Inhaled nitric oxide reduction in systolic pulmonary artery pressure is less in patients with decreased left ventricular ejection fraction

OBJECTIVE: To assess whether inhaled nitric oxide decreases pulmonary artery pressure in patients with depressed left ventricular ejection fraction. DESIGN: Randomized, blinded, crossover clinical trial. SETTING: Tertiary care university referral hospital. PATIENTS: Thirty-three patients with pulmonary hypertension and left ventricular dysfunction or valvular heart disease were recruited by convenience. INTERVENTIONS: Systolic pulmonary artery pressure was measured by Doppler echocardiography during randomized inhalation of either 20 ppm or 40 ppm nitric oxide in 30% oxygen as well as during control periods without nitric oxide. MAIN RESULTS: Systolic pulmonary artery pressure was significantly (P < 0.05) decreased with 20 ppm nitric oxide (53.4 +/- 13.9 mmHg) and 40 ppm nitric oxide (53.1 +/- 14.4 mmHg) compared with either initial control (55.8 +/- 15.3 mmHg) or terminal control (56.3 +/- 15.2 mmHg) values. The regression equation for the change in systolic pulmonary artery pressure (y) as predicted by the left ventricular ejection fraction (x) alone for 20 ppm nitric oxide was y = 13.8x-2.9; R2adj = 0.30, P < 0.0001. For 40 ppm nitric oxide alone, the regression equation was y = 16.3x-3.3; R2adj = 0.25, P < 0.0001. Left ventricular ejection fraction was the most explanatory independent variable in the multivariate equation for nitric oxide-induced change in systolic pulmonary artery pressure (R2 = 0.61, P = 0.0000). The change in systolic pulmonary artery pressure was -5.1 +/- 5.2 versus 0.8 +/- 4.9 mmHg (P < 0.0000) in patients with left ventricular ejection fractions greater than 0.25, and 0.25 or less, respectively. CONCLUSIONS: These data imply that in patients with left ventricular ejection fraction of 0.25 or less, nitric oxide may not decrease systolic pulmonary artery pressure. Nitric oxide inhalation may result in a paradoxical increase in systolic pulmonary artery pressure in patients with severely depressed left ventricular ejection fraction. This effect would significantly limit the therapeutic role of nitric oxide in patients with severe heart failure.     

Doppler estimation of pulmonary artery end-diastolic pressure using contrast enhancement of pulmonary regurgitant signals

Pulmonary artery (PA) end-diastolic pressure is used as an estimate of PA wedge pressure. We evaluated contrast enhanced pulmonary regurgitant signals in the assessment of PA end-diastolic pressure in 24 patients in a critical care unit. Right atrial pressure was estimated by the percent decrease of the inferior vena caval diameter with inspiration. Weak or absent pulmonary regurgitant signals were enhanced by sonicated albumin (Albunex) in 23 patients (96%). The Doppler-determined PA end-diastolic pressure (the sum of the pulmonary regurgitant pressure gradient at end-diastole and the right atrial pressure) was significantly correlated with the catheter-determined PA end-diastolic pressure (y = 0.85x + 1.72, r = 0.93). Compared with invasive hemodynamic monitoring, the contrast-enhanced Doppler technique using Albunex is effective for measuring PA end-diastolic pressure, even in critically ill patients.     

Characteristics of pulmonary artery pressure waveform for differential diagnosis of chronic pulmonary thromboembolism and primary pulmonary hypertension

OBJECTIVES: The accurate diagnosis of chronic pulmonary thromboembolism (CPTE) is a prerequisite for life-saving surgical interventions. To help in the differential diagnosis of CPTE and primary pulmonary hypertension (PPH), we characterized the configuration of the pulmonary artery pressure waveform. BACKGROUND: Because CPTE predominantly involves the proximal arteries, whereas PPH involves the peripheral arteries, we hypothesized that patients with CPTE would have stiff or high resistance proximal arteries, whereas those affected by PPH would have high resistance peripheral arteries. These differences in the primary lesions would make arterial pulsatility relative to mean pressure larger in CPTE than in PPH. METHODS: In 34 patients with either CPTE (n = 22) or PPH (n = 12) whose pulmonary systolic pressure was > or = 50 mm Hg, we measured pulmonary artery pressure using a fluid-filled system that included a balloon-tipped flow-directed catheter. RESULTS: To quantify the magnitude of pulsatility relative to mean pressure, we normalized pulse pressure by mean pressure, hereinafter referred to as fractional pulse pressure (PPf). PPf was markedly higher in CPTE than in PPH (mean [+/-SD] 1.41 +/- 0.20 and 0.80 +/- 0.18, respectively, p < 0.001) and was diagnostic in separating the two groups without overlap. Similarly, the coefficient of variation of pulmonary artery pressure also separated the two groups without overlap (0.45 +/- 0.06 and 0.25 +/- 0.06, respectively, p < 0.001). Fractional time to half the area under the pressure curve separated the two groups reasonably well (0.35 +/- 0.02 and 0.43 +/- 0.03, respectively, p < 0.001). CONCLUSIONS: The analysis of pulsatility of pulmonary artery pressure is useful in the differential diagnosis of CPTE and PPH.     

