Frequency and predictors of normalization of left ventricular ejection fraction in recent-onset nonischemic cardiomyopathy.

Emerging evidence has shown the potential of marked improvement in left ventricular ejection fraction (LVEF) in patients with recent-onset cardiomyopathy (ROCM) on medical therapy. This study was designed to determine the frequency and to identify predictors of normalization of LVEF in a cohort of Chinese patients with ROCM receiving contemporary medication. A consecutive series of patients admitted from October 2008 to November 2012 with the clinical diagnosis of ROCM and LVEF ≤ 40% by echocardiography at presentation were followed up at least 12 months to identify those with normalization of LVEF, defined as an increase in LVEF to a final level of ≥ 50%. An array of clinical and echocardiographic variables regarded as potentially relevant to normalization was evaluated to identify predictors using logistic regression analysis. After a mean follow-up of 31 ± 13 months, 48% of 128 patients had normalized their LVEF, showing a significant increase in LVEF from 32 ± 6% to 58 ± 5%, of which 68% occurred within 1 year after initial diagnosis. Multivariate analysis demonstrated that normalization of LVEF was associated with a history of hypertension, higher systolic blood pressure at presentation, shorter electrocardiographic QRS duration, smaller left ventricular end-diastolic diameter, and higher LVEF by echocardiography at baseline. In conclusion, nearly 1/2 of a relatively large number of Chinese patients with ROCM have shown normalization of LVEF on current medical therapy after a medium-term follow-up, which was associated with some clinical and echocardiographic parameters.

[A survey on knowledge of recommended heart failure guidelines among Chinese physicians].

OBJECTIVE: To obtain the knowledge status on recommended heart failure (HF) guidelines among Chinese physicians. METHODS: Questionnaire on heart failure including 20 multiple choice questions and 10 fill in the blank questions was designed based on the Chinese guidelines for the diagnosis and treatment of chronic heart failure in 2007 and the Chinese guidelines for the diagnosis and treatment of acute heart failure in 2010. The rate of correct answer for each item was calculated and compared among physicians specialized for cardiovascular diseases and not. RESULTS: The Questionnaire was completed in 400 physicians, including 208 physician specialized for cardiovascular disease and 192 physicians not specialized in cardiovascular disease. The rate of correct answer for 20 multiple choice questions was lower than 60% in 8 questions, 60%-80% in 8 questions, higher than 80% in 4 questions. The rate of correct answers for 10 fill in the blank questions focusing on the aimed dosage of 10 ACEI/ARB/ß-blockers was 49%. The 8 multiple choice questions with correct answer rate <60% are detailed items of myocardial remodeling, symptoms suggestive of HF, diagnosis tools for patients with suspected HF, the AHA stages of heart failure, the Forrester's hemodynamic classes of acute heart failure, the goals of ACEI/ARBs treatment in patients with HF, names of heart diseases which might benefit from ACEI/ARBs treatment defined by evidenced based medicine, and detailed application methods of ACEI/ARBs and ß-blockers for HF patients. In general, the rate of correct answer was significantly higher in physicians specialized for cardiovascular disease compared physicians not specialized for cardiovascular disease. CONCLUSION: There is a considerable knowledge gap on the Chinese guidelines for the diagnosis and treatment of chronic heart failure and the Chinese guidelines for the diagnosis and treatment of acute heart failure among Chinese physicians. Efforts must be made to educate physicians to improve their knowledge and improve HF patient care.

Neuregulin-1 attenuates doxorubicin-induced autophagy in neonatal rat cardiomyocytes.

