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We report on a patient with ankylosing spondylitis in association with mitral stenosis, mitral regurgitation, and aortic regurgitation. Despite extensive search of literature, we could not find association of mitral stenosis with ankylosing spondylitis. This report is the first to describe this association. Our findings are based on clinical and echocardiographic findings.
The dynamics of the delayed accentuated mitral component (M1) of the first heart sound and the MOS were studied in 11 patients with mitral stenosis of varying severity. Echophonocardiographic (M-mode and 2D) studies were performed with analysis of LA dimensions, dynamics, and mitral valve excursion at the time of M1 and MOS. LA area and length, mitral annular diameter, and mitral dome area (from anulus plane to fused valve tip) and length were measured at M1 and MOS. Significant dynamic increases in mitral dome area and length occurred from M1 to MOS, with less striking but consistent increases in LA area, LA length, and mitral annular diameter. Conversely, mitral dome area and length decreased significantly from MOS to M1, with less striking but consistent decreases in LA area, LA length, and mitral annular diameter. Frame-by-frame video tape analysis showed that dome movement was separate from anulus motion. Mitral dome descent into the left ventricle terminated at MOS and reversal of dome motion terminated at M1. The conformational and dimensional changes that terminated abruptly at MOS reversed and terminated abruptly in a reciprocal manner at the time of the delayed, accentuated M1. When considered in light of known hemodynamic, pressure pulse, and imaging correlates in mitral stenosis, these observations strengthen the hypothesis that the mechanisms involved in the production of M1 and MOS in mitral stenosis are paired or reciprocal in nature, and the delayed, accentuated M1 and the MOS of mitral stenosis are reciprocal cardiovascular sounds.
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Natural and post-surgical history has been investigated in 410 pts with mitral stenosis and 209 pts with mixed mitral stenosis and regurgitation. They had undergone cardiac catheterization in the years 1968-1980. Hemodynamic data and clinical status (NYHA class) have been statistically analyzed in order to obtain prognostically useful parameters. In mitral stenosis peak pulmonary artery pressure is the most important parameter for natural history, whereas cardiac index is the leading parameter in the operated patients. Commissurotomy has a very low surgical mortality, largely due to the better conditions of the patients undergoing this type of conservative surgery. Results are similar in mixed mitral stenosis and regurgitation. Surgery markedly improves survival in comparable patients. Therefore, intervention seems to be indicated especially in patients with elevated pulmonary artery pressure, because they can get the maximum advantage at a minimal risk.
Mitral stenosis still remains a major problem in Southeast Asia including Thailand. It contributes to the morbidity and mortality related to thromboembolism which was associated with the left atrial thrombus. However, the pathogenesis of left atrial thrombus in these patients is not completely understood. Therefore, the objective of this study was to investigate the coagulation and platelet activity including the function of the endocardium in the left atrium and peripheral circulation in patients with mitral stenosis who were free of left atrial thrombus and to compare those hematologic markers activity in the peripheral venous blood between the patients with mitral stenosis and the control. Thirty-six patients with moderate to severe mitral stenosis were included in the study. Most of the patients were in functional class II and 50 per cent had atrial fibrillation. Blood was obtained from the femoral vein, femoral artery, pulmonary artery and left atrium of these patients before heparin was administered to determine the value of various hematologic markers. In the control group, blood for determining the hematologic markers was collected only from the antecubital vein. The results of this study demonstrated that the levels of prothrombin activation fragment 1+2 (F1+2), thrombin-antithrombin III complex (TAT) and Beta-thromboglobulin (beta-TG) in the left atrium of the patients with mitral stenosis were significantly higher than those in the femoral vein and femoral artery, whereas the level of thrombomodulin was significantly lower in the left atrium compared with the femoral artery and vein. When comparing with the control group, the levels of TAT, plasminogen activator inhibitors-1 (PAI-1) from the peripheral vein were significantly higher and the level of thrombomodulin was also significantly lower in the patients with mitral stenosis. In conclusion, the present study demonstrated an abnormal hypercoagulable state of the left atrium and systemic circulation related to the abnormalities of coagulation, platelets and the endocardium which may cause the formation of left atrial thrombus in patients with mitral stenosis.
