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)     

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 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)     

Improvement in exercise capacity and exercise hemodynamics 3 months after double-balloon, catheter balloon valvuloplasty treatment of patients with symptomatic mitral stenosis

Clinical status, exercise treadmill performance, and hemodynamics were determined in 24 patients with symptomatic mitral stenosis before catheter balloon valvuloplasty (CBV) and at 3 months follow-up. Hemodynamic determinations at rest showed that mitral CBV performed by the double-balloon technique resulted in significant immediate decreases in mean pulmonary arterial wedge pressure (28 +/- 7 to 16 +/- 5 mm Hg, p less than .01), mean pulmonary arterial pressure (41 +/- 11 to 33 +/- 10 mm Hg, p less than .05), and mitral valve gradient (16 +/- 7 to 6 +/- 3 mm Hg, p less than .01), and significant increases in cardiac output (4.3 +/- 1.1 to 5.0 +/- 1.4 liters/min, p less than .01). Mitral valve area increased from 1.0 +/- 0.3 to 2.2 +/- 0.7 cm2 (p less than .01). The mitral valve area was unchanged (2.0 +/- 0.7 cm2, p = NS) at 3 months. The lower pulmonary arterial wedge pressure, pulmonary arterial pressure, and mitral valve gradient persisted at 3 month follow-up catheterization. Clinical examinations showed that before CBV, 21 of 24 patients were in New York Heart Association functional class III or IV; 3 months after CBV, 22 patients were in class I or II. Before CBV, the mean exercise treadmill time was 5.9 +/- 3.2 min and it had increased to 9.8 +/- 2.9 min (p less than .01) by the 3 month follow-up.(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)     

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.     

The usefulness of dobutamine in the assessment of the severity of mitral stenosis

Patients with mitral stenosis often require supine exercise in order to increase their heart rate and cardiac output to assess the severity of their valvular obstruction during cardiac catheterization. We substituted dobutamine for exercise in 14 patients with suspected mitral stenosis. The dobutamine infusion was started at 5 micrograms/kg/min and was increased to 10, 15, and 20 micrograms/kg/min every 3 minutes as tolerated. The heart rate increased from 84 +/- 4 to 123 +/- 7 bpm (p less than 0.001), the cardiac index increased from 2.4 +/- 0.2 to 3.4 +/- 0.2 L/min/m2 (p less than 0.001), and the mean pulmonary artery pressure increased from 27 +/- 3 to 30 +/- 2 mm Hg (p less than 0.02). The pulmonary wedge pressure of 19 +/- 2 mm Hg and the mitral valve index of 0.8 +/- 0.1 cm2/m2 remained unchanged, but the left ventricular end-diastolic pressure decreased from 11 +/- 2 to 6 +/- 2 mm Hg (p less than 0.02). The hemodynamic response during the infusion of dobutamine identified a subgroup of patients with more severe mitral stenosis. Thus, the administration of dobutamine is useful in the evaluation of the severity of mitral valve obstruction during catheterization.     

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)     

Spectrum of hemodynamic changes in cardiac tamponade

To investigate the pathophysiology of cardiac tamponade, the hemodynamics of 77 consecutive patients with greater than 150 ml of pericardial effusion were studied. Patients were classified into 3 groups based on the equilibration of intrapericardial with right atrial and pulmonary arterial wedge pressures (mm Hg): group I (n = 16), intrapericardial pressure was less than right atrial and pulmonary arterial wedge pressures; group II (n = 13), intrapericardial pressure was equilibrated with right atrial but not pulmonary arterial wedge pressures; group III (n = 48), intrapericardial pressure was equilibrated with right atrial and pulmonary arterial wedge pressures. Pericardiocentesis produced the following changes: group I--significant (p less than 0.03) decreases in intrapericardial pressure (7 +/- 2 mm Hg), right atrial pressure (3 +/- 2 mm Hg), pulmonary arterial wedge pressure (2 +/- 2 mm Hg), and the inspiratory decrease in arterial systolic pressure (3 +/- 4 mm Hg) but no significant change in cardiac output; group II--significant (p less than 0.02) decreases in intrapericardial pressure (11 +/- 5 mm Hg), right atrial pressure (6 +/- 4 mm Hg), pulmonary arterial wedge pressure (4 +/- 5 mm Hg), and inspiratory decrease in arterial systolic pressure (8 +/- 7 mm Hg), and increase in cardiac output (1.1 +/- 1.2 liters/min); group III--significant (p less than 0.001) decreases in intrapericardial pressure (16 +/- 7 mm Hg), right atrial pressure (9 +/- 4 mm Hg), pulmonary arterial wedge pressure (8 +/- 5 mm Hg), inspiratory decrease in arterial systolic pressure (17 +/- 11 mm Hg), and increase in cardiac output (2.8 +/- 1.5 liters/min). The changes after pericardiocentesis in all parameters were significantly (p less than 0.05) greater in group III than in groups I or II except for the change in right atrial pressure, which was not significantly different in groups II versus III. The changes after pericardiocentesis indicate pericardial effusion caused the greatest abnormalities in group III but also caused significant abnormalities of pressure and flow in group II and of pressure alone in group I.(ABSTRACT TRUNCATED AT 250 WORDS)     

