1688 patients who underwent balloon mitral valvotomy. Haemodynamic measurements could be obtained in 7 of these patients and they constituted group I. Eight other patients undergoing elective mitral valve replacement during the same period for chronic mitral regurgitation constituted group II. Standard haemodynamic measurements were obtained at the following stages: (1) Baseline- 20-30 min after endotracheal intubation; (2) stage 1- 20-30 min after termination of the cardiopulmonary bypass: (3) stage 2- four hours after the patient was transferred to ICU and (4) stage 3-30 min after extubation. All the patients were suffering from severe pulmonary hypertension. However, the indices of pulmonary artery hypertension such as mean pulmonary artery pressure, pulmonary capillary wedge pressure, pulmonary vascular resistance as well as right ventricular systolic and end-diastolic pressures did not decrease after surgery in group I. In contrast, in group II, there was significant decrease in mean pulmonary artery pressure (p<0.05), pulmonary capillary wedge pressure (p<0.05), right ventricular systolic (p<0.001) and end-diastolic pressures (p<0.05) at stage 1. These changes persisted throughout the study period. Pulmonary vascular resistance showed a decreasing trend, but attained statistical significance at stage 1 only. Two patients died; one of intractable cardiac failure and another from septicaemia and multiple organ failure in group I, but there were no deaths in group II. Reactive pulmonary hypertension secondary to acute mitral regurgitation may not recover immediately following mitral valve replacement and may be responsible for poor outcome in these patients.     

Extreme pulmonary hypertension caused by mitral valve disease. Natural history and results of surgery.

Five hundred and eighty six patients with mitral valve disease were studied with cardiac catheterization between 1961 and 1972; 48 (8.2%) had extreme pulmonary hypertension (resting systolic pulmonary artery pressure of 80 mmHg or above and pulmonary vascular resistance of 10 units or greater) and of these patients, 27 underwent cardiac surgery. The operative mortality for mitral valvotomy was 11 per cent and for mitral valve replacement 56 per cent. The overall mortality was 31 per cent. The risks of operation were increased in those with a long history of cardiac symptoms, those over 50 years of age, and in the presence of associated aortic valve disease. The mean survival for those patients not having operation was only 2.4 plus or minus 0.5 years. The mean follow-up period for those surviving operation has been 5.8 plus or minus 0.6 years, and symptomatic improvement has been good.     

Repair of anomalous origin of left coronary artery from the pulmonary artery

Patients with anomalous origin of the left coronary artery from the pulmonary artery often have mitral valve regurgitation. Although establishing dual coronary circulation is the procedure of choice, there remains controversy as to how the mitral valve is handled. Between April 1999 and August 2005, 8 patients underwent surgical correction at our institution. There were 4 males and 4 females, aged from 9 months to 13 years (mean, 6.4 years). Six patients underwent direct aortic reimplantation and 2 had a Takeuchi procedure. Simultaneous mitral annuloplasty was performed in 7 patients with moderate or severe mitral regurgitation. There were no deaths or postoperative complications. Follow-up ranged from 4 to 80 months (mean, 34 +/- 26 months). Left ventricular function improved significantly from a preoperative fractional shortening of 0.21 +/- 0.09 to 0.35 +/- 0.06. Mitral regurgitation decreased on follow-up in the 7 patients who had mitral annuloplasty. We recommend performing mitral annuloplasty at the time of operation in patients with moderate or severe mitral regurgitation and anomalous origin of the left coronary artery from the pulmonary artery.     

Is dobutamine stress echocardiography predictive of middle and late term outcomes in mitral stenosis patients?

AIM: In mitral stenosis (MS) patients with a poor symptom-echocardiography correlation, dobutamine stress echocardiography (DSE) still does not have a confirmed utility and predictive value. Our aim is to evaluate usefulness of DSE in assessing 2 and 5 years clinical outcomes. METHODS: Forty-four consecutive patients with known MS were submitted, between April 1998 and July 1999, to basal and DSE. Patients were divided in 2 groups: group A if during DSE was reached a mean mitral gradient (MG) = or > 15 mmHg and/or a pulmonary arterial pressure (PAP) = or > 60 mmHg, and group B if MG and/or PAP were respectively lower than 15 and 60 mmHg. Endpoints considered were death, hospitalization for acute pulmonary edema, complications associated with mitral valve disease and mitral valve interventions (percutaneous or surgical). Mean follow-up was 73.6+/-16.6 months. RESULTS: Mean age was 55.2+/-10.5 years; 83.7% were women; NYHA class was I-II-III respectively in 18.6%, 58.1% and 23.3% of the patients; mean mitral valve area was 1.39+/-0.26 cm2; mean MG 8.05+/-2.54 mmHg; PAP 39.3+/-7.9 mmHg. Twenty-five patients met criteria for group A and 18 for group B. The event-free interval (27.9+/-32.1 months in group A vs 53.5+/-25.8 months in group B; P=0.008) and the 2 years event-free survival (40% for group A vs 88.9% for group B; P=0.002) showed significantly different patterns between the 2 groups. The 5 years survival analysis did not reach significance. CONCLUSION: DSE seems to detect MS patients that will have rapid evolution of their valvular disease within 24 months.     

