Effect of single lung transplantation on pulmonary hypertension in patients with end stage fibrosing lung disease.

OBJECTIVE--To investigate the effect of successful single lung transplantation on pulmonary haemodynamic variables and right ventricular function. DESIGN--Pulmonary haemodynamic variables and right ventricular function were measured at right heart catheterisation after single lung transplantation. The results were compared with the preoperative pulmonary haemodynamic variables measured at the time of assessment for transplantation. SETTING--A tertiary referral centre. PATIENTS--Five survivors of single lung transplantation performed for end stage lung disease. INTERVENTIONS--Cardiac catheterisation in all five patients at a mean of 18 months postoperatively. Preoperative catheter data were available for comparison in four. Right heart pressures and cardiac output were measured and right ventricular angiography was performed. Perfusion scans performed for clinical reasons were used to assess the percentage of cardiac output passing through each lung. MAIN OUTCOME MEASURES--Right heart pressures, cardiac output, right ventricular function, percentage perfusion to lungs. RESULTS--After operation mean peak right ventricular pressure fell from 53 mm Hg to 33 mm Hg, mean pulmonary artery pressure from 33 mm Hg to 18 mm Hg, total pulmonary resistance from 11.2 U x m2 to 5.8 U x m2, and pulmonary arteriolar resistance from 8.9 U x m2 to 3.6 U x m2. Pulmonary artery wedge pressure and cardiac index were unchanged. Right ventricular function improved in all patients. The transplanted lung received most of the cardiac output. CONCLUSION--In patients with moderate pulmonary hypertension and right ventricular dysfunction secondary to end stage fibrosing lung disease single lung transplantation was followed by an improvement in pulmonary haemodynamic variables and right ventricular function.     

Central haemodynamic changes during lower body positive pressure in patients with congestive cardiac failure

Fifteen patients with moderately severe and severe chronic congestive heart failure were studied to determine the central haemodynamic results of short term increases in lower body positive pressure. Central haemodynamic variables were determined by Swan-Ganz thermodilution catheterisation and arterial cannulation. Graded increases in lower body positive pressure were applied to supine patients using Medical Anti-Shock Trousers (MAST). Increasing lower body positive pressure by 25 mm Hg and 55 mm Hg caused increases in mean right atrial pressure (6.0 to 13.2 to 17.9 mm Hg; p less than 0.001 and p less than 0.0001 respectively) and mean pulmonary artery pressure (26.8 to 35.5 to 41.3 mm Hg; p less than 0.05 and p less than 0.01 respectively). No significant changes were seen in left heart filling pressures or in pulmonary vascular resistance. Furthermore, there were no significant increases in indices of cardiac work (cardiac index, left ventricular stroke work index, right ventricular stroke work index or cardiac power output) despite the increased right heart filling pressures. These results show that in patients with longstanding severe congestive heart failure, short term increases in cardiac return may increase right heart pressures but do not appear to cause either beneficial or detrimental changes in left heart haemodynamic indices.     

Immediate effects of lung transplantation on right ventricular morphology and function in patients with variable degrees of pulmonary hypertension

Objectives. This study sought to determine the immediate effects of lung transplantation on right ventricular morphology and function in patients with variable degrees of pulmonary hypertension and to evaluate these features as potential markers of immediate outcome.Background. Selected lung transplant recipients with severe preoperative pulmonary hypertension have previously been shown to have a reduction in right ventricular size and improved function at follow-up evaluation.Methods. Thirty-two consecutive patients (mean [± SD] age 44 ± 11 years) were prospectively classified into three groups according to their pretransplantation pulmonary artery systolic pressure: severe pulmonary hypertensive group ≥ 75 mm Hg, intermediate pulmonary hypertensive group 40 to 74 mm Hg and non-pulmonary hypertensive group < 40 mm Hg. Hemodynamic and transesophageal echocardiographic variables were measured immediately before and after lung transplantation.Results. Pulmonary artery systolic and mean pressures markedly decreased after transplantation in the severe pulmonary hypertensive group (from 115 ± 26 to 45 ± 19 mm Hg and from 76 ± 14 to 31 ± 11 mm Hg, respectively, both p < 0.05). Mean pulmonary artery pressure decreased in the intermediate group (from 34 ± 7 to 26 ± 7 mm Hg, p < 0.05). Right ventricular end-diastolic area, end-systolic area and eccentricity index decreased in the severe pulmonary hypertensive group after transplantation. End-diastolic area also decreased in the intermediate pulmonary hypertensive group. Right ventricular fractional area change was not significantly different between groups and did not change consistently after transplantation. Three patients with severe pulmonary hypertension who had continued depression of right ventricular function after transplantation died in the immediate postoperative period.Conclusions. Lung transplantation is associated with an immediate decrease in pulmonary artery pressures and right ventricular size and normalization of septal geometry but variable changes in right ventricular function. Continued depression of right ventricular fractional area change may be a potential marker of poor outcome.     

