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.     

Blade atrial septostomy: experience with the first 50 procedures

We have performed 50 blade and balloon atrial septostomies in 46 patients with diagnoses of transposition of the great arteries--32 patients; mitral atresia or stenosis--10 patients; total anomalous pulmonary venous drainage--2 patients; tricuspid atresia--1 patient; and pulmonary valve atresia with hypoplastic right ventricle--1 patient. The patients' age ranged from 1 day to 72 months (median = 8 months) and weights ranged from 2.7 to 14.5 kg. In patients with transposition the systemic saturation increased from an average of 62% to 74.6% (p less than 0.001) and the inter-atrial mean pressure gradient was reduced from 7.74 +/- 5.3 to 1.4 +/- 2.04 mm Hg. Patients with mitral atresia had no significant increase in systemic arterial saturation but a significant decrease in the mean inter-atrial gradient from 19.6 +/- 12.4 to 3.8 +/- 5.3 mm Hg. In three patients the blade septostomy was unsuccessful for technical reasons and the condition of the patient. Complications included one death due to atrial laceration, blood loss requiring transfusion in 5 patients, transient CVA in one patient, and failure of the blade to close in one patient. We have found the palliative use of the blade catheter in conjunction with balloon atrial septostomy to be an effective and safe procedure.     

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 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)     

Clinical and hemodynamic characteristics of patients with inducible pulsus alternans

Pulsus alternans can be found in some patients with abnormal left ventricular function and also can develop after spontaneous premature beats. The purposes of this study were to: (1) determine the inducibility of pulsus alternans in a series of patients referred for routine cardiac catheterization and (2) define the clinical and hemodynamic characteristics of those who develop pulsus alternans. In 104 patients referred for right and left heart catheterization, atrial premature beats and rapid atrial pacing were used to try to provoke pulsus alternans. The 29 patients who developed pulsus alternans in response to these maneuvers were older (63 +/- 6 vs 59 +/- 10 years, p less than 0.01) and had a greater incidence of valvular heart disease (45% vs 23%, p less than 0.01) and congestive heart failure (38% vs 17%, p less than 0.05). Aortic stenosis was the most prevalent valve lesion found. Those who developed pulsus alternans in response to pacing were further characterized by higher left ventricular systolic (143 +/- 42 vs 121 +/- 23 mm Hg, p less than 0.02) and end-diastolic pressures (17 +/- 9 vs 13 +/- 6 mm Hg, p less than 0.05), higher pulmonary artery systolic pressure (35 +/- 14 vs 29 +/- 11 mm Hg, p less than 0.04), and lower left ventricular ejection fractions (0.42 +/- 0.13 vs 0.53 +/- 0.14, p less than 0.001). Eight patients (28%) with inducible pulsus alternans had a normal left ventricular ejection fraction (greater than 0.50) and left ventricular end-diastolic pressure (less than 13 mm Hg).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of induced ventricular tachycardia on atrial natriuretic peptide in humans

The effects of induced sustained ventricular tachycardia on the release of plasma-immunoreactive atrial natriuretic peptide were evaluated in 11 adult patients undergoing diagnostic electrophysiologic study. Plasma concentrations of atrial natriuretic peptide withdrawn from the right atrium before and during sustained ventricular tachycardia (mean tachycardia cycle length 320 +/- 68 ms, duration greater than 30 s) were determined by radioimmunoassay. Hemodynamic measurements included phasic femoral artery blood pressure and mean right atrial blood pressure before and during ventricular tachycardia. During ventricular tachycardia, atrial natriuretic peptide increased from 93 +/- 49 pg/ml to 234 +/- 195 pg/ml (p less than 0.05), systolic arterial blood pressure decreased from 120 +/- 16 to 70 +/- 23 mm Hg (p less than 0.001), diastolic arterial blood pressure decreased from 63 +/- 8 to 51 +/- 16 mm Hg (p = NS) and mean right atrial blood pressure increased from 3 +/- 1 to 8 +/- 5 mm Hg (p less than 0.02). In six patients, all hemodynamic variables and the atrial natriuretic peptide were measured during repeated stimulation protocols to investigate the effect of ventricular stimulation for ventricular tachycardia induction on atrial natriuretic factor release. Compared with the values obtained during sinus rhythm, there was no significant increase in atrial natriuretic factor during ventricular stimulation at a cycle length of 600 ms (45 +/- 20 versus 52 +/- 21 pg/ml) or at a cycle length of 400 ms (45 +/- 20 versus 57 +/- 18 pg/ml). No significant linear relation could be found among the changes in mean right atrial pressure, systolic arterial blood pressure and the increase in atrial natriuretic peptide.(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)     

