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[The study of platelet function in patients with chronic pulmonary heart disease].

OBJECTIVE: To study the platelet function in patients with chronic pulmonary heart disease. METHOD: Subjects were divided into three groups (cor pulmonale exacerbation, cor pulmonale remission stage and normal control). Platelet adhesion rate (PAdT), platelet aggregation rate(PAgT), alpha-granule membrane protein (GMP-140) and glycoproteinII were measured by radioimmunoassay, flow cytometry and other methods. RESULT: In cor pulmonale exacerbation, the values of PAdT, PAgT, GMP-140 and GPII were31% +/- 16%, 14% +/- 8%, 190 +/- 49 molecule/platelet and 145% +/- 36% respectively. In cor pulmonale remission stage, the values were 33% +/- 13%, 38% +/- 16%, 178 +/- 33 molecule/platelet and 137% +/- 48% respectively. These findings showed that the values of PAdT, GMP-140 and GPII in cor pulmonale exacerbation were markedly increased, whereas PAgT was significantly reduced. However, PAdT, PAgT, GMP-140 and GPII in remission stage were all higher than that of normal group. CONCLUSION: In vivo platelet activation is indeed present in patients with chronic pulmonary heart disease.

Aged↗

Changing pattern of heart diseases in Shanghai from the 1950s to 1980s.

OBJECTIVE: To determine the pattern of dynamic change in types of heart diseases in the past 4 decades for providing a reference to treatment and prevention of heart diseases in China. METHODS: All adult cardiac patients admitted to the Zhong Shan Hospital and Hua Shan Hospital from 1948 to 1989 were analyzed. The constituent ratio of different heart diseases in the 1950s, 1960s, 1970s and 1980s was compared. RESULTS: The percentage of heart diseases among medical inpatients increased in each of the recent 4 decades, from 9.89%, 15.69%, 20.90% to 23.54% respectively. The constituent ratio of different heart diseases changed, coronary heart disease constituted the highest proportion, next came rheumatic heart disease, and congenital heart disease was in third place. Congenital heart disease, myocarditis, cardiac dysrhythmia without organic heart disease, cardiomyopathy and endocarditis increased, rheumatic heart disease, pulmonary heart disease and hypertensive heart disease apparently decreased; syphilitic heart disease could rarely be encountered. CONCLUSION: China is now facing a low overall death rate, a long life expectancy and an aging population. The incidence of heart diseases increased gradually and patterns of heart diseases kept changing. The overall trend is that heart diseases which were not related to infection are increasing while heart diseases related to bacterial infection are decreasing.

Arrhythmias, Cardiac↗

Digitalis in pulmonary heart disease (cor pulmonale).

The use of digitalis in pulmonary heart disease has been a topic of great interest for a number of years. The physician's decision to use or not to use digitalis in pulmonary disease has often been an emotional rather than a reasoned one. The diagnostic difficulties from a clinical point of view in separation of pulmonary from cardiac symptoms and findings have also been confusing. The fact that small doses of digitalis may have an inotropic effect on the cardiac muscle has been a difficult concept for many physicians to adopt. On the other hand, the larger doses of digitalis that are often necessary to control the ventricular response in supraventricular arrhythmias sometimes gives rise to confusion. We shall attempt to review the subject in detail and examine indications, contraindications, toxicity, dosage, assessment of benefit, and role of digitalis serum levels in patient management.

Arrhythmias, Cardiac↗

Xamoterol improves right ventricular systolic and diastolic function in pulmonary heart disease.