Balloon dilation of mitral stenosis in adult patients: postmortem and percutaneous mitral valvuloplasty studies

Preliminary reports have documented the utility of percutaneous balloon valvuloplasty of the mitral valve in adult patients with mitral stenosis, but the mechanism of successful valve dilation and the effect of mitral valvuloplasty on cardiac performance have not been studied in detail. Accordingly, mitral valvuloplasty was performed in five postmortem specimens and in 18 adult patients with rheumatic mitral stenosis, using either one (25 mm) or two (18 and 20 mm) dilation balloons. Postmortem balloon dilation resulted in increased valve orifice area in all five postmortem specimens, secondary to separation of fused commissures and fracture of nodular calcium within the mitral leaflets. In no case did balloon dilation result in tearing of valve leaflets, disruption of the mitral ring or liberation of potentially embolic debris. Percutaneous mitral valvuloplasty in 18 patients with severe mitral stenosis (including 9 with a heavily calcified valve) resulted in an increase in cardiac output (4.3 +/- 1.1 to 5.1 +/- 1.5 liters/min, p less than 0.01) and mitral valve area (0.9 +/- 0.2 to 1.6 +/- 0.4 cm2, p less than 0.0001), and a decrease in mean mitral pressure gradient (15 +/- 5 to 9 +/- 4 mm Hg, p less than 0.0001), pulmonary capillary wedge pressure (23 +/- 7 to 18 +/- 7 mm Hg, p less than 0.0001) and mean pulmonary artery pressure (36 +/- 12 to 33 +/- 12 mm Hg, p less than 0.01). Left ventriculography before and after valvuloplasty in 14 of the 18 patients showed a mild (less than or equal to 1+) increase in mitral regurgitation in five patients and no change in the remainder.(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.     

Hemodynamic response to exercise after propranolol in patients with mitral stenosis.

Hemodynamic response to exercise before and 10 minutes after propranolol (5 mg intravenously) was studied in 10 young patients with pure mitral stenosis who had normal sinus rhythm and no cardiac failure. After propranolol the mean heart rate and cardiac index at rest were lower than during the control state (respectively, 95 +/- 4 versus 82 +/- 3 beats/min, P less than 0.005; 3.4 +/- 0.2 versus 2.8 +/- 0.1 liters/min per m2, P less than 0.025). As a result, the mean pulmonary wedge pressure and mean mitral valve gradient at rest were lower (respectively, 22 +/- 2 versus 18 +/- 2 mm Hg, P less than 0.005; 24 +/- 2 versus 17 +/- 2 mm Hg, P less than 0.001). During exercise after propranolol the values of pulmonary wedge pressure and mitral valve gradient were lower than control values during exercise (respectively, 39 +/- 3 versus 30 +/- 2 mm Hg, P less than 0.005; 44 +/- 3 versus 32 +/- 3 mm Hg, P less than 0.005), again because of the lower heart rate and cardiac index (130 +/- 6 versus 104 +/- 6 beats/min, P less than 0.001; 4.6 +/- 3 versus 3.7 +/- 2 liters/min per m2, P less than 0.01). Left ventricular end-diastolic pressure and stroke index showed no significant changes. Thus, propranolol may benefit patients with pure mitral stenosis with sinus rhythm and no cardiac failure whose symptoms occur during those reversible conditions characterized by an increase in heart rate or cardiac output, or both.     