A new configuration for right ventricular assist with skeletal muscle ventricle. Short-term studies

BACKGROUND. Previous attempts to provide right heart assistance with skeletal muscle ventricles (SMVs) have been frustrated by the low preload supplied by the systemic venous blood pressure. In the present study, right ventricular pressure was exploited to provide more optimal preload, the SMV being connected by valved conduits between right ventricular free wall and the main pulmonary artery. METHODS AND RESULTS. SMVs were constructed from the right latissimus dorsi muscle in seven mongrel dogs. Following a delay period of 4 weeks, SMVs were preconditioned with 2-Hz continuous stimulation for 5-6 weeks. The SMV was then connected to the right ventricle using a porcine valved Dacron conduit. A similar valved conduit connected the SMV to the main pulmonary artery that had been ligated proximally. SMVs were stimulated with 33-Hz burst frequency to contract synchronously with ventricular diastole in a 1:2 mode. The stimulator was intermittently turned off to permit comparison of assisted and nonassisted circulation. Cardiac output increased by 27% at 1 hour (1,437 +/- 54 versus 1,140 +/- 64 ml/min, p less than 0.005) and by 30% at 4 hours (1,403 +/- 161 versus 1,074 +/- 99 ml/min, p less than 0.005), systemic arterial systolic pressure increased at 1 hour by 12% (87.1 +/- 4.9 versus 78.0 +/- 4.9 mm Hg, p less than 0.05) and by 13% at 4 hours (81.4 +/- 2.8 versus 72.3 +/- 3.4 mm Hg, p less than 0.005), and peak pulmonary arterial pressure increased at 1 hour by 35% (28.0 +/- 2.1 versus 20.9 +/- 1.8 mm Hg, p less than 0.01) and by 37% at 4 hours (31.5 +/- 2.6 versus 23.0 +/- 0.4 mm Hg, p less than 0.05). Peak SMV pressure was 52.8 +/- 2.0 mm Hg at 1 hour and 49.9 +/- 3.3 mm Hg at 4 hours (p = NS). CONCLUSIONS. The improved preload supplied by this configuration of right ventricular assist enabled an SMV to provide stable and effective circulatory support throughout the 4-hour duration of the experiment.     

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)     

Increased circulating endothelin-1 in rheumatic mitral stenosis: irrelevance to left atrial and pulmonary artery pressures

