Increase In Pulmonary Artery Systolic Pressure Research Articles

No Correlation between Pulmonary Artery Pressure and Markers of Pulmonary Interstitial Fluid Accumulation at Altitude

PURPOSE: A previous study yielded indirect evidence by changes in closing volume that “subclinical” high altitude pulmonary edema (HAPE) occurs in a large number of mountaineers after ascent to 4559 m. Since an abnormal increase of pulmonary artery pressure (PAP) in hypoxic environment is the key mechanism of pulmonary fluid accumulation, we hypothesized that markers of interstitial pulmonary fluid accumulation correlate with the increase in PAP at high altitude. METHODS: We therefore performed pulmonary function testing by body plethysmography and measured lung compliance by oesophageal pressure measurements and systolic PAP by echocardiography in 34 healthy subjects at baseline at low altitude (LA) and after rapid ascent to 4559 m. Measurements at high altitude (HA) were performed 2–4 h (HA1), 20 h (HA2) and 44 h (HA3) after arrival at 4559 m. RESULTS: HAPE was diagnosed by clinical examination and chest x-ray in 4 subjects, which were excluded from the further analysis presented here. Pulmonary function testing showed normal values for all subjects at LA and there were no differences for the whole group in measurements at high altitude for total lung capacity, vital capacity, diffusion capacity, closing volume and dynamic or static compliance. PAP also was normal in all subjects at LA (22 ± 4 mmHg) and significantly increased by 16 ± 8 (HA1), 14 ± 6 (HA2) and 12 ± 6 (HA3), respectively (p<0.001). Maximum values of systolic PAP at high altitude varied from 30 to 60 mmHg between subjects. There was no correlation in any parameter of pulmonary function testing with the increase in systolic PAP. CONCLUSIONS: In contrast to previous studies we found that lung volumes, diffusion capacity, closing volume, and pulmonary compliance are unchanged at high altitude, which indicates that no relevant interstitial fluid accumulation occurred in our subjects despite a wide range in elevation of PAP. The lack of correlation of systolic PAP and decrements in pulmonary function parameters is evidence against the claim that the majority of climbers ascending to altitudes in the range of 4000 to 5000 meters develop subclinical HAPE.

The Noninvasive Evaluation of Exercise-induced Changes in Pulmonary Artery Pressure and Pulmonary Vascular Resistance

During exercise, pulmonary artery systolic pressure (PASP) may increase. The purpose of this study was to examine the responses of PASP and pulmonary vascular resistance by Doppler echocardiography during exercise in conditioned athletes and in patients with pulmonary disease. Fifteen participants in each group were evaluated using Doppler echocardiography at rest and during recumbent bicycle exercise. PASP was calculated using 4 times the tricuspid regurgitant velocity squared (TRV)2 and a surrogate for pulmonary vascular resistance was calculated using the equation: pulmonary vascular resistance = TRV/right ventricular outflow tract time-velocity integral. During exercise, PASP increased in both groups with higher values achieved by patients with pulmonary conditions (54.8 vs 70.6 mm Hg, P = .009). At baseline the ratio TRV/right ventricular outflow tract time-velocity integral was 0.2 or less in both the athlete and pulmonary groups. During exercise, the ratio of TRV/right ventricular outflow tract time-velocity integral remained less than 0.2 in the athletes and increased more than 0.2 in the pulmonary group. Doppler echocardiography can be used to discriminate a flow- versus resistance-mediated mechanism for exercised-induced increase in PASP.

Diagnostic Value of Echo-Doppler and Tissue Doppler Imaging in Dogs with Pulmonary Arterial Hypertension

Diagnosis of pulmonary arterial hypertension (PAH) relies on Doppler measurement of pulmonic and tricuspid regurgitation (TR). However, these are not always detectable. Tissue Doppler imaging (TDI), a novel noninvasive ultrasound technique, provides indirect but sensitive and specific assessment of elevated systolic pulmonary artery pressure (SPAP) in dogs. One hundred and five dogs with TR. Prospective observational study. Dogs were categorized as presenting normal (group 1, n = 45), mildly increased (group 2, n = 19), or moderately to severely increased (group 3, n = 41) SPAP, based on TR peak velocities (< 2.5, 2.5-3.0, and > 3.0 m/s, respectively). Ten quantitative echo-Doppler- and TDI-derived variables were assessed, including the main pulmonary arterial diameter to aortic diameter ratio, pulmonary flow acceleration time, and acceleration-to-ejection time ratio, the Tei index of right ventricular function, and 6 longitudinal basal right ventricular TDI variables. A significant correlation was observed between SPAP and each of the 10 tested variables (P < .05). Conventional echo-Doppler variables were less discriminating than the TDI for predicting increased SPAP. The combined systolic and diastolic right TDI index had the highest sensitivity and specificity (89% and 93% respectively, for a cutoff of 11.8 cm/s) and could discriminate between dogs in group 1 from dogs in group 2. TDI provided effective predictors of systolic PAH and demonstrated that both alterations in right-sided systolic and diastolic myocardial function can occur with mild increases in SPAP.

