Left ventricular rupture following mitral valve replacement

During a 10-year period, we have encountered 6 patients (mean age, 61.2 years) with left ventricular rupture following mitral valve replacement, with an overall incidence of 1.8 percent. Four patients had early rupture, one had delayed rupture, and one had late rupture with a false aneurysm formation. Among four patients with early rupture, there were two patients with external repair by using a large ventricular patch and two patients with internal and the external repair by removing the prosthetic valve and patching both the inside and outside of the ventricle. In a patient with delayed rupture, bleeding from an epicardial hematoma was recognized along the atrioventricular groove in the intensive care unit. It was possible to control bleeding by packing the gauze, hemostatic cellulose [Surgical], and fibrin glue. Late rupture was recognized as a false aneurysm; however, there were no clinical symptoms. All patients survived the surgery, but two patients with early rupture subsequently died. One of these died of renal failure and the other died of multiple organ failure. The sites of rupture in all patients were in accordance with type 1 rupture (Treasure's classification); however, an autopsy review demonstrated the initial laceration in one case was recognized in the membranous septum 5 mm below the mitral ring and extended to the posterior atrioventricular groove. These findings suggest that the injury in the anterior mitral annulus could lead to type 1 rupture, although in the posterior mitral annulus more commonly. Since 1987, we have preserved the posterior leaflet with attached chordae when the mitral valve was fragile and myxomatous. As a result, no instances of left ventricular rupture were encountered.     

Left ventricular rupture following mitral valve replacement

Rupture of the posterior wall of the left ventricle is an unusual but often lethal complication following mitral valve replacement. The incidence is about 1% of MVRs. Most of the ruptures are attributed either to technical maneuvers in the operation or to stretch injury produced by removal of the mural leaflet of the mitral valve. Surgical repair of the rupture requires the cardiopulmonary bypass, and it seems to be suited that we select extracardiac approach to type 2 or 3 rupture and intracardiac approach to type 1 rupture. Preventive measures include the modifications in operative techniques, reduction of pre and afterload of the left ventricle, and retention of posterior mitral leaflet.     

Left ventricular false aneurysm complicating mitral valve repair

Left ventricular false aneurysm is a rare complication of mitral valve replacement or myocardial infarction. A case of left ventricular false aneurysm complicating mitral valve repair is presented. The patient was clinically asymptomatic, and the diagnosis was made on postoperative transesophageal echocardiography. The patient subsequently underwent successful mitral valve replacement and false aneurysm repair.     

Left ventricular outflow tract obstruction due to a left ventricular myxoma: a case report and review of the literature

A 17-year-old-man who presented with syncope, had a left ventricular (LV) myxoma causing left ventricular outflow tract obstruction. The tumor was removed through left ventriculotomy using conventional cardiopulmonary bypass with good result. There have been 47 cases of LV myxoma reported in the world literature since 1957. Most of them are symptomatic (92.7%). Systemic embolism is the most common manifestation (50%) and often leads to death. The surgical removal should be performed urgently. Resection of the mass with limited normal tissue surrounding its pedicle is recommended. There are only three recurrences and five operative deaths.     

Improvement in mitral regurgitation after aortic valve replacement

This study sought to determine whether there is a quantitative improvement in mitral regurgitation (MR) after aortic valve replacement (AVR) for aortic stenosis (AS) and, if so, the mechanisms for this change. MR frequently accompanies AS. The addition of mitral valve replacement to AVR significantly increases the risk of surgery. Although previous studies have suggested a qualitative improvement in MR severity after AVR, semiquantitative analysis of this improvement has not been documented nor have the underlying mechanisms been examined. We evaluated 28 patients who had undergone 2-dimensional echo and color flow Doppler imaging an average of 1.5 +/- 2.5 months before and 2.5 +/- 4.2 months after AVR. Maximum MR area, MR percentage (MR area/left atrial area), mitral annular area, left atrial area, aortic gradient, and parameters of left ventricular geometry were measured to evaluate MR severity and to assess functional mechanisms for improvement in MR. There was a significant decrease in MR area (5.5 +/- 2.8 cm2 vs 2.5 +/- 1.9 cm2, p < or =0.0001) and MR percentage (25 +/- 11% vs 12 +/- 10% after operation, p < or =0.0001) between preoperative and postoperative studies. There was a significant reduction in aortic gradient, mitral annular area, left atrial area, and left ventricular length postoperatively. In univariate analysis, MR improvement was related to the lower preoperative left ventricular fractional area change (p = 0.027) and to the changes in fractional area change (p = 0.001) and left ventricular systolic area (p = 0.001). Thus, improvement in MR after AVR is related to changes in left ventricular function postoperatively. These data suggest that reduction in MR is due not only to decreased intraventricular pressure, but also to changes in ventricular morphology.     