Recombinant human neuregulin-1 (rhNRG-1) improves cardiac function in animal models of doxorubicin (DOX)-induced cardiomyopathy, but the underlying mechanism remains largely unknown. Here, we confirm a role for rhNRG-1 in attenuating DOX-induced autophagy and define the signaling pathways through which it mediates some of its effects. Neonatal rat ventricular myocytes were subjected to different treatments both to induce autophagy and to determine the effects of rhNRG-1 on the process. The rhNRG-1 inhibited DOX-induced autophagy, reduced reactive oxygen species production and increased protein expression of Bcl-2, effects that were recapitulated when the cells were treated with the antioxidant N-acetylcysteine. These effects were blocked by the phosphatidylinositol 3-kinase inhibitor LY294002, pointing to the involvement of the Akt pathway in mediating the process. Inhibition of Bcl-2 expression with small interfering RNA silencing also inhibited rhNRG-1's ability to attenuate DOX-induced autophagy. The rhNRG-1 is a potent inhibitor of DOX-induced autophagy and multiple signaling pathways, including Akt and activation of reactive oxygen species, play important roles in the anti-autophagy effect. The rhNRG-1 is a novel drug that may be effectively therapeutically in protecting further damage in DOX-induced damaged myocardium.

[Value of plasma NT-proBNP for diagnosing heart failure in patients with previous myocardial infarction].

OBJECTIVE: The study aimed to evaluate the value of plasma NT-proBNP in diagnosing heart failure in patients with previous myocardial infarction. METHODS: Plasma concentration of NT-proBNP was measured in patients with previous myocardial infarction by ELISA method at admission. Patients were divided into non heart failure group (NYHA class I) and heart failure group (NYHA class II-IV). The NT-proBNP levels were compared between NYHA class I, II, III and IV, and between heart failure group and non heart failure group. ROC analyses were performed to evaluate the diagnosing value of plasma NT-proBNP for heart failure and to identify the optimal cut-off point for diagnosing heart failure patients. RESULTS: Total 586 patients [aged from 25 - 83 (58 ± 11) years, 80% male] with previous myocardial infarction were enrolled in his study (n = 374 of NYHA class I, n = 99 of NYHA classes II, n = 82 of NYHA class III, n = 31 of NYHA class IV). Plasma NT-proBNP levels in these four NYHA classes were 484.7 (381.6, 647.8) pmol/L, 907.6 (516.6, 1290.3) pmol/L, 1420.2 (879.5, 2336.2) pmol/L, 2442.6 (1695.4, 3670.7) pmol/L, respectively (P < 0.01). The plasma NT-proBNP level in heart failure group was significantly higher than in non heart failure group [1148.2 (707.9, 2145.3) pmol/L vs. 484.7 (381.6, 647.8) pmol/L, P < 0.01]. Plasma NT-proBNP level in patients with age ≥ 60 years was significantly higher than patients with age < 60 years [702.3 (472.4, 1208.5) pmol/L vs. 526.6 (392.1, 855.6) pmol/L, P < 0.01]. ROC analysis showed that the area under the curve (AUC) for diagnosing heart failure was 0.844 (95%CI: 0.809 - 0.880, P < 0.01), the optimal plasma NT-proBNP cut-off point for diagnosing heart failure was 700 pmol/L with a sensitivity of 75.9%, a specificity of 79.9%, an accuracy of 78.3%, a positive predictive value of 67.9% and a negative predictive value of 85.3%. The optimal plasma NT-proBNP cut-off point was 600 pmol/L for patients ≥ 60 years old and 800 pmol/L for patients < 60 years old. CONCLUSION: Plasma NT-proBNP level is a valuable parameter for diagnosing heart failure in patients with previous myocardial infarction.

[Comparison on efficacy and safety between domestic levosimendan versus dobutamine for patients with acute decompensated heart failure].