Determinants of pulmonary artery hypertension at rest and during exercise in patients with heart failure

Pulmonary hypertension, a marker of poor prognosis in heart failure, may develop or increase during exercise. We sought to examine the determinants of pulmonary hypertension at rest and during exercise in heart failure patients. Forty-six patients with left ventricular (LV) dysfunction (ejection fraction: 30 +/- 6%) underwent a semi-recumbent, incremental bicycle exercise Doppler echocardiography. LV systolic and diastolic function, pulmonary artery systolic pressure (PASP), functional mitral regurgitation (MR), and left atrial volume were quantified at rest and during exercise. Wide changes in PASP at exercise were unrelated to PASP at rest (r = 0.12). Independent predictors of PASP at rest were left atrial volume (P = 0.006), E-wave velocity (P = 0.02), mitral tenting area (P = 0.005), and mitral effective regurgitant orifice (ERO) (P = 0.02). The incidence of dyspnoea was similar in patients with and without moderately severe pulmonary hypertension at baseline. At peak exercise, LV ejection fraction (P = 0.03) and mitral ERO (P = 0.008) were independently associated with PASP. Patients with a larger exercise increase in PASP (>60 mmHg) interrupted frequently exercise for dyspnoea (70 vs. 27%; P = 0.04). A larger rise in mitral regurgitant volume during exercise emerged as the single determinant of exercise-induced increases in PASP. In patients with HF, left atrial volume, mitral deformation, and mitral regurgitant orifice correlated with pulmonary pressure at rest, whereas dynamic MR and limited contractile reserve correlated with pulmonary pressure at exercise. The magnitude of pulmonary pressure during exercise in these patients mainly depends on dynamic MR.

Reduced Exercise Capacity and Stress-Induced Pulmonary Hypertension in Patients With Scleroderma

We sought to determine the incidence of stress-induced pulmonary artery (PA) systolic hypertension in a referral population of patients with scleroderma, and to examine the relation between stress-induced pulmonary systolic hypertension and exercise capacity in this population. Early detection of patients with scleroderma at risk for pulmonary hypertension (PHTN) could lead to more timely intervention and thus reduce morbidity and improve mortality. The change in PA systolic pressure (PASP) with exercise provides a possible tool for such detection. Sixty-five patients with scleroderma (9 men and 56 women; mean age 51 +/- 12 years [SD]), normal resting PASP, and normal resting left ventricular function underwent exercise Doppler echocardiography using a standard Bruce protocol. Tricuspid regurgitation velocity was measured before and after exercise. Exercise variables including workload achieved in metabolic equivalents (METS), total exercise time, percentage of target heart rate achieved, and PASP at rest and within 60 s after exercise were recorded. Thirty patients (46%) demonstrated an increase in PASP to > 35 mm Hg plus an estimated right atrial pressure of 5 mm Hg. Postexercise PASP inversely correlated to both the maximum workload achieved (r = - 0.34, p = 0.006) and exercise time (r = - 0.31, p = 0.01). In women, the correlation was more significant (r = - 0.38, p = 0.003). Patients in the lowest quartile of exercise time, with the least cardiac workload achieved, produced the highest postexercise PASP. Stress-induced PHTN is common in patients with scleroderma, even when resting PASP is normal. Stress Doppler echocardiography identifies scleroderma patients with an abnormal rise in PASP during exertion. Peak PASP is linearly related to exercise time and maximum workload achieved. Measurement of PASP during exercise may prove to be a useful tool for the identification of future resting PHTN.