Non-invasive estimation of pulmonary arterial hypertension in chronic obstructive pulmonary disease

The feasibility and reliability of the combination of several noninvasive methods using a multivariate method of analysis to predict pulmonary artery hypertension (PAH) is evaluated in 20 patients with chronic obstructive pulmonary disease. These methods comprised arterial blood gases (Pao2, Paco2), pulmonary functional parameters (FEV1), echo-Doppler parameters (tricuspid regurgitation jets, acceleration time on pulmonary valve), computed tomography measurements (transhilar distance, hilar thoracic index, and measurement of the descending branch of the right pulmonary artery to the lower lobe). A multiple stepwise regression analysis (including one Doppler parameter, two parameters of arterial blood gases, and one functional parameter) revealed a coefficient of determination (R2) equal to 0.954 for mean pulmonary artery pressure (MPAP) with a standard error of estimate (S.E.E.) of 5.25 mmHg. A stepwise regression analysis including computed tomography and radiographic parameters revealed an R2 equal to 0.970 for PAP with a S.E.E. of 4.26 mmHg. Logistical regression analysis classified correctly 80% of patients with PAH using noninvasive methods such as the diameter of the main pulmonary artery and the diameter of the left pulmonary arterial branch calculated by computed tomography. Not only the presence of PAH but also the level of MPAP can be estimated by the combination of multiple stepwise and logistical regression analyses.     

Determinants of the pulmonary artery pressure rise in left ventricular dysfunction

Pulmonary artery hypertension in patients with left ventricular dysfunction is related to poor outcome but the role of cardiac functional abnormalities in the genesis of pulmonary hypertension remains unknown. The aim of this prospective study was to identify the determinants of pulmonary hypertension in 102 consecutive patients with primary left ventricular dysfunction (ejection fraction < 50%). Systolic pulmonary artery pressure was measured by continuous wave Doppler. Left ventricular systolic and diastolic function, severity of functional mitral regurgitation, cardiac output, and left atrial volume were assessed using Doppler echocardiography. In patients with left ventricular dysfunction, systolic pulmonary artery pressure was increased (51 +/- 14 mmHg, range 23 to 87 mmHg). Mitral deceleration time (r = -0.61; p = 0.0001) and mitral effective regurgitant orifice (r = 0.50; p = 0.0001) were the strongest parameters related to systolic pulmonary artery pressure. Multivariate analysis identified these two variables as the strongest predictors of systolic pulmonary artery pressure in association with the mitral E/A ratio (p = 0.006) and age (p = 0.005). In conclusion, pulmonary hypertension is common and variable in patients with left ventricular dysfunction. It is closely related to diastolic dysfunction and severity of functional mitral regurgitation but not independently to the degree of left ventricular systolic dysfunction. These findings underline the importance of assessing diastolic function and quantifying mitral regurgitation in patients with left ventricular dysfunction.     