BACKGROUND: Increased plasma endothelin (ET)-1 concentrations have been observed in patients with rheumatic mitral stenosis (MS). However, the mechanisms of increased circulating ET-1 in patients with MS remain unclear. METHODS: We measured plasma concentrations of ET-1 in blood samples from the femoral vein and artery, and right and left atria obtained from 20 patients with moderate-to-severe rheumatic MS before and after percutaneous transluminal mitral valvuloplasty (PTMV) [group 1; 16 patients in chronic atrial fibrillation and 4 patients in sinus rhythm]. In addition, we measured plasma concentrations of ET-1 in the peripheral venous blood samples obtained from 22 control patients (including 14 healthy volunteers in sinus rhythm [group 2] and 8 patients in chronic lone atrial fibrillation [group 3]). Plasma ET-1 concentrations were measured by solid-phase, sandwich enzyme-linked immunosorbent assay. RESULTS: The peripheral venous plasma concentrations of ET-1 were significantly higher in group 1 patients (2.46 +/- 0.90 pg/mL) than in group 2 and group 3 patients (0.74 +/- 0.42 pg/mL and 0.99 +/- 0.41 pg/mL, respectively [mean +/- SD]; p < 0.0001). However, there was no significant difference in the peripheral venous concentrations of ET-1 between group 2 and group 3 patients. In group 1 patients, the plasma ET-1 concentration in the femoral vein (2.46 +/- 0.90 pg/mL) was significantly higher than that in the right atrium (2.02 +/- 0.69 pg/mL), left atrium (2.11 +/- 0.99 pg/mL), and femoral artery (2.05 +/- 0.75 pg/mL) [p = 0.0001]. The plasma ET-1 concentration in the femoral vein was not correlated with the mean left atrial pressure (r = 0.05; p = 0.838) and mean pulmonary artery pressure (r = 0.07; p = 0.757). The plasma ET-1 concentration in the left atrium was also not correlated with the mean left atrial pressure (r = 0.11; p = 0.656), mean pulmonary artery pressure (r = 0.06; p = 0.788), or mitral valve area (r = 0.02; p = 0.936). Although the area of mitral valve increased significantly (1.06 +/- 0.17 cm(2) vs 1.48 +/- 0.32 cm(2); p < 0.0001), and the mean left atrial pressure (23.0 +/- 5.1 mm Hg vs 17.6 +/- 5.9 mm Hg; p < 0.0001) and mean pulmonary arterial pressure (31.0 +/- 7.9 mm Hg vs 25.5 +/- 7.0 mm Hg; p < 0.001) fell significantly and immediately after PTMV, there were no significant changes in the plasma ET-1 concentrations in the femoral vein, right atrium, left atrium, and femoral artery immediately after PTMV. CONCLUSION: Increased production of ET-1 in the pulmonary circulation in response to increased pulmonary artery pressure was not the mechanism of increased circulating ET-1 concentration in patients with MS. We proposed that one of the mechanisms of increased ET-1 concentration in the femoral vein was increased peripheral ET-1 release due to increased systemic venous pressure and mechanical damage of the endothelium.     

Exercise-induced secretion of atrial natriuretic factor and its relation to hemodynamic and sympathetic stimulation in untreated essential hypertension.

This study evaluates the release of atrial natriuretic factor (ANF) during maximal exercise in 7 patients with untreated moderate to severe hypertension with invasive monitoring of hemodynamic characteristics in relation to sympathetic activity. Peripheral venous ANF (fmol/ml) was determined at rest and maximal exercise producing a respiratory exchange ratio of 1.14 +/- 0.10. In 5 of 7 patients, simultaneous right ventricular and peripheral venous ANF samples could be obtained to assess exercise myocardial secretion of ANF. With exercise, mean blood pressure increased from 150 +/- 26 to 192 +/- 29 mm Hg (p less than 0.001), pulmonary wedge pressure increased from 7 +/- 3 to 18 +/- 10 mm Hg (p less than 0.05) and ANF increased from 11.7 +/- 8.2 to 25.7 +/- 15.9 (p less than 0.02). This ANF response correlated weakly with pulmonary wedge pressure (r = 0.497, p = not significant), since patients without an increase in pulmonary wedge pressure had no increase in ANF. However, changes in pulmonary wedge pressure and plasma norepinephrine during exercise were inversely correlated (r = -0.811, p less than 0.02), with the greatest increase in norepinephrine occurring with a minimal increase in pulmonary wedge pressure. Similarly, ANF and plasma norepinephrine were inversely correlated during exercise (r = -0.869, p less than 0.05). A significant increase in right ventricular ANF indicated myocardial secretion. Plasma ANF therefore increased because of active myocardial production during exercise in patients with moderate to severe hypertension. These findings further suggest a directionally opposing relation between ANF release resulting from increased atrial tension and sympathetic nervous system influence on cardiac performance during exercise.     

Effect of abrupt mitral regurgitation after balloon valvuloplasty on myocardial load and performance