Acute haemodynamic effects of nifedipine in patients with ventricular septal defect.

The haemodynamic effects of nifedipine were studied in 14 patients (aged 8-14 years, seven male and seven female) with ventricular septal defect with and without pulmonary hypertension. All underwent left and right heart catheterisation. In each patient the pressures and heart rate were measured and blood samples were taken for oximetry before and after sublingual administration of 10 mg nifedipine. In eight patients with ventricular septal defect without pulmonary hypertension (mean pulmonary artery pressure less than 20 mm Hg) nifedipine significantly reduced the mean aortic pressure and systemic vascular resistance, and significantly increased heart rate. The other haemodynamic indices did not change significantly. In six patients with ventricular septal defect complicated by pulmonary hypertension (mean pulmonary artery pressure greater than 20 mm Hg) nifedipine significantly increased systemic output, stroke volume, and heart rate, and significantly reduced systemic vascular resistance and the pulmonary to systemic flow ratio. The other haemodynamic indices did not change significantly. Nifedipine had a beneficial effect in patients with ventricular septal defect complicated by pulmonary hypertension. It reduced the left to right shunt and increased the stroke volume. This effect was not seen in patients with ventricular septal defect uncomplicated by pulmonary hypertension.     

Acute haemodynamic effects of nifedipine in patients with ventricular septal defect

The haemodynamic effects of nifedipine were studied in 14 patients (aged 8-14 years, seven male and seven female) with ventricular septal defect with and without pulmonary hypertension. All underwent left and right heart catheterisation. In each patient the pressures and heart rate were measured and blood samples were taken for oximetry before and after sublingual administration of 10 mg nifedipine. In eight patients with ventricular septal defect without pulmonary hypertension (mean pulmonary artery pressure less than 20 mm Hg) nifedipine significantly reduced the mean aortic pressure and systemic vascular resistance, and significantly increased heart rate. The other haemodynamic indices did not change significantly. In six patients with ventricular septal defect complicated by pulmonary hypertension (mean pulmonary artery pressure greater than 20 mm Hg) nifedipine significantly increased systemic output, stroke volume, and heart rate, and significantly reduced systemic vascular resistance and the pulmonary to systemic flow ratio. The other haemodynamic indices did not change significantly. Nifedipine had a beneficial effect in patients with ventricular septal defect complicated by pulmonary hypertension. It reduced the left to right shunt and increased the stroke volume. This effect was not seen in patients with ventricular septal defect uncomplicated by pulmonary hypertension.     

