[APROPOS OF THE PHONOCARDIOGRAPHIC DIAGNOSIS OF MITRAL STENOSIS(DISCUSSION ON V.F. LITVINOV'S ARTICLE "ON THE ROLE OF PHONOCARDIOGRAPHY IN THE DIAGNOSIS OF MITRAL STENOSIS")].
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The echocardiographic findings of six patients with pure mitral stenosis associated with pure aortic stenosis were compared with the findings from a series of ten cases of pure aortic stenosis without mitral disease. Each patient also underwent haemodynamic studies in order to quantitate the severity of the stenoses. The aortic stenosis was of the same degree of severity in both series (0.71 +/- 0.24 cm2 and 0.73 +/- 0.16 cm2). The systolic separation of the aortic valve was greater than 1 cm in 4 of the 6 cases on echocardiography, corresponding to a false negative of tight aortic stenosis. This appearance corresponded to a doming of the aortic valve on 2D echocardiography. The wall thickness was significantly less in the AS + MS series than in pure SA series (1.13 +/- 0.13 cm compared with 1.52 +/- 0.21 cm; p less than 0.01). The wall was found to be thicker, the tighter the MS. Overall, the diagnostic criteria of the severity of AS on echocardiography (restricted opening of the valve and the severity of ventricular wall hypertrophy) were absent in the association of AS + MS. The absence of myocardial hypertrophy can not be fully explained. It could be related to a decreased filling on the left ventricle and therefore a smaller systolic ejection volume because of the mitral obstruction.
Congenital supravalvular mitral stenosis is a rare malformation characterized by the presence of a shelf-like fibrous membrane, with 1 or 2 small orifices, covering and obstructing the mitral valve. The membrane is positioned closely to the mitral valve (and sometimes it is attached to it); therefore, a preoperative diagnosis is inevitably difficult, even with the use of biplane echocardiography. Two patients with supravalvular mitral stenosis aged 3 years and 3 months are described. In 1 patient, a preoperative diagnosis was made, and both successfully underwent correction.
Estimation of mitral valve area (MVA) in the cardiac catheterization laboratory is prone to pitfalls because of the time required for calculations and inaccuracies in the measurement of cardiac output. Because the rate of decrease in the mitral gradient directly correlates with the severity of mitral stenosis, an on-line estimate of MVA at the time of catheterization may be possible with regression analysis of digitized pressure recordings. A total of 61 comparisons of mitral gradient measurements and MVA were obtained in 37 patients at diagnostic catheterization and in 24 patients after balloon mitral valvotomy. Linear and nonlinear regression parameters yielded pressure half-time values and empiric constants similar to those used in Doppler echocardiography for estimation of MVA. The correlations derived from linear analysis were as good as those obtained from nonlinear analysis: from linear analysis, MVAregression = 0.79.MVAGorlin -0.03; r2 = 0.64, p = 0.0001; and from double exponential analysis, MVAregression = 0.86.MVAGorlin -0.07; r2 = 0.74; p = 0.0001. The correlations were not significantly affected by the presence of mild to moderate mitral regurgitation or whether they were obtained after balloon valvotomy. In summary, linear regression analysis yields accurate estimates of MVA despite the theoretical superiority of nonlinear methods. On-line digital analysis of mitral gradient tracings may thus be useful at the time of diagnostic cardiac catheterization or balloon mitral valvotomy to assess the severity of mitral stenosis and the response to interventions.