OBJECTIVE: Abnormal right ventricular function in patients with pulmonary heart disease (PHD) may contribute to their reduced exercise capacity. We have evaluated the effect of subacute dosing with xamoterol, a beta-1 adrenoreceptor partial agonist with inotropic properties, on right ventricular function in patients with PHD. PATIENTS: Twelve patients with advanced chronic obstructive pulmonary disease and clinical evidence of PHD received xamoterol 200 mg twice daily or placebo for 7 days in a randomised double-blind crossover study. Right heart krypton-81m radionuclide ventriculography was used to derive right ventricular ejection fraction (RVEF) both at rest and during submaximal exercise, and indices of right ventricular systolic and diastolic function at rest. RESULTS: During treatment with placebo, mean RVEF was 0.53 at rest and was unchanged during exercise. After xamoterol, mean RVEF was 0.55 at rest and increased to 0.59 during exercise. Xamoterol increased right ventricular peak ejection rate from 3.04 to 3.45 EDV.s-1 and mean early diastolic filling rate from 1.00 to 1.20 EDV.s-1. CONCLUSION: Subacute treatment with xamoterol in patients with PHD improves right ventricular systolic and diastolic function at rest and results in a favourable augmentation in right ventricular function during submaximal exercise.

Aged↗

[Functional evaluation of the left ventricle in chronic pulmonary heart disease].

20 patients (18 m., 2 f., age 64.8 +/- 6.3 years), with chronic pulmonary heart disease (CPHD) secondary to chronic obstructive pulmonary disease and/or arterial hypertension were studied in comparison with a control group of subjects, age and sex matched, with normal respiratory function tests and without heart disease. CPHD patients did not show any difference of left ventricle (LV) systolic function, assessed by echocardiography, in comparison with the control group. However, among CPHD patients, significant correlations were found between lower arterial pH and cardiac output/m2 and between spirometric tests of bronchial obstruction and echocardiographic parameters of LV function. These results confirm that LV function in CPHD is maintained if other pathologic conditions are absent. On the other hand, correlations between echocardiography and spirometry and blood gas analysis strengthen the functional interdependence concept between left and right heart chambers.

Aged↗

The inhibition of pulmonary vessel remodeling by carbon monoxide system in rats with chronic pulmonary heart disease.

OBJECTIVE: To study the effect of carbon monoxide on pulmonary vessel remodeling of chronic pulmonary heart disease. METHODS: Thirty-six sprague-dawley rats were randomly divided into three groups: control group, and hypoxic hypercapnic group, and hypoxic hypercapnia + hemin group. Blood CO concentration (COHb%), activity of HO-1 in blood serum and lung homogenate, pulmonary arteriole micromorphometric index, HO-1 and HO-1 mRNA were measured. RESULTS: (1) mPAP and RV/(LV + S) were (20.1 +/- 0.8) mm Hg and (35.5 +/- 1.7)% in hypoxic hypercapnic group, they were significantly higher than those of control group's (15.3 +/- 1.4) mm Hg, (26.7 +/- 1.7)%, and those of hypoxic hypercapnia + hemin (activator of HO-1) group's (16.5 +/- 3.7) mm Hg, (30.2 +/- 1.6)% (P < 0.01). (2) Pulmonary arteriole micromorphometric index in rats of hypoxic hypercapnic group were significantly higher than those of control group and hypoxic hypercapnia + hemin group (P < 0.01). (3) Blood CO concentration, activity of HO-1 in blood serum and lung homogenate, content of HO-1 and HO-1 mRNA in pulmonary arterioles in rats of hypoxic hypercapnic group were (2.1 +/- 0.9)%, (73 +/- 18) nmol.L(-1).h(-1), (1 751 +/- 311) pmol.mg(-1).h(-1), 0.191 +/- 0.012 and 0.301 +/- 0.017, were significantly higher than those of control group: (0.5 +/- 0.3)%, (25 +/- 8) nmol.L(-1).h(-1), (385 +/- 46) pmol.mg(-1).h(-1), 0.059 +/- 0.005, 0.131 +/- 0.011, but were significantly lower than those of hypoxic hypercapnia + hemin group: (4.9 +/- 2.1)%, (132 +/- 39) nmol.L(-1).h(-1), (2 849 +/- 426) pmol.mg(-1).h(-1), 0.272 +/- 0.013, 0.339 +/- 0.020 (P < 0.01). (4) Correlation analysis revealed that the relationship between carbon monoxide system and pulmonary arteriole micromorphometric index was significantly negative (P < 0.01). CONCLUSION: Up-regulation of endogenous carbon monoxide system can inhibit pulmonary vessel remodeling in rats with chronic pulmonary heart disease induced by hypoxia and hypercapnia.

Animals↗