[A new possibility to evaluate ultrasonic curves in combined mitral valve insufficiency, mitral valve stenoses and implanted mitral valve prostheses].
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Mitral valve repair (MVR) is the golden standard for the surgical treatment of mitral valve regurgitation and is superior to mitral valve replacement in terms of perioperative and long-term morbidity and mortality. However, the underlying disease has a significant impact on the functional long-term result of the repair. To evaluate the results of MVR, patients have to be divided by the underlying disease, degenerative mitral valve regurgitation, rheumatic mitral valve regurgitation, ischemic mitral valve regurgitation, and mitral valve regurgitation due to advanced cardiomyopathy. The best functional result for MVR can be achieved for degenerative mitral valve regurgitation (10-year freedom from reoperation for recurrent mitral regurgitation up to 94%) followed by patients with rheumatic mitral valve regurgitation (10-year freedom from reoperation for recurrent mitral regurgitation up to 82%). The progress in the underlying disease of the mitral valve is responsible for recurrent mitral valve regurgitation in these patients. For both underlying disease the 10-year survival rate is > 75%. For patients with ischemic mitral valve regurgitation the functional and survival rates are worse with a 5-year survival rate < 60% and recurrent mitral valve regurgitation > MI (mitral valve insufficiency) II degrees in 28% of patients within 6 months. However, ischemic mitral valve regurgitation is not a disease of the valve, it is a disease of the myocardium; thus, the myocardium is the key factor influencing the functional results of MVR and not pathologic changes in the mitral valve per se. There are no long-term results on patients operated on MI in conjunction with advanced cardiomyopathy; however, the initial mid-term results are encouraging with improved survival. Besides the underlying disease the timing of surgery is of utmost importance for the long-term survival; patients with preoperative NYHA functional class III/IV have a significantly worse short-term and long-term outcome compared to patients operated on for significant mitral valve regurgitation who have only minor or even no symptoms (NYHA class I/II). However, the compliance to undergo complex open-heart surgery via a median sternotomy in asymptomatic patients is very low. Minimally invasive endoscopic mitral valve repair may be an option to increase compliance in these patients, which will result in improved long-term survival with a normal life expectancy.
A 33-year-old man was admitted because of jaundice. Five months ago a reconstruction of the mitral valve was performed because of mitral valve insufficiency. There was a history of heroin dependence until three years ago. Laboratory tests showed normochromic normocytic anemia, increased nonconjugated serum bilirubin, decreased plasma haptoglobin, hemoglobinuria and hemosiderinuria. The peripheral blood smear contained numerous fragmented red cells, and the bone marrow showed a markedly increased erythropoiesis and absent iron stores. The clinical examination as well as echocardiography revealed severe mitral valve insufficiency; therefore, a mitral valve replacement was performed. Introperatively the mitral valve showed ruptured chordae tendineae of the posterior leaflet and a leaking stitch of the anterior leaflet. We diagnosed a macrovascular hemolytic anemia with subsequent mechanical injury and fragmentation of red cells on a dysfunctioning mitral valve.
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Eighteen patients underwent surgery for traumatic mitral regurgitation following percutaneous mitral valvuloplasty (PMV). Three patients required emergency surgery (delay less than 6 hours). In the remaining cases, the operation was performed one week after PMW (n = 11) or delayed for up to 3 months (n = 4). The operative findings were: ruptured papillary muscle (n = 1); torn anterior leaflets (n = 4), torn posterior leaflet (n = 1), anterior paracommissural tear (n = 3), posterior paracommissural tear (n = 9). Associated lesions included left atrial thrombosis (n = 2) and greater than 1 cm atrial septal defect (n = 4). Conservative mitral valve surgery was possible in over half the cases (n = 10), including two extensive tears of the anterior leaflet. The other patients required mitral valve replacement (n = 8). There were no postoperative complications in any of the patients.