The concept that mitral regurgitation masks myocardial dysfunction by reducing afterload and augmenting ejection performance has not been well established in humans. The effect of abruptly produced mitral regurgitation on left ventricular loading and performance was therefore evaluated in five patients who developed this complication after an otherwise successful percutaneous balloon mitral valvuloplasty. Mitral valve area by Gorlin formula calculated with forward flow increased from 0.92 +/- 0.14 to 2.75 +/- 0.82 cm2. Mean left atrial pressure did not decrease (19 +/- 4 to 19 +/- 6 mm Hg). The size of the left atrial V wave relative to mean left atrial pressure (peak V - mean left atrial pressure) increased from 7 +/- 4 to 19 +/- 6 mm Hg. Angiographic mitral regurgitation increased from 0+ or 1+ to greater than 3+ in each patient and regurgitant fraction increased from 0.23 +/- 0.11 to 0.55 +/- 0.09 (p less than 0.01). End-diastolic volume increased modestly from 148 +/- 15 to 159 +/- 15 ml (p = NS). Heart rate increased from 54 +/- 5 to 71 +/- 8 beats/min (p less than 0.05), which may have prevented further increases in preload by shortening the filling period. End-systolic stress decreased by 32% from 277 +/- 34 to 188 +/- 52 kdyn/cm2 (p less than 0.01) as a result of a 25% decrease in end-systolic pressure from 121 +/- 8 to 91 +/- 7 mm Hg and a 16% decrease in end-systolic volume from 67 +/- 13 to 56 +/- 8 ml (p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)     

Acute hemodynamic effect of oral MDL 17,043 in severe congestive heart failure

MDL 17,043, when administered intravenously in humans, produces a significant and salutary hemodynamic response. To determine its acute effect when administered orally (3 mg/kg), 10 patients with severe congestive heart failure were studied by right-sided cardiac catheterization for 8 hours. At 4 hours after drug ingestion, there was significant improvement in several hemodynamic measurements. Cardiac index increased 38% over baseline (from 1.9 +/- 0.4 to 2.6 +/- 0.4 liters/min/m2, p less than 0.01), arteriovenous oxygen difference decreased by 30% (from 8.0 +/- 1.4 to 5.6 +/- 1.2 vol%, p less than 0.01), heart rate increased by 8% (from 85 +/- 16 to 92 +/- 16 beats/min, p less than 0.05), stroke volume index increased by 22% (from 23 +/- 5 to 28 +/- 4 ml/beat/m2, p less than 0.05), left ventricular stroke work increased by 24% (from 18 +/- 5 to 22 +/- 5 g-m/m2, p less than 0.01), mean arterial pressure decreased by 10% (from 79 +/- 6 to 71 +/- 9 mm Hg, p less than 0.01), mean right atrial pressure decreased by 40% (from 10 +/- 5 to 6 +/- 4 mm Hg, p less than 0.01), and mean pulmonary artery wedge pressure decreased by 36% (from 22 +/- 5 to 14 +/- 6 mm Hg, p less than 0.01). Cardiac index, arteriovenous oxygen difference, mean arterial pressure, right atrial pressure, and pulmonary artery wedge pressure remained significantly improved at 8 hours. These findings indicate that MDL 17,043 is active when administered orally and produces beneficial hemodynamic effects for as long as 8 hours.     

Preserved atrial natriuretic peptide secretory function after cardiac transplantation.

The purpose of this investigation was to determine whether atrial natriuretic peptide (ANP) secretory function is preserved after cardiac transplantation. Thirteen hemodynamically stable outpatients performed supine exercise on a bicycle an average of 7 months after orthotopic cardiac transplantation. Right atrial pressure increased 2.2-fold (6 +/- 1 to 13 +/- 2 mm Hg) and pulmonary artery wedge pressure 2.1-fold (11 +/- 1 to 23 +/- 7 mm Hg) with exercise in the transplant recipients. Resting venous ANP level (114 +/- 19 pg/ml) and peak exercise venous level (373 +/- 61 pg/ml) was elevated in transplant recipients (p less than 0.001) compared with control subjects (21 +/- 1 and 92 +/- 14 pg/ml, respectively. This represents a 3.3-fold (114 +/- 19 to 373 +/- 61 pg/ml) increase in the ANP level from resting to exercise in transplant recipients and a 4.4-fold (21 +/- 1 to 92 +/- 14 pg/ml) increase in control subjects. A correlation between venous ANP levels and hemodynamics (right atrial pressure) was observed r = 0.49 p = 0.01. It is concluded that ANP levels at rest are elevated after cardiac transplant, the levels correlate with the intracardiac hemodynamics, and exercise-induced augmentation of plasma levels occurs.     