Influence of changes in the pulmonary artery pressure on ventilation requirements in patients undergoing mitral valve replacement

The study was designed to evaluate the influence of changes in pulmonary artery pressure on the ventilation requirements in patients undergoing mitral valve surgery. Thirty patients with mitral valve disease with significant pulmonary arterial hypertension undergoing mitral valve replacement under cardiopulmonary bypass were included in this prospective study. All patients had a pulmonary artery catheter placed after the anaesthetic induction. The minute ventilation was adjusted to achieve an arterial carbon dioxide tension (PaCO2) of 35-40 mm Hg. After a stabilisation period of 15 minutes, the pulmonary artery pressure and the minute volume needed for maintaining a PaCO2 of 35-40 mm Hg in the precardiopulmonary bypass, post-cardiopulmonary bypass and six hours postoperatively were measured after ensuring stable haemodynamics and normothermia. There was a significant decrease in the mean pulmonary artery pressure from pre-cardiopulmonary bypass value of 41.3+/-15 mm Hg to 29.3+/-8 mm Hg in the postcardiopulmonary bypass period and subsequently to 25.5+/-7 mm Hg in the intensive care unit. There was a corresponding increase in the minute volume requirements from a pre-cardiopulmonary bypass value of 6.8+/-1 L/min to 8.0+/-1 L/min in the post cardiopulmonary bypass period and then to 9.4+/-1.2 L/min in the postoperative period. We conclude that there is a significant decrease in the pulmonary blood volume and a subsequent decrease in the pulmonary artery pressure after a successful mitral valve replacement in patients with pulmonary arterial hypertension. This is associated with a significant increase in the requirement of minute ventilation to maintain normocarbia.     

Evidence for rheumatic valve disease in patients with severe tricuspid regurgitation long after mitral valve surgery: the role of 3D echo reconstruction

BACKGROUND AND AIM OF THE STUDY: Although severe tricuspid regurgitation (TR) is a well-recognized, long-term complication of rheumatic mitral valve replacement that impairs the functional results of surgery, its exact basis remains unclear and its management is unsatisfactory. The study aim was to obtain a detailed assessment of tricuspid valve morphology and function using 2D transesophageal echocardiography (TEE) with 3D reconstruction, and to determine long-term clinical outcome in patients after surgery for rheumatic mitral valve disease. METHODS: A total of 42 patients (mean age 50 +/- 10 years) was followed up; 39 patients had mitral replacement and three had valvotomy. Thirty patients had developed impaired exercise tolerance, fluid retention and echocardiographic evidence of severe TR at 8.2 +/- 2.6 years after surgery; the remainder had mild regurgitation. RESULTS: Follow up showed greater mortality in the severe TR group, with approximately 50% survival at 60 months after diagnosis compared with mild TR. None of the patients with severe TR had a dysfunctional mitral prosthesis. In these patients, transthoracic echo-Doppler showed enlarged right atrium and right ventricle, a mean transtricuspid retrograde pressure drop of 15 +/- 4 mmHg and apparently normal leaflet anatomy. Twenty patients (15 with severe TR) underwent a TEE and 3D reconstruction study for further evaluation. Abnormal leaflet anatomy was demonstrated in all patients with severe TR, with restricted leaflet motion in 10, leaflet shortening and thickening in the remainder, and dilatation of tricuspid valve annular insertion suggestive of rheumatic involvement. Although diastolic transtricuspid velocities were increased (peak flow 0.8 +/- 0.1 m/s) in these patients due to increased stroke volume, significant tricuspid stenosis was present in only two cases (mean gradient 4 and 3 mmHg respectively). Histopathology confirmed the presence of leaflet vascularization and extensive fibrosis in two patients who underwent tricuspid valve replacement. CONCLUSION: Rheumatic leaflet involvement contributes to severe TR occurring long after mitral valve replacement, though overt stenosis is uncommon. Knowledge of the structural basis of this condition may thus improve its long-term management, possibly with early tricuspid valve repair.     

