[Natural history of pulmonary hypertension in chronic obstructive lung diseases and the usefulness of the simple noninvasive methods of its diagnosis]. / Historia naturalna nadcisnienia plucnego w przewleklych chorobach pluc i przydatnosc prostych nieinwazyjnych metod jego rozpoznawania.

In 47 patients with chronic obstructive pulmonary disease and 19 patients with idiopathic pulmonary fibrosis pulmonary haemodynamics were studied. Pulmonary arterial pressure was compared with non-invasive lung function tests, ecg and the chest X-ray. Correlations between pulmonary arterial pressure and some of those parameters were found. Investigations were repeated after 3 or 5 years depending on severity of pulmonary hypertension initially found. The progression of pulmonary hypertension was found. It was accompanied by intensification of non-invasive indices of pulmonary hypertension. More than half of patients with initially severe pulmonary hypertension (> or = 30 mmg Hg) did not survive 3 years.

Effects of corticosteroid treatment on pulmonary haemodynamics in patients with sarcoidosis.

Effects of 12 months steroid treatment on pulmonary haemodynamics in 24 patients with pulmonary sarcoidosis, stage II and III, were investigated. All patients had a chest radiograph, lung function tests, and pulmonary haemodynamics (measured at rest and during submaximal exercise) prior to the treatment. Resting pulmonary hypertension was found in 3 patients. In 18 an abnormal increase in pulmonary arterial mean pressure (PAP) on exercise was observed. All investigations were repeated after a year of treatment. In almost all patients (22) a regression of radiological changes in the lungs and improvement of pulmonary function were observed. The changes in pulmonary circulation were less uniform. In only half of the patients studied was regression of the disease seen on chest X-ray and improvement in lung function accompanied by improvement in pulmonary haemodynamics.

[Assessment of pulmonary hemodynamics in patients with idiopathic pulmonary fibrosis]. / Ocena krazenia plucnego u chorych z samoistnym wlóknieniem pluc.

Pulmonary hemodynamics were assessed in 52 patients with idiopathic pulmonary fibrosis of which 25 were confirmed histopathologically. The study group consisted of 26 males and 26 females, of a mean age of 41 +/- 15 years. Pulmonary function studies revealed restrictive changes and increased elastic recoil. Mean vital capacity was 2.6 +/- 1.2 L, compliance - static 97 +/- 59 ml/cm H2O, dynamic 71 +/- 50 ml/cm H2O. Esophageal pressure was - 8.0 +/- 5.3 mm Hg. Mean pulmonary artery pressure was slightly elevated - 22.6 +/- 8.3 mm Hg. Transmural pulmonary pressure was 31.3 +/- 9.8 mm Hg, cardiac output was 7.6 +/- 3.8 L/min, pulmonary resistance 206 +/- 119 dyn sec cm-5. A mild hypoxemia was observed--PaO2 71.8 +/- 13.3 mm Hg. In part of the study group (27 subjects) the response to exercise was assessed. A mean increase of pulmonary artery pressure from 20.4 +/- 7.2 to 38.0 +/- 14.7 mm Hg and a decrease of PaO2 from 74.2 +/- 11.7 mm Hg to 62.5 +/- 15.3 mm Hg were found. Negative correlation was found between mean artery pulmonary pressure and arterial oxygen partial pressure, vital capacity and one-second forced expiratory volume, and a higher correlation between mean transmural pulmonary pressure and PaO2, VC, FEV1 and Cdyn.

[Effect of steroid therapy on pulmonary circulation in pulmonary sarcoidosis]. / Wplyw leczenia kortykosteroidami na krazenie plucne u chorych na sarkoidoze pluc.

Effect of 12 month steroid therapy on pulmonary circulation at rest and during exercise was assessed in 24 patients with histologically confirmed stage II and III pulmonary sarcoidosis. Pulmonary hypertension was found in 3 patients before starting therapy. In the remaining 21 pulmonary artery pressure was within normal limits. In 18 of these an abnormal increase of pulmonary arterial pressure during exercise was found. After 12 months of steroid therapy in all except 2 patients radiological regression was observed. In most patients pulmonary function improved. Normal pulmonary arterial pressure was found in 22 patients. An abnormal increase of pulmonary arterial pressure during exercise was seen in 12 patients. No correlation could be demonstrated between radiological evaluation, respiratory function and effect of steroids on pulmonary circulation.