Comparative evaluation of left ventricular performance after mitral valve repair or valve replacement with or without chordal preservation

Germinating barley produces two alpha-amylase isozymes, AMY1 and AMY2, having 80% amino acid (aa) sequence identity and differing with respect to a number of functional properties. Recombinant AMY1 (re-AMY1) and AMY2 (re-AMY2) are produced in yeast, but whereas all re-AMY1 is secreted, re-AMY2 accumulates within the cell and only traces are secreted. Expression of AMY1::AMY2 hybrid cDNAs may provide a means of understanding the difference in secretion efficiency between the two isozymes. Here, the efficient homologous recombination system of the yeast, Saccharomyces cerevisiae, was used to generate hybrids of barley AMY with the N-terminal portion derived from AMY1, including the signal peptide (SP), and the C-terminal portion from AMY2. Hybrid cDNAs were thus generated that encode either the SP alone, or the SP followed by the N-terminal 21, 26, 53, 67 or 90 aa from AMY1 and the complementary C-terminal sequences from AMY2. Larger amounts of re-AMY are secreted by hybrids containing, in addition to the SP, 53 or more aa of AMY1. In contrast, only traces of re-AMY are secreted for hybrids having 26 or fewer aa of AMY1. In this case, re-AMY hybrid accumulates intracellularly. Transformants secreting hybrid enzymes also accumulated some re-AMY within the cell. The AMY1 SP, therefore, does not ensure re-AMY2 secretion and a certain portion of the N-terminal sequence of AMY1 is required for secretion of a re-AMY1::AMY2 hybrid.     

Dynamic left intraventricular obstruction after reconstructive mitral valve surgery

To investigate the effect of pioglitazone, a thiazolidinedione oral antidiabetic agent, on the glucose and insulin metabolism in insulin resistance, a perfusion study of the liver and hindquarter was performed in high-fructose-fed rats. Male Wistar albino rats were assigned randomly to one of the following diets for 2 weeks: (1) normal chow (control group), (2) a diet high in fructose (fructose group), or (3) a high-fructose diet plus pioglitazone (pioglitazone intake of approximately 10 mg/kg body weight; pioglitazone group). The elevated levels of plasma insulin, triglyceride, and free fatty acids (FFA) in the fructose group were normalized by pioglitazone administration. In the perfused liver, the glucagon-induced increment in the glucose output of the fructose (57.1+/-9.1 micromol/g liver/20 min) and pioglitazone (44.7+/-10.1 micromol/g liver/20 min) groups was significantly (P < .01) higher than that in the control group (27.6+/-5.7 micromol/g liver/20 min). The level in the pioglitazone group was significantly (P < .05) lower than that in the fructose group. In the presence of 100 or 500 microU/mL insulin, the insulin-mediated decrement in the glucagon-induced glucose output of the fructose group (29.8+/-7.8 or 38.9+/-9.3 micromol/g liver/20 min) was significantly (P < .05) lower than that in the control (45.8+/-14.2 or 54.5+/-8.5 micromol/g liver/20 min) and pioglitazone (44.4+/-9.2 or 56.2+/-10.8 micromol/g liver/20 min) groups, respectively. In the perfused hindquarter, glucose uptake in the fructose group (8.2+/-2.0 micromol/g muscle/30 min) was significantly (P < .05) lower than that in the control (12.1+/-2.3 micromol/g muscle/30 min) and pioglitazone (11.8+/-3.1 micromol/g muscle/30 min) groups. In the presence of 100 or 500 microU/mL insulin, glucose uptake in the fructose group (12.0+/-5.2 or 17.4+/-3.0 micromol/g muscle/30 min) was significantly (P < .05) lower than that in the control (20.2+/-2.4 or 23.0+/-3.1 micromol/g muscle/30 min) and pioglitazone (17.8+/-2.4 or 20.7+/-2.0 micromol/g muscle/30 min) groups, respectively. Insulin uptake by the liver and hindquarter was not significantly different in the control, fructose, and pioglitazone groups. These results indicate that pioglitazone improves the increased glucagon-induced hepatic glucose output and decreases insulin-induced muscular glucose uptake without altering insulin uptake in high-fructose-fed insulin-resistant rats.     