OBJECTIVE: To compare the efficacy and safety of domestic levosimendan versus dobutamine for patients with acute decompensated heart failure (ADHF). METHODS: ADHF patients from 8 medical centers were recruited in this multicenter, blind, positive-controlled, randomized study and received 24 h intravenous levosimendan (n = 114) or dobutamine (n = 114) therapy. SWAN-GANZ catheter was performed in patients with pulmonary capillary wedge pressure (PCWP) ≥ 15 mm Hg (1 mm Hg = 0.133 kPa) and cardiac index (CI) ≤ 2.5 L·min(-1)×m(-2) (n = 39 each). RESULTS: Compared with baseline level, LVEF increased [(31.56 ± 9.69)% vs. (28.44 ± 7.08)%, P < 0.01] at 24 h in both groups. LVEF increase at 24 h was similar between two groups [(3.11 ± 6.90)% vs. (3.00 ± 6.63)%, P > 0.05]. The PCWP decrease at 24 h was significantly greater in levosimendan group than in dobutamine group [(-8.90 ± 7.14) mm Hg vs. (-5.64 ± 6.83) mm Hg, P = 0.04]. Decrease in NT-proBNP at 3 days was also more significant in levosimendan group than in dobutamine group [the percentage change compared to baseline: (-22.36 ± 38.98)% vs. (-8.56 ± 42.42)%, P < 0.01]. Dyspnea improvement at 24 h was more significant in levosimendan group than in dobutamine group. The incidences of adverse reactions and events were similar between two groups. CONCLUSION: LVEF improvement is similar between dobutamine and domestic levosimendan while greater decreases in PCWP and NT-proBNP are achieved with domestic levosimendan in patients with ADHF.

[Hemodynamic and efficacies of domestic levosimendan versus dobutamine in patients with acute decompensated heart failure].

OBJECTIVE: To compare the hemodynamic effects of domestic levosimendan versus dobutamine on patients with acute decompensated heart failure (ADHF). METHODS: A total of 78 ADHF patients with pulmonary capillary wedge pressure (PCWP) ≥ 15 mm Hg and cardiac index (CI) ≤ 2.5 L×min(-1)×m(-2) were enrolled into this blind, positive-controlled, randomized and multicenter study to receive 24 h intravenous levosimendan or dobutamine therapy. They were randomized into 2 groups: levosimendan and dobutamine (n = 39 each). RESULTS: In the levosimendan group, the PCWP 24 h decreased significantly ((14.2 ± 7.6) vs (23.1 ± 8.1) mm Hg, P < 0.01)and CI increased significantly versus the baseline levels ((2.8 ± 0.7) L×min(-1)×m(-2) vs (2.0 ± 0.4) L×min(-1)×m(-2), P < 0.01). As compared with the dobutamine group, the change percentages versus baseline in PCWP, pulmonary arterial mean pressure (PAMP), systemic vascular resistance (SVR) at 24 h (median) decreased or increased significantly in the levosimendan group 45.5% vs 22.1% (P < 0.05); 20.8% vs 15.0% (P < 0.05); 34.5% vs 12.7% (P < 0.01); CI increased 39.8% vs 13.5% (P < 0.01). As compared with the baseline level, LVEF increased at 24 h in the levosimendan group (27.4% ± 6.1% vs 32.5% ± 8.7%, P < 0.05). Both PCWP and CI at 24 h correlated significantly with NT-proBNP at Day 3 (r = 0.31, P < 0.01; r = -0.29, P < 0.05). Dyspnea improved greatly at 24 h in the levosimendan group than that in the dobutamine group. CONCLUSION: As compared with dobutamine, domestic levosimendan may bring about better outcomes of hemodynamics and dyspnea.

[Influencing factors for the plasma concentration of N-terminal brain natriuretic peptide precursor in patients with heart failure due to various heart diseases].