227 Strain rate imaging reveals myocardial ischemia as mechanism of right ventricular dysfunction after acute pulmonary embolism

evaluation before treadmill EE using the modified Bruce protocol. Pulmonary artery systolic pressure (PASP) was estimated in left lateral desubitus, in upright position before exercise was started and at peak workload from peak tricuspid regurgitant jet velocities according to the equation: PASP=4V2+5mmHg. PASP 60mmHg Conclusions: A high percentage (62%) of CMD pts with normal PASP at rest revealed a pathological increase of PASP during treadmill exercise, classified as severe in 3 of them. The clinical significance of these findings are not known but might reveal the usefulness of EE in the early screening of PAH and underscore the need for long term follow-up of these pts with the purpose of clarifying the clinical implications of our study.

Progression of Pulmonary Hypertension in Patients with Sickle Cell Disease.

Introduction: The prevalence of pulmonary hypertension (PHT) is high in patients with sickle cell disease (SCD). Although most patients have only mild increases in their pulmonary artery systolic pressure (PASP), the presence of PHT is strongly associated with an increased risk of death. While PHT seen in SCD is thought to progress over time, both the rate of development of PHT and the factors that affect disease progression remain unknown.Methods: The 41 subjects in this study were drawn from an original cohort of 60 patients followed in the Sickle Cell Clinic at UNC-Chapel Hill. All patients were previously evaluated for PHT (defined using an age-, sex-, and BMI-adjusted reference range). Of the 60 patients in the original cohort, six are now deceased and 13 others were not available for repeat evaluation. The PASP was determined using Doppler echocardiography and then applying the modified Bernoulli equation (PASP = 4V2 + right atrial pressure). Individuals were not studied if they: 1) showed clinical evidence of left ventricular failure; 2) had a recent acute illness (e.g., vaso-occlusive crisis); or 3) had experienced an episode of acute chest syndrome within the preceding 4 weeks. Means and standard deviations were calculated for all measures at the time of initial evaluation and at the time of follow-up.Results: Of the 41 subjects in our study, PHT was originally present in 12, while no evidence of PHT was present in 29. Of the 29 subjects who initially had no evidence of PHT, 4 (or 14%) have now developed PHT (mean follow-up period of 3.3 ± 0.4 years). In these 4 subjects, the mean PASP at the time of initial and follow-up evaluations respectively were: 37.0 ± 2.0 mm Hg vs. 55.8 ± 11.0 mm Hg. The patients who developed PHT during the course of the study had lower systolic BP (143 ± 12 mm Hg vs. 128 ± 12 mm Hg), lower fetal hemoglobin levels (6.2 ± 5.7 % vs. 4.2 ± 3.7 %), and higher platelet counts (276 ± 119 X 103/μL vs. 426 ± 96 X 103/μL) at the time of their follow-up analyses. By contrast, 3 of the 12 subjects (or 25%) who were thought to have PHT at the time of their original evaluations were found to have normal PASP determinations at the time of their repeat echocardiograms (mean follow-up period of 3.2 ± 0.6 years). In these latter 3 subjects, the mean PASP values at the time of the initial and follow-up evaluations respectively were: 40.0 ± 4.6 mm Hg vs. 33.7 ± 4.7 mm Hg.Conclusion: In this small group of patients with SCD, we found that PHT developed in 14% of subjects who had no evidence of PHT 3 years earlier. Based on this observation, it seems that periodic echocardiograms to screen for the development of PHT would be appropriate. On the other hand, our observation that some patients initially classified as having PHT failed to have elevated PASP measurements at the time of follow-up illustrates the limitation of a single echocardiographic evaluation in establishing this diagnosis. Because of the increase in PASP that occurs during acute vaso-occlusive episodes, and the difficulty usually encountered in distinguishing steady state from crisis, the initial elevation of the PASP in these patients could have resulted from sub-clinical crisis states. For these reasons, a patient found to have an elevated PASP at the time of a screening echocardiogram should have a repeat study, and perhaps a right heart catheterization, before the diagnosis of PHT is firmly established.

Identification of individuals susceptible to high-altitude pulmonary oedema at low altitude

Individuals susceptible to high-altitude pulmonary oedema (HAPE) are characterised by an abnormal increase of pulmonary artery systolic pressure (PASP) in hypoxia and during normoxic exercise, reduced hypoxic ventilatory response, and smaller lung volume. In 37 mountaineers with well-documented altitude tolerance, it was investigated whether any combination of these noninvasive measurements, including exercise in hypoxia, could improve the identification of HAPE-susceptible subjects at low altitude. HAPE-susceptible subjects showed a significant higher increase of PASP during hypoxia at rest (48+/-10 mmHg) compared with controls (38+/-3 mmHg), as well as during normoxic exercise (57+/-14 versus 38+/-7 mmHg) and hypoxic exercise (69+/-13 versus 49+/-8 mmHg). PASP could not be assessed in three and eight subjects during normoxic or hypoxic exercise, respectively, due to insufficient Doppler profiles or systemic arterial hypertension. Sensitivity (77-94%) and specificity (76-93%) were not significantly different between the various testing conditions. Additional assessment of hypoxic ventilatory response and lung function parameters did not improve identification of HAPE-susceptible subjects in a multivariate analysis. Due to the greater number of missing values in pulmonary artery systolic pressure measurements during hypoxic exercise, it was concluded that pulmonary artery systolic pressure measurements at rest during hypoxia or exercise in normoxia are most feasible for the identification of high-altitude pulmonary oedema-susceptible subjects.