Long-term hemodynamic function of the transplanted heart

The aim of this study was to identify the long-term haemodynamic changes of the transplanted heart. Between 1987 and 1997, 136 patients required cardiac transplantation at Dijon hospital. During follow-up, 76 patients aged 51.2 +/- 9.46 years underwent catheter studies (12 women, 15.8%; and 64 men, 84.2%). Right and left heart catheterisation was performed at 3 months, 1, 2, 3 and 5 years after transplantation. Right heart catheterisation included measurement of mean pulmonary artery and pulmonary capillary pressures and pulmonary arteriolar resistances. During left heart catheterisation, cardiac output, mean aortic pressure, the ejection fraction, the dp/dt max of the left ventricular wall, systemic arterial resistances and left ventricular end diastolic pressures were measured. At each catheter study, the indexed myocardial mass, indexed end systolic and end diastolic left ventricular volumes, the mass/volume ratio, the residual serum cyclosporine concentrations and the serum creatinine were analysed. In addition, an endomyocardial biopsy was also performed. Initially raised, the mean pulmonary artery and pulmonary capillary pressures decrease from the 3rd month to the 2nd year. From the 3rd year onwards, they readjust to the upper limits of normal. The pulmonary artery resistances underwent the same changes. The left heart parameters remained constant over the period of follow-up but with a heart rate, mean aortic pressure and left ventricular end diastolic pressure higher than normal. The indexed myocardial mass was increased at all periods. The indexed left ventricular end systolic and diastolic volumes decreased with a M/V ratio which increased. Cyclosporine concentrations decreased whereas serum creatinine increased. The frequency of severe rejection and of coronary atherosclerosis was low. Significant correlations were observed between different parameters at different periods. In the long-term, the function of the transplanted heart is not normal in the strict sense of the term. The apparent normality is obtained by anti-hypertensive treatment. The transplanted heart adapts to the increase in cyclosporine-induced afterload by permanent myocardial hypertrophy, and increased diastolic pressure probably relates to diastolic dysfunction without noticeable intracardiac fibrosis.     

Right ventricular function in an operating room model of mechanical left ventricular assistance and its effects in patients with depressed left ventricular function

Approximately 20% of patients who receive left ventricular assist devices (LVADs) for refractory cardiac failure after open heart surgery have had complications of right ventricular failure. To evaluate this problem in the diseased heart we simulated an LVAD in the operating room by bypassing and unloading the left ventricle with the heart-lung machine before routine open heart surgery. Right ventricular function was assessed in 12 patients with preoperative left ventricular ejection fractions of less than 0.55 (poor left ventricular function) (mean +/- SEM 0.40 +/- 0.03) and 10 patients with ejection fractions greater than 0.55 (normal left ventricular function) (0.63 +/- 0.02). Measurements before and during left ventricular bypass in the normal left ventricular function group revealed no change in cardiac output (from 5.7 +/- 0.6 to 5.8 +/- 0.4 liters/min), with a decrease in right ventricular end-diastolic pressure (from 8 +/- 2 to 6 +/- 1 mm Hg). However, in the poor left ventricular function group, cardiac output was increased significantly during left ventricular bypass from 4.5 +/- 0.2 to 5.3 +/- 0.4 liters/min and right ventricular end-diastolic pressure was decreased significantly from 13 +/- 2 to 8 +/- 2 mm Hg. During bypass there were significant reductions in mean pulmonary arterial pressure from 17 +/- 3 to 10 +/- 2 mm Hg in the normal left ventricular function group and from 27 +/- 3 to 12 +/- 2 mm Hg in the poor left ventricular function group. These measurements reflect passive changes in pulmonary pressures due to reductions in left ventricular filling pressure during left ventricular bypass.(ABSTRACT TRUNCATED AT 250 WORDS)     

Dimensional changes of the left ventricle during acute pulmonary arterial hypertension in dogs

Left ventricular dimensions and volumes were measured by an endocardial marker technique in eight closed chest dogs during progressive increases of 10 mm Hg in mean pulmonary arterial pressure. Right ventricular volumes were measured by biplane cineanglography.

Increasing mean pulmonary arterial pressure caused a progressive increase in right ventricular volume; at a mean pulmonary arterial pressure of 60 mm Hg, right ventricular end-diastolic volume increased by 48 percent and end-systolic volume by 50 percent. Left ventricular volumes began to decrease significantly at a mean pulmonary arterial pressure of 30 mm Hg, and when a mean pulmonary arterial pressure of 60 mm Hg was reached, left ventricular end-diastolic volume had decreased by 30 percent and left ventricular end-systolic volume by 19 percent. Changes in ventricular filling pressure dlrectionally followed the volume changes of the respective ventricle. Left ventricular stroke volume decreased 45 percent at a mean pulmonary arterial pressure of 60 mm Hg but increasing heart rate prevented a decrease in cardiac output.