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.     

Prospective study comparing different echocardiographic measurements of pulmonary capillary wedge pressure in patients with organic heart disease other than mitral stenosis

In 25 patients with cardiac disease, but free of left ventricular inflow obstruction, the electrocardiogram and M-mode echocardiogram of the aortic root, left atrium and both the mitral and the aortic valves were obtained simultaneously with the pulmonary artery wedge pressure (PAWP) during right heart catheterization. The echocardiographic measurements of the left atrial size, PR-AC interval, left atrial emptying index and the ratio between the electrocardiographic Q wave to mitral valve closure (Q-MVC) and between aortic valve closure to the mitral E point (AVC-E) were correlated to the pulmonary artery wedge pressure by means of linear regression analysis. A formula in which PAWP = 36.6 (Q-MVC/AVC-E)-- 2 was prospectively used to study the measured pressure in the current group of patients. The pulmonary artery wedge pressure derived from these latter measurements correlated well with the invasive measurement of this pressure (r = 0.91). The pulmonary artery wedge pressure calculated by echocardiography differed from the pulmonary artery wedge pressure measured by catheterization by 3 mm Hg or less in 19 of the 25 patients, by 4 mm Hg or less in 22 patients and by 6 mm Hg or less in 24 patients. Although the correlation between the (Q-MVC/AVC-E) ratio and measured pulmonary artery wedge pressure was highly significant (r = 0.91, probability [p] less than 0.001, n = 25), the left atrial emptying index, PR-AC and left atrial size revealed poor correlation coefficients (r = 0.45, r = 0.45 and r = 0.56 [p less than 0.05]), 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.     

Progressive improvement in pulmonary vascular resistance after percutaneous mitral valvuloplasty

Percutaneous mitral valvuloplasty has been proposed as a nonsurgical technique for treating high-risk patients with mitral stenosis who are deferred from mitral valve replacement. The effect of this technique on patients with pulmonary hypertension, however, has not been fully evaluated. Accordingly, serial assessment of pulmonary vascular resistance was made in 14 patients with critical mitral stenosis and pulmonary hypertension (pulmonary vascular resistance greater than 250 dynes.sec/cm5 or mean pulmonary artery pressure greater than 40 mm Hg or both) who underwent percutaneous balloon dilatation of the mitral valve. Balloon valvuloplasty was performed with either one (n = 10) or two (n = 4) balloons through the transseptal approach, and it resulted in significant improvement in mean mitral gradient (from 18 +/- 4 to 9 +/- 4 mm Hg, p less than 0.001), systemic blood flow (from 3.7 +/- 1.2 to 5.0 +/- 2.2 l/min, p less than 0.001), and calculated mitral valve area (from 0.7 +/- 0.2 to 1.6 +/- 0.7 cm2, p less than 0.001). Immediately after balloon mitral valvuloplasty, pulmonary vascular resistance fell from 630 +/- 570 to 447 +/- 324 dynes.sec/cm5. Repeat catheterization 7 +/- 4 months after valvuloplasty showed further improvement of pulmonary hypertension in 12 of the 14 patients, with a mean pulmonary vascular resistance for the group as a whole of 280 +/- 183 dynes.sec/cm5, p less than 0.005. In two patients, mitral valve restenosis to a mitral valve area less than 1.0 cm2 was associated with a return of pulmonary hypertension to predilatation values.(ABSTRACT TRUNCATED AT 250 WORDS)     

Influence of left ventricular filling profile on the effect of atrioventricular synchronous pacing.