Mitral stenosis may be recognized simply on routine physical examination from abnormalities on auscultation, which are subsequently confirmed by Doppler echocardiographic examination. The diagnosis may also be suspected in patients in whom the history is suggestive of rheumatic fever and in whom physical diagnosis reveals findings indicative of mitral stenosis. Occasional cases of mitral stenosis are picked up in the Doppler echocardiography laboratory when a patient has not been suspected of having mitral stenosis but in whom a routine echocardiogram has been taken, for whatever reason. If there is any doubt about the presence of mitral stenosis, confirming the presence of a diastolic pressure gradient across the mitral valve during cardiac catheterization permits one to make a definitive diagnosis as well as estimate the area of the stenotic valve orifice. Intervention with either surgery or balloon valvotomy is indicated when the mitral valve area falls to < or = 1.2 cm2 in a symptomatic patient.
Mitral valve echo score has been proposed as a predictor or of the outcome of balloon mitral valvotomy in patients with mitral stenosis. The relationship between mitral echo score and the hemodynamic variables was evaluated. In 41 patients with pure mitral stenosis (nine men and 32 women, aged 57.9 +/- 9.4 years), mitral echo score was estimated from two-dimensional echocardiographic findings, and mitral valve area was measured by planimetry on the two-dimensional short-axis view. Apex phonocardiography and continuous-wave Doppler echocardiographic recording of transmittral flow were simultaneously performed to measure left atrial/left ventricular mean transmittral pressure gradient, pressure half-time and (Q-1)-(2-OS) interval. Linear regression analysis revealed that both mitral echo score and mitral valve area were significantly correlated with mean transmittral gradient (r = 0.522, p = 0.0005 and r = -0.651, p < 0.0001, respectively), pressure half-time (r = 0.491, p < 0.005 and r = -0.757, p < 0.0001) and (Q-1)-(2-OS) interval (r = 0.551, p < 0.0005 and r = -0.487, p < 0.005, respectively). Mitral echo score has a significant correlation with hemodynamic variables, which were comparable to but slightly different from mitral valve area, in patients with mitral stenosis.
BACKGROUND: Mitral stenosis after mitral valve repair for non-rheumatic mitral regurgitation is rare. METHODS: From 1990 to 1999, 478 patients had mitral valve repair for myxomatous and 40 patients had mitral valve repair for ischemic mitral regurgitation. The Carpentier annuloplasty ring (Edwards Lifesciences, Irvine, CA) was used in 72 patients, the Duran ring (Medtronic, Minneapolis, MN) in 152, a posterior band in 221 and no ring or band in 73 patients. RESULTS: Four patients developed mitral stenosis late after mitral valve repair: 2 for myxomatous disease and 2 for ischemic mitral regurgitation. All 4 patients had Duran annuloplasty rings (sizes 25 to 31). The diagnosis of mitral stenosis was made by Doppler echocardiography. The mitral valve area in these 4 patients decreased from 2.7 cm2 (range, 2.3 to 3.2 cm2) early postoperatively to 0.85 cm2 (0.4 to 1.2 cm2) after a mean follow-up of 66 months (range, 38 to 110 months). Three patients had mitral valve replacement and the etiology of the mitral stenosis was the same in all patients (ie, pannus overgrowth on the annuloplasty ring with extension onto both leaflets rendering them stiff and immobile). The fourth patient had a mitral valve area of 1.2 cm2, which was mildly symptomatic with normal pulmonary artery pressure, and this patient has not had reoperation. CONCLUSIONS: Mitral stenosis may develop after mitral valve repair for myxomatous disease or ischemic mitral regurgitation when a Duran ring is used for annuloplasty. The stenosis is caused by pannus on the annuloplasty ring with extension onto the leaflets.