OBJECTIVE: To compare the plasma concentrations of N-terminal brain natriuretic peptide precursor (NT-proBNP) in patients with heart failure due to various heart diseases and analyze the influencing factors. METHODS: We enrolled a total of 804 heart failure patients due to various heart diseases, including valvular heart disease (VHD), dilated cardiomyopathy (DCM), ischemic heart diseases (IHD), restrictive cardiomyopathy (RCM), hypertensive heart disease (HHD), hypertrophic cardiomyopathy (HCM), pulmonary heart disease (PHD) and adult congenital heart disease (CHD). The plasma concentration of NT-proBNP was measured by enzyme-linked immunosorbent assay (ELISA). Multiple linear regression analysis was used to detect the influencing factors for the plasma concentration of NT-proBNP. RESULTS: The plasma concentration of NT-proBNP had no significant difference between patients with VHD, DCM, IHD, RCM, HCM, PHD, HHD and CHD. The median (25 percent, 75 percent) values were 1866 (803 - 3973), 2247 (1087 - 3865), 2400 (1182 - 4242), 2456 (1385 - 5839), 2204 (1053 - 3186), 2285 (1155 - 3424), 2313 (655 - 3850) and 2768 (795 - 4371) pmol/L respectively (P > 0.05). It increased with New York Heart Association (NYHA) class from II through III to IV. The median (25 percent, 75 percent) values were 646 (447 - 1015), 2160 (1118 - 3750) and 3342 (1549 - 5455) pmol/L respectively (P < 0.01). The patients with a body mass index (BMI) of ≥ 25 kg/cm(2) had a lower NT-proBNP concentration than those with a BMI of < 25 kg/cm(2). The median (25 percent, 75 percent) values were 1468 (784 - 3177) and 2424 (1090 - 4213) pmol/L respectively (P < 0.01). Patients with a serum creatinine concentration of ≥ 107 µmol/L had a higher NT-proBNP concentration than those < 107 µmol/L. The median (25 percent, 75 percent) values were 3337 (1470 - 5380) and 1644 (781 - 3375) pmol/L respectively (P < 0.01). Multiple linear regression analysis demonstrated that NYHA class, creatinine, BMI, hepatic damage and diastolic pressure were independently associated with the plasma concentration of NT-proBNP (all P < 0.01). CONCLUSION: The plasma concentration of NT-proBNP has no significant difference between heart failure patients due to various heart diseases. Its level may be affected by NYHA class, serum creatinine, BMI, hepatic damage and diastolic pressure.

[Diagnostic value of NT-proBNP in identifying aortic stenosis patients with heart failure].

OBJECTIVE: To evaluate the diagnostic value of NT-proBNP in aortic stenosis (AS) patients with heart failure. METHOD: We measured the whole venous blood of NT-proBNP with enzyme linked immuno sorbent assay (Biomedica, Vienna, Austria) in 40 AS patients with heart failure and 76 normal subjects and assessed the diagnostic value of NT-proBNP for heart failure. RESULTS: NT-proBNP levels were significantly higher in AS patients with heart failure compared to controls (P < 0.01). The level of NT-proBNP increased in proportion to the increase of NYHA functional classes (all P < 0.01). The level of NT-proBNP was similar between compensated heart failure group and control group (P > 0.05) and significantly (8 times) increased in decompensated heart failure group (P < 0.01 vs. control group). NT-proBNP level was also significantly higher in LVEDD > 50 mm group than that in LVEDD ≤ 50 mm group (P < 0.05) and in LVEF ≤ 60% group than that in LVEF > 60% group (P < 0.01). Patients with atrial fibrillation also had higher NT-proBNP levels compared to those with sinus rhythm (P < 0.05). The NT-proBNP value of 1360 ng/L was determined as the best cutoff value for the diagnosis of AS patients with heart failure (AUC = 0.762, P < 0.01) and decompensated heart failure (AUC = 0.997, P < 0.01), the sensitivity, specificity and accuracy were 67.50% and 100.00%, 96.05% and 96.05% and 86.21% and 95.83%, respectively. Log (NT-proBNP) was positively related with NYHA functional class and negatively related with LVEF in univariate analysis and multiple regression analyses (P < 0.05). NT-proBNP was independent correlative with NYHA functional class and LVEF. CONCLUSIONS: NT-proBNP has a fairly good diagnostic potential for the identification of AS patients with heart failure. The accuracy is 86.21% for the diagnosis of AS patients with heart failure and 95.83% for decompensated heart failure with the diagnostic cutoff value of 1360 ng/L.

[Clinical value of NT-proBNP in the diagnosis and analysis of correlation of NT-proBNP with clinical and echocardiographic findings in patients with aortic stenosis].