Reconsideration of criteria for the Fontan operation. Influence of pulmonary artery size on postoperative hemodynamics of the Fontan operation

BACKGROUND: The outcome of the Fontan operation largely depends on the selection of patients because this procedure is a physiological correction. Among the several selection criteria for the Fontan operation, the importance of adequate size of the pulmonary artery remains controversial. In this series, in order to clarify whether the pulmonary artery size is indispensable or not as one of the selection criteria for the Fontan operation, we considered the physiological meaning of pulmonary artery size and investigated how it influenced postoperative hemodynamics of the Fontan operation. METHODS AND RESULTS: In congenital heart disease of decreasing pulmonary blood flow, 40 patients were examined for this analysis. Pulmonary artery indexes (cross-sectional area of the right and left pulmonary arteries divided by body surface area) were measured as the expression of pulmonary artery size, and the relations of pulmonary artery index (PAI) to pulmonary vascular resistance (Rp) and compliance (Cp) were studied. There was no significant correlation between PAI and Rp, whereas a significant correlation was found between PAI and Cp (r = .71, P = .001). Furthermore, Cp influenced postoperative hemodynamics of the Fontan operation by affecting the peak central venous pressure (pCVP) and total impedance, which was the afterload to the ventricle. Impedance increased abruptly when PAI was < approximately 100 mm2/m2. CONCLUSIONS: The smaller pulmonary artery size causes more disadvantageous hemodynamics after the Fontan operation, with resultant effects of the rise in pCVP and the increase in afterload to the single ventricle.     

False-positive diagnosis of pulmonary hypertension by Doppler echocardiography

A 37-yr-old female presented with a history of several months of exertional dyspnoea. A diagnosis of primary pulmonary hypertension was suspected on the basis of a negative extensive cardiorespiratory work-up with a systolic pulmonary artery pressure of 41-46 mmHg calculated from repeated measurement of the maximum velocity of tricuspid regurgitation jets at 2.8-3 m x s(-1) by continuous-wave Doppler echocardiography. However, a right heart catheterization with a high-fidelity transducer-tipped catheter revealed pulmonary artery pressures of 22/8 mmHg at rest, which remained within normal limits at exercise. This case indicates a possible misleading overestimation of pulmonary artery pressures from Doppler echocardiographic studies of tricuspid regurgitation.     

Extrinsic compression of the pulmonary artery by non-microcytic lung carcinoma

A patient with a remitting non-microcytic pulmonary carcinoma was subjected to Doppler-echocardiography. The detection of a pericardial effusion with compression of the pulmonary artery due to an extrinsic mass indicated that the disease was progressing. The Doppler technique was used to evaluate the degree of arterial stenosis by determining the pressure gradient caused by it (49 mmHg) and to calculate the right ventricle pressure (75 mmHg). Tumor infiltration of mediastinal structures was posteriorly confirmed by computed tomography.     

Successful in vivo and ex vivo transfection of pulmonary artery segments in lung isografts

OBJECTIVE: Gene transfer to lung grafts may be useful in ameliorating ischemia-reperfusion injury and rejection. Efficient gene transfection to the whole organ may prove problematic. Proximal pulmonary artery endothelial transfection might provide beneficial downstream effects on the whole graft. The aim of this study was to determine the feasibility of transfecting proximal pulmonary artery segments in lung isografts. METHODS: Male Fischer rats were divided into six groups. In vivo transfection: In group I (n = 7), a proximal segment of the left pulmonary artery was isolated and injected with saline solution by means of a catheter inserted through the right ventricle. After an exposure period of 20 minutes, clamps were removed and blood flow was restored. In group II (n = 7), the isolated arterial segments were injected with adenovirus carrying the Escherichia coli LacZ gene encoding for beta-galactosidase. Ex vivo transfection: In group III (n = 5), arterial segments were injected ex vivo with saline solution and in group IV (n = 5) with the adenovirus construct. In group V (n = 6), arteries were injected with saline solution and in group VI (n = 11) with liposome chloramphenicol acetyl transferase cDNA. In groups I to IV, animals were killed on postoperative day 3 and transgene expression was assessed by Bluo-Gal staining. In groups V and VI, animals were killed on postoperative day 2 and transgene expression was assessed by chloramphenicol acetyl transferase activity assay. RESULTS: Transgene expression was detected grossly and microscopically in endothelial and smooth muscle cells of pulmonary artery segments from all surviving animals of groups II and IV. In group VI, chloramphenicol acetyl transferase activity was significant in all assessed arterial segments. CONCLUSION: Significant transgene expression is observed in proximal pulmonary artery segments after both in vivo and ex vivo exposure.     