Stress Doppler echocardiography for identification of susceptibility to high altitude pulmonary edema

OBJECTIVEThis prospective single-blinded study was performed to quantitate noninvasive pulmonary artery systolic pressure (PASP) responses to prolonged acute hypoxia and normoxic exercise.BACKGROUNDHypoxia-induced excessive rise in pulmonary artery pressure is a key factor in high-altitude pulmonary edema (HAPE). We hypothesized that subjects susceptible to HAPE (HAPE-S) have increased pulmonary artery pressure response not only to hypoxia but also to exercise.METHODSPASP was estimated at 45, 90 and 240 min of hypoxia (Fi02=12%) and during supine bicycle exercise in normoxia using Doppler-echocardiography in nine HAPE-S and in 11 control subjects.RESULTSIn the control group, mean PASP increased from 26 ± 2 to 37 ± 4 mm Hg (ΔPASP 10.3 ± 2 mm Hg) after 90 min of hypoxia and from 27 ± 4 to 36 ± 3 mm Hg (ΔPASP 8 ± 2 mm Hg) during exercise. In contrast, all HAPE-S subjects revealed significantly greater increases (p = 0.002 vs. controls) in mean PASP both during hypoxia (from 28 ± 4 to 57 ± 10 mm Hg, ΔPASP 28.7 ± 6 mm Hg) and during exercise (from 28 ± 4 to 55 ± 11 mm Hg, ΔPASP 27 ± 8 mm Hg) than did control subjects. Stress echocardiography allowed discrimination between groups without overlap using a cut off PASP value of 45 mm Hg at work rates less than 150 W.CONCLUSIONSThese data indicate that HAPE-S subjects may have abnormal pulmonary vascular responses not only to hypoxia but also to supine bicycle exercise under normoxic conditions. Thus, Doppler echocardiography during supine bicycle exercise or after 90 min of hypoxia may be useful noninvasive screening methods to identify subjects susceptible to HAPE.

Pulmonary artery hypertension in adult patients with symptomatic valvular aortic stenosis

Pulmonary hypertension (PH) has been reported in patients with valvular aortic stenosis (AS) and has been found to be associated with a more severe clinical picture and a poor prognosis after aortic valve replacement. The aim of this study was to assess the prevalence of PH in adult patients with symptomatic AS undergoing cardiac catheterization, and to evaluate the relation between pulmonary artery (PA) systolic pressure and hemodynamic and clinical variables to further clarify the pathogenetic mechanisms. We assessed right-sided heart hemodynamics during cardiac catheterization in 388 patients with symptomatic isolated or predominant AS. PA systolic pressure between 31 and 50 mm Hg was used to define mild to moderate PH, whereas PA systolic pressure >50 mm Hg was used to define severe PH. PA systolic pressure showed no significant difference according to age and sex, although it was significantly higher in patients in New York Heart Association functional classes III and IV and in patients with coexistent systemic hypertension than in the others. PH was absent in 136 patients (35%, group 1), mild to moderate in 196 patients (50%, group 2), and severe in 58 patients (15%, group 3). Only the prevalence of overt heart failure was significantly higher in group 3 patients. AS severity was similar among the 3 groups, and PA systolic pressure showed no relation to aortic valve area in the entire population. Also, a poor correlation was found between PA pressure and left ventricular (LV) ejection fraction (r = −0.28), with several patients having moderate or severe PH despite a preserved LV systolic function. PA systolic pressure significantly correlated with LV end-diastolic pressure (r = 0.50) and with PA wedge pressure (r = 0.84). Furthermore, transpulmonary pressure gradient, an index of resistance across the pulmonary vascular bed (obtained as the difference between PA mean and PA wedge pressure), was significantly higher in patients with PH, especially in those with a marked increase in PA systolic pressure, suggesting a reactive component of PH.