Effect of nitroglycerin during hemodynamic estimation of valve orifice in patients with mitral stenosis

In patients with mitral stenosis, valve orifice calculations using pulmonary capillary wedge pressure as a substitute for left atrial pressure may overestimate the severity of disease. Previous studies have shown that mitral valve area determined from transseptal left atrial pressure measurements exceeds that area derived from pulmonary wedge pressure measurements. This is probably due to pulmonary venoconstriction, which is reversed by nitroglycerin. Nitroglycerin, 0.4 mg, was administered sublingually to 20 patients with mitral valve disease during preoperative cardiac catheterization using the pulmonary capillary wedge pressure as the proximal hydraulic variable. At the time of a peak hypotensive effect, 3 to 5 minutes after nitroglycerin administration, the mean pulmonary capillary wedge pressure decreased from 23 +/- 2 (mean +/- SEM) to 19 +/- 2 mm Hg (p less than 0.005). The mean diastolic transmitral pressure gradient (12.6 +/- 1.2 mm Hg before and 11.5 +/- 1.0 mm Hg after nitroglycerin; p = NS) and cardiac output (4.0 +/- 0.3 to 4.1 +/- 0.3 liters/min; p = NS) did not change significantly. Nevertheless, the hemodynamic mitral orifice area, calculated using the Gorlin formula, increased from 0.8 +/- 0.1 to 1.1 +/- 0.2 cm2 (p less than 0.05). In 12 patients with isolated mitral stenosis, without regurgitation, the mitral valve orifice area after nitroglycerin was 0.4 +/- 0.2 cm2 larger than it was before drug administration (p less than 0.05). Administration of nitroglycerin during evaluation of mitral stenosis eliminates pulmonary venoconstriction, which raises the pulmonary capillary wedge pressure above the left atrial pressure in some patients.(ABSTRACT TRUNCATED AT 250 WORDS)     

Hemodynamic and volumetric effects of venodilation with nitroglycerin in chronic mitral regurgitation

To evaluate the potential value of nitrate therapy in patients with chronic mitral regurgitation, the hemodynamic and angiographic effects of intravenous nitroglycerin were studied in 10 such patients. Nitroglycerin infusion, titrated to reduce mean pulmonary artery wedge pressure at least 20%, resulted in a significant reduction in mean blood pressure (from 91 +/- 12 to 77 +/- 13 mm Hg, p less than 0.0001), mean right atrial pressure (12 +/- 6 to 7 +/- 4 mm Hg, p less than 0.001), left ventricular end-diastolic pressure (22 +/- 7 to 13 +/- 5 mm Hg, p less than 0.0001) and peak V wave of indirect left atrial pressure (34 +/- 9 to 20 +/- 10 mm Hg, p less than 0.001). Changes in systemic vascular resistance (1,986 +/- 468 vs 1,582 +/- 534 dynes s cm-5) and forward stroke volume (39 +/- 14 vs 45 +/- 8 ml) were not statistically significant. Angiographic data showed a decrease in both end-diastolic and end-systolic left ventricular volumes (248 +/- 51 to 216 +/- 54 ml, p = 0.06 and 127 +/- 69 to 99 +/- 48 ml, p less than 0.05, respectively) and an improvement in ejection fraction, from 0.52 +/- 0.15 to 0.55 +/- 0.15 (p less than 0.05). There was no significant change in the group values for mitral regurgitant volume and fraction (from 85 +/- 32 to 72 +/- 32 ml and 67 +/- 10 to 64 +/- 5%, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)     

Acute reduction of atrial overload during vasodilator and diuretic therapy in advanced congestive heart failure