Left ventricular volume reduction for end-stage heart failure: intrapapillary or extrapapillary resection, mitral valve repair or replacement?

We report on two patients with end-stage dilated cardiomyopathy and functional mitral valve insufficiency who underwent left ventricular volume reduction. Intrapapillary resection and correction of the mitral valve regurgitation produced inadequate reduction of the ventricular cavity and resulted in inability to wean the patients from cardiopulmonary bypass. Following extension of the resection to include the papillary muscles and mitral valve replacement, there was a significant improvement in cardiac function. Both patients survived surgery; subsequent echocardiography provided evidence of improved myocardial function and NYHA functional class.     

Echocardiography after mitral valve replacement and criteria of paraprosthetic regurgitation

19 patients with Bj?rk-Shiley mitral tilting disc valve prostheses were studied by echocardiography before the valve replacement operation and postoperatively every three months up to one year. In 14 patients with normal prosthetic function the left atrial diameter decreased markedly after operation (p less than 0.001), but echocardiographic dimensional indices of left ventricular performance remained unchanged. Paradoxical or markedly hypokinetic motion of the interventricular septum was observed within 3 months of operation in 46% of the patients, but in only 28% in studies performed 9 - 12 months after the replacement. The ampliture of the disc was on average 11 +/- 2 mm. In 5 patients with paraprosthetic regurgitation the left atrial diameter increased with the development of regurgitation and decreased again after successful reoperation. In these patients the left ventricular end diastolic and stroke volumes were great (p less than o.01) than in patients with normal prostheses. The septal motion was in the normal direction in all these 5 patients and the septal amplitudes were greater (p less than 0.01) than in the patients with normal prostheses. The amplitudes of the disc were normal, but abnormal anterior movement of the disc at the beginning of the diastole was observed. These data demonstrate that echocardiography is useful in the diagnosis of paraprosthetic mitral valve regurgitation.     

Left ventricular outflow obstruction as a result of external cardiac compression by a mediastinal tumor

A case of left ventricular outflow tract stenosis resulted from compression of the heart is presented. This symptomatic cardiovascular lesion was produced by extensive growth of mediastinal tumour. Numerous noninvasive methods were necessary to establish this difficult diagnosis. The patient underwent surgery that disclosed a benign process (of neurofibroma). After tumour's resection marked hemodynamic signs subsided.     

Pulmonary valve atresia with ventricular septum defect: interventional recanalization of the right ventricular outflow tract]

A case of pulmonary atresia with ventricular septal defect is reported where continuity between the right ventricle and the hypoplastic pulmonary artery was established interventionally. The atretic valve was perforated using a special "perforation needle" with a sharp and stiff distal and a flexible proximal part. Perforation of the bifurcation was well tolerated without later sequelae. After perforation of the atresia, dilation was successfully performed using 2, 4, and 7.2 mm balloons with a pressure of 10 atm; the arterial oxygen saturation increased from 72% to 84%. Four weeks later repeated "valvuloplasty" was performed (balloon diameters 8 mm, 9.5 mm, and 12 mm) and the "valve" ring was dilated to a diameter of 10.5 mm. Although no general conclusions can be drawn from this single application, mechanical perforation of the atresia could become an attractive interventional approach for the treatment of pulmonary atresia.     

Effects of valve replacement on ventricular mechanics in mitral regurgitation and aortic stenosis

BACKGROUND: This study in humans assessed changes in left ventricular function early and late after correction of mitral regurgitation (MR) (n = 9) or aortic stenosis (AS) (n = 10). METHODS: Ventricular function was measured with radionuclide and micromanometer-derived pressure-volume loops during preload manipulation, thermodilution cardiac outputs, and echocardiograms. Late radionuclide and echocardiographic data were acquired at 24 hours and 20 months. RESULTS: Perioperative left ventricular performance (stroke work-end-diastolic volume relationship) did not change for patients with MR or AS. Significant changes in afterload occurred: ejection fraction (MR, 0.49 to 0.37; AS, 0.54 to 0.60; both, p = 0.013), mean left ventricular ejection pressure (MR, 73 to 91 mm Hg; AS, 138 to 93 mm Hg; both, p < 0.01), and end-systolic wall stress (MR, 26 to 42 x 10(3) dynes/cm2; AS, 37 to 22 x 10(3) dynes/cm2; both, p < 0.01). Ejection efficiency improved for MR patients (0.69 +/- 0.26 to 1.0 +/- 0.15; p < 0.05). The 20-month data showed improved New York Heart Association functional class, normal resting ejection fraction, and normal exercise response for both groups. CONCLUSIONS: Early after operation, a significant change in left ventricular load was seen with correction of MR and AS. Data obtained late after operation showed improvement consistent with ventricular remodeling.     