OBJECTIVE: To evaluate the diagnostic value of NT-proBNP in patients with aortic stenosis (AS), analyze the relation of NT-proBNP to NYHA functional class and echocardiographic findings. METHODS: Measured the whole venous blood of NT-proBNP with enzyme linked immuno sorbent assay in 40 aortic stenosis patients (AS group) and 76 normal subjects (control group). We assessed the diagnostic value of NT-proBNP for aortic stenosis, and related NT-proBNP to clinical NYHA functional class and echocardiographic findings. RESULTS: Compared to controls, NT-proBNP levels had significantly higher in patients with aortic stenosis (P < 0.01). The level of NT-proBNP was gradually and significantly increased with the NYHA functional II, III and IV class compared to controls (all P < 0.01). NT-proBNP was significantly (3.5 times) higher in mild/moderate stenosis group than that in control group (2.95 ± 0.48 vs 2.63 ± 0.10, P < 0.05), and was significantly (6.0 times) higher in severe stenosis group than that in control group (3.16 ± 0.50 vs 2.63 ± 0.10, P < 0.01). LVMI was significantly (1.7 times) higher in mild/moderate stenosis group than that in control group (169 ± 51 vs 100 ± 22, P < 0.01), and was significantly (2.1 times) higher in severe stenosis group than that in control group (212 ± 86 vs 100 ± 22, P < 0.01). The NT-proBNP values of 1150 ng/L and 1356 ng/L were determined as the best cutoff values for the diagnosis of patients with mild/moderate (AUC = 0.657, P < 0.05) and severe aortic stenosis (AUC = 0.848, P < 0.01), the sensitivity, specificity and accuracy were 61.11% and 77.30%, 69.74% and 96.10%, 68.09% and 91.80%. Log (NT-proBNP) was significantly positively related with LVEDD, LVMI and mean transvalvular pressure gradient (MTPG) (all P < 0.05), and negatively related with LVEF (P = 0.01) in univariate analysis. In multiple regression analyses, NYHA functional class, LVEF and Log (MTPG) was independently associated with NT-proBNP. CONCLUSION: NT-proBNP is valuable for the diagnosis of patients with aortic stenosis. NT-proBNP has correlation with the heart function and severity of the aortic stenosis.

[The association study of serum total bilirubin, plasma N-terminal proBNP and invasive hemodynamic parameters in patients with heart failure].

OBJECTIVE: To explore the correlation among serum total bilirubin (TBil), invasive hemodynamic parameters, plasma N-terminal proBNP (NT-proBNP) and C reactive protein (CRP) in patients with heart failure. METHODS: Invasive hemodynamic parameters derived from Swan-Ganz catheter, TBil, plasma NT-proBNP and CRP within 12 hours after hospital admission were analyzed in 130 patients with chronic heart failure [New York Heart Association (NYHA) class II-IV]. RESULTS: Compared with those in non-hyperbilirubinemia group, pulmonary capillary wedge pressure (PCWP), NT-proBNP and left ventriculus ejection fraction were different significantly in total hyperbilirubinemia group [(26.09 vs 16.00) mm Hg (1 mm Hg = 0.133 kPa), (3.36 vs 2.91) pmol/L, (34.12 vs 28.92)%, P < 0.05]. The serum TBil increased significantly in higher PCWP, right atrial pressure and NT-proBNP groups than those in lower level groups [(32.22 vs 24.17), (37.52 vs 24.19), (32.14 vs 16.74) pmol/L, P < 0.05]. Partial correlation analysis showed serum TBil was associated with PCWP, right atrial pressure, pulmonary vascular resistance index and NT-proBNP respectively (r = 0.21, P = 0.02; r = 0.33, P < 0.01; r = 0.20, P = 0.04; r = 0.37, P < 0.01, respectively). Multiple linear regression analysis showed both right atrial pressure and NT-proBNP correlated independently with serum TBil (beta = 0.39, P < 0.01; beta = 0.29, P = 0.01, respectively). CONCLUSION: For patients with heart failure, serum TBil correlated well with right atrial pressure, PCWP and NT-proBNP; it is a reliable indicator for exact clinical evaluation of heart failure.

