[Heart-type fatty acid binding protein for the assessment of the short-term prognosis in acute pulmonary embolism patients with hemodynamic stability on admission].

OBJECTIVE: To explore the clinical value of heart-type fatty acid binding protein (H-FABP) for the assessment of the short-term prognosis in acute pulmonary embolism (APE) patients with hemodynamic stability on admission. METHOD: A total of 156 APE patients with hemodynamic stability on admission were hospitalized in Beijing Anzhen hospital from December 2009 to December 2010, and the final study population comprised 90 patients [37 men and 53 women; age (61.1 ± 14.6) years], who were taken blood samples before thrombolysis or anticoagulation for plasma H-FABP level measurement by a solid-phase enzyme-linked immunoabsorbent assay based on the sandwich principle, cardiac troponin I (cTnI) and N-terminal pro-brain natriuretic peptide (NT-proBNP) by heterogeneous immunoassay. All had 30-day follow-up and divided them into the complicated clinical course group (n = 7) and the simple clinical course group (n = 83). The clinical and follow-up data was analyzed by Mann-Whitney U test, Pearson Chi-Square test, Continuity Correction test and logistic regression. RESULTS: The level of H-FABP was higher in the complicated clinical course group than it in the simple clinical course group (U = 54.000, P < 0.01). With ROC analysis, 7 µg/L was identified as the best cutoff value of H-FABP in this study, and the differences of AUC among H-FABP, cTnI and NT-proBNP were no statistical significance. By univariable logistic regression, H-FABP ≥ 6 µg/L, heart rate ≥ 106 beats/min and syncope ( all P < 0.01) may predict the short-term prognosis in APE patients with hemodynamic stability. H-FABP ≥ 6 µg/L and syncope (both P < 0.05) may also be 30-day predictor by multivariable logistic regression. NT-proBNP or cTnI combined with H-FABP may increase 30-day prognosis value in APE patients with hemodynamic stability. CONCLUSIONS: H-FABP, alone or in combination with other clinical data may predict 30-day prognosis in APE patients with hemodynamic stability on admission. H-FABP is superior to cTnI and NT-proBNP in the predication of 30-day prognosis in APE patients with hemodynamic stability on admission.

[Protective effects of beraprost plus simvastatin on monocrotaline-induced pulmonary arterial hypertension in rats].

OBJECTIVE: To explore the protective effects of beraprost plus simvastatin on monocrotaline-induced pulmonary arterial hypertension in rats. METHODS: Forty male Sprague-Dawley rats were allocated to control (C), untreated pulmonary arterial hypertension (P), beraprost (B), simvastatin (S) and combination groups (Com) (n = 8 each). Normal saline was injected subcutaneously into group C and then there was no other intervention for 21 days. Group P, B, S and Com rats received subcutaneous injections of monocrotaline (MCT, 60 mg/kg) and then isovolumetric normal saline, beraprost (100 µg·kg(-1)·d(-1)), simvastatin (2 mg·kg(-1)·d(-1)) and beraprost (100 µg·kg(-1)·d(-1)) plus simvastatin (2 mg·kg(-1)·d(-1)) by daily gastric lavage for 21 days. At Day 22, heart rate (HR), mean arterial pressure (MAP) and mean pulmonary pressure (mPAP) were detected and right heart ventricular hypertrophy index (RVHI) was calculated. The histopathology changes and tunica media thickness percentage of pulmonary arteries (WT%) were evaluated by pulmonary tissue staining. The results were analyzed statistically. RESULTS: The differences of HR and MAP were not significant among 5 groups (all P > 0.05). The levels of mPAP, RVHI and WT% in group B ((27.4 ± 3.7) mm Hg, 0.35 ± 0.03, 26.7% ± 2.4%), group S ((29.9 ± 4.4) mm Hg, 0.36 ± 0.03, 28.2% ± 1.9%) and group Com ((23.1 ± 3.9) mm Hg, 0.32 ± 0.03, 17.4% ± 3.3%) were lower than those in group P ((35.4 ± 5.7) mm Hg, 0.41 ± 0.05, 42.8% ± 5.9%) (all P < 0.05). CONCLUSIONS: The combined use of beraprost and simvastatin may delay the increase of mPAP and remodeling of pulmonary vessels and inhibit right ventricular hypertrophy in pulmonary arterial hypertension rats. Its efficacy is superior to that of monotherapy.

[A randomized controlled study of the VKORC1 and CYP2C9 genotypes in guiding warfarin therapy for pulmonary thromboembolism].

OBJECTIVE: To evaluate the clinical application of a dosing algorithm by genotypes in prediction of warfarin maintenance dose in Chinese patients with pulmonary thromboembolism. METHOD: During October 2010 and August 2012, 220 inpatients or outpatients with pulmonary embolism in Beijing Anzhen Hospital, were enrolled by the inclusion criteria. The patients included 86 males and 134 females. The clinical data and blood samples were collected. The fluorescent PCR genotyping method was used to detect the genotypes of vitamin K epoxy compounds reductase complex subunit 1 (VKORC1) and cytochrome P450 enzyme 2C9 (CYP2C9). According to the random number table, the patients were randomly divided into a study group and a control group. In the study group, the first 3 doses of warfarin were prescribed according to the predicted warfarin dose, while in the control group the drug was prescribed according to the dose estimated empirically by clinicians. Warfarin was adjusted until it reached a stable dose according to the INR value, and the following-up lasted for 50 days. RESULT: AT the end of follow-up, the percentage of patients who obtained a stable dose in the study group and the control group was 82.1% (n = 78) and 66% (n = 64), respectively. The mean time to reach a stable dose in the study group and the control group was (16.8 ± 1.5) and (25.6 ± 1.8) days, and the median time was (11.0 ± 1.0) days and (20.0 ± 2.0) days, the difference between the 2 groups being statistically significant (χ(2) = 18.175, P < 0.001). The incidence of side effects of the study group was lower than that of the control group, and the time to the occurrence of side effects in study group was longer. The average predicted dose of the 142 patients who reached a stable dose was (3.6 ± 0.9) mg/d, and the average effective dose was (3.7 ± 1.3) mg/d, the average predicted dose being lower than the actual dose (0.1 ± 1.2) mg/d, but the difference was not significant(t = -1.202, P > 0.05). CONCLUSION: The warfarin stable dose prediction algorithm, containing genetic factors and non-heritage factors, can significantly shorten the adjustment time to reach warfarin stable dose, and reduce the incidence of side effects, and is clinically applicable.