We correlated the percentage of atrial contribution to left ventricular filling (percent AC) assessed by Doppler echocardiography with the hemodynamic benefit from atrioventricular synchronous pacing assessed by direct hemodynamic measurements. Subjects comprised 40 patients who underwent electrophysiologic catheterization because of unexplained syncope or bradycardia (< 40 beats/min). Femoral arterial and pulmonary capillary wedge pressure were recorded by catheterization, and cardiac output was measured by thermodilution during temporary atrioventricular synchronous (DDD, 70 beats/min with 150 ms of atrioventricular delay) and ventricular (VVI, 70 beats/min) pacing. Mitral inflow velocity by pulsed-wave Doppler echocardiography was recorded during DDD pacing and percent AC was obtained by calculating the ratio of mitral inflow velocity area during atrial systole to total mitral inflow velocity area during early diastole and atrial systole. The mean arterial pressure and the cardiac output increased significantly (99 +/- 16 mm Hg vs 90 +/- 15 mm Hg, p < 0.001; 4.6 +/- 1.0 L/min vs 3.9 +/- 0.9 L/min, p < 0.001), and the mean pulmonary capillary wedge pressure decreased (7 +/- 4 mm Hg vs 10 +/- 4 mm Hg, p < 0.001) during DDD compared with VVI pacing. A significant positive correlation was observed between the percent AC and the increase in cardiac output (r = 0.58, n = 40, p < 0.01) or the increase in mean arterial pressure (r = 0.62, n = 38, p < 0.01) during DDD pacing. The percent AC did not significantly correlate with the decrease in pulmonary capillary wedge pressure. In conclusion, patients with larger percent AC may receive major benefit from atrioventricular synchronous pacing.     

Serial assessment of mitral regurgitation by pulsed Doppler echocardiography in patients undergoing balloon aortic valvuloplasty

Mitral regurgitation was serially assessed by pulsed Doppler echocardiography in 144 patients undergoing balloon aortic valvuloplasty for symptomatic aortic stenosis. Regurgitant scores of 0, 1, 2 and 3 were assigned to pulsed Doppler patterns corresponding to no, mild, moderate and severe mitral regurgitation, respectively. Before balloon aortic valvuloplasty, mitral regurgitant score correlated significantly (p less than 0.005) but weakly with aortic valve area (r = -0.24), left ventricular ejection fraction (r = -0.34) and left ventricular systolic pressure (r = 0.23). There was no significant correlation between mitral regurgitation and either mean catheterization or mean Doppler aortic valve gradient. Balloon aortic valvuloplasty produced significant decreases in both catheterization and Doppler mean transvalvular aortic valve gradients (56 +/- 19 to 31 +/- 12 and 60 +/- 19 to 48 +/- 16 mm Hg, respectively; both p less than 0.0001) and a significant increase (p less than 0.0001) in aortic valve area assessed by catheterization (0.6 +/- 0.2 to 0.9 +/- 0.3 cm2). Left ventricular ejection fraction did not change, but cardiac output increased (p less than 0.001) and pulmonary capillary wedge pressure decreased (p less than 0.0001). Pulsed Doppler findings of mitral regurgitation were present in 102 of the 144 patients. Eighty-eight patients had a score compatible with mild or more severe degrees of mitral regurgitation, and 49 had a score indicative of moderate or severe valvular insufficiency. In the entire group of 144 patients, mitral regurgitant score decreased significantly from 1.1 +/- 1.0 to 1.0 +/- 1.0 (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Motion analysis of the Carpentier ring in the tricuspid position: an echocardiographic and hemodynamic study

The echocardiographic and hemodynamic results before and after (30 +/- 4 months) mitral valve replacement and tricuspid valvuloplasty using a Carpentier ring were compared in 37 patients. The motion of the Carpentier ring in the echocardiogram was related to the pulmonary artery pressure curve and the intracardiac phonocardiogram for exact temporal relation. Pressure measurements were done using a tip micromanometer. Postoperatively 29 patients were clinically improved showing a decrease of the mean pulmonary artery pressure from 63 +/- 14 mm Hg to 41 +/- 18 mm Hg (p less than 0.001) as well as of the right atrial pressure from 13 +/- 4 mm Hg to 8 +/- 3 mm Hg (p less than 0.01). The postoperative decrease of the opening amplitude of the septal tricuspid leaflet from 22 +/- 3 mm to 10 +/- 4 mm (p less than 0.001) and of the EF-slope from 125 +/- 45 mm/s to 34 +/- 41 mm/s (p less than 0.001) in 9 patients was a sign of an inflow obstruction in the right ventricle. During the synchronous pressure measurement in the right ventricle and in the right atrium, a mean diastolic pressure gradient of 3.9 +/- 1.4 mm Hg was registered postoperatively in these patients. Five patients showed persisting right heart failure, in one a severe tricuspid regurgitation was still present, in 4 patients the pressure gradient exceeded 5 mm Hg.(ABSTRACT TRUNCATED AT 250 WORDS)     

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.