Latent Pulmonary Hypertension Research Articles

Exercise-Induced Pulmonary Hypertension: A Valid Entity or Another Factor of Confusion?

Exercise-induced pulmonary hypertension EIPH has been defined as an increase in mean pulmonary arterial pressure (mPAP) during exercise in otherwise normal values at rest. EIPH reflects heart and/or lung dysfunction and may precede the development of manifest pulmonary hypertension (PH) in a proportion of patients. It is also associated with decreased life expectancy in patients with heart failure with reduced ejection fraction (HFrEF) or left ventricle (LV) valvular diseases. Diastolic dysfunction exacerbated during exercise relates to increased LV filling pressure and left atrial pressure (LAP). In this context backward, transmitted pressure alone or accompanied with backward blood flow promotes EIPH. The gold standard of EIPH assessment remains the right heart catheterization during exercise, which is an accurate but invasive method. Alternatively, non-invasive diagnostic modalities include exercise stress echocardiography (ESE) and cardiopulmonary exercise testing (CPET). Both diagnostic tests are performed under gradually increasing physical stress using treadmill and ergo-cycling protocols. Escalating workload during the exercise is analogous to the physiological response to real exercise. The results of the latter techniques show good correlation with invasive measurements, but they suffer from lack of validation and cut-off value determination. Although it is not officially recommended, there are accumulated data supporting the importance of EIPH diagnosis in the assessment of other mild/subclinical or probably fatal diseases in patients with latent PH or heart failure or LV valvular disease, respectively. Nevertheless, larger, prospective studies are required to ensure its role in clinical practice.

An Article on the Benefit of Advanced Therapy for Pulmonary Hypertension in Patients with Systemic Sclerosis Who Have Latent Pulmonary Hypertension Unmasked by Fluid Bolus

An Article on the Benefit of Advanced Therapy for Pulmonary Hypertension in Patients with Systemic Sclerosis Who Have Latent Pulmonary Hypertension Unmasked by Fluid Bolus

Latent pulmonary hypertension in atrial septal defect: Dynamic stress echocardiography reveals unapparent pulmonary hypertension and confirms rapid normalisation after ASD closure

ObjectiveClosure of atrial septal defects (ASD) prevents pulmonary hypertension, right heart failure and thromboembolic stroke. The exact timing for ASD closure is controversial.MethodsIn a prospective study to address the question whether unapparent pulmonary hypertension can be revealed prior to right ventricular (RV) remodelling, patients were investigated before and 6, 12, and 24 months after ASD closure using exercise stress echocardiography (ESE) and ergospirometry (n = 24).ResultsAt rest, RV systolic pressure (RVSP) was normal in 58.8 %, slightly elevated in 26.5 %, and moderately elevated in 11.8 %. One patient showed severe pulmonary hypertension. During ESE, all patients with normal RVSP at rest exhibited an increase (25.7 ± 1.2 mmHg vs. 45.3 ± 2.3 mmHg, p < 0.001). After closure the RVSP was lower, both at rest and ESE. RV diameters decreased too. Tricuspid annulus plane systolic excursion (TAPSE) at rest remained lower after closure (24.0 ± 0.9 vs. 22.0 ± 0.9 mm, p < 0.05). TAPSE in ESE was elevated, and stayed stable after closure (30.1 ± 1.8 mm vs. 29.3 ± 1.6 mm). Before closure, RV systolic tissue velocities (sa) at rest were normal and decreased after closure (14.0 ± 1.0 cm/s vs. 11.5 ± 0.7 (6 month) vs. 10.6 ± 0.5 cm/s (12 month), p < 0.05). During ESE, sa velocity was similar before and after closure (23.0 ± 1.3 cm/s vs. 23.3 ± 1.9 cm/s). Maximal oxygen uptake (VO2/kg) did not differ between baseline and follow-ups.ConclusionLatent pulmonary hypertension may become apparent in ESE. ASD closure leads to a significant reduction in this stress-induced pulmonary hypertension and to a decrease in the right heart diameters indicating reverse RV remodelling. RV functional parameters at rest did not improve. The VO2/kg did not change after ASD closure.

