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Results for “PULMONARY HEART DISEASE”

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PubMed1999

[Clinical study of fibrinolysis indicators in patients with chronic pulmonary heart disease].

OBJECTIVE: To investigate the change of D-dimer and other fibrinolysis indicators in patients with chronic pulmonary heart disease. METHODS: The fibrinolytic activity of plasma was measured in 42 patients with chronic pulmonary heart disease and in 20 controls (matched with sex and age). RESULTS: The D-dimer level was significantly higher in exacerbated patients than in controls (P < 0.001). The fibrinolytic activity in patients was lower than in controls. The plasma fibrinolytic activity was positively correlated with PaO2 and negativly correlated with PaCO2. CONCLUSIONS: The depressed fibrinolysis may be associated with hypercoagulability state of chronic pulmonary heart disease and contributes to thrombi in small pulmonary arteries and arterioles. D-dimer can be used in diagnosis of thrombi formation in small pulmonary arteries and arterioles. Patients with chronic pulmonary heart disease can be treated with fibrinolysis drugs.

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PubMed2001

[A multicenter clinical study on clinical effects of meglumine cyclic adenylate in treating patients with chronic pulmonary heart disease].

OBJECTIVE: To observe the clinical effects of meglumine cyclic adenylate (MCA) in treating patients with chronic pulmonary heart disease. METHODS: 785 patients with chronic pulmonary heart disease were divided into two groups: MCA group and control group. Both groups of patients were treated with the same ordinary methods, but MCA was given in the MCA group. The period of treatment was 5-7 days. The degree of improvement in clinical symptoms, signs, ECG, pulmonary ventilation function and arterial blood gas analysis of the two groups before and after treatment were compared. RESULTS: The rates of improvement in clinical symptoms and signs were 92.2% and 73.6% in MCA group and control group respectively. VC increased (426 +/- 123) ml and (313 +/- 145) ml respectively as compared with the values before the treatment. FEV(1) increased (134 +/- 54) ml and (95 +/- 55) ml, PEF increased (0.78 +/- 0.32) L/s and (0.47 +/- 0.32) L/s and PaO(2) increased (23.4 +/- 9.5) mm Hg and (17.3 +/- 10.4) mm Hg respectively. The rates of ECG improvement were 63.7% and 41.2% respectively. There was significant difference between the two groups (P < 0.01 and 0.05). CONCLUSION: Significant therapeutic effects were obtained in treating patients of chronic pulmonary heart disease with respiratory and cardiac failure by using ordinary treatment measures combined with MCA injection.

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PubMed1990

[Therapeutic principles in pulmonary heart disease and right heart insufficiency].

Until now the pathomechanism of pulmonary heart disease is insufficiently elucidated. Therefore, at present, rational therapeutical concepts are possible only in chronic obstructive lung diseases. Without any modification, the principle of comprehensive treatment of the basic pulmonary disease remains valid. In the symptomatic therapy of the pulmonary heart disease, in first place the long-term oxygen therapy becomes mandatory. Treatment with vasodilatory drugs remains in the long-term activity disappointing. Reasonable expectations are directed to clinical trials of angiotensin-converting-enzyme-inhibitors. Cardiac glycosides remain reserved for manifest cardiac failure. The stabilization of the acid-base-balance is of great importance for the efficacy of treatment. The decision on the use of additives depends upon a critical evaluation of the actual clinical state and upon the consideration of the risks from polymorbidity.

Combined Modality Therapy↗
PubMed1994

[Hemodynamic studies of pulmonary heart diseases and the effects of nifedipine].

Swan-Ganz catheterization, blood gas analysis, pulmonary function tests and two-dimensional echocardiography were performed in 10 patients with pulmonary heart disease and the effects of nifedipine were then observed. Mean pulmonary artery pressure (mPAP) correlated significantly to PaO2. PaO2 may be a useful parameter for predicting mPAP. Continuous oxygen breathing can correct hypoxemia, prevent and alleviate pulmonary artery hypertension (PAH). After using nifedipine, PaO2 and blood pressure of systemic circulation decreased significantly, while pulmonary physiological shunt increased and pulmonary artery pressure did not decrease. As a consequence, the use of nifedipine to treat pulmonary heart disease and PAH is not advocated.

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