BACKGROUND: Mitral valve repair is considered the gold standard in surgery of degenerative mitral valve insufficiency (MVI), but the long-term results (>20 years) are unknown. METHODS AND RESULTS: We reviewed the first 162 consecutive patients who underwent mitral valve repair between 1970 and 1984 for MVI due to nonrheumatic disease. The cause of MVI was degenerative in 146 patients (90%) and bacterial endocarditis in 16 patients (10%). MVI was isolated or, in 18 cases, associated with tricuspid insufficiency. The mean age of the 162 patients (104 men and 58 women) was 56+/-10 years (age range 22 to 77 years). New York Heart Association functional class was I, II, III, and IV in 2%, 39%, 52%, and 7% of patients, respectively. The mean cardiothoracic ratio was 0.58+/-0.07 (0.4 to 0.8), and 72 (45%) patients had atrial fibrillation. Valve analysis showed that the main mechanism of MVI was type II Carpentier's functional classification in 152 patients. The leaflet prolapse involved the posterior leaflet in 93 patients, the anterior leaflet in 28 patients, and both leaflets in 31 patients. Surgical technique included a Carpentier's ring annuloplasty in all cases, a valve resection in 126 patients, and shortening or transposition of chordae in 49 patients. During the first postoperative month, there were 3 deaths (1.9%) and 3 reoperations (2 valve replacements and 1 repeat repair [1.9%]). Six patients were lost to follow-up. The remaining 151 patients with mitral valve repair were followed during a median of 17 years (range 1 to 29 years; 2273 patient-years). The 20-year Kaplan-Meier survival rate was 48% (95% CI 40% to 57%), which is similar to the survival rate for a normal population with the same age structure. The 20-year rates were 19.3% (95% CI 11% to 27%) for cardiac death and 26% (95% CI 17% to 35%) for cardiac morbidity/mortality (including death from a cardiac cause, stroke, and reoperation). During the 20 years of follow-up, 7 patients were underwent surgery at 3, 7, 7, 8, 8, 10, or 12 years after the initial operation. Valve replacement was carried out in 5 patients, and repeat repair was carried out in 2 patients. At the end of the study, 65 patients remained alive (median follow-up 19 years). Their median age was 76 years (age range 41 to 95 years). All except 1 were in New York Heart Association functional class I/II. CONCLUSIONS: Mitral valve repair using Carpentier's technique in patients with nonrheumatic MVI provides excellent long-term results with a mortality rate similar to that of the general population and a very low incidence of reoperation.
A 62-year-old patient with low grade fever, fatigue, arthralgia and newly discovered mitral regurgitation was diagnosed with subacute endocarditis. Streptococcus bovis grew from all six blood culture bottles. Streptococcus bovis is known to be associated with gastrointestinal neoplasias. Therefore a colonoscopy was performed and two polyps were removed. Histological analysis revealed a tubulovillous adenoma and a serrated adenoma. Colonoscopy is mandatory for all patients with Streptococcus bovis endocarditis even without any symptoms for colorectal neoplasia. The significance of Streptococcus bovis for the carcinogenesis of colorectal neoplasias and the possible alternative pathway for colorectal carcinomas through serrated adenomas will be discussed.
The increase of coronary artery size in myocardial hypertrophy represents an adaptive mechanism to keep coronary blood flow normal. The relationship between coronary cross-sectional area and left ventricular muscle mass was determined angiographically in 10 patients with severe mitral regurgitation before and 28 +/- 15 months after successful mitral valve surgery. 10 subjects with atypical chest pain without coronary artery disease served as controls (C). Left ventricular muscle mass was increased preoperatively in mitral regurgitation (257 g vs C = 129 g; p < 0.001) and decreased postoperatively (205 g; p < 0.01 vs preop. and vs C). The cross-sectional area of the left coronary (= left anterior descending+left circumflex) artery was augmented preoperatively (26.5 vs C = 14.0 mm2; p < 0.001) and decreased postoperatively (22.9 mm2; p < 0.05 vs preop. and vs C). The cross-sectional area of the left coronary artery per 100 g LV muscle mass was not different in the three groups. The cross-sectional area of the right coronary artery was also increased before surgery (12.7 vs C = 8.8 mm2; p < 0.05) and decreased postoperatively (11.3 mm2; p < 0.05 vs preop. ns vs C). Our data show that in mitral regurgitation the size of the left coronary artery increases proportionally to the increase in left ventricular muscle mass. Also, the right coronary artery shows slight enlargement which is probably due to the pressure overload of the right ventricle. After surgery there is regression but not normalization of the size of the coronary arteries.
Breaks in a mechanical heart valve prosthesis with resulting acute valvar insufficiency are extremely rare. The case is reported of a 49-year-old man who, two-and-a-half years after implantation of a mitral valve prosthesis, suddenly went into acute cardiogenic shock, after having been in good health since the valve replacement. Although the symptoms were unequivocal, the correct diagnosis was not made for more than 40 hours. Emergency re-operation could not prevent death from severe interstitial pulmonary oedema with hyaline membranes. Within the last 20 years 25 similar cases have been reported.
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Twenty horses with mitral valve insufficiency, but without signs of congestive heart failure, and five horses without signs of heart disease were examined before and after medication with an angiotensin-converting enzyme (ACE) inhibitor. The examination included echocardiography assessment as well as heart catheterization. The echocardiographic examination included B-mode, M-mode, conventional and colour Doppler techniques. For 8 weeks, all horses were treated with Accupro 20 (active substance: Quinapril) at an oral dose rate of 120 mg/horse/day. A follow-up of the horses with mitral valve insufficiency after 8 weeks revealed a statistically significant increase in the stroke volume and the cardiac output as well as a decrease in regurgitation velocity time integral (VTI). The regurgitation blood velocity remained the same. The severity of mitral valve insufficiencies revealed a moderate improvement in five horses, from moderate to mild, after therapy. Significant changes of cardiac dimension (B-mode) and shortening fraction (M-mode) before and after treatment could not be observed. The owners' judgement of the horses' performance was that of a minor improvement. In the horses without clinical findings the results of examination before and after treatment remained the same.
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