Patients with mitral stenosis and some degree of right ventricular failure may benefit from inotropic or pulmonary vasodilator drugs in the early postoperative period. Thirty patients undergoing an operation for mitral stenosis were randomized into three groups. In group I (n = 10), isoproterenol (5 micrograms/kg/min) was started in the immediate postoperative period. In group P (n = 10), prostaglandin E1 (0.08 microgram/kg/min) was given, and in group C, the control group (n = 10), no drugs were used. After the operation and before drug therapy was begun, basal measurements of cardiac index, mean pulmonary arterial and mean arterial pressures, and pulmonary vascular resistance were taken. Measurements were repeated at 6, 12, and 24 hours. Mean measurements of cardiac index (basal up to 24 hours) were as follows: 1.39 +/- 0.3, 1.92 +/- 0.4, 2.4 +/- 0.5, and 2.34 +/- 0.3 L/min/m2 for group C; 1.54 +/- 0.5, 2.64 +/- 0.4, 2.68 +/- 0.7, and 2.2 +/- 0.6 L/min/m2 for group I, and 1.57 +/- 0.3, 2.2 +/- 0.6, 2.72 +/- 0.7, and 2.27 +/- 0.4 L/min/m2 for group P (p less than 0.05 between groups C and I at 6 and 12 hours). Mean pulmonary artery pressures were as follows: 19.5 +/- 3.2, 24.8 +/- 7, 27.7 +/- 7.3 and 28.8 +/- 5.7 mm Hg in group C; 21.4 +/- 8.7, 25.7 +/- 7.2, 26.4 +/- 7, and 29.4 +/- 8.6 mm Hg in group I, and 19.1 +/- 4, 19.2 +/- 3, 20.4 +/- 6, and 20.7 +/- 5 mm Hg in group P (p less than 0.05, group P versus groups C and I at 6, 12, and 24 hours). Mean pulmonary vascular resistances were as follows: 3.9 +/- 2.4, 3.9 +/- 1, 3.36 +/- 2, and 3.2 +/- 1.4 Wood units in group C; 4.84 +/- 4, 3.37 +/- 2.2, 3.69 +/- 3, and 4.69 +/- 4.1 Wood units in group I, and 3.29 +/- 1.3, 1.71 +/- 0.5, 1.61 +/- 0.5, and 1.96 +/- 0.8 Wood units in group P (p less than 0.05, group P versus groups C and I at 6, 12, and 24 hours). There was no difference in mean systemic arterial pressure among the three groups. Our results indicate that patients subjected to mitral valve operations have a low cardiac index. Isoproterenol increases cardiac index but has little effect on pulmonary resistance. At low doses, prostaglandin E1 effectively decreases pulmonary vascular resistance without altering systemic arterial pressure or heart rate.
Percutaneous transvenous mitral commissurotomy (PTMC) using the Inoue technique was performed in 557 patients with rheumatic mitral stenosis. Of these, 107 were children aged 10-18 years (mean +/- SD 14.5 +/- 2.3). All patients were symptomatic New York Heart Association (NYHA) Class II (n = 78) and Class III (n = 29). All were in sinus rhythm. Following PTMC, the mitral valve area (MVA) increased from 0.73 +/- 0.18 to 1.7 +/- 0.53 cm2 (P < 0.001). There was a significant fall in mean transmitral gradient from 15.6 +/- 5.2 to 5.1 +/- 2.3 mmHg, and in mean pulmonary artery pressure from 41 +/- 15 to 28.4 +/- 10 (P < 0.001). Cardiac tamponade developed in one patient. One patient developed severe mitral regurgitation requiring emergency mitral valve replacement. Five patients (4.7%) developed moderate mitral regurgitation. There was no mortality or cerebral embolism in any of the children. Four patients (3.7%) had oximetry evidence of atrial septal defect. Mean mitral valve area and transmitral gradient at 14 months mean follow up was 1.68 +/- 0.4 cm2 and 6 +/- 3.5 mmHg, respectively, and were comparable to the immediate post-PTMC results. Two patients (1.8%) developed restenosis. The immediate haemodynamic results in children were compared to 450 adult patients who underwent PTMC in the same period. The outcome was similar in both groups. Children were found to have significantly higher pulmonary artery pressure compared to adults. We found that PTMC using an Inoue balloon is very effective and safe in children, and consider that it should be the procedure of choice for young patients with symptomatic rheumatic mitral stenosis.
The aim of this study was to specify in patients with tight mitral stenosis whether lung diffusing capacity could play a role in their exercise intolerance. A similar study was recently carried out in patients with moderate chronic heart failure. Ten patients with tight mitral stenosis were studied before and 6 months after successful percutaneous transvenous balloon valvuloplasty and compared to six control subjects. Measurements of diffusing capacity, evaluated by the lung transfer factor (TLCO) and by the transfer coefficient (TLCO/VA), obtained at rest and during early recovery after cardiopulmonary exercise testing were performed. Cardiac output was determined non-invasively, both at rest and during exercise, using the carbon dioxide exponential rebreathing technique. Prior to valvuloplasty, TLCO and TLCO/VA were not different at rest between the two groups. During exercise, patients differed from control subjects, with lower oxygen uptake (P < 0.001) and lower cardiac output at peak exercise (P < 0.001). These values at peak exercise were significantly correlated (P = 0.02; r = 0.75). Moreover, patients differed from control subjects at early recovery after peak exercise with an absence of increase in TLCO (P < 0.05). Six months after valvuloplasty, a decrease of both TLCO (P < 0.01) and TLCO/VA (P < 0.05) was observed at rest. During exercise, comparison of patients demonstrated a significant increase of both peak exercise oxygen uptake (SLVO2, P < 0.01) and cardiac output (P < 0.001). At early recovery after peak exercise there was a significant increase in TLCO (P < 0.05) and TLCO/VA (P < 0.01), such that a delta TLCO and a delta TLCO/VA appeared (P < 0.05) identical to that observed in control subjects. Moreover, delta SLVO2 was significantly correlated in patients with delta Q+ delta TLCO/VA (P = 0.02; r = 0.72). In conclusion, this study suggests a role, at least partial, of lung diffusing capacity in exercise intolerance in patients with tight mitral stenosis and in the improvement of their aerobic exercise capacity demonstrated after successful percutaneous balloon valvuloplasty.
BACKGROUND: This study evaluated the correlation and variability between noninvasive and invasive measures of mitral stenosis severity before and after balloon mitral commissurotomy (BMC) in a large group of patients with symptomatic mitral stenosis. Factors related to variability between measurements were determined. METHODS: The Doppler transmitral gradient, Doppler half-time valve area, and 2-dimensional echocardiographic (2D) mitral valve area (MVA) were measured immediately before and 1 day after BMC in 272 consecutive patients with mitral stenosis and compared with their respective measures during cardiac catheterization. RESULTS: The correlation coefficient for the comparison of noninvasive and invasive measurements of the transmitral gradient was 0.63 before BMC and 0.60 after the procedure; for 2D versus Gorlin-derived MVA, 0.39 and 0.57, respectively; and for Doppler half-time versus Gorlin-derived MVA, 0.31 and 0.18, respectively. A large degree of variability in the measurement of MVA was present among the 3 techniques before BMC and increased after BMC. Before BMC, for the comparison of 2D and Gorlin-derived MVA, variables predictive of the discrepancy were age, echocardiographic score, transmitral gradient during catheterization, and cardiac index. For the comparison of Doppler half-time versus Gorlin-derived MVA, age, heart rate during cardiac catheterization and echocardiography, cardiac output and left ventricular end-diastolic pressure predicted the difference between the 2 measures. CONCLUSIONS: In symptomatic patients with mitral stenosis, there is significant variability between noninvasive and invasive measures of mitral stenosis severity despite careful, reproducible measurements. The difference between noninvasive and invasive measures of MVA before BMC is strongly related to cardiac output.
Thirty-seven patients with symptomatic mitral stenosis underwent balloon dilatation of the mitral valve. Significant increases (p less than 0.001) were noted in both catheterization- and Doppler-determined valve area (0.9 +/- 0.3 to 1.8 +/- 0.8 and 0.9 +/- 0.2 to 1.7 +/- 0.5 cm2). However, catheterization and Doppler areas before and after valvuloplasty correlated less well (r = 0.51, p less than 0.002 and r = 0.47, p less than 0.005, respectively) than the catheterization-Doppler area correlation in a previous study of 59 consecutive patients with varying degrees of mitral stenosis (r = 0.84, p less than 0.001). Mitral valve area increases were independent of valve thickness estimated using 2-dimensional echocardiography. Flail mitral leaflet movement was not observed and the degree of mitral regurgitation qualitatively assessed using pulsed Doppler mapping techniques increased by greater than 1 of 4 grades in only 1 patient. The lateral mitral valve orifice diameter increased more than the anteroposterior diameter, suggesting commissural splitting as the mechanism of successful valvuloplasty. Increases (all p less than 0.0001) were noted in mitral valve EF slope (7 +/- 5 to 18 +/- 10 mm/s), excursion (11 +/- 5 to 13 +/- 4 mm), S20S interval (0.07 +/- 0.02 to 0.08 +/- 0.02 s) and cardiac output (4.2 +/- 1.3 to 5.3 +/- 2.0 liters/min). There were significant decreases (all p less than 0.001) in left atrial diameter (5.4 +/- 1.0 to 5.1 +/- 1.0 cm), mean catheterization gradient (15 +/- 5 to 8 +/- 4 mm Hg) and mean Doppler gradient (10 +/- 4 to 6 +/- 3 mm Hg).(ABSTRACT TRUNCATED AT 250 WORDS)
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The echocardiographic diagnosis of mitral stenosis is based on the finding of a decreased early diastolic slope of the anterior mitral leaflet. This finding is also seen in other conditions in which the rate of left ventricular filling is reduced by decreased compliance of the ventricular myocardium rather than by mitral valve obstruction. Patients with "true" mitral stenosis have been differentiated from those with decreased ventricular compliance resulting in "false" mitral stenosis by the direction of movement of the posterior mitral valve leaflet. This report describes a patient with mitral stenosis proved at cardiac catheterization whose echocardiogram showed posterior motion of thickened posterior mitral leaflet during diastole, a finding previously considered to exclude organic mitral stenosis. This false negative echocardiographic finding in proved mitral stenosis has not previously been reported.
Compared with mitral valve replacement as treatment for severe mitral stenosis, balloon mitral valvuloplasty (BMV) is a less invasive and well-established alternative therapeutic procedure. The best results are obtained with BMV in association with pliable, non-calcified valves. However, in the western world, mitral stenosis is predominantly a condition of the elderly, in whom less favourable valve anatomy is generally found. In this report we describe the case of an 86-year-old woman with severe symptomatic mitral stenosis and breathlessness on minimal exertion who underwent successful BMV. Following the procedure she was able to function independently. This serves to highlight the fact that BMV should be considered in the treatment of symptomatic mitral stenosis, irrespective of age.
The diastolic rumbling murmur of mitral stenosis (MS) may be attenuated in the presence of low cardiac output, right ventricular enlargement, Lutembacher's syndrome, pulmonary emphysema, and obesity. In this report we would like to stress that the presence of tricuspid stenosis (TS) is an additional significant cause of silent MS. The clinical material consisted of 73 patients with rheumatic TS who had undergone cardiac surgery. Five of these cases had clinical findings of TS without auscultatory findings of MS. They were found to have severe MS at the time of operation and to require mitral valve surgery. At cardiac catheterization the mean diastolic gradient (MDG) across the mitral valve (MV) was less than 3 mmHg and pulmonary arterial systolic pressure was 29-42 mmHg. The MDG across the tricuspid valve was 6-17 mmHg. In conclusion, TS can mask clinical and hemodynamic findings of MS. The reason for this is the mechanical barrier imposed by TS proximal to the MV.
Patients with rheumatic mitral stenosis often have no pulmonary oedema despite considerably increased pulmonary venous pressure. Pulmonary microvascular permeability was measured non-invasively by a previously validated method of double isotope scintigraphy with indium-113m and technetium-99m. This permits calculation of an index reflecting transferrin efflux and thus, indirectly, the microvascular permeability. Fifteen patients with severe mitral stenosis (defined as valve area less than 1.0 cm2) were compared with a control group of 11 patients with mild coronary artery disease. The permeability index was significantly lower in patients with mitral stenosis than in the control group. Furthermore, the extent of reduction of the permeability index correlated with the severity of mitral stenosis as reflected by the Gorlin valve area. This finding may account for the relative resistance of these patients to pulmonary oedema despite chronic pulmonary venous hypertension.
Mitral stenosis, being a progressive disease, remains even at present an important specialized diagnostic field of cardiology which deserves special attention. Although a substantial regression of rheumatic disease was recorded in our country, we have to take into account that there are patients after surgery of mitral stenosis made in the past, that restenosis may develop and that there is also a certain number of non-rheumatic forms of mitral stenosis. Clinical cardiological examination still remains the basis for evaluation of mitral stenosis. A central position in the diagnosis of mitral stenosis for assessment of structural morphological changes in the area of the mitral valve and functional flow changes in the cardiac area is played by echocardiography which, when modern techniques are used, usually suffices for indication of invasive treatment on the stenotic mitral valve. The drug of choice in selected patients with mitral stenosis is balloon mitral commissurotomy which clearly dominates in the majority of patients needing a radical procedure and leads to release of the close block in this area and substantial improvement or sometimes complete disappearance of the symptomatology of the disease. Similarly as in surgical commissurotomy this invasive procedure must be described as palliative and not as a curative procedure.
The continuity equation was used to estimate non-invasively the stenotic mitral valve area by comparison with two other echocardiographic methods (planimetry and pressure half-time) and with Gorlin's formula as the gold standard. The accuracy of the equation of continuity was determined before and 24 h after valvuloplasty in a study group of 21 patients with severe mitral stenosis. According to the equation of continuity, mitral valve area was calculated by the product of the cross-sectional area and the aortic or pulmonary annulus and the ratio of the time velocity integral of the aortic or pulmonary flow to that of the mitral stenotic jet. In pre-valvotomy basal conditions, the Doppler continuity equation demonstrated significant correlations with 2D planimetry (r = 0.72, P less than 0.01), with the pressure half-time method (r = 0.62, P less than 0.01) and with the Gorlin formula (r = 0.66, P less than 0.01). There was no significant difference between the haemodynamic data and the echocardiographic measurements. Twenty-four hours after valvotomy, the Doppler continuity equation also demonstrated significant correlations with 2D planimetry (r = 0.83, P less than 0.01), with pressure half-time (r = 0.82, P less than 0.01) and with the Gorlin formula (r = 0.69, P less than 0.01). However, the haemodynamic measurements significantly overestimated (P less than 0.01) the echographic measurements. Thus, we conclude that the continuity equation provides an accurate estimation of mitral valve area in mitral stenosis before and after balloon valvotomy.