[Multiple organ damage in patients dying from acute decompensated heart failure].

OBJECTIVE: To detect the occurring and developing patterns of multiple organ damage in patients dying from acute decompensated heart failure (ADHF). METHODS: The clinical data of 30 hospitalized patients of ADHF were analyzed. The dying causes included renal, hepatic, respiratory dysfunctions, infection and anemia. All patients received continuous cardiac rhythm monitoring. Their renal, hepatic and respiratory function, infection and anemia were evaluated at admission and during the last 24 hours pre-death respectively. And the results were compared. RESULTS: There were 19 males and 11 females. The average age was (55±22) years old. Among them, 7 cases were of NYHA class III and 23 cases NYHA class IV at admission. The causes of heart failure included valvular heart disease (n=17), dilated cardiomyopathy (n=6), ischemic cardiomyopathy (n=4), valvular heart disease and previous cardiac infarction (n=2) and restrictive cardiomyopathy (n=1). From admission to death, the average hospitalization duration was (8.8±7.4) days. Eleven cases suffered from sudden cardiac death due to lethal arrhythmias including ventricular tachycardia, ventricular fibrillation and sinus arrest. Another 19 cases had no lethal arrhythmias, but they suffered cardiac shock eventually. Among all 30 cases, there were 15 cases with pulmonary infection, 13 cases with hepatic dysfunction, 6 cases with renal dysfunction, 7 cases with respiratory failure, 7 cases with anemia and 15 cases with multiple organ damage at admission. However, the pre-death values increased to 26 (87%, P<0.01), 19 (63%, P<0.05), 24 (80%, P<0.01), 20 (67%, P<0.01), 9 (30%, P>0.05) and 29 (97%, P<0.01) respectively. CONCLUSION: Multiple organ damage evolves and worsens to result in death in ADHF patients.

[Value of admission NT-proBNP in predicting in-hospital mortality in decompensated systolic heart failure].

OBJECTIVE: To evaluate the value of NT-proBNP in predicting in-hospital mortality in patients with decompensated systolic heart failure. METHODS: Plasma NT-proBNP levels within 24 hours of admission were obtained in 366 patients with decompensated systolic heart failure. The levels were compared between dying patients in hospital and survival patients at discharge. ROC analyses were performed to evaluate if NT-proBNP was a predictor for in-hospital mortality and identify the optimal NT-proBNP cut-off point for predicting in-hospital mortality. A binary logistic regression analysis was used to evaluate if NT-proBNP was an independent predictor for in-hospital mortality. RESULTS: 19 cases of the 366 patients died in hospital. NT-proBNP levels of the dying cases were much higher than those of the survivals 3970 (3452, 6934) pmol/L vs 2340 (1132, 4002) pmol/L respectively, P < 0.01). ROC analysis of NT-proBNP to predict in-hospital mortality had an area under the curve (AUC) of 0.762 (95% CI: 0.657-0.857, P < 0.01), the optimal NT-proBNP cut-off point for predicting in-hospital mortality was 3500 pmol/L with a sensitivity of 73.7%, a specificity of 66.9%, an accuracy of 67.6% and a negative predictive value of 97.9%. Patients whose NT-proBNP levels were equal or more than 3500 pmol/L had an in-hospital mortality of 10.9%, compare with 2.1% in those NT-proBNP levels less than 3500 pmol/L (P < 0.01). Binary logistic regression analysis demonstrated that NT-proBNP was an independent predictor for in-hospital mortality in patients with decompensated systolic heart failure (P < 0.01). CONCLUSION: Admission plasma NT-proBNP level is an independent predictor for in-hospital mortality in patients with decompensated systolic heart failure. The optimal NT-proBNP cut-off point for predicting in-hospital mortality is 3500 pmol/L.