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Mitral stenosis is a well known cause of hemoptysis; however, sudden death due to fatal massive pulmonary hemorrhage is an extremely rare complication. In this report, we describe a 28-year-old female with severe mitral stenosis who died suddenly due to such complication. A review of the literature shows such complication is extremely rare and unpredictable. We recommend that patients with severe mitral stenosis and history of hemoptysis be considered as candidates for early surgical intervention.
Mitral valve replacement with preserving all chordae tendineae in patients with mitral regurgitation has been proved to be beneficial for left ventricular performance in the postoperative period. To evaluate the effectiveness of this technique in patients with mitral stenosis a comparison of the hemodynamic and echocardiographic data between patients having operation with this technique (Group P, n = 15, mean age = 37.5 +/- 12 years), and those having operation with the conventional method of mitral valve replacement (Group C, n = 15, mean age = 39 +/- 10.4 years) was made. The study population was limited to patients who had no clinical evidence of coronary artery disease and if over 40 years of age had normal coronary artery anatomy on coronary arteriography; patients with no evidence of aortic stenosis and/or regurgitation; and patients who had pure mitral stenosis or mitral stenosis with slight regurgitation (Grade 2 or less) with a mean gradient across the mitral valve greater than 10 mmHg. Hemodynamic parameters improved in both groups after the operation. However, echocardiographic measurements obtained six months postoperatively revealed a significant decrease in left ventricular ejection fraction in Group C (61.33 +/- 9.29% preoperatively versus 53.2 +/- 10.3% postoperatively; p < 0.05). The difference between left ventricular ejection fraction diminution of the two groups was statistically significant (-0.71 +/- 6.28% in Group P versus -8.07 +/- 13.35% in Group C; p < 0.01). Left ventricular end systolic and end diastolic dimensions decreased in patients with preserved valves and increased in patients operated on with conventional method without reaching a statistical significance. Sizes of prosthetic valves inserted were in the same range and no significant differences were found in preoperative and postoperative comparison of the two groups in respect to effective mitral orifice area and transvalvular gradient. There were no evidence of prosthetic valve dysfunction and paravalvular leakage and no operative or late deaths. It is concluded that if it is suitable, mitral valve replacement with preservation of chordae tendineae is expected to have a beneficial effect on postoperative left ventricular performance in patients with mitral stenosis.
Mitral valve area (MVA) was calculated using the proximal flow convergence method in 60 patients with severe mitral stenosis. Using the apical 4 chamber view, colour Doppler was used to measure the peak forward flow rate. From this, the mitral valve area was calculated according to the formula: mitral valve area = peak forward flow rate/peak mitral velocity. This method compared well with the established 2D planimetry derived valve area (r = 0.89) and Doppler pressure half time method (r = 0.88). Hence, this can be used as an alternative method to estimate the valve area in patients with mitral stenosis.
Mitral stenosis with or without regurgitation is the most common form of valve disease associated with arrhythmias, as atrial fibrillation (AF) is the most frequent complication of mitral stenosis. AF may occur as transient episodes with the patients reporting a history of palpitation, paroxysmal dyspnea or tachycardia or as sustained arrhythmia.
Mitral commissurotomy is the treatment of choice for mitral stenosis. If this is not feasible, replacement of the valve becomes necessary. Open commissurotomy has been performed at Loyola University Medical Center, Maywood, Ill, in 105 patients since 1970. The mean age was 45 years. The indication for surgery was heart failure in 92 of the cases. Sixty of the patients were in class 3 of the New York Heart Association (NYHA) classification. Eighty-five underwent open mitral commissurotomy alone. This was not feasible in 42 patients scheduled for it who required valvular replacement. Twenty-five patients had a left atrial thrombus. Two patients died, one from aortic dissection and the other from acute infarction in the perioperative period. Ninety-eight patients are NYHA class 1 or 2 at present. Two patients required valvular replacement following the commissurotomy. The low mobidity and mortality with excellent long-term results support our contention that open mitral commissurotomy is the treatment of choice for mitral stenosis.