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1.
Journal of Southern Medical University ; (12): 941-946, 2016.
Artigo em Chinês | WPRIM | ID: wpr-286869

RESUMO

<p><b>OBJECTIVE</b>To investigate the impact of heart valve calcification (HVC) on cardiovascular outcomes in patients on maintenance hemodialysis (MHD).</p><p><b>METHODS</b>We enrolled 302 Chinese patients on MHD between 2009 and 2011 including 99 with HVC identified by echocardiography screening. All the patients were followed up for 2 years and survival analysis was performed with all-cause mortality, cardiovascular mortality and new onset cardiovascular events as the endpoints. Cox regression analysis was used for analyzing the impact of heart valve calcification on the cardiovascular outcomes of the patients.</p><p><b>RESULTS</b>The mean age of the total patients was 58.2∓15.0 years when receiving the initial MHD, and 53.6% were male patients. The overall mortality, cardiovascular mortality and new on-set cardiovascular events in HVC and non-HVC groups were 30.3% vs 16.3%, 22.2% vs 6.9%, and 48.5% vs 25.6%, respectively (P<0.05). Kaplan-Meier survival analysis showed a significant difference in all-cause mortality (P=0.006), cardiovascular mortality (P<0.001) and new-onset cardiovascular events (P<0.001) between HVC and non-HVC groups. After adjustment, Cox regression analysis identified HVC as a risk factor for increased all-cause mortality (HR=1.88; 95%CI: 1.11-3.19), cardiovascular mortality (HR=3.47, 95%CI: 1.76-6.84) and cardiovascular events (HR=1.64, 95% CI: 1.09-2.47).</p><p><b>CONCLUSIONS</b>HVC is an independent risk factor for increased cardiovascular mortality and new cardiovascular events in patients on MHD.</p>


Assuntos
Adulto , Idoso , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Calcinose , Patologia , Ecocardiografia , Doenças das Valvas Cardíacas , Mortalidade , Patologia , Valvas Cardíacas , Patologia , Estimativa de Kaplan-Meier , Diálise Renal , Fatores de Risco
2.
Journal of Southern Medical University ; (12): 1910-1913, 2011.
Artigo em Chinês | WPRIM | ID: wpr-265754

RESUMO

<p><b>OBJECTIVE</b>To investigate the prevalence of cardiovascular diseases (CVD) in patients with systemic lupus erythematosus (SLE) and estimate the associated risk factors for CVD.</p><p><b>METHODS</b>This cross-sectional study was conducted in 879 SLE patients treated in our hospital between March, 2006 and March, 2011. The demographic data and the clinical data including SLE duration, therapeutic regimen, renal pathological data, estimated glomerular filtration rate (eGFR), SLE Disease Activity Index (SLEDAI), and associated biochemical parameters were analyzed. Cardiovascular ultrasound was used for detecting and analyzing the cardiovascular structural and functional abnormalities.</p><p><b>RESULTS</b>Eighty-five cases of CVD were found in the 879 SLE cases (9.7%). After age stratification, CVD was identified in 5.8%, 9.0%, 14.0% and 20.0% in SLE patients aged ≤19, 20-39, 40-59 and ≥60 years, respectively, showing a tendency to increase with age (P=0.002). The prevalence of CVD differed significantly between patients with and those without lupus nephritis (P=0.001). Among the 85 patients with CVD, 23.5% (20/85) had left ventricular hypertrophy, 49.5% (42/85) had congestive heart failure, 20.0% (17/85) had stroke, 3.5% (3/85) had angina pectoris, and 3.5% (3/85) had peripheral CVD. Compared to those without CVD, patients with CVD had a longer SLE duration (P=0.002), a longer time of steroids treatment (P=0.026), a higher blood pressure (P=0.0006), a lower eGFR (P=0.001), and a lower concentration of HDL (P=0.007). Logistic regression analysis showed that SBP, eGFR, HDL, SLE duration, SLEDAI index, serum C3 and hs-CRP were the risk factors for CVD in SLE patients (P=0.033).</p><p><b>CONCLUSION</b>SLE is associated with a high risk of CVD which increases with age, and SLE patients with lupus nephritis have an even higher risk for CVD. SBP, eGFR, HDL, SLE duration, SLEDAI index, serum C3 and hs-CRP are the risk factors for CVD in SLE patients.</p>


