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Objective@#To assess the relationship between serum albumin level and clinical outcome in heart failure (HF) patients receiving cardiac resynchronization therapy (CRT).@*Methods@#In this retrospective cohort study, 357 consecutive chronic heart failure patients receiving CRT between January 2010 and December 2015 were enrolled and divided into two groups based on pre-CRT serum albumin (albumin≥40 g/L, n=244; albumin<40 g/L, n=113). Clinical outcomes were defined as all-cause mortality (including heart transplantation) and rehospitalization due to worsening HF.Baseline characteristics were compared and all-cause mortality (including heart transplantation) and rehospitalization due to worsening heart failure (HF) were analyzed using Kaplan-Meier curves.Prognostic value of albumin level was evaluated in Cox proportional-hazards regression models.@*Results@#Over a median follow-up time of 21 months, 45 patients (12.6%) died, 4 patients (1.1%) underwent heart transplantation and 100 patients (28.0%) were rehospitalized due to worsening HF. HF patients with pre-CRT albumin<40 g/L were related with worse NYHA function class, lower HDL-C level and ACEI/ARB use compared to HF patients with pre-CRT albumin≥40 g/L. Kaplan-Meier analyses evidenced lower survival rate in HF patients (log-rank test: P=0.000 4, χ2=12.60) and higher rehospitalization rate due to worsening HF (log-rank test: P=0.009, χ2=6.82) in HF patients with pre-CRT albumin<40 g/L.Multivariate Cox analyses indicated that serum pre-CRT albumin <40 g/L was an independent risk factor for all-cause mortality (HR=2.019, 95%CI 1.125-3.622, P=0.018) and HF rehospitalization (HR=1.517, 95%CI 1.014-2.270, P=0.043).@*Conclusion@#Pre-CRT serum albumin level is associated