[Questions and answers on heart diseases. 9. Pulmonary heart disease].
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Pulmonary hypertension was diagnosed in 97 elderly patients (age 60-79) using electrokymography of the heart and vessels, ECG and rheography of the lungs. All the patients suffered from chronic cor pulmonale (CCP). Electrokymography proved an effective diagnostic tool in detection of pulmonary hypertension in CCP patients, whereas quantitation of the hypertension was successful at electrokymography with application of L. Burstin nomogram and electrocardiography according to S. A. Dushanin. ECG according to R. Bernar et al. appeared poorly sensitive, especially at early CCP stages. A. M. Novikov's rheopulmonography technique can provide only an approximate value of mean pressure in the pulmonary artery of elderly CCP patients.
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Pulmonary artery pressure was measured in 70 patients with chronic bronchitis. Those with pulmonary hypertension underwent two hours oxygen therapy (flow 10-12 l/min). Those in whom a decrease of pulmonary artery pressure was observed were qualified for long term oxygen therapy (LTOT). In 32 patients which were qualified for LTOT, after a two week period of 18 hour per day oxygen therapy a decrease of systolic pulmonary arterial pressure from 336.1 mm Hg to 30.9 mm Hg and a decrease of mean pulmonary artery pressure from 25.9 to 23.2 mm Hg was observed.
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The plasma neuron-specific enolase (NSE) activity in the 15 patients of chronic pulmonary heart disease complicated by pulmonary encephalopathy and 10 chronic pulmonary heart disease without pulmonary encephalopathy (controls) were detected. The results showed that NSE activity in patients with moderate, severe pulmonary encephalopathy were significantly higher than those of patients with mild pulmonary encephalopathy, stable patients and controls. The plasma NSE activity from the patients with pulmonary encephalopathy were negatively correlated with the PaO2 and were positively correlated with PaCO2. This study suggests that plasma NSE activity may reflect the degree of brain damage by chronic hypoxia and remain of CO2 in the patients with chronic pulmonary heart disease.
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