The decrease in left ventricular volume as pulmonary arterial pressure was Increased was associated with a disproportionate reduction in the left ventricular septal-lateral axis. At end-diastole, this dimension decreased by 22 percent at a mean pulmonary arterial pressure of 60 mm Hg, the anterior-posterior axis decreased by 8 percent and the base-apex axis by 4 percent. A similar disproportionate decrease of the septal-lateral axis occurred at end-systole. Even at the modest increase in mean pulmonary arterial pressure to 20 mm Hg, only the septal-lateral dimension was significantly shortened, and the right ventricular end-diastolic volume had increased by 17 percent but left ventricular end-diastolic volume was not significantly changed. Thus, during acute pulmonary hypertension, the right ventricle progressively dilates resulting in a distinctive change in the shape of the left ventricle that suggests septal buiging and that may impair left ventricular function.     

A quantitative analysis of hemodynamic effects of the right ventricle included in the circulation of the Fontan procedure

BACKGROUND. Right heart hemodynamics were analyzed with a catheter-mounted velocity meter in seven patients after direct atrioventricular anastomosis for Fontan procedure (RV group) and were compared with those obtained in eight patients after direct atriopulmonary anastomosis (RA group). METHODS AND RESULTS. In the RV group, cardiac output was 2.7 +/- 0.6 l/min/m2; mean right atrial and pulmonary artery pressures were both 13 +/- 3 mm Hg; mean pulmonary artery wedge pressure was 7 +/- 5 mm Hg; left ventricular end-diastolic volume, determined angiographically, was 129 +/- 40% of normal; and its ejection fraction was 0.50 +/- 0.09. In the RA group, data were similar to those of the RV group except that right heart pressure were lower in the RV group, which was related to the preoperative condition of the pulmonary circulation. In the RV group, the fraction of ventricular forward flow of the total forward flow in the main pulmonary artery ranged from 0.21 to 0.46 and was not correlated with cardiac output or with any other parameter. The backward flow into the inferior vena cava at ventricular systole was greater than the atrial flow in two patients in whom cardiac output was less than 2.2 l/min/m2, whereas caval backward flow at atrial contraction was greater than ventricular flow in the other five patients, of whom four had a cardiac output greater than 3.1 l/min/m2. CONCLUSIONS. We conclude that the inclusion of right ventricle in the circulation of the Fontan procedure does not necessarily improve overall hemodynamics in most patients.     

Hemodynamic spectrum of “dominant” right ventricular infarction in 19 patients

In 19 patients right ventricular infarction was diagnosed on the basis of electrocardiographic features of acute inferior infarction and clinical evidence of elevation of systemic venous pressure and an absence of pulmonary congestion. Right heart catheterization documented elevated right ventricular end-diastolic pressure (mean 15.5 mm Hg) and commensurate right atrial pressure (mean 14.9 mm Hg). In all patients the pulmonary capillary wedge pressure (mean 13.2 mm Hg) was exceeded or equaled by the right ventricular end-diastolic pressure, suggesting a disproportionate reduction in right ventricular compliance or contractile function, or both. Thirteen patients were hypotensive (systolic blood pressure less than 100 mm Hg on admission), including six patients with cardiogenic shock.

Right ventricular infarction is an uncommon and potentially reversible cause of cardiogenic shock;yet, in the experimental model, isolated right ventricular damage is relatively well tolerated. To identify the factors associated with systemic hypotension, data from patients with and without compromised systemic hemodynamic function were compared. In hypotensive patients, the right ventricular end-diastolic pressure was significantly higher (16.8 versus 12.8 mm Hg;p < 0.01) and reflected more extensive right ventricular damage. A pulmonary wedge pressure of 15 mm Hg or more was noted only among the hypotensive patients, and their wedge pressure (mean 14.8 mm Hg) was significantly greater than that of normotensive patients (mean 9.7 mm Hg, p < 0.05). Therefore, in patients with right ventricular infarction, an additional impairment of left ventricular function due to associated infarction of the inferior left ventricle is a significant factor causing hypotension. The elevated wedge pressure may influence right ventricular output by affecting pulmonary arterial diastolic pressure and right ventricular afterload. Right ventricular peak systolic pressure as an index of right ventricular afterload was significantly higher in hypotensive than in normotensive patients (30.5 versus 23.8 mm Hg, p < 0.03), and there was a linear correlation between this pressure and the pulmonary capillary wedge pressure (r = 0.895, p < 0.001).