Chordal rupture. II: comparison between repair and replacement

During the period 1970-81, 183 patients underwent mitral valve surgery for chordal rupture. Of these, 82 (45%) patients were treated by mitral valve repair and 101 (55%) by mitral valve replacement. Mean age at surgery was 57 years. The early mortality was nine of 183 (4.9%) patients, of whom five had undergone replacement and four repair. During the follow up period (mean 3.6 years, range 0.8-12.2 years) a further 27 patients died; 23 of these had undergone mitral valve replacement and four mitral valve repair. Cerebrovascular events accounted for 35% of the deaths after mitral valve replacement and none of those after mitral valve repair. In 11 patients repair was technically unsatisfactory, and mitral valve replacement was undertaken at the same operation; a further five patients required late replacement (mean 1.4 years) for pronounced mitral regurgitation. Actuarial curves predict a six year survival of 68 +/- 5.7% (mean +/- SD) for all patients after mitral valve replacement compared with 88 +/- 6.9% (mean +/- SD) after repair (p less than 0.01). Actuarial survival curves favour mitral valve repair as the procedure choice for chordal rupture, and in isolated posterior cusp repair breakdown of the repair is a rare occurrence.     

Mitral valve replacement in children with a Bj?rk-Shiley prosthesis

This report documents our experience with mitral valve replacement in children. Between 1978 and 1982, 30 replacements have been performed in patients under 15 years of age. Twenty seven patients (90%) with rheumatic heart disease and 3 (10%) had congenital disease. Their functional capacity prior to operation was as follows: Nine patients fell into class II, 18 into class III and 2 into class IV. Preoperative cardiac catheterization, was undertaken in 26 patients, the mean pulmonary arterial wedge pressure was 27.4 +/- 8 mmHg, the pulmonary artery mean pressure was 48 +/- 20 mmHg, the left ventricular end diastolic pressure was 11.7 +/- 5.6 mmHg. One child died in the operative period. Twenty six patients (90%) have been followed for a mean period of 22.7 months. Late mortality occurred in three patients (11%). Bacterial endocarditis, thromboembolism and valve maldisfunction were not present. The post operative NYHA functional class was as follows: twenty two children fell into class I, and one patient fell into class II. The actuarial survival rate 5 years after operation was 79%. We believe that the Bj?rk-Shiley prosthesis offer excellent results in children when repair of the natural valve is not possible.     

Functional tricuspid insufficiency: conservative or operative management

Between 1978 and 1982 mitral valve replacement was performed in a total of 43 patients with mitral valve disease in the presence of functional tricuspid insufficiency (TI). The concomitant tricuspid valve regurgitation was treated conservatively in 17 patients, a Carpentier ring prosthesis was implanted in 9 patients. De Vega annuloplasty was performed in 13 patients and 4 times the valve was replaced with a Hancock bioprosthesis. The hospital mortality of 26% (11 patients) was high, due to the poor clinical condition of the patients. In a mean follow-up of 43.1 +/- 18,0 months, 20 patients could be restudied by clinical and echocardiographical investigation. Tricuspid insufficiency was found in all of the 9 patients who had been treated conservatively. Seven out of 11 patients operated showed no signs of TI, 3 had mild TI and 1 patient had severe TI. In the conservatively treated group, the preoperative mean pulmonary vascular resistance (PVR = 296 +/- 161 dynes x sex x cm-5), pulmonary artery pressure (PAP = 46.1 +/- 16.2 mmHg) and rise of right atrial V-wave (15.8 +/- 3.6 mmHg) were only slightly higher than n the operatively treated group (PVR - 274 +/- 146 dynes x sex x cm-5), PAP = 43.2 +/- 13.6 mmHg, V-wave = 18.5 +/- 6.4 mmHg) with no statistically significant difference. Preoperative hemodynamic findings in patients with and without TI a follow-up were also not significantly different. These results indicate that the recurrence of functional TI depends on the method of treatment, rather than preoperative increased PVR, PAP or V-wave rise.     

Chordal rupture. II: comparison between repair and replacement.