[Predictive value of admission amino-terminal pro-B-type natriuretic peptide on in-hospital mortality in patients with decompensated heart failure].

OBJECTIVE: To evaluate the predictive value of admission plasma amino-terminal pro-B-type natriuretic peptide (NT-proBNP) on in-hospital mortality in patients with decompensated heart failure. METHODS: Plasma NT-proBNP levels were measured in patients with decompensated heart failure within 24 hours after admission with ELISA method. The NT-proBNP levels were compared between survivals and dying patients in hospital. ROC analyses were performed to evaluate the predictive value of admission plasma NT-proBNP on in-hospital mortality and to identify the optimal NT-proBNP cut-point for predicting in-hospital mortality. A binary logistic regress analyses was used to evaluate if NT-proBNP was an independent predictor for in-hospital mortality. RESULTS: A total of 804 patients with decompensated heart failure were enrolled in his study (293 valvular heart diseases, 219 ischemic cardiomyopathy, 141 dilated cardiomyopathy, 14 hypertrophic cardiomyopathy, 21 restrictive cardiomyopathy, 39 hypertensive heart disease, 41 chronic pulmonary heart disease and 36 adult congenital heart disease) and 96 patients were in class II, 450 in class III and 258 in cases IV according to NYHA Classification. During hospitalization, 64 deaths were recorded and the on admission plasma NT-proBNP levels of patients died during hospitalization were significantly higher than those of survivals [4321.1 (3063.8, 6606.5) pmol/L vs. 1921.6 (873.9, 3739.2) pmol/L, P<0.01]. Area under receiver operating characteristic curve (AUC) of NT-proBNP to predict in-hospital death was 0.772 (95% CI: 0.718 - 0.825, P<0.01), the optimal plasma NT-proBNP cut-point for predicting in-hospital mortality was 3500 pmol/L, with a sensitivity of 70.3%, a specificity of 72.0%, an accuracy of 71.9%, a positive predictive value of 17. 8% and a negative predictive value of 96.6%. Patients whose NT-proBNP levels were equal or more than 3500 pmol/L had a much higher in-hospital mortality (17.8%) compared with those with NT-proBNP levels of less than 3500 pmol/L (3.4%), P<0.01. Binary logistic regress analyses demonstrated that admission plasma NT-proBNP, pneumonia, heart rate and NYHA class were independent predictors for in-hospital mortality in patients with decompensated heart failure (P<0.05 or 0.01) and admission plasma NT-proBNP was the strongest predictor for in-hospital mortality. CONCLUSIONS: Admission plasma NT-proBNP level was an independent predictor for in-hospital mortality in patients with decompensated heart failure. The optimal NT-proBNP cut-point for predicting in-hospital mortality was 3500 pmol/L in this patient cohort.

[Association of plasma amino-terminal pro-A-, B- and C-type natriuretic peptide levels with NYHA grade and echocardiographic derived parameters of cardiac function in heart failure patients].

OBJECTIVE: To observe the correlation of plasma amino-terminal pro-A-, B- and C-type natriuretic peptide (NT-proANP, NT-proBNP and NT-proCNP) levels with New York Heart Association (NYHA) functional class and echocardiographic derived parameters of cardiac function in heart failure patients. METHODS: Data of NYHA grade, echocardiographic derived parameters of cardiac function, plasma levels of NT-proANP, NT-proBNP and NT-proCNP (measured by enzyme immunoassay method) were obtained in 112 heart failure patients and 44 normal control subjects. The correlation analysis was made between NT-proANP, NT-proBNP, NT-proCNP and NYHA functional class, left atrium diameter (LAD), left ventricular end-diastolic diameter (LVEDD) and left ventricular ejection fraction (LVEF), respectively. RESULTS: The plasma concentrations of NT-proANP, NT-proBNP and NT-proCNP in heart failure patients were significantly higher than in control group (all P<0.05). Correlation analysis revealed a strong correlation between NT-proANP and NT-proBNP (r = 0.790, P = 0.000) and a weak correlation between NT-proCNP and NT-proBNP (r = 0.278, P = 0.003) as well as between NT-proCNP and NT-proANP (r = 0.236, P = 0.012) in heart failure patients. Univariant analysis showed that NT-proANP and NT-proBNP were positively correlated to LAD, LVEDD and negatively correlated to LVEF (all P<0.05) while there was no significant correlation between NT-proCNP and echocardiographic derived parameters of cardiac function in heart failure patients. Multivariate stepwise regression analysis including age, gender, NYHA classification, LAD, LVEDD and LVEF revealed that NYHA classification, LVEF, LAD and age were independent predictors of NT-proANP; while NYHA classification, LVEF and age were independent predictors of NT-proBNP while there was no association among these factors and NT-proCNP. CONCLUSION: In heart failure patients, the plasma concentration of NT-proANP, NT-proBNP and NT-proCNP were significantly increased and NT-proANP, NT-proBNP but not NT-proCNP were significantly correlated to NYHA classification and echocardiographic derived parameters of cardiac function.