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)     

The hemodynamic effects of cardiac tamponade: mainly the result of atrial, not ventricular, compression

We studied the hemodynamic effects of surgically induced regional cardiac tamponade in anesthetized dogs. Tamponade restricted to either the right or the left ventricle was compared with tamponade of either ventricle and both atria. Intrapericardial pressures were elevated to approximately 20 mm Hg. With tamponade of the right ventricle alone, aortic pressure rose from 161 +/- 3.8 to 164 +/- 3.4 mm Hg (p greater than .05) and cardiac output fell from 149.4 +/- 16.1 to 134.9 +/- 11.9 ml/kg/min (p greater than .05). However, tamponade of the right ventricle plus both atria decreased mean aortic pressure from 152.5 +/- 3.6 to 115.9 +/- 8.7 mm Hg (p less than .01) and cardiac output fell from 118 +/- 14.8 to 38.9 +/- 4.8 ml/kg/min (p less than .01). With tamponade of the left ventricle alone, aortic mean pressure changed significantly from 158.5 +/- 6.1 (control) to 148.9 +/- 5.0 mm Hg (tamponade) (p less than .05) and cardiac output was 135.5 +/- 28.3 (control) and 111 +/- 24.7 ml/kg/min (tamponade) (p greater than .05). However, when the atria were included, mean aortic pressure fell significantly more from 155.5 +/- 5.4 to 105.5 +/- 10.4 mm Hg (p less than .01) and cardiac output fell from 142.2 +/- 16 to 47.8 +/- 6.4 ml/kg/min (p less than .01). Atrial pressure rose when the atria were included, but not with tamponade of the left ventricle alone. Right but not left atrial pressure rose slightly with isolated right ventricular tamponade. We conclude that the principal hemodynamic effects of cardiac tamponade are not the result of compression of either the right or the left ventricle, but are the consequence of compression of the atria and/or the venae cavae and the pulmonary veins.     

Effect of AV synchronization and rate increase on hemodynamics and on atrial natriuretic peptide in patients with total AV block

We studied nine patients (56 +/- 7 years) with complete AV-block and permanent dual-chamber pacemaker (DDD) under different pacing modes: ventricle pacing (VVI) 70 bpm, DDD 106 +/- 4 bpm, rate adaptive pacing (VVI-FA) 108 +/- 3 bpm. Exercise was performed supine on the bicycle ergometer at 50 watts for 5 min at each setting. DDD-paced patients showed significantly higher mixed venous oxygen saturation, being 45 +/- 2% after the fourth minute, (VVI 38 +/- 2%, p less than 0.01 and VVI-FA paced patients 40 +/- 1%, p less than 0.01). Pressures were normal under DDD pacing during exercise (RAP 7 +/- 2 mm Hg; PCP 14 +/- 3 mm Hg) and showed further increase to abnormal levels during VVI (RAP 13 +/- 2 mm Hg, p less than 0.01; PCP 21 +/- 3 mm Hg, p less than 0.02) and VVI-FA pacing (RAP 10 +/- 2 mm Hg, p less than 0.05; PCP 20 +/- 3 mm Hg, p less than 0.01). Stroke volume increased from 71 +/- 5 ml to 105 +/- 7 ml during VVI and from 64 +/- 7 ml to 81 +/- 7 ml during DDD pacing. Stroke volume remained unchanged (69 +/- 5 ml) during VVI-FA pacing. The peak levels of ANP during and after exercise were significantly higher under VVI (951 +/- 248 pg/ml) than under DDD pacing (650 +/- 140 pg/ml, p less than 0.01) and were not different between DDD and VVI-FA pacing (677 +/- 97 pg/ml). These results show that VVI pacing effects a more pronounced increase of ANP level than other pacing modes. Under moderate exercise, rate-responsive pacing compared to VVI pacing showed no differences in mixed venous oxygen saturation and in atrial pressures. Only DDD pacing showed higher oxygen saturation and a normalization of atrial pressures when compared to other types of single chamber pacing.     