There was one hospital death (mortality rate 5.3 percent). Clinical management generally consisted of administration of fluids and digitalis and implantation of a temporary pacemaker. This study emphasizes the relatively favorable prognosis of this condition and suggests that aggressive diagnosis and management are appropriate.     

Right ventricular function in adult atrial septal defect: Preoperative and postoperative assessment and clinical implications

Right ventricular function was assessed with gated cardiac blood pool scanning in 20 adult patients with an atrlal septal defect. All patients had scans both before and 6 or more months after surgical repair of the defect. Clinical findings, pre- and postoperative course and cardiac catheterization data were correlated with scan findings. In all 20 patients, the right ventricle was dilated preoperatively. In nine patients (aged 18 to 42 years, mean 25), right ventricular wall motion was normal preoperatively. All nine were asymptomatic and had normal sinus rhythm. Their pulmonary to systemic flow ratio ranged between 2:1 and 5:1, pulmonary arterial systolic pressure between 18 and 30 mm Hg and right ventricular end-diastolic pressure between 0 and 8 mm Hg. After repair of the atrlal septal defect, all nine remained asymptomatic, right ventricular size decreased dramatically and wall motion was normal.In the remaining 11 patients (aged 36 to 63 years, mean 52), there was moderate to severe preoperatlve right ventricular hypokinesia. All had preoperatlve symptoms (functional class II and III, New York Heart Association); six had atrial fibrillation and five had normal sinus rhythm; seven had clinical heart failure. Pulmonary to systemic flow ratio ranged between 1.7:1 and 5.0:1, pulmonary arterial pressure between 26 and 70 mm Hg and right ventricular end-diastolic pressure between 4 and 16 mm Hg. Symptoms were lessened and right ventricular size and function improved postoperatively in these 11 patients. Unlike those with normal preoperatlve right ventricular wall motion, however, only 1 of the 11 had normal postoperative right ventricular function and became asymptomatic.     

Hemodynamics and gas exchange in acute lung embolism

The main hemodynamic consequence of pulmonary embolism is the acute mechanical reduction of the pulmonary vascular cross-sectional area. This results in a sudden increase of the pulmonary vascular resistance, and if the cardiac output is to be maintained, in an increase in pulmonary artery pressure and right ventricular work. The extent of hemodynamic changes in pulmonary embolism are determined primarily by the size of the emboli and whether or not the patient has underlying cardiopulmonary disease. Although humoral factors and neural reflexes play a role in determining the severity of hemodynamic responses to pulmonary embolism in experimental animals, their role in patients is uncertain. In patients free of preembolic cardiopulmonary disease, the extent of embolic obstruction can be related directly to the mean pulmonary artery pressure. Accordingly, either the extent of obstruction or the mean pulmonary artery pressure may be used as a measure of right ventricular afterload. Obstruction of 25 to 40% leads to an increase in mean pulmonary artery pressure of 20 to 30 mm Hg, massive obstruction over 75% to a pressure of 40 to 45 mm Hg. Continuous hemodynamic monitoring helps to estimate the speed of the resolution of emboli and to a certain extent the adequacy of treatment. Right arterial pressure is consistently elevated by a mean pulmonary artery pressure over 30 mm Hg and provides also a rough estimate of the degree of pulmonary vascular obstruction. A previously normal right ventricle will dilate at a mean pulmonary artery pressure of 40 to 45 mm Hg. which may result in acute tricuspid insufficiency.(ABSTRACT TRUNCATED AT 250 WORDS)     

Correlation of left ventricular diastolic filling characteristics with right ventricular overload and pulmonary artery pressure in chronic thromboembolic pulmonary hypertension