The impact of ischemic heart disease on main pulmonary artery blood flow patterns: a comparison between magnetic resonance phase velocity mapping and transesophageal color Doppler

OBJECTIVE: To give a detailed evaluation on main pulmonary artery blood velocity patterns, in patients with ischemic heart disease and to provide recommendations for pulsed Doppler sample volume placement, in order to optimize cardiac output estimation. METHODS: Using magnetic resonance phase and esophageal color Doppler velocity mapping in 12 patients with ischemic heart disease and undergoing coronary artery by-pass grafting, very similar data on pulmonary artery blood velocity patterns were provided for comparison with each other. RESULTS: Peak blood velocities were located in the inferior half of the main pulmonary artery cross-sectional area. Early after peak systole the highest velocities shifted towards the superior/left (major curvature) with a simultaneous decrease in velocities inferiorly. The velocity decrease further evolved into retrograde flow to the inferior/right (minor curvature). This feature was significantly enhanced compared to earlier findings in healthy volunteers. The mean temporal blood velocity profiles were asymmetrically skewed, thereby giving unreliable cardiac output estimates based on single point Doppler blood velocity recordings. The error incurred may amount to more than 100% in extreme cases. According to our data, optimal assessment of cardiac output should be based on multiple sample volumes placed along the inferior/right to superior/left diameter. CONCLUSIONS: MR-phase velocity mapping and multiplane transesophageal color Doppler recordings provided similar blood velocity patterns in patients with ischemic heart disease. The skewness of the mean temporal blood velocity profile is enhanced compared with healthy subjects, resulting in error in the assessment of CO by means of pulsed Doppler echocardiography. By using multiple Doppler sample volumes, the error can be minimized.     

Sleep-related O2 desaturation and daytime pulmonary haemodynamics in COPD patients with mild hypoxaemia

It has been hypothesized but not firmly established that sleep-related hypoxaemia could favour the development of pulmonary hypertension in chronic obstructive pulmonary disease (COPD) patients without marked daytime hypoxaemia. We have investigated the relationships between pulmonary function data, sleep-related desaturation and daytime pulmonary haemodynamics in a group of 94 COPD patients not qualifying for conventional O2 therapy (daytime arterial oxygen tension (Pa,O2) in the range 7.4-9.2 kPa (56-69 mmHg)). Nocturnal desaturation was defined by spending > or = 30% of the recording time with a transcutaneous O2 saturation < 90%. An obstructive sleep apnoea syndrome was excluded by polysomnography. Sixty six patients were desaturators (Group 1) and 28 were nondesaturators (Group 2). There was no significant difference between Groups 1 and 2 with regard to pulmonary volumes and Pa,O2 (8.4+/-0.6 vs 8.4+/-0.4 kPa (63+/-4 vs 63+/-3 mmHg)) but arterial carbon dioxide tension (Pa,CO2) was higher in Group 1 (6.0+/-0.7 vs 53+/-0.5 kPa (45+/-5 vs 40+/-4 mmHg); p<0.0001). Mean pulmonary artery pressure (Ppa) was very similar in the two groups (2.6+/-0.7 vs 2.5+/-0.6 kPa (19+/-5 vs 19+/-4 mmHg)). No individual variable or combination of variables could predict the presence of pulmonary hypertension. It is concluded that in these patients with chronic obstructive pulmonary disease with modest daytime hypoxaemia, functional and gasometric variables (with the noticeable exception of arterial carbon dioxide tension) cannot predict the presence of nocturnal desaturation; and that mean pulmonary artery pressure is not correlated with the degree and duration of nocturnal hypoxaemia. These results do not support the hypothesis that sleep-related hypoxaemia favours the development of pulmonary hypertension.     

Efficacy and position of endurance training as a non-drug therapy in the treatment of arterial hypertension

BACKGROUND: The prevalence of chronic lung disease increases with advancing age. The purpose of this study was to detect latent pulmonary hypertension noninvasively in elderly patients with chronic lung disease. METHODS: The changes of flow-velocity by passive leg raising were assessed using pulsed Doppler echocardiography in the right ventricular outflow tract in 19 patients with chronic lung disease and 13 normal healthy subjects. Pulmonary artery pressure was measured simultaneously using a thermodilution cardiac output catheter. RESULTS: In patients with chronic lung disease examined at rest, we found pulmonary hypertension in seven, and none in 12. The normal pattern observed at rest changed to pulmonary hypertension pattern after leg raising in six out of the 12 patients. Pulmonary arterial catheterization confirmed the data obtained by pulsed Doppler echocardiography. CONCLUSIONS: Some elderly patients with chronic lung disease have latent pulmonary hypertension which can be detected noninvasively by analyzing the changes of flow velocity profiles in the right ventricular outflow tract by passive leg raising.     