High Plasma Brain Natriuretic Peptide Levels in Stable COPD without Pulmonary Hypertension or Cor Pulmonale

Early diagnosis of chronic obstructive pulmonary disease (COPD) with latent pulmonary hypertension (PH) and cor pulmonale is important because the prognosis of this condition is poor. To investigate the utility of brain natriuretic peptide (BNP) for prognostication of COPD, plasma BNP was measured in patients with COPD without symptoms or physical findings of PH or cor pulmonale. Plasma BNP was measured in 60 patients with COPD, 10 asthmatics, and 30 healthy subjects. Echocardiography, arterial blood gas analysis, and spirometry were also performed. Mortality and exacerbation were compared between COPD patients with high and low plasma BNP levels over a 3-year follow-up period. Plasma BNP (mean +/- SEM, pg/mL) in COPD patients (41.0+/-6.6) was significantly higher than in normal subjects (14.8+/-2.7) and asthmatics (17.4+/-4.5) (p<0.0001 and p<0.05, respectively). No significant correlations were observed between plasma BNP level and pulmonary function or hypoxia. There was, however, a significant correlation between plasma BNP level and % ejection fraction (r=-0.41, p=0.0197) and pulmonary artery systolic pressure (r=0.5, p=0.004). The period until initial COPD exacerbation in subjects with a high plasma BNP level was significantly shorter (p<0.05). Plasma BNP level during exacerbations (79.9+/-16.2) was also significantly higher than during stable disease (41.2+/-8.7) (p=0.004). We suggest that plasma BNP is a non-invasive biomarker that can be used as a screening parameter for latent PH and left ventricular dysfunction, and also as a predictor of exacerbation in stable COPD.

Magnetic Resonance–Derived 3-Dimensional Blood Flow Patterns in the Main Pulmonary Artery as a Marker of Pulmonary Hypertension and a Measure of Elevated Mean Pulmonary Arterial Pressure

Pulmonary hypertension is a disease characterized by an elevation in pulmonary arterial pressure that is diagnosed invasively via right heart catheterization. Such pathological altered pressures in the pulmonary vascular system should lead to changes in blood flow patterns in the main pulmonary artery. Forty-eight subjects (22 with manifest pulmonary hypertension, 13 with latent pulmonary hypertension, and 13 normal control subjects) underwent time-resolved 3D magnetic resonance phase-contrast imaging of the main pulmonary artery. Velocity fields that resulted from measurements were calculated, visualized, and analyzed with dedicated software. Main findings were as follows: (1) Manifest pulmonary hypertension coincides with the appearance of a vortex of blood flow in the main pulmonary artery (sensitivity and specificity of 1.00, 95% confidence intervals of 0.84 to 1.00 and 0.87 to 1.00, respectively), and (2) the relative period of existence of the vortex correlates significantly with mean pulmonary arterial pressure at rest (correlation coefficient of 0.94). To test the diagnostic performance of the vortex criterion, we furthermore investigated 55 patients in a blinded prospective study (22 with manifest pulmonary hypertension, 32 with latent pulmonary hypertension, and 1 healthy subject), which resulted in a sensitivity of 1.00 and specificity of 0.91 (95% confidence intervals of 0.84 to 1.00 and 0.76 to 0.98, respectively). Comparison of catheter-derived mean pulmonary artery pressure measurements and calculated mean pulmonary artery pressure values resulted in a standard deviation of differences of 3.6 mm Hg. Vortices of blood flow in the main pulmonary artery enable the identification of manifest pulmonary hypertension. Elevated mean pulmonary arterial pressures can be measured from the period of vortex existence.

Assessment of Pulmonary Artery Systolic Pressures by Stress Doppler Echocardiography After Bilateral Lung Transplantation

Even after successful single-lung transplantation (SLTx) or bilateral lung transplantation (BLTx), patients continue to have peripheral muscle weakness and exercise impairment. After SLTx, exercise limitation is also attributed to persistent or recurrent pulmonary vascular abnormalities with elevated pulmonary arterial pressures at rest or during exercise. Therefore, the aim of this study was to evaluate systolic pulmonary artery pressures (PASPs) at rest and during supine bicycle exercise, exercise capacity and cardiopulmonary function in post-BLTx patients. Nine patients underwent BLTx due to end-stage pulmonary arterial hypertension (PAH) and 37 age- and gender-matched control subjects underwent a physical examination, electrocardiographic (ECG) test, a 6-minute walk test, a lung function test, a cardiopulmonary exercise test and echocardiographic assessment at rest and during exercise. Exercise capacity was significantly reduced in the BLTx group, with an impaired 6-minute walk test and maximal oxygen uptake and workload. Ventilatory factors did not appear to limit exercise capacity. Right and left ventricular size and pump function and PASP values at rest were normal in both groups, but exceeded 40 mm Hg in 3 of 9 BLTx recipients and in 1 of 37 controls during exercise at low workloads. Mean PASP during exercise was only slightly higher in the BLTx group (40 +/- 5 vs 36 +/- 4 mm Hg, p = not statistically significant). Reduced exercise capacity of patients after BLTx due to end-stage pulmonary hypertension is not attributed to persistent or recurrent manifest pulmonary hypertension or cardiopulmonary dysfunction. Nevertheless, latent pulmonary hypertension with exaggerated pulmonary artery pressures during exercise may occur in some patients.