[Plasma N-terminal pro-B-type natriuretic peptide reference value in subjects without heart diseases].

OBJECTIVE: To determine the reference value of plasma N-terminal pro-B-type natriuretic peptide (NT-proBNP) in subjects without heart diseases. METHODS: The plasma concentration of NT-proBNP was measured with ELISA method in 300 adults excluded heart disease through various examinations including electrocardiography, echocardiography, X-ray and coronary artery angiography. The plasma NT-proBNP concentration was compared between age-groups 30-39, 40-49, 50-59, 60-69 and > or = 70 years old, between male and female in the same age-group and between subjects with and without hypertension, diabetes and obesity. A multiple linear regression analysis was used to detect factors influencing NT-proBNP among age, sex, body mass index, blood pressure, heart rate, serum creatinine, hypertension, diabetes mellitus, use of angiotensin-converting-enzyme inhibitors, Ca(2+)-antagonist, and beta-blocker. RESULTS: The plasma NT-proBNP concentration increased in proportion to aging in male subjects more than 60 years old (P < 0.05), remained unchanged in males less than 60 years old and females (P > 0.05). Plasma NT-proBNP concentration was significantly higher in female (170-660 pmol/L) than in male (160-470 pmol/L) in subjects less than 60 years old (P < 0.05) and significantly lower in female (180-560 pmol/L) than in male (180-760 pmol/L) in subjects more than 60 years old (P < 0.05). Multiple linear regression analysis demonstrated that age was the only independent predictor for plasma NT-proBNP in these subjects (P < 0.01). CONCLUSION: The plasma concentration of NT-proBNP in subjects without heart diseases was different between male and female, and was increasing with age in male subjects more than 60 years old.

Is slow coronary flow associated with inflammation?

Cardiologists are familiar with the phenomenon of slow progression of angiographic contrast in the coronary arteries in the absence of stenosis in the epicardial vessels in some patients presenting with chest pain. This phenomenon is called as coronary slow flow phenomenon, and firstly described in 1972, while it remains scantily studied. The pathophysiological mechanisms of coronary slow flow phenomenon remain uncertain. Several hypotheses however, have been suggested for slow coronary flow phenomenon, including a form of early phase of atherosclerosis, small vessel dysfunction, Hagen-Poiseuille's equation model, imbalance between vasoconstrictor and vasodilatory factors, and platelet function disorder. More recently, there has been mounting evidence that inflammation plays an important role in the initiation, development as well as evolution of atherosclerosis, suggesting that atherosclerosis is an inflammation disease. New evidence has also indicated that inflammation may be involved in the development of slow coronary flow phenomenon. Coronary slow flow phenomenon is an important clinical entity because it may be the cause of angina at rest or during exercise, acute myocardial infarction, and hypertension. Despite the good prognosis of this kind of patients, the chronic, frequent nature of the persistent uncomfortable chest can significantly impair the quality of life. Whether this is really a new kind of coronary disease involving in inflammation, however, is still unknown and deserves further investigation.