Exercise tolerance assessed by unilateral pulmonary artery occlusion test before and after pulmonary resection

Pre- and post-operative exercise tests and unilateral pulmonary artery occlusion tests were performed on 15 surgical patients with pulmonary cancer. The relationship between these cardio-pulmonary parameters and exercise tolerance was studied, and pulmonary functional resectability was discussed. Pre- and post-operative anaerobic thresholds correlated with driving pressure (D.P: pulmonary artery pressure--pulmonary wedge pressure), and the pulmonary vascular-resistance index (PVRI). From the regression line and post-operative energy metabolic ratio, the standard limitation point of pulmonary resection can be estimated, (D.P = 22.6 mmHg PVRI = 621 dyne.sec.cm-5.m2). These data yielded a pulmonary pressure = 33.4 mmHg, total pulmonary vascular resistance index = 885 dyne.sec.cm-5.m2. These correlations were obtained because D.P and PVRI indicate the over all condition of the pulmonary vascular bed, gas exchange, ventilation and cardiac function. These data were in close agreement with previous results pertaining to the above indications. Unilateral pulmonary occlusion testing predicted the post-operative exercise tolerance of patients undergoing lung resection.     

Doppler assessment of pulmonary artery pressure in neonates at risk of chronic lung disease

AIM: To evaluate the pulmonary artery pressure (PAP) change in very low birth-weight (VLBW) infants at risk of chronic lung disease (CLD). METHODS: The time to peak velocity:right ventricular ejection time (TPV:RVET) ratio calculated from the pulmonary artery Doppler waveform, which is inversely related to PAP, was used. The TPV:RVET ratio was corrected for different heart rate (TPV:RVET(c)). Seventy three VLBW infants studied on days 1, 2, 3, 7, 14, 21 and 28 were enrolled for the analysis. RESULTS: Twenty two infants developed CLD with a characteristic chest radiograph at day 28. Fifty one did not, of whom 17 were oxygen dependent on account of apnoea rather than respiratory disease, and 34 were non-oxygen dependent. The TPV:RVET(c) ratio rose progressively in all three groups over the first three days of life, suggesting a fall in PAP. In the oxygen and non-oxygen dependent groups, the mean (SD) ratio rose to 0.53 (0.09) and 0.57 (0.09), respectively, on day 7, then remained relatively constant thereafter. The CLD group rose more slowly after day 3 and had a significantly lower mean ratio from day 7 onwards compared with the other two groups (day 7: P < 0.001, days 14-28: P < 0.0001), and fell significantly from 0.47 (0.11) on day 7 to 0.41 (0.07) on day 28 (P = 0.01), suggesting a progressive rise in PAP. The mean (SD) ratios at day 28 of all infants were: CLD group 0.41 (0.07); oxygen dependent group 0.66 (0.15); and the non-oxygen group 0.67 (0.11). The CLD group had a significantly lower ratio than the oxygen dependent group and the non-oxygen group (P < 0.0001). Using the TPV:RVET(c) ratio of < 0.46, infants at risk of developing CLD could be predicted on day 7 (predictive value 82.8%, sensitivity 54.5%, specificity 94.1%). CONCLUSION: The non-invasive assessment of PAP using the TPV:RVET(c) ratio may be useful in the longitudinal monitoring of PAP change in VLBW infants, and for prediction of chronic lung disease.     

Pulmonary artery pressure: early predictor of chronic lung disease in preterm infants

AIM: To determine if pulmonary artery pressure (PAP) in ventilated preterm infants is independently associated with the development of chronic lung disease (CLD) and whether early assessment has any prognostic value. METHODS: Two cohorts (development n = 55; and validation n = 28) of preterm infants were studied at 24 hours of age. PAP was assessed non-invasively using its inverse correlation with the corrected acceleration time to right ventricular ejection time ratio (AT:RVET(c)), calculated from the pulmonary artery Doppler waveform. Clinical and respiratory variables were also collected. Using logistic regression analysis to identify factors independently associated with CLD, a prognostic score was developed to predict CLD. The ability of the score to predict CLD was described using receiver operating characteristic (ROC) curves. RESULTS: Birthweight, inspired oxygen concentration, and AT:RVET(c) were independently predictive of CLD. The area under the ROC curve was 0.96 for the development and 0.89 for the validation cohort. Exclusion of AT:RVET(c) resulted in a reduction to 0.88 and 0.73, respectively. CONCLUSION: PAP is independently associated with CLD. An early assessment of PAP using AT:RVET(c) may permit the early prediction of CLD as part of a multifactorial scoring system.     