During the period 1970-81, 183 patients underwent mitral valve surgery for chordal rupture. Of these, 82 (45%) patients were treated by mitral valve repair and 101 (55%) by mitral valve replacement. Mean age at surgery was 57 years. The early mortality was nine of 183 (4.9%) patients, of whom five had undergone replacement and four repair. During the follow up period (mean 3.6 years, range 0.8-12.2 years) a further 27 patients died; 23 of these had undergone mitral valve replacement and four mitral valve repair. Cerebrovascular events accounted for 35% of the deaths after mitral valve replacement and none of those after mitral valve repair. In 11 patients repair was technically unsatisfactory, and mitral valve replacement was undertaken at the same operation; a further five patients required late replacement (mean 1.4 years) for pronounced mitral regurgitation. Actuarial curves predict a six year survival of 68 +/- 5.7% (mean +/- SD) for all patients after mitral valve replacement compared with 88 +/- 6.9% (mean +/- SD) after repair (p less than 0.01). Actuarial survival curves favour mitral valve repair as the procedure choice for chordal rupture, and in isolated posterior cusp repair breakdown of the repair is a rare occurrence.     

Influence of valve replacement on plasma endothelin-1 level in mitral stenosis

BACKGROUND AND AIM OF THE STUDY: The rise of pressure in the pulmonary circulation during the course of mitral stenosis leads to pathomorphological changes and a reduction in vascular compliance. Endothelial dysfunction is also promoted, with increased expression of endothelin. This aim of this study was to evaluate whether the increase in endothelin-1 levels in pulmonary hypertension due to advanced mitral stenosis is reversible after valve replacement. METHODS: Thirty-nine patients with isolated, longlasting post-rheumatic mitral stenosis were enrolled. During preoperative Swan-Ganz catheterization blood samples were withdrawn from the pulmonary artery and capillaries for measurement of endothelin-1 (ET-1). Similar examinations were performed six months after mitral valve replacement. Hemodynamic parameters were measured also during 25-W exercise effort. RESULTS: The mean preoperative hemodynamic parameters of the pulmonary circulation were moderately increased. Mean plasma levels of ET-1 were about three-fold higher than normal. Capillary levels of ET-1 were significantly higher than those in the pulmonary artery (1.78+/-1.22 versus 1.03+/-1.16 pg/ml, p <0.05). There was no significant correlation between ET-1 level and any hemodynamic or clinical parameters, except NYHA functional class. After surgery, pulmonary capillary levels of ET-1 fell significantly, but were still high (1.78+/-1.22 versus 1.41+/-1.00 pg/ml); ET-1 levels in the pulmonary artery were unchanged. Patients with persistently high ET-1 levels had significantly worse exercise hemodynamic parameters, especially of pulmonary arterial compliance. CONCLUSION: In patients with long-lasting, severe mitral stenosis, ET-1 levels remained increased and the ET-1 concentration gradient across the pulmonary circulation persisted for six months after valve replacement. High ET-1 capillary levels are correlated with poor exercise tolerance and poor exercise compliance of the pulmonary vessels.     

Late results of combined mitral valve replacement and coronary bypass surgery

The incremental risk of coronary bypass surgery was analyzed in 718 patients undergoing mitral valve replacement between 1971 and 1983. Ninety-eight patients (14%) had significant coronary artery disease requiring coronary bypass surgery. In 70 of these patients, the origin of the mitral valve disease was nonischemic, whereas 28 patients had ischemic mitral regurgitation unsuitable for conservative valve surgery. There were six operative deaths (9%) and four perioperative myocardial infarctions (6%) after mitral valve replacement and coronary bypass surgery for nonischemic mitral valve disease. Operative mortality was related to low output cardiac failure before operation or perioperative myocardial infarction. Actuarial curves predict survival (+/- standard error) of 55 +/- 7% at 5 years and 43 +/- 8% at 10 years. Preoperative functional class was the only significant predictor of long-term survival in this group (p less than 0.05). The actuarial survival of the 620 patients without coronary artery disease who underwent mitral valve replacement alone was 63 +/- 3% at 10 years. This was significantly better than that of the 70 patients who underwent mitral valve replacement and coronary bypass surgery for nonischemic mitral valve disease (p less than 0.001). Conversely, 5 year survival of the 28 patients with ischemic mitral regurgitation was 43 +/- 10%. This confirms the negative detrimental effect of an ischemic origin of mitral valve disease on survival after mitral valve replacement and coronary bypass surgery (p less than 0.0001).     