OBJECTIVES: This study was designed to determine a quantitative relationship between right ventricular (RV) pressure overload and left ventricular (LV) diastolic filling characteristics in patients with chronic thromboembolic pulmonary hypertension (CTEPH). BACKGROUND: Right ventricular pressure overload in patients with CTEPH causes abnormal LV diastolic filling. However, a quantitative relationship between RV pressure overload and LV diastolic function has not been established. METHODS: We analyzed pre- and postoperative diastolic mitral inflow velocities and right heart hemodynamic data in 39 consecutive patients with CTEPH over the age of 30 (55 +/- 11 years) with mean pulmonary artery pressure >30 mm Hg who underwent pulmonary thromboendarterectomy (PTE). RESULTS: After PTE, mean pulmonary artery pressure (mPAP) decreased from 50 +/- 11 to 28 +/- 9 mm Hg (p < 0.001) while cardiac output (CO) increased from 4.4 +/- 1.1 to 5.7 +/- 0.9 l/m (p < 0.001). Mitral E/A ratio (E/A) increased from 0.74 +/- 0.22 to 1.48 +/- 0.69 (p < 0.001). E/A was < 1.25 in all patients pre-PTE. After PTE, all patients with E/A >1.50 had mPAP <35 mm Hg and CO >5.0 l/min. E/A correlated inversely with mPAP (r = 0.55, p < 0.001) and directly with CO (r = 0.53, p < 0.001). CONCLUSIONS: E/A is consistently abnormal in patients with CTEPH and increases post-PTE. Moreover, E/A varies inversely with mPAP and directly with CO. Following PTE, E/A >1.5 correlates with the absence of severe pulmonary hypertension (mPAP >35 mm Hg) and the presence of normal cardiac output (> 5.0 l/m).     

Hypoplastic left heart syndrome: hemodynamic and angiographic assessment after initial reconstructive surgery and relevance to modified Fontan procedure

After undergoing initial reconstructive surgery for hypoplastic left heart syndrome performed between August 1985 and March 1989, 59 patients (age range 3 to 27 months, mean 13.8 +/- 4.5) underwent elective cardiac catheterization in anticipation of a modified Fontan procedure. Five important hemodynamic and anatomic features considered to be components of successful reconstructive surgery were specifically addressed. 1) Interatrial communication: Only two patients had a measured pressure difference of greater than 4 mm Hg across the atrial septum. 2) Tricuspid valve function: Angiography demonstrated significant tricuspid valve regurgitation in only five patients (moderate in two and severe in three). 3) Aortic arch: Pressure tracings from the right ventricle to the descending aorta revealed a gradient greater than 25 mm Hg in only two patients. 4) Pulmonary vasculature: Ten patients had a calculated pulmonary vascular resistance greater than 4 U.m2; 51 (86%) of the 59 patients had no evidence of distortion (stenosis or hypoplasia) of either the left or the right pulmonary artery. 5) Right ventricular function: Five patients had an end-diastolic pressure in the right ventricle greater than 12 mm Hg and two patients had qualitative assessment of decreased ventricular function. Comparison of catheterization data between survivors and nonsurvivors of the subsequent modified Fontan procedure showed that only significant tricuspid regurgitation is a possible predictor of poor outcome. After first stage reconstructive surgery for hypoplastic left heart syndrome, most survivors have favorable anatomy and hemodynamics at follow-up cardiac catheterization for a subsequent Fontan procedure.     

Lack of correlation between P pulmonale and right atrial overload in chronic obstructive airways disease.

The correlation between P pulmonale and right atrial overload in chronic lung disease was studied. Right atrial pressure, pulmonary artery pressure, and cardiac output were measured with a Swan-Ganz catheter in nine patients with chronic lung disease and P pulmonale on the electrocardiogram (P wave amplitude of greater than or equal to 2.5 mm (0.25 mV) in leads II, III, and a VF. The results were compared with those in six patients with an atrial septal defect (left to right shunt greater than or equal to 50%) and six patients with pulmonary hypertension (mean pressure greater than or equal to 30 mm Hg without left sided heart disease). Right atrial volume and wall thickness were measured in 10 cases of P pulmonale among 1000 necropsy cases and compared with 141 normal hearts from the same series. The patients with P pulmonale did not show a significant increase in right atrial or pulmonary artery pressures. None of the patients with an atrial septal defect or pulmonary hypertension had P pulmonale on the electrocardiogram. In the necropsy cases of P pulmonale mean (1 SD) in right atrial volume (32 (12) ml) and wall thickness (1.5 (0.7) mm) were not significantly increased (40 (14) ml and 1.4 (0.5) mm in the normal hearts). There was a significant inverse relation between the presence of P pulmonale and the cardiothoracic ratio. In all the patients with P pulmonale chest x ray showed a low cardiothoracic ratio, a considerably depressed diaphragm, and a pendulous heart. This study showed no correlation between P pulmonale and right atrial overload in chronic lung disease. A more vertical anatomical position of the heart, particularly of the right atrium, seems to be the major factor responsible for generation of P pulmonale in chronic airways disease.     