Single, total paracentesis for tense ascites: sequential hemodynamic changes and right atrial size

Hemodynamic changes induced by a single, total paracentesis were evaluated in 21 patients with tense ascites from whom 4 to 16 L of ascites were drained over 2 to 8 hr with no serious complications. At 60 min, compared to baseline, there was an increase in cardiac output (7.7 +/- 0.5 to 8.5 +/- 0.6 L/min, p less than 0.02) and a tendency for right atrial pressure to decrease (9.3 +/- 0.8 to 7.50 +/- 0.8 mm Hg, NS), with no change in pulmonary capillary wedge pressure (10.9 +/- 0.9 to 10.7 +/- 0.9 mm Hg). Between 3 and 12 hr later, there was a drop in right atrial pressure, pulmonary capillary wedge pressure and cardiac output to 5.6 +/- 0.6 (p less than 0.02), 7.2 +/- 0.8 mm Hg (p less than 0.002) and 7.2 +/- 0.6 L/min (NS) respectively, indicative of the development of relative hypovolemia and suggesting that therapeutic plasma expansion is appropriate at this time. Two-dimensional echocardiography before paracentesis (n = 8) showed a reduction in the right to left atrium area ratio as compared with values in patients with minimal ascites (0.54 +/- 0.04 vs 0.82 +/- 0.02, p less than 0.0001). This technique may help in identifying patients with right atrial compression caused by tense ascites.     

Effects of atrial natriuretic factor on coronary hemodynamics and myocardial energetics in patients with heart failure

Synthetic analogues of atrial natriuretic factor (ANF) have been developed for potential use as therapeutic agents in the treatment of congestive heart failure and hypertension. We studied the effects of 14 intravenous infusions of synthetic ANF (anaritide, human ANF 102-126) on coronary hemodynamics and myocardial energetics in six patients with heart failure. ANF infusion caused no change in coronary blood flow and a fall in coronary vascular resistance from 1.22 +/- 0.22 to 1.08 +/- 0.18 mm Hg-min/ml (p less than 0.05). Myocardial oxygen and lactate consumption were unchanged from baseline values. Mean arterial pressure fell from 91 +/- 4 to 78 +/- 3 mm Hg (p less than 0.01), right atrial pressure fell from 10 +/- 1 to 8 +/- 1 mm Hg (p less than 0.01), pulmonary capillary wedge pressure fell from 21 +/- 3 to 16 +/- 2 mm Hg (p less than 0.01), heart rate and cardiac index were unchanged, and systemic vascular resistance fell from 1346 +/- 130 to 1087 +/- 98 dyne-sec/cm5 (p less than 0.05). We conclude that infusion of ANF in hemodynamically effective doses in patients with heart failure decreases coronary vascular resistance with no change in coronary blood flow or myocardial oxygen or lactate metabolism.     

Pattern of left ventricular diastolic filling associated with right ventricular enlargement

Right ventricular (RV) dilatation associated with pressure overload may alter left ventricular (LV) geometry resulting in abnormal diastolic function as demonstrated by a smaller LV diastolic volume for a given LV diastolic pressure. To determine whether abnormalities in LV geometry due to RV dilatation result in abnormalities in the LV diastolic filling pattern, we obtained pulsed Doppler transmitral recordings from 23 patients with RV dilatation with RV systolic pressure estimated to be less than 40 mm Hg (group 1), 18 patients with RV dilatation and RV systolic pressures greater than or equal to 40 mm Hg (group 2) and 33 normal patients. RV systolic pressures were estimated from continuous wave Doppler peak tricuspid regurgitation velocities using the modified Bernoulli equation. Diastolic filling parameters in group 1 patients were similar to normals. In group 2 patient, increased peak atrial filling velocity (76 +/- 14 vs 57 +/- 12 cm/s, p less than 0.001), decreased peak rapid filling velocity/peak atrial filling velocity (1.1 +/- 0.4 vs 1.5 +/- 0.4, p less than 0.01), increased atrial filling fraction (41 +/- 14 vs 30 +/- 10%, p less than 0.01) and prolongation of the atrial filling period (171 +/- 47 vs 152 +/- 39 ms, p less than 0.05) were noted compared with the normal group. RV end-diastolic size and LV end-systolic shape were significantly correlated with the atrial filling fraction in group 2 patients. In patients with RV dilatation and RV systolic pressures greater than or equal to 40 mm Hg, there is increased reliance on atrial systolic contribution to the LV filling volume.