Assuntos
Adulto , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Adulto Jovem , Doenças Cardiovasculares , Epidemiologia , China , Epidemiologia , Estudos Transversais , Lúpus Eritematoso Sistêmico , Prevalência , Estudos Retrospectivos , Fatores de Risco
3.
Journal of Southern Medical University ; (12): 1272-1278, 2010.
Artigo em Chinês | WPRIM | ID: wpr-336202

RESUMO

<p><b>OBJECTIVE</b>To evaluate the clinical efficacy of continuous venous-venous hemofiltration (CVVH) combined with coupled plasma filtration adsorption (CPFA) in the management of systemic inflammation response syndrome (SIRS) complicated by acute renal failure (ARF).</p><p><b>METHODS</b>Thirty patients with SIRS complicated by ARF (including 25 with severe acute pancreatitis, 2 with colonic perforation with infection, and 3 with acute infective endocarditis) were randomly divided into CVVH plus CPFA group (n=14) and CVVH alone group (n=16). The APACHE II score, mean arterial pressure, PaO2/FiO2, TNF-alpha and IL-10 were detected prior to or after the intervention. The feasibility and tolerance of CVVH plus CPFA and the therapy-related adverse reactions were evaluated.</p><p><b>RESULTS</b>The two groups showed no significant differences in the baseline clinical characteristics (P>0.05). The mean arterial pressure and PaO2/FiO2 increased significantly after treatment as compared with the control (P<0.05), with TNF-alpha being reduced and IL-10 elevated. In CVVH plus CPFA group, APACHEII score improved significantly after 10 days (P<0.05). No therapy-related adverse reactions were noted, suggesting good tolerance of CVVH plus CPFA.</p><p><b>CONCLUSION</b>CVVH combined with CPFA is an effective and safe method for improving the clinical outcome of patients with SIRS and ARF.</p>


Assuntos
Adulto , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Injúria Renal Aguda , Terapêutica , Hemofiltração , Métodos , Síndrome de Resposta Inflamatória Sistêmica , Terapêutica , Resultado do Tratamento
4.
Journal of Southern Medical University ; (12): 1002-1004, 2010.
Artigo em Chinês | WPRIM | ID: wpr-290008

RESUMO

<p><b>OBJECTIVE</b>To examine the relationship between reduction of serum fetuin A and coronary artery calcification (CAC) in patients starting hemodialysis.</p><p><b>METHODS</b>Twenty-nine patients on chronic hemodialysis (duration of hemodialysis less than 6 months) were enrolled in this study. Serum fetuin A and such potential CAC-related risk factors as C-reactive protein (CRP), Ca, P, iPTH, body mass index (BMI) were examined. CAC was detected by multislice spiral CT scan (MSCT) and quantified by the modified Agaston's scoring system. All the 29 patients were followed up for 18 months to appraise the cardiovascular events defined as cardiac failure, angina pectoris or myocardial infarction.</p><p><b>RESULTS</b>Eleven patients (78.57%) were found to have CAC as detected by MSCT in low serum fetuin A (below the average serum concentration of 0.71 g/L) group, a rate significantly higher than that in high serum fetuin A group (7 patients, 46.67%, P<0.05). Serum fetuin A in these 29 patients was related with CAC score (Pearson correlation coefficient of -0.734, P=0.001) and stepwise regression analysis indicated that serum fetuin A (standardized beta=-0.568, P=0.003) and age (standardized beta=0.416, P=0.019) were independently correlated to CAC. Such factors as CRP, Ca, P, iPTH, Chol, TG, HDL-C, LDL-C, BMI and blood pressure were excluded from the regression equation. Reduction of serum fetuin A was associated with cardiovascular events (Spearman's rho -0.758, P<0.01). No significant difference was found between low and high serum fetuin A groups by Kaplan-Meier survival analysis (P=0.065).</p><p><b>CONCLUSION</b>Reduced serum fetuin A may be a potential risk factor of coronary artery calcification, and can contribute to cardiovascular events in patients starting hemodialysis.</p>


Assuntos
Adulto , Idoso , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Proteínas Sanguíneas , Metabolismo , Calcinose , Sangue , Vasos Coronários , Patologia , Diálise Renal , Fatores de Risco , alfa-2-Glicoproteína-HS
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