Although acute afterload reduction is known to improve cardiac output in patients with congestive heart failure (CHF), the effect of therapy on the atrial overload directly causing congestive symptoms has not been systematically studied. Atrial volumes and mitral and tricuspid regurgitation, in addition to left ventricular ejection fraction and indexes of left ventricular contractility (mean acceleration, ejection time and peak systolic pressure/end-systolic volume index), were measured using 2-dimensional and Doppler echocardiography and color flow imaging in 30 patients with advanced CHF, before and after acute vasodilator and diuretic therapy tailored to hemodynamic goals. Therapy increased stroke volume by 64% (36 +/- 10 to 55 +/- 14 cc), decreased right atrial pressure by 45% (15 +/- 5 to 8 +/- 4 mm Hg), systemic vascular resistance by 36% (1,700 +/- 400 to 1,030 +/- 300 dynes s cm-5) and pulmonary capillary wedge pressure by 37% (31 +/- 6 to 19 +/- 6 mm Hg) (all p less than 0.001). Echocardiography showed simultaneous reductions in left and right atrial volumes: 24 +/- 19 and 18 +/- 12%, respectively (p less than 0.001). Mitral and tricuspid regurgitation measured by color flow fraction both decreased by a mean of 44% (p less than 0.001). While ejection fraction increased from 15 +/- 5 to 19 +/- 7% (p less than 0.001), there were no changes in relatively load-independent indexes of contractility. Therefore, acute therapy with vasodilators and diuretics in advanced CHF causes reductions in atrial volumes and atrioventricular valve regurgitation that are evident from serial noninvasive studies and may play a major role in the improvement of congestive symptoms.     

Short- and long-term results of catheter balloon percutaneous transvenous mitral commissurotomy

Percutaneous transvenous mitral commissurotomy (PTMC) was performed in 219 patients with symptomatic, severe rheumatic mitral stenosis. There were 59 men and 160 women, aged 19 to 76 years (mean 43). Pliable, noncalcified valves were present in 139 (group 1), and calcified valves or severe mitral subvalvular lesions, or both, in 80 patients (group 2). Atrial fibrillation was present in 133 patients (61%) and 1+ or 2+ mitral regurgitation in 59 (27%). Technical failure occurred with 3 patients in our early experience. There was no cardiac tamponade or emergency surgery. The only in-hospital death occurred 3 days after the procedure in a group 2 premoribund patient in whom last-resort PTMC created 3+ mitral regurgitation. Mitral regurgitation appeared or increased in 72 patients (33%); 3+ mitral regurgitation resulted in 12 patients (6%). There were 3 systemic embolisms. Atrial left-to-right shunts measured by oximetry developed in 33 patients (15%). Immediately after PTMC, there were significantly reduced (p = 0.0001) left atrial pressure (24.2 +/- 5.6 to 15.1 +/- 5.1 mm Hg), mean pulmonary artery pressure (39.7 +/- 13.0 to 30.6 +/- 10.9 mm Hg) and mitral valve gradient (13.0 +/- 5.1 to 5.7 +/- 2.6 mm Hg). Mitral valve area increased from 1.0 +/- 0.3 to 2.0 +/- 0.7 cm2 (p = 0.0001) and cardiac output from 4.4 +/- 1.4 to 4.7 +/- 1.2 liters/min (p less than 0.01). The results mirrored clinical improvements in 209 patients (97%). Multivariate analysis showed an echo score greater than 8, and valvular calcification and severe subvalvular lesions as independent predictors for suboptimal hemodynamic results.(ABSTRACT TRUNCATED AT 250 WORDS)     

Accuracy of left atrial and pulmonary artery wedge pressure in pure mitral regurgitation in predicting left ventricular end-diastolic pressure

In most clinical conditions pulmonary artery (PA) wedge pressure accurately reflects left ventricular (LV) end-diastolic pressure. In the presence of mitral regurgitation (MR), large V waves can distort PA wedge pressure and result in incorrect estimation of LV end-diastolic pressure. In 52 patients with MR simultaneous measurement of PA wedge pressure or left atrial pressure and LV end-diastolic pressure was recorded. Twenty-one (40%) patients had large V waves (V wave greater than A wave by greater than 10 mm Hg, group 1), and 31 (60%) patients had small V waves (group 2). Group 1 had significantly higher V waves than group 2 (46 +/- 3 vs 21 +/- 2 mm Hg, p less than 0.001). The LV end-diastolic pressure was similar in both groups (21 +/- 2 vs 19 +/- 2 mm Hg, difference not significant). The mean PA wedge or left atrial pressure in group 1 (26 +/- 2 mm Hg) overestimated LV end-diastolic pressure (21 +/- 2 mm Hg) by 30% (p less than 0.01), but the trough of the X descent (20 +/- 2 mm Hg) was similar to the LV end-diastolic pressure. In group 2 patients with small V waves the mean PA wedge pressure was not significantly different from the LV end-diastolic pressure (16 +/- 2 vs 19 +/- 2 mm Hg, p = 0.06), but the trough of the X descent (13 +/- 2 mm Hg) underestimated LV end-diastolic pressure.(ABSTRACT TRUNCATED AT 250 WORDS)     

Pulmonary venous flow dynamics before and after balloon mitral valvuloplasty as determined by transesophageal Doppler echocardiography.