[Pulmonary arterial pressure and the effect of short term oxygen therapy on it in patients qualified for home oxygen treatment]. / Cisnienie w tetnicy plucnej i wplyw na nie krótkotrwalego oddychania tlenem u chorych zakwalifikowanych do przewleklej tlenoterapii domowej.

Forty patients with chronic bronchitis and emphysema qualified for domiciliary oxygen treatment according to widely accepted criteria were assessed. Only two patients had normal pulmonary artery pressure. Pulmonary arterial pressure correlated well with oxygen arterial partial pressure. It seems that pulmonary hemodynamic studies are not necessary in patient qualification for domiciliary oxygen therapy. Short oxygen therapy (30 min.) produced only a small decrease of pulmonary artery pressure from 31 +/- 10 to 29 +/- 8 mm Hg. Only in 7 patients was the fall greater than 5 mm Hg. Fall of pressure in pulmonary artery produced by oxygen correlated only with initial pulmonary artery pressure and rose proportionally with increase of pressure.

Captopril effects on pulmonary and systemic hemodynamics in chronic cor pulmonale.

A placebo-controlled single-blind study on acute effects of captopril on hypoxic pulmonary hypertension was performed in 15 patients with severe chronic obstructive lung disease recovering from right heart failure. Ten patients received active drug (25 mg captopril orally), five patients received placebo and served as control subjects. Before drug administration, there was no difference in lung function data and pulmonary hemodynamics between patients in both groups. Captopril produced highly significant fall in systemic arterial pressure. No change in breathing frequency, minute ventilation, and pulmonary gas exchange was observed. There was no significant change in studied variables after placebo. The presented data suggest that captopril does not decrease pulmonary vascular resistance in patients with hypoxic pulmonary hypertension. A fall in pulmonary wedge pressure reflects a decrease in left ventricular afterload.

Acute effects of almitrine infusion on pulmonary haemodynamics in normal man.

The aim of the study was to assess haemodynamic and ventilatory effects of almitrine infusion in normal subjects. Five males aged 19-49 years were studied using a floating catheter technique. The investigation consisted of three consecutive periods, lasting 20 min each. During the first one, the subject was allowed to settle down and baseline measurements were made. During the second period, a total dose of 0.33 mg X kg-1 of almitrine was infused over 20 min. During the third period, postinfusion effects were observed. Almitrine produced the expected increase in minute ventilation that was entirely due to that in tidal volume. Haemodynamic changes consisted of an increase in pulmonary vascular resistance and pulmonary arterial pressure. As there was no concomitant change in cardiac output or wedge pressure, the increase in pulmonary vascular resistance was apparently due to constriction of pulmonary muscular arteries. Pulmonary vasoconstrictor effects of almitrine were of short duration and were already tapering off before completion of the infusion, so that pulmonary arterial pressure was back to the baseline value 10 min after the infusion was completed.

Pulmonary haemodynamics at rest and during exercise in patients with sarcoidosis.

Pulmonary haemodynamics at rest and during exercise was studied in 30 patients with histologically confirmed sarcoidosis. All subjects were divided into three groups according to the stage of the disease assessed by radiological image of pulmonary lesions. At rest, in stage I and II patients, the mean pulmonary pressure (PAP) was normal. In stage III patients, a slight pulmonary hypertension was found. During exercise, a rise in PAP in stage I and II subjects was within the normal limits for a given workload, although in individual stage II subjects a rise in PAP was abnormally high. In all stage III patients a rise in PAP was pathologically elevated.

Effects of prolonged oxygen therapy on pulmonary hypertension and blood viscosity in patients with advanced cor pulmonale.

In 16 patients with chronic bronchitis and advanced cor pulmonale admitted to hospital due to heart failure, a controlled 6-weeks oxygen therapy, 17 h a day, was performed. The trial was started when patients were out of the exacerbation of the disease in a respiratory and circulatory steady state. Pulmonary hemodynamics, blood viscosity, packed cell volume and basic lung function data before and after oxygen therapy were compared. A significant fall of mean pulmonary arterial pressure from 42 to 30 mm Hg without a change in the cardiac output was found. Blood viscosity and packed cell volume-significantly decreased. Arterial oxygen tension did not significantly change. It seems that 17-hours per day oxygen therapy is sufficient to induce regression of anatomic changes in pulmonary arteries, a main cause of pulmonary hypertension in hypoxic cor pulmonale.