Isolated right ventricular dysfunction in systemic sclerosis: latent pulmonary hypertension?

Right ventricular function is frequently abnormal in patients with systemic sclerosis, but whether this is related to pulmonary vascular complications of the disease is unclear. Standard echocardiography with tissue Doppler imaging was performed at rest and during exercise for the study of right ventricular function and pulmonary circulation in 25 consecutive systemic sclerosis patients and in 13 age-matched healthy controls. When compared with the controls, the patients had no difference in systolic right ventricular pressure gradient, but a decreased pulmonary flow acceleration time, and increased right ventricular free wall thickness and end-diastolic dimensions. At the tricuspid annulus, the E maximal velocity was decreased (8.9 +/- 4 versus 11.7 +/- 2.3 cm.s(-1)) and the isovolumic relaxation time corrected to RR interval was increased (6.5 +/- 2.9 versus 4.5 +/- 2.5%). The tissue Doppler imaging profile at the mitral annulus was similar in both groups. At exercise, 18 patients had a decreased maximum workload and cardiac output, no change in systolic right ventricular pressure gradient, but an increase in the slope of pulmonary artery pressure/flow relationships. These results suggest that patients with systemic sclerosis may present with latent pulmonary hypertension as a likely cause of right ventricular diastolic dysfunction, as revealed by stress echocardiography and tissue Doppler imaging.

Doppler echocardiographic evaluation of latent pulmonary hypertension by passive leg raising.

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. 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. 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. 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.

Noninvasive diagnosis of latent pulmonary hypertension in copd by exercise-load impedance rheopneumogram: a comparative study with right heart catheterization

Impedance rheopneumogram (IRP) and right heart Swan-Ganz catheter examinations were simultaneously carried out in 63 patients. Two equations for calculating after-exercise-pulmonary-pressure (PAPm) were obtained by stepwise regression analysis: 1) PAPm (kPa) = -1.40-0.88.InHs+8.30.(B-F)+5.78.Q-B/B-Y (r = 0.730, IRP is measured at rest); 2) PAPm(kPa) = 6.46-5.04.Hs/square root of R-R +4.35.Q-B/B-Y-19.34.(Q-C) (r = 0.648, IRP is measured after exercise). This is a new method for diagnosing latent pulmonary hypertension noninvasively.

Functional surgery of bullous emphysema.

Multiple large and small emphysematous bullae were resected in 27 patients with chronic obstructive lung disease (COLD). Twenty-two patients were operated on one side, and 5 patients underwent bilateral consecutive operations. Twenty-five patients were male, 2 female, and they were between 22 and 67 years old (mean 49.5 years). All patients had a follow-up examination between 3 and 48 months postoperatively. As operative techniques, resection by means of a clamp, plication of cysts according to Nissen, resection with homologous dura plasty (7 patients) and pericardial plasty (7 patients) were used. In 19 patients preoperative and postoperative pulmonary function was compared. Functional improvement occurred in 17 patients - including all of the 5 bilateral procedures. Postoperative improvement was more pronounced with decreasing preoperative pulmonary function, measured as VC, RV, IGV and Raw. Partial pulmonary insufficiency could be improved in 9 patients and global pulmonary insufficiency was improved in 5. In 16 cases physical work capacity was increased. The hemodynamics of the pulmonary circulation were improved in all patients with increased preoperative pulmonary artery pressure (latent pulmonary hypertension in 7 patients, overt pulmonary hypertension in 5). FEV1 was least influenced by surgery, especially in patients more than 50 years old. The long-term prognosis, thus has to be judged cautiously. One patient died postoperatively (mortality 4%). The technique of dura and pericardial plasty, aiming at functional adaptation, is described. Sutures inverting or folding pulmonary tissue are avoided. The aspect of at least temporary (up to 3 years) functional improvement leads us to advocate the use of extended criteria of operability.