Validation of new pulsed Doppler echocardiographic techniques for assessment of pulmonary hemodynamics

In preparation for a vasodilator study on chronic obstructive pulmonary disease (COPD), we investigated the reliability of recently described pulsed Doppler techniques for estimating pulmonary artery pressure (PAP) and cardiac output (CO). Our aims were to determine the following: (1) the imaging success rate for pulsed Doppler measurements; (2) the repeatability of the measurements, and interobserver and intraobserver variability; and (3) the accuracy of Doppler compared with catheter measurements. Doppler studies were attempted in 81 patients (cardiac disease [23], COPD [22], sleep apnea [32], and normal subjects [4]). Suitable images were obtained in 68 subjects (84 percent) and in 76 subjects (94 percent) for PAP and CO estimations, respectively. The lowest imaging success rates were in COPD patients (68 percent for PAP and 86 percent for CO estimation). Repeatability of the techniques was assessed in four cardiac patients and three healthy volunteers by performing four replicate studies in each subject over 1 h. Intrasubject coefficient of variation was < 10 percent for PAP and < 5 percent for CO. The intraobserver variability for Doppler estimation of systolic and mean PAP was 5.5 percent and 5.8 percent, respectively. The corresponding values for interobserver variability were 6.7 percent and 6.2 percent. Intraobserver and interobserver variability for "nongeometric" method of estimating CO was 5.1 percent and 5.9 percent, respectively. Agreement was good between catheter-measured and Doppler-estimated PAP in the 27 patients tested (cardiac [19] and COPD [8]) for both mean and systolic pressures (r = 0.96 and r = 0.97, respectively). The correlations between thermodilution and Doppler estimations of CO in eight COPD patients were 0.77 ("geometric" technique) and 0.97 ("nongeometric" technique). We conclude that pulsed Doppler techniques can be used to obtain accurate and reproducible quantitative information on pulmonary hemodynamics in a wide range of patients. Suitable Doppler images can be obtained in more than two thirds of COPD patients.     

Estimation of left ventricular filling pressures using two-dimensional and Doppler echocardiography in adult patients with cardiac disease. Additional value of analyzing left atrial size, left atrial ejection fraction and the difference in duration of pulmonary venous and mitral flow velocity at atrial contraction

OBJECTIVES: The purpose of this study was to determine whether left atrial size and ejection fraction are related to left ventricular filling pressures in patients with coronary artery disease. BACKGROUND: In patients with coronary artery disease, left ventricular filling pressures can be estimated by using Doppler mitral and pulmonary venous flow velocity variables. However, because these flow velocities are age dependent, additional variables that indicate elevated left ventricular filling pressures are needed to increase diagnostic accuracy. METHODS: Echocardiographic left atrial and Doppler mitral and pulmonary venous flow velocity variables were correlated with left ventricular filling pressures in 70 patients undergoing cardiac catheterization. RESULTS: Left atrial size and volumes were larger and left atrial ejection fractions were lower in patients with elevated left ventricular filling pressures. Mean pulmonary wedge pressure was related to mitral E/A wave velocity ratio (r = 0.72), left atrial minimal volume (r = 0.70), left atrial ejection fraction (r = -0.66) and atrial filling fraction (r = -0.66). Left ventricular end-diastolic and A wave pressures were related to the difference in pulmonary venous and mitral A wave duration (both r = 0.77). By stepwise multilinear regression analysis, the ratio of mitral E to A wave velocity was the most important determinant of pulmonary wedge (r = 0.63) and left ventricular pre-A wave (r = 0.75) pressures, whereas the difference in pulmonary venous and mitral A wave duration was the most important variable for both left ventricular A wave (r = 0.75) and left ventricular end-diastolic (r = 0.80) pressures. The sensitivity of a left atrial minimal volume > 40 cm3 for identifying a mean pulmonary wedge pressure > 12 mm Hg was 82%, with a specificity of 98%. CONCLUSIONS: Left atrial size, left atrial ejection fraction and the difference between mitral and pulmonary venous flow duration at atrial contraction are independent determinants of left ventricular filling pressures in patients with coronary artery disease. The additive value of left atrial size and Doppler variables in estimating filling pressures and the possibility that left atrial size may be less age dependent than other mitral and pulmonary venous flow velocity variables merit further investigation.     