The effects of phenylephrine on right ventricular performance in patients with pulmonary hypertension

Pulmonary hypertension causes right ventricular ischemia and failure as a result of increased afterload combined with reduced coronary blood flow. Increasing coronary driving pressure by raising aortic pressure with phenylephrine has been shown to reverse right ventricular ischemia from pulmonary hypertension in animals. Since vasodilators often fail to reduce afterload, we tested whether raising the coronary driving pressure would improve right ventricular function in man. Ten patients with pulmonary hypertension had hemodynamics and right ventricular coronary driving pressure measured before and 10 minutes after a steady state was reached with a phenylephrine infusion titrated to raise aortic pressure by 25 percent. Phenylephrine caused a significant (p less than .01) increase in mean aortic pressure (84 to 108 mm Hg) and right ventricular coronary driving pressure (46 to 69 mm Hg). In response, there was a significant (p less than .01) rise in mean pulmonary artery pressure (58 to 67 mm Hg), right ventricular end-diastolic pressure (10 to 16 mm Hg) and wedge pressure (5 to 9 mm Hg), and an insignificant fall in cardiac output (3.26 to 3.09 L/min) and pulmonary artery O2 saturation (57 to 49 percent). Although phenylephrine increased right ventricular coronary driving pressure, it worsened right ventricular function as manifest by a rise in end-diastolic pressure and fall in cardiac output. Any benefit of raising right ventricular coronary driving pressure may have been offset by alpha vasoconstriction of right ventricular coronary blood flow and/or pulmonary arterial vasoconstriction. Phenylephrine does not appear to be a useful therapy of right ventricular failure from pulmonary hypertension in patients who fail vasodilators.     

Comparison of Doppler derived haemodynamic variables and simultaneous high fidelity pressure measurements in severe pulmonary hypertension.

OBJECTIVE--To assess relations between right ventricular pressure measured with a high fidelity transducer tipped catheter and the characteristics of tricuspid regurgitation recorded with Doppler echocardiography. DESIGN--A prospective non-randomised study of patients with severe pulmonary hypertension referred for consideration of lung transplantation. SETTING--A tertiary referral centre for cardiac and pulmonary disease, with facilities for invasive and non-invasive investigation, and assessment for heart and heart-lung transplantation. PATIENTS--10 patients with severe pulmonary hypertension being considered for lung transplantation. ENDPOINTS--Peak right ventricular, pulmonary artery, and right atrial pressures; peak positive and negative right ventricular dP/dt; peak Doppler right ventricular-right atrial pressure drop; Doppler derived peak positive and negative right ventricular dP/dt; and time intervals of Q to peak right ventricular pressure and to peak positive and negative right ventricular dP/dt. RESULTS--The mean (SD) pulmonary artery systolic pressure was 109 (29) mm Hg. The peak Doppler right ventricular-right atrial pressure drop underestimated peak right ventricular pressure by 38 (21) mm Hg, and by 21 (18) mm Hg when the Doppler value was added to the measured right atrial pressure (P values < 0.05). This discrepancy was greater for higher pulmonary artery pressures. The timing of peak right ventricular pressure differed, with the Doppler value consistently shorter (mean difference 16 ms, P < 0.05). Values of peak positive and negative right ventricular dP/dt and the time intervals Q-peak positive right ventricular dP/dt and pulmonary closure to the end of the pressure pulse differed between the two techniques in individual patients, but not in a consistent or predictable way. CONCLUSIONS--Doppler echocardiography significantly underestimates the peak right ventricular pressure and the time interval to peak right ventricular pressure in pulmonary hypertension, particularly when severe. These differences may be related to orifice geometry. Digitisation of Doppler records of tricuspid regurgitation provides useful semiquantitative estimates of absolute values and timing of peak positive and negative right ventricular dP/dt. Clinically significant differences may exist, however, and must be considered in individual patients.     