Mitral valve anomalies obstructing left ventricular outflow

This paper reports on two cases of more uncommon types of subaortic stenosis. A 2-year-old boy was found with accessory mitral valve leaflet (AMVL) attaching to the anterior leaflet, ballooning into the subaortic ventricular septum associated with a discrete subaortic membrane. The obstruction was successfully relieved by removal of the AMVL and resection of the membrane. A 19-day-old newborn with accessory tissue on the mitral valve (AMVT) causing subaortic stenosis, subaortic ventricular septal defect (VSD) and patent ductus arteriosus was operated on successfully. Accessory tissue excision through the VSD, VSD patch closure and ductus ligation were performed.     

Successful surgical repair of left atrial dissection after mitral valve replacement

A rare case of left atrial dissection after mitral valve replacement is reported. Low output syndrome developed in the immediate postoperative period. Cardiac catheterization showed marked elevation of the pulmonary wedge pressure, and left ventriculography revealed massive paraprosthetic leakage with left atrial dissection. At the reoperation, the dissecting cavity was successfully closed from inside the left atrium under cardiopulmonary bypass. We consider this complication another variation of an atrioventricular discontinuity after mitral valve replacement.     

Stress-induced left ventricular outflow tract obstruction: a potential cause of dyspnea in the elderly

OBJECTIVES: We sought to identify the pattern of disturbed left ventricular physiology associated with symptom development in elderly patients with effort-induced breathlessness. BACKGROUND: Limitation of exercise tolerance by dyspnea is common in the elderly and has been ascribed to diastolic dysfunction when left ventricular cavity size and systolic function appear normal. METHODS: Dobutamine stress echocardiography was used in 30 patients (mean [+/-SD] age 70 +/- 12 years; 21 women, 9 men) with exertional dyspnea and negative exercise test results, and the values were compared with those in 15 control subjects. RESULTS: Before stress, left ventricular end-diastolic and end-systolic dimensions were reduced, fractional shortening was increased, and the basal septum was thickened (2.3 +/- 0.5 vs. 1.4 +/- 0.2 cm, p < 0.001, vs. control subjects) in the patients, but posterior wall thickness did not differ from that in control subjects. Left ventricular outflow tract diameter, measured as systolic mitral leaflet septal distance, was significantly reduced (13 +/- 4.5 vs. 18 +/- 2 mm, p < 0.001). Isovolumetric relaxation time was prolonged, and peak left ventricular minor axis lengthening rate was reduced (8.1 +/- 3.5 vs. 10.4 +/- 2.6 cm/s, p < 0.05), suggesting diastolic dysfunction. Transmitral velocities and the E/A ratio did not differ significantly. At peak stress, heart rate increased from 66 +/- 8 to 115 +/- 20 beats/min in the control subjects, but blood pressure did not change. Transmitral A wave velocity increased, but the E/A ratio did not change. Left ventricular outflow tract velocity increased from 0.8 +/- 0.1 to 2.0 +/- 0.2 m/s, and mitral leaflet septal distance decreased from 18 +/- 2 to 14 +/- 3 mm, p < 0.001. In the patients, heart rate rose from 80 +/- 12 to 132 +/- 26 beats/min and systolic blood pressure from 143 +/- 22 to 170 +/- 14 mm Hg (p < 0.001 for each), but left ventricular dimensions did not change. Peak left ventricular outflow tract velocity increased from 1.5 +/- 0.5 m/s (at rest) to 4.2 +/- 1.2 m/s; mitral leaflet septal distance fell from 13 +/- 4.5 to 2.2 +/- 1.9 mm (p < 0.001); and systolic anterior motion of mitral valve appeared in 24 patients (80%) but in none of the control subjects (p < 0.001). Measurements of diastolic function did not change. All patients developed dyspnea at peak stress, but none developed a new wall motion abnormality or mitral regurgitation. CONCLUSIONS: Although our patients fulfilled the criteria for "diastolic heart failure," diastolic dysfunction was not aggravated by pharmacologic stress. Instead, high velocities appeared in the left ventricular outflow tract and were associated with basal septal hypertrophy and systolic anterior motion of the mitral valve. Their appearance correlated closely with the development of symptoms, suggesting a potential causative link.