Coronary-to-pulmonary artery shunts via the bronchial artery: analysis of cineangiographic studies

Coronary-to-pulmonary artery shunts via the bronchial artery (CA-BA-PA shunts) were observed in 16 of 2,922 consecutive patients who underwent selective coronary cineangiography. Underlying diseases included Takayasu arteritis (n = 8), chronic pulmonary inflammatory diseases (n = 4), pulmonary thromboembolism (n = 2), pulmonary artery tumor (n = 1), and tetralogy of Fallot with pulmonary atresia (n = 1). Ventilation-perfusion scans were available in 15 of the 16 patients. Mismatched defects were identified in 11 patients, and matched defects were identified in four. Bronchial-to-pulmonary artery shunts were detected on selective bronchial angiograms and/or thoracic aortograms in 13 patients. Feeding arteries of the CA-BA-PA shunts included left atrial branches (n = 13), right sinus node branches (n = 7), left sinus node branches (n = 2), right conal branch (n = 1), left conal branch (n = 1), and posterolateral branches (n = 2). These coronary branches seemed to serve as collateral vessels from a coronary arterial system with a higher pressure to a pulmonary arterial system with a lower pressure in conditions of decreased pulmonary flow or in cases of chronic pulmonary inflammatory disease. The importance of the coronary artery along with other superior thoracic collateral networks in contributing to the development of shunts to the pulmonary artery is underscored.     

Effects of airway obstruction on transmural pulmonary artery pressure in exercising horses

OBJECTIVE: To determine whether laryngeal hemiplegia would increase transmural pulmonary artery pressure (TPAP). ANIMALS: 6 horses. DESIGN: Horses were studied under 5 conditions: control conditions, after induction of left laryngeal hemiplegia, during obstruction of the left nostril, after placement of an instrumented tracheostomy, and after placement of an open tracheostomy. Horses were evaluated after being given saline solution and after being given furosemide. PROCEDURES: Horses were exercised on a high speed treadmill, using a maximum speed of 13 m/s. During each exercise, airway pressures, airflow, esophageal and pulmonary artery pressures, and blood gas partial pressures were measured. RESULTS: When adjusted for horse, speed, and obstruction condition, mean TPAP (pulmonary artery pressure-esophageal pressure) and minimum TPAP were significantly lower after administration of furosemide than after administration of saline solution. In horses given saline solution, respiratory obstruction that increased intrapleural pressure significantly increased mean TPAP, and respiratory obstruction that decreased intrapleural pressure significantly decreased minimum TPAP. CONCLUSIONS: Changes in intrapleural pressure appear to play an important role in pulmonary artery pressure and TPAP. CLINICAL RELEVANCE: Because induction of laryngeal hemiplegia did not increase TPAP, laryngeal hemiplegia is unlikely to contribute to development of exercise-induced pulmonary hemorrhage.     

Estimation of pulmonary artery pressure by spectral analysis of the second heart sound

The objective of the present work was to test and validate a noninvasive method based on spectral analysis of the second heart sound (S2) to estimate the pulmonary artery (PA) systolic pressure in 89 patients with a bioprosthetic heart valve. The technique was compared with continuous-wave Doppler estimation of PA systolic pressure in these patients. The heart sounds recorded at the pulmonary area on the chest wall were digitized by computer. The spectra of S2 and those of the aortic (A2) and the pulmonary (P2) components of S2 were computed with a fast-Fourier transform. Seven features were extracted from these spectra. The statistical analysis performed with the Pearson linear correlation coefficient showed that the best estimation of PA systolic pressure obtained by spectral phonocardiography (r = 0.84, SEE +/- 5.6 mm Hg, p <0.0001) was provided by the following equation: PA systolic pressure = 47 + 0.68 Fp - 4.4 Qp - 17 Fp/Fa - 0.15 Fs, where Fs and Fp are dominant frequencies associated with the maximal amplitude of the power spectra of S2 and P2, respectively, Qp is the quality of resonance of P2, and Fp/Fa is the ratio of the dominant frequencies of P2 and A2, respectively.