Lack of correlation between P pulmonale and right atrial overload in chronic obstructive airways disease

The correlation between P pulmonale and right atrial overload in chronic lung disease was studied. Right atrial pressure, pulmonary artery pressure, and cardiac output were measured with a Swan-Ganz catheter in nine patients with chronic lung disease and P pulmonale on the electrocardiogram (P wave amplitude of greater than or equal to 2.5 mm (0.25 mV) in leads II, III, and a VF. The results were compared with those in six patients with an atrial septal defect (left to right shunt greater than or equal to 50%) and six patients with pulmonary hypertension (mean pressure greater than or equal to 30 mm Hg without left sided heart disease). Right atrial volume and wall thickness were measured in 10 cases of P pulmonale among 1000 necropsy cases and compared with 141 normal hearts from the same series. The patients with P pulmonale did not show a significant increase in right atrial or pulmonary artery pressures. None of the patients with an atrial septal defect or pulmonary hypertension had P pulmonale on the electrocardiogram. In the necropsy cases of P pulmonale mean (1 SD) in right atrial volume (32 (12) ml) and wall thickness (1.5 (0.7) mm) were not significantly increased (40 (14) ml and 1.4 (0.5) mm in the normal hearts). There was a significant inverse relation between the presence of P pulmonale and the cardiothoracic ratio. In all the patients with P pulmonale chest x ray showed a low cardiothoracic ratio, a considerably depressed diaphragm, and a pendulous heart. This study showed no correlation between P pulmonale and right atrial overload in chronic lung disease. A more vertical anatomical position of the heart, particularly of the right atrium, seems to be the major factor responsible for generation of P pulmonale in chronic airways disease.     

Effect of xamoterol (ICI 118587), a new beta1 adrenoceptor partial agonist, on resting haemodynamic variables and exercise tolerance in patients with left ventricular dysfunction

The effect of xamoterol, a beta1 adrenoceptor partial agonist, on resting haemodynamic measurements and exercise tolerance was studied in 10 patients with dyspnoea of effort. All patients had poor left ventricular function due to myocardial infarction with ejection fractions ranging from 15% to 35% (mean 28%). The cardiac index and stroke work index both rose significantly. The mean pulmonary artery pressure fell from 20(2) mm Hg to 16(2) mm Hg and pulmonary artery wedge pressure from 14(2) mm Hg to 10(2) mm Hg within the first four hours. Exercise tolerance, measured on the treadmill, increased significantly in seven patients but was unchanged in the three who had the lowest left ventricular ejection fractions. Exercise heart rate response was attenuated by the drug in all patients. It is concluded that xamoterol may be beneficial in patients with poor left ventricular function but can be harmful in extremely poor left ventricular function where high sympathetic drive may be important.     

Effect of xamoterol (ICI 118587), a new beta1 adrenoceptor partial agonist, on resting haemodynamic variables and exercise tolerance in patients with left ventricular dysfunction.

The effect of xamoterol, a beta1 adrenoceptor partial agonist, on resting haemodynamic measurements and exercise tolerance was studied in 10 patients with dyspnoea of effort. All patients had poor left ventricular function due to myocardial infarction with ejection fractions ranging from 15% to 35% (mean 28%). The cardiac index and stroke work index both rose significantly. The mean pulmonary artery pressure fell from 20(2) mm Hg to 16(2) mm Hg and pulmonary artery wedge pressure from 14(2) mm Hg to 10(2) mm Hg within the first four hours. Exercise tolerance, measured on the treadmill, increased significantly in seven patients but was unchanged in the three who had the lowest left ventricular ejection fractions. Exercise heart rate response was attenuated by the drug in all patients. It is concluded that xamoterol may be beneficial in patients with poor left ventricular function but can be harmful in extremely poor left ventricular function where high sympathetic drive may be important.