| Objective The objective of the study is to observe the myocardial injury index of different periods of chronic pulmonary heart disease(CPHD), and discuss the clinical significance of myocardial injury index of chronic pulmonary heart disease.Method One hundred and twenty-five patients of chronic pulmonary heart disease from November 2011 to December 2013 were selected in respiration medicine of Liaoning Provincial People’s Hospital. They were divided into CPHD decompensated period group(n=64), and 42 of them with artherosclerosis as CPHD decompensated period with artherosclerosis group, and another 22 of them without artherosclerosis as simplex CPHD decompensated period group; CPHD compensated period group(n=61),and 34 of them with artherosclerosis as CPHD compensated period with artherosclerosis group, and another 27 of them without artherosclerosis as simplex CPHD compensated period group. And 57 patients of chronic obstructive pulmonary disease(COPD) were selected as the observed subject, and 24 of them with artherosclerosis as COPD with artherosclerosis group, and another 33 of them without artherosclerosis as simplex COPD group. B-type natriuretic peptide(BNP, using double antibody sandwich method)level, N-terminal pro-brain natriuretic peptide creatinine(Nt-pro-BNP, using enzyme linked immunosorbent assay) level; cardiac troponin I(CTn I, using doble antibody chemiluminescence method) level; PH, arterial partial pressure of oxygen(PO2),arterial partial pressure of carbon dioxide(PCO2), total hemoglobin(ct Hb) level using blood gas analyzer; right ventricular end diastolic diameter(RVEDD), right ventricular outflow trace(RVOT), pulmonary artery pressure(PAP) using cardiac colour ultrasonic scanner were examined and recorded. All the patients of COPD group were received carotid artery ultrasound examination, the bilateral carotid artery intima-media thickness and artery atherosclerotic plaque were observed.All the patients were given oxygen inhalation, removing phlegm, anti-asthmatic, anti-infection, and nutritional support while in hospital, and given the reexamination after remission. BNP, NT-pro BNP, CTn I level, results of blood gas analyzer and cardiac colour ultrasonic scanner were compared before and after treatment of different groups.Results There was no significant different of clinical data in different groups(P>0.05). In CPHD decompensated period with artherosclerosis group before treatment,NT-pro BNP concentration was(7784.65±393.21) pg/ml, and c Tn I concentration was(1.87±0.13) μg/ml, all of them were significantly higher than simplex CPHD decompensated period group, compensated period group and COPD group(P<0.05).After treatment, NT-pro BNP, and c Tn I concentrations of three groups were significant reduced, the difference was significant comparing with before treatment(P<0.05). In CPHD decompensated period with artherosclerosis group after treatment, NT-pro BNP concentration was(1989.52±196.36) pg/ml, and c Tn I concentration was(1.64±0.17)μg/ml, all of them were still significantly higher than simplex CPHD decompensated period group, compensated period group and COPD group(P<0.05); and in CPHD compensated period with artherosclerosis group, NT-pro BNP concentration was(1053.96±84.29) pg/ml, and c Tn I concentration was(1.32±0.13) μg/ml, all of them were significantly higher than simplex CPHD compensated period group and COPD group(P<0.05).There was no significant different of ct Hb level in acute exacerbation of three groups(P>0.05), and all the patients with severe hypoxia state. In CPHD decompensated period with artherosclerosis group, PH(6.82±0.07) and PO2(46.86±11.39 mm Hg) were significantly lower than simplex CPHD decompensated period group, compensated period group and COPD group(P<0.05), but PCO2(78.38±16.29 mm Hg) were significantly higher than simplex CPHD decompensated period group, compensated period group and COPD group(P<0.05); And in compensated period group, PCO2 was significantly higher than COPD group(P<0.05),PH and PO2 were significantly lower than COPD group(P<0.05). In acute exacerbation showed by cardiac colour ultrasonic scanner, RV(30.28±6.32mm), RVOT(38.37±4.31mm), and PAP(73.34±11.23 mm Hg) of patients of CPHD decompensated period with artherosclerosis group were significantly higher than simplex CPHD decompensated period group, compensated period group and COPD group(P<0.05);and patients of CPHD compensated period group were significantly higher than COPD group(P<0.05). The linear correlation analysis in acute exacerbation showed that NT-pro BNP concentration of CPHD patients had significant positive correlation with RV, RVOT, and PAP(P<0.05), and had significant negative correlation with PO2(P<0.05); and NT-pro BNP concentration of COPD patients had significant positive correlation with PAP(P<0.05).Conclusions NT-pro BNP could have effects for the progress of CPHD, mesaure the NT-pro BNP level could more accurately react severity of CPHD. COPD caused changes of the body organs, especially blood vessel changes. Artherosclerosis will aggravate hypoxia, and lead to the significant changes of heart indicators, and the myocardial injuries of patients with carotid atherosclerosis were more serious. Carotid atherosclerosis is one of the risk factor of CPHD. Blood gas analysis and cardiac colour ultrasonic scanner could suggest the degree of CPHD lesions, and react the acid-base balance, Pa O2 and hemorheology changes. It has guiding significance to clinical treatment. CTn I level could accurately reflect myocardial injury degree in CPHD patients, and it could be a regular monitoring indicator of CPHD. |
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