Ventricular septal defect with congenital mitral valve disease: long-term results of corrective surgery

BACKGROUND: A retrospective analysis of the mortality, morbidity and long-term follow-up of patients undergoing corrective surgery for ventricular septal defect and congenital mitral valve disease is presented. METHODS AND RESULTS: Between January 1991 and December 2000, 69 consecutive patients aged 2 months to 45 years (median 18 months) underwent repair of ventricular septal defect and associated mitral valve disease. In 52 patients (75%), the ventricular septal defects were located in the perimembranous and subarterial area. Forty-six patients had congenital mitral incompetence and 23 had congenital mitral stenosis. The ventricular septal defect was repaired through the right atrium in all. Sixty-five patients underwent reconstruction of the mitral valve and 4 underwent primary mitral valve replacement. Another 4 patients underwent mitral valve replacement after a failed repair. Associated procedures included: patent ductus arteriosus ligation (n=12), aortic valve replacement (n=6), coarctation repair (n=13), interrupted aortic arch repair (n=1), atrial septal defect closure (n=17) and Takeuchi repair (n=1). There were 6 early deaths (8.6%). Three deaths were due to pulmonary arterial hypertensive crisis and one due to residual mitral stenosis. One death was due to intractable congestive heart failure. Another patient died due to persistent low cardiac output. Follow-up ranged from 6 months to 120 months (mean 64.4+/-33.6 months). Reoperation was required in 22 patients, mainly for recurrent/residual mitral valve dysfunction or hemodynamically significant left ventricular outflow tract obstruction. There were 4 late deaths, 2 due to residual mitral stenosis and the other 2 as a result of a thrombosed prosthetic valve. At 10 years, the actuarial survival rate was 850+/-5.0%, and freedom from reoperation was 45%+/-10.0%. CONCLUSIONS: Reconstruction of the mitral valve along with closure of VSD is possible in most cases. However, careful follow-up is recommended to detect changes in the mitral valve status over a course of time.     

Five years of experience with mitral valve homografts

INTRODUCTION: The main advantages of mitral homografts are preservation of the subvalvular apparatus and avoidance of life-long anticoagulation. In this communication, we will present our five-year experience using mitral homografts in mitral valve surgery. PATIENTS AND METHODS: Since 1996, 14 patients (mean age 46 +/- 8 years, range 27 - 65 years have had mitral homografts implanted. Thirteen patients had mitral valve replacement; the septal leaflet of the tricuspid valve was replaced in one case. The indications were mitral (n = 6) or tricuspid endocarditis (n = 1), mitral valve stenosis (n = 3), and combined mitral valve disease (n = 4). Complete mitral homografts were implanted in eight patients; partial homografts were used in six cases. Preoperatively, the dimensions of the left ventricle and the mitral valve were measured by transoesophageal echocardiography (TOE). The mean left ventricular ejection fraction was 56 +/- 9%, the mean end-diastolic diameter 58 +/- 6 mm. The technique described by Acar/Carpentier was adapted for implantation; a Carpentier ring was implanted in all cases for annular stabilization. The patients had anticoagulative therapy which was discontinued when stable sinus rhythm was present after three months postoperatively. Follow-up included clinical examination, ECG, and echocardiography, and was initiated six months postoperatively and continued on a yearly basis. The following parameters were determined by echocardiography--left atrial size, left ventricular end-diastolic and end-systolic diameter, pressure gradient across the mitral valve (c/w Doppler, Bernoulli's equation), and mitral regurgitation. RESULTS: All patients survived surgery; the mean operation-time was 281 +/- 37 minutes. Intraoperative TOE revealed a first degree insufficiency in 7 patients. Follow-up was completed in all patients, with a mean period of 30 months (6 - 60 months). Two patients had an acute endocarditis two years postoperatively, requiring repeat valve replacement with a mechanical prosthesis. An additional patient had to be reoperated due to chordal rupture three years postoperatively. All three patients had mitral valve stenosis as the initial indication for surgery and had received a complete homograft. In the remaining eleven patients, the morphological and functional state of the implanted grafts remained unchanged during follow-up. The freedom from valve-related events was 93% after one year, 86% after two years, and 79% after three years. At six-month follow-up, ECG and echocardiography revealed sinus rhythm and sufficient atrial contractions in 13 cases. At the last follow-up, the pressure gradients were 3.4 +/- 0.6 mmHg for complete homografts and 2.8 +/- 0.6 mmHg for partial homografts. In five cases, a mild insufficiency was documented, while six patients presented with competent grafts. CONCLUSIONS: Mitral homografts can be used with acceptable mid-term results in selected cases with good left ventricular function and only slightly dilated left ventricles. Partial mitral homografts represent an additional technique, especially for mitral valve repair in patients with acute endocarditis. The susceptibility to bacterial infections of a homograft makes strict prophylaxis against endocarditis mandatory.