The pattern of left atrial filling was studied in 14 patients with severe mitral stenosis in sinus rhythm before and immediately after successful balloon mitral valvuloplasty by transesophageal pulsed Doppler echocardiography of the left superior pulmonary vein. Mean mitral valve orifice area increased from 0.8 +/- 0.1 to 2.2 +/- 0.3 cm2 (p less than 0.0001), and left atrial mean pressure decreased from 30 +/- 5 to 12 +/- 4 mm Hg (p less than 0.0001) after the procedure. After balloon mitral valvuloplasty, significant increases in peak systolic pulmonary velocity (35 +/- 16 to 44 +/- 10 cm/s; p less than 0.01), systolic flow velocity time integral (3.3 +/- 1.5 to 5.9 +/- 2.0 cm; p less than 0.001) and the ratio of systolic/diastolic pulmonary venous flow velocity time integrals (0.8 +/- 0.4 to 1.4 +/- 0.5; p less than 0.001) were observed. An acute increase in mitral valve orifice area caused no significant changes in peak diastolic forward flow velocity (40 +/- 7 to 41 +/- 9 cm/s; p = not significant [NS]), diastolic forward flow velocity time integral (4.3 +/- 1.7 to 4.6 +/- 1.8 cm; p = NS) and atrial flow reversal velocity (30 +/- 3 to 35 +/- 3 cm/s; p = NS) compared with at baseline. The results suggest that in patients with severe mitral stenosis and sinus rhythm, left atrial filling is biphasic with a diastolic preponderance, and successful mitral valvuloplasty is associated with an immediate increase in pulmonary venous systolic forward flow.     

Use of pulmonary capillary wedge pressure to assess severity of mitral stenosis: is true left atrial pressure needed in this condition?

There is disagreement concerning the use of the pulmonary capillary wedge pressure (in place of left atrial pressure) in assessing the presence and severity of mitral valve disease. This study was done to assess the accuracy and reliability of an oximetrically confirmed pulmonary capillary wedge pressure in measuring the transvalvular pressure gradient and valve area in patients with mitral stenosis. In 10 patients with mitral stenosis (1 man and 9 women; mean age +/- SD 47 +/- 7 years), pulmonary capillary wedge pressure was measured through an 8F Goodale-Lubin catheter with its wedge position confirmed by oximetry (oxygen saturation greater than or equal to 95%). In addition, a transseptal left atrial pressure was measured through a Brockenbrough catheter and left ventricular pressure was measured through a pigtail catheter. The mean and phasic left atrial and pulmonary capillary wedge pressures were similar (mean left atrial pressure 18 +/- 6 mm Hg; mean pulmonary capillary wedge pressure 18 +/- 8 mm Hg; p = NS). When the pulmonary capillary wedge pressure was used without adjustment for time delay, the transvalvular pressure gradient (9.8 +/- 3.3 mm Hg) and valve area (1.5 +/- 0.5 cm2) were significantly different (p less than 0.05) from the values obtained with use of left atrial pressure (7.2 +/- 2.9 mm Hg and 1.7 +/- 0.6 cm2, respectively). In contrast, when the pulmonary capillary wedge pressure was adjusted for the time delay through the pulmonary vasculature, the difference in gradients averaged only 1.7 mm Hg and the mitral valve areas were similar.(ABSTRACT TRUNCATED AT 250 WORDS)     

Large V waves in the pulmonary capillary wedge pressure tracing without mitral regurgitation: the influence of the pressure/volume relationship on the V wave size

We have previously demonstrated that a large V wave in the pulmonary capillary wedge tracing may occur in the absence of mitral regurgitation. This study evaluates the role of left atrial and pulmonary vein compliance on such a finding. We studied 11 patients with coronary disease, without clinical or angiographic mitral regurgitation. Heart rate, pulmonary capillary wedge mean, A and V waves, V-wave slope, left ventricular and aortic pressures, cardiac output, and left atrial echo and apical phonocardiogram were recorded simultaneously. Preload was modified acutely by volume overload and by the administration of i.v. nitroglycerine. Volume administration induced a marked increase in V-wave pressure (13.0 +/- 9.6 vs. 27.0 +/- 9.6 mmHg, p less than 0.05), without producing mitral regurgitation, and without appreciable change in left atrial dimension by echo (33.0 +/- 4.9 vs. 35.5 +/- 5.2 mm, NS), or stroke volume (101.7 +/- 26.2 vs. 97.8 +/- 34.3 ml, NS). An increase was also seen in the A wave (13.6 +/- 8.9 vs. 23.3 +/- 8.5 mmHg, p less than 0.05), pulmonary capillary wedge mean pressure (9.8 +/- 7.2 vs. 20.6 +/- 7.8 mmHg, p less than 0.05), and left ventricular diastolic pressure (7.4 +/- 5.5 vs. 14.6 +/- 6.3 mmHg, p less than 0.05). All values returned to baseline after nitroglycerine. The compliance of the left atrium/pulmonary veins decreased with increasing pulmonary capillary wedge pressures. With large filling volumes, a small stroke volume brings on a large pressure change, thus explaining the finding of large V waves in patients with elevated pulmonary capillary wedge pressure and without mitral regurgitation.     

Effect of nitroglycerin on the pulmonary venous gradient in patients after mitral valve replacement

Because the equality of the pulmonary artery wedge pressure and left atrial pressure has been questioned in patients with mitral valve disease and pulmonary hypertension, this study examined how vasomotor activity in the pulmonary capacitance vessels might contribute to a discrepancy between these pressures. The difference between the pulmonary wedge and left atrial pressures (designated as the pulmonary venous gradient) was measured after nitroglycerin administration in nine patients who had pulmonary hypertension (mean pulmonary artery pressure 40 mm Hg) after mitral valve replacement. Five minutes after sublingual nitroglycerin, 0.4 mg, the mean pulmonary wedge pressure decreased from 19 +/- 2 to 13 +/- 2 mm Hg (p less than 0.005), exceeding the decrease in left atrial pressure (15 +/- 2 to 11 +/- 2 mm Hg; p less than 0.005). Pulmonary blood flow increased from 4.6 +/- 0.4 to 4.9 +/- 0.4 liters/min (p less than 0.005). The decrease in mean pulmonary venous gradient from 4.0 +/- 0.8 to 1.7 +/- 0.6 mm Hg (p less than 0.025) was attributed to nitrate-mediated pulmonary venodilation. The ratio of venous gradient to blood flow, an index of pulmonary venous tone, decreased after nitroglycerin from 0.9 +/- 0.2 to 0.4 +/- 0.1 (p less than 0.01). These data indicate that reversible pulmonary vasoconstriction contributes to elevation of the pulmonary wedge pressure above the left atrial pressure in patients with chronic mitral valve disease and pulmonary hypertension and that nitroglycerin may produce pulmonary venodilation decreasing the pulmonary venous gradient.     

Effect of mitral regurgitation and volume loading on pressure half-time before and after balloon valvotomy in mitral stenosis

Doppler pressure half-time (PHT) is frequently used to assess mitral valve area (MVA), but the reliability of PHT has recently been challenged, specifically in the setting of balloon mitral valvotomy when hemodynamics have been abruptly altered. The effect of volume loading both before and after balloon mitral valvotomy on computation of MVA by Gorlin and by PHT in 18 patients with high-fidelity micromanometer measurements of left atrial and left ventricular pressure was therefore examined. Echocardiographic MVA increased from 0.91 +/- 0.15 to 1.97 +/- 0.42 cm2 after valvotomy. Volume loading produced significant increases in left atrial pressure (16 to 23 before and 12 to 20 mm Hg after valvotomy), in cardiac output (3.7 to 4.1 before and 3.9 to 4.6 liters/min after valvotomy), and in mitral valve gradient (11 to 14 before and 5 to 7 mm Hg after valvotomy). These hemodynamic changes were associated with modest but significant decreases in PHT and increases in MVA estimated by 220/PHT (0.66 to 0.81 before and 1.64 to 1.96 cm2 after valvotomy), whereas the MVA by Gorlin was not affected in a consistent fashion by volume loading (0.85 to 0.89 before and 1.66 to 1.69 cm2 after valvotomy). The correlation between Gorlin MVA and 220/PHT was only fair (r = 0.73, p less than 0.001) and was significantly poorer among patients with greater than 1+ mitral regurgitation (r = 0.72) than among those with less or no regurgitation (r = 0.79) (p = 0.001 by analysis of covariance for mitral regurgitation effect).(ABSTRACT TRUNCATED AT 250 WORDS)     

Percutaneous mitral valvotomy with the Inoue balloon catheter in children and adults: immediate results and early follow-up.

Percutaneous mitral balloon valvotomy (PMV) using the Inoue balloon catheter was attempted in 60 consecutive patients with severe symptomatic mitral stenosis. There were 10 children (mean age 13 years) and 50 adults (mean age 31 years). Forty patients were females and 20 were males; 53 were in sinus rhythm. The procedure was technically successfully performed in 57 (95%) patients. There were no deaths or thromboembolic complications. Balloon valvotomy was done using a 22 to 30 mm diameter catheter with the echo/Doppler guided stepwise mitral dilatation technique. After PMV the mean left atrial pressure decreased from 23.0 +/- 5.0 to 14.0 +/- 4.0 mm Hg (p less than 0.001). The mean mitral valve gradient (MVG) decreased from 15.0 +/- 4.0 to 6.0 +/- 2.0 mm Hg (p less than 0.001). The mitral valve area (Gorlin formula) increased from 0.7 +/- 0.2 to 1.6 +/- 0.4 cm2 (p less than 0.001). The mitral valve area as determined by echocardiography increased from 0.8 +/- 0.1 to 1.9 +/- 0.3 cm2 (p less than 0.001). Mild mitral regurgitation (MR) developed in six patients (11%) and increased by one grade in another five patients (9%). No patient developed severe mitral regurgitation. Mitral valve area at mean follow-up of 4.8 months remained unchanged at 1.9 +/- 0.3 cm2. We conclude that PMV, using the Inoue balloon catheter, is safe and effective in the treatment of severe mitral stenosis in children and adults, without inducing significant mitral regurgitation.     

Responsiveness of plasma atrial natriuretic factor to short-term changes in left atrial hemodynamics after percutaneous balloon mitral valvuloplasty

To assess the effect of short-term alteration of left atrial pressure and volume on the circulating plasma level of atrial natriuretic factor, 11 patients with left atrial hypertension due to mitral stenosis were studied at the time of percutaneous balloon mitral valvuloplasty. Hemodynamic measurements and plasma atrial natriuretic factor levels were obtained before, immediately (5 to 10 min) after and 24 h after valvuloplasty, and echocardiographic left atrial size was determined before and 24 h after valvuloplasty. Immediately after valvuloplasty, left atrial pressure decreased from 28 +/- 2 to 10 +/- 1 mm Hg (p less than 0.0005), mitral pressure gradient decreased from 20 +/- 2 to 7 +/- 1 mm Hg (p less than 0.0005), mitral valve area increased from 0.8 +/- 0.1 to 1.9 +/- 0.2 cm2 (p less than 0.0005) and plasma atrial natriuretic factor level rose from 249 +/- 42 to 348 +/- 50 pg/ml (p less than 0.01). This short-term rise in atrial natriuretic factor level may reflect a transient increase in left atrial pressure associated with balloon occlusion of the mitral valve.(ABSTRACT TRUNCATED AT 250 WORDS)     

Late hemodynamic changes in percutaneous mitral valvuloplasty

Percutaneous mitral valvuloplasty (PMV) was performed in 57 patients with mitral stenosis. Twenty-three women and 34 men (mean age 28 +/- 10 mean +/- SD) were included in the study. A single-balloon (trefoil or bifoil) technique was used in 49 patients and a double-balloon (trefoil + monofoil) technique in eight. After a 3-month follow-up period, right- and left-sided cardiac catheterization was repeated. In the single-balloon group there was improvement in the mitral valve gradient (16.10 +/- 5.99 to 4.41 +/- 2.03 mm Hg), mean left atrial pressure (22.65 +/- 6.13 to 9.76 +/- 3.01 mm Hg), and mitral valve area (0.89 +/- 0.22 to 1.95 +/- 0.46 cm2/m2). Mean pulmonary artery pressure and mean pulmonary wedge pressure decreased to 19.33 +/- 4.19 mm Hg and 10.73 +/- 2.60 mm Hg from 32.94 +/- 7.90 mm Hg and 21.49 +/- 5.98 mm Hg. Cardiac output increased to 6.86 +/- 0.56 L/min from 5.57 +/- 0.66. All improvements were statistically significant (p less than 0.001). In the double-balloon study group, mitral valve gradient (23.75 +/- 2.77 to 4.50 +/- 1.94 mm Hg), mean left atrial pressure (31.63 +/- 3.57 to 9.50 +/- 1.94 mm Hg), mean pulmonary artery pressure (44.00 +/- 6.36 to 18.88 +/- 7.10), and mean pulmonary wedge pressure (29.25 +/- 3.73 to 10.25 +/- 1.85 mm Hg) all improved significantly (p less than 0.001). Mitral valve area and cardiac output increased from 0.89 +/- 0.15 to 2.44 +/- 0.44 cm2/m2 (p less than 0.001) and from 5.46 +/- 0.76 to 7.15 +/- 0.52 L/min (p less than 0.002), respectively.(ABSTRACT TRUNCATED AT 250 WORDS)     

Double-transseptal, double-balloon valvuloplasty for congenital mitral stenosis.

BACKGROUND. Eight patients with severe congenital mitral stenosis underwent double transseptal, double-balloon valvuloplasty; two had isolated congenital mitral stenosis, six had additional cardiac defects, and one had previous surgical valvotomy. Ages ranged from 0.6 to 36 years (median, 9 years). METHODS AND RESULTS. All procedures were tolerated well. After valvuloplasty, the left atrial a wave minus the left ventricular end-diastolic pressure (LVEDP) gradient was reduced from 25 +/- 6 mm Hg to 9 +/- 3 mm Hg (p less than 0.001), the mitral valve mean gradient was reduced from 18 +/- 7 mm Hg to 8 +/- 3 mm Hg (p = 0.003), and the LVEDP was unchanged. All patients had marked clinical improvement. Only one patient developed significant mitral regurgitation. Two of the first four patients underwent repeat balloon valvuloplasty 7 months later. Follow-up evaluation on six patients from 4 to 54 months revealed no recurrence of symptoms or increased mitral regurgitation. CONCLUSIONS. Double transseptal, double-balloon valvuloplasty is an effective treatment for many forms of congenital mitral stenosis. Mitral regurgitation is uncommon after this procedure. The double transseptal approach results in less trauma to the atrial septum and femoral veins and allows easy assessment of any residual postvalvuloplasty gradient.     

Unusual sequelae after percutaneous mitral valvuloplasty: a Doppler echocardiographic study.

Percutaneous mitral valvuloplasty is a promising new technique for the treatment of mitral stenosis, with a relatively low complication rate reported to date. To assess the sequelae of this procedure, Doppler echocardiographic studies were prospectively performed before and after percutaneous mitral valvuloplasty in a series of 172 patients (mean age 53 +/- 17 years). After balloon dilation, mitral valve area increased from 0.9 +/- 0.3 to 2 +/- 0.8 cm2 (p less than 0.0001), mean gradient decreased from 16 +/- 6 to 6 +/- 3 mm Hg (p less than 0.0001) and mean left atrial pressure decreased from 24 +/- 7 to 14 +/- 6 mm Hg (p less than 0.0001). Although most patients were symptomatically improved, six (4%) were identified who had unusual sequelae evident on Doppler echocardiographic examination immediately after percutaneous mitral valvuloplasty. These included rupture of a posterior mitral valve leaflet, producing a flail distal leaflet portion with severe mitral regurgitation detected on Doppler color flow mapping (n = 1); asymptomatic rupture of the chordae tendineae attached to the anterior mitral valve leaflet with systolic anterior motion of the ruptured chordae into the left ventricular outflow tract (n = 1); a double-orifice mitral valve (n = 1); and evidence of a tear in the anterior mitral valve leaflet (n = 3), producing on both pulsed Doppler ultrasound and color flow mapping a second discrete jet of mitral regurgitation in addition to regurgitation through the main mitral valve orifice. All six patients made a satisfactory recovery and none has required mitral valve replacement.(ABSTRACT TRUNCATED AT 250 WORDS)     

Percutaneous balloon versus surgical closed commissurotomy for mitral stenosis. A prospective, randomized trial

BACKGROUND. We performed a prospective, randomized trial comparing percutaneous balloon commissurotomy with surgical closed commissurotomy in 40 patients with severe rheumatic mitral stenosis. METHODS AND RESULTS. Data were analyzed by investigators who were masked to treatment assignment or phase of study. Patients randomized to balloon (n = 20) or surgical (n = 20) commissurotomy had severe mitral stenosis without significant baseline differences (left atrial pressure, 26.1 +/- 4.2 versus 27.6 +/- 6.2 mm Hg; mitral valve gradient, 18.0 +/- 4.2 versus 19.7 +/- 6.3 mm Hg; mitral valve area, 1.0 +/- 0.2 versus 1.0 +/- 0.4 cm2, respectively). At 1-week follow-up after balloon commissurotomy, pulmonary wedge pressure was 14.3 +/- 7.2 mm Hg; mitral valve gradient was 9.6 +/- 5.1 mm Hg; and mitral valve area was 1.6 +/- 0.6 cm2 (all p less than 0.0001). At 1-week follow-up after surgical closed commissurotomy, wedge pressure was 13.7 +/- 5.4 mm Hg; mitral valve gradient was 9.4 +/- 4.2 mm Hg (both p less than 0.0001); and mitral valve area was 1.6 +/- 0.7 cm2 (p less than 0.003). At 8-month follow-up, improvement occurred in both groups: Mitral valve area was 1.6 +/- 0.6 cm2 in the balloon commissurotomy group (p less than 0.002) and was 1.8 +/- 0.6 cm2 in the surgical closed commissurotomy group (p less than 0.0001). There was no difference between the groups at 1-week or 8-month follow-up (all p greater than 0.4). One case of severe mitral regurgitation occurred in each group; complications were otherwise related to transseptal catheterization. There was no death, stroke, or myocardial infarction. Cost analysis revealed that balloon commissurotomy may substantially exceed the cost of surgical commissurotomy in developing countries, whereas it may represent a significant savings in industrialized nations. CONCLUSIONS. We conclude that percutaneous balloon commissurotomy and surgical closed commissurotomy result in comparable hemodynamic improvement that is sustained through 8 months of follow-up.     

Importance of the "atrial kick" in determining the effective mitral valve orifice area in mitral stenosis

Atrial fibrillation with a rapid ventricular response in patients with mitral stenosis (MS) is often accompanied by pulmonary congestion and reduced cardiac output owing to a diminished diastolic filling period and the loss of the end-diastolic left ventricular (LV) pressure increment. To test the hypothesis that loss of atrial contraction (atrial kick) also results in a decrease in effective mitral valve orifice area, 6 patients with pure, isolated MS were studied in sinus rhythm during atrial pacing and simultaneous atrioventricular pacing. Atrial pacing at 140 beats/min caused no significant change from baseline in cardiac output or mitral valve area, but there was a decrease in LV end-diastolic volume and ejection fraction as well as an increase in left atrial pressure and mean diastolic gradient. Simultaneous atrioventricular pacing (to eliminate atrial kick) induced a decrease in cardiac output (4.4 +/- 0.9 vs 5.2 +/- 0.8 liters/min at 110 beats/min, 4.2 +/- 0.9 vs 5.1 +/- 0.9 liters/min at 140 beats/min; p less than 0.05) and LV end-diastolic volume (77 +/- 27 vs 93 +/- 29 ml at 110 beats/min, 54 +/- 17 vs 65 +/- 19 ml at 140 beats/min; p less than 0.05), an increase in left atrial pressure (28 +/- 3 vs 20 +/- 5 mm Hg at 110 beats/min, 30 +/- 4 vs 25 +/- 5 mm Hg at 140 beats/min; p less than 0.05), and a decrease in mitral valve area (1.2 +/- 0.4 vs 1.4 +/- 0.5 cm2 at 110 beats/min, 1.2 +/- 0.4 vs 1.4 +/- 0.4 cm2 at 140 beats/min; p less than 0.05). Thus, loss of atrial kick may cause pulmonary congestion and reduced cardiac output in patients with MS, partly because of a decrease in effective mitral valve area.     

Results of percutaneous mitral commissurotomy in 200 patients

To assess the feasibility and efficacy of percutaneous mitral commissurotomy (PMC), the procedure was attempted in 200 patients with severe mitral stenosis. There were 154 women and 46 men, their mean age was 43 +/- 16 years (range 13 to 79) and 15 were older than 70 years of age. Forty-four had had previous surgical commissurotomy. Forty were in New York Heart Association class II, 152 in class III and 8 in class IV. In regard to valvular anatomy, 67 had calcified valves, 58 had pliable valves and only mild subvalvular disease, and 75 had flexible valves but extensive subvalvular disease. Grade 1+ mitral regurgitation was present in 62 and grade 2+ in 2. In 11 patients the procedure was discontinued because of complications in 3 and technical failure in 8. Six of the 8 technical failures occurred during the first 15 attempts. Effective PMC was performed in 189 patients using 1 balloon in 23 and 2 balloons in 166. After PMC, there was a significant improvement in mean left atrial pressure (21 +/- 7 to 12 +/- 5 mm Hg, p less than 0.0001), mean mitral gradient (16 +/- 6 to 6 +/- 2 mm Hg, p less than 0.0001), cardiac index (2.6 +/- 0.8 to 3.1 +/- 0.8 liters/min/m2, p less than 0.001) and valve area assessed by hemodynamics (1.1 +/- 0.3 to 2.2 +/- 0.5 cm2, p less than 0.0001) and 2-dimensional echocardiography (1 +/- 0.3 to 1.9 +/- 0.4 cm2, p less than 0.0001). No patient died. Embolism occurred in 8 (4%), with no further sequelae. Sixteen (8%) had atrial septal defect detected by oxymetry.(ABSTRACT TRUNCATED AT 250 WORDS)     

Short- and mid-term follow-up results after percutaneous transvenous mitral commissurotomy.

This study reports the clinical follow-up for 6 months of 52 patients who underwent percutaneous transvenous mitral commissurotomy (PTMC). PTMC resulted in an increase in mitral valve area from 1.1 +/- 0.3 to 1.7 +/- 0.4 cm2 (p < 0.0001), a decrease in mean left atrial pressure from 16 +/- 7 to 13 +/- 5 mmHg (p < 0.0001), and an increase in exercise time from 4.6 +/- 2.1 to 6.3 +/- 2.3 min (p < 0.0001). At 6 months follow-up, mitral valve area was unchanged (1.7 +/- 0.4 cm2). Of 52 patients, 33 showed clinical improvement and 19 had no clinical improvement after PTMC. Univariate analysis showed (1) younger age, (2) echocardiographic score of 8 or less, (3) existence of mitral regurgitation of less than grade 2 after PTMC, and (4) amelioration in left atrial dimension, mean pulmonary artery pressure and exercise time after PTMC as correlative factors for clinical improvement. In conclusion, PTMC was an effective procedure for mitral stenosis, especially in younger patients with an echocardiographic score of 8 or less. Change in left atrial dimension was a good indicator of the effectiveness of PTMC.     

Importance of the left ventricular filling pressure on diastolic filling in idiopathic dilated cardiomyopathy

Both mitral regurgitation and elevated left ventricular (LV) filling pressures may normalize or enhance rapid filling in patients with idiopathic dilated cardiomyopathy. To assess the individual effects of the LV filling pressure and mitral regurgitation, 33 normal subjects, 14 patients with cardiomyopathy and normal LV filling pressures (measured as mean pulmonary capillary pressure) and 26 patients with elevated LV filling pressures (greater than 15 mm Hg) were studied with transmitral spectral tracings derived from pulsed Doppler echocardiography. Both cardiomyopathy groups demonstrated similarly dilated left ventricles with reduced systolic dysfunction. Patients with cardiomyopathy and normal LV filling pressures had prolonged isovolumic relaxation periods and a reduced ratio of the rapid filling to atrial filling integrals. Patients with cardiomyopathy and elevated LV pressures demonstrated an increased peak rapid filling velocity (97 +/- 21 cm/s) and rapid filling fraction (74.8 +/- 16.2%) compared with normal subjects (80 +/- 16 cm/s, p less than 0.01; 62.4 +/- 12.5%, p less than 0.05) and patients with cardiomyopathy and normal LV filling pressures (81 +/- 27 cm/s, p less than 0.05; 59.3 +/- 8.8%, p less than 0.05). Conversely, the atrial filling fraction was decreased in the cardiomyopathy group with elevated LV filling pressures compared with normal subjects and patients with cardiomyopathy and normal LV filling pressures. Mitral regurgitation increased the peak rapid filling velocity in both cardiomyopathy groups without altering the distribution of diastolic filling. In conclusion, elevated LV filling pressures appear to affect the distribution of diastolic filling, whereas mitral regurgitation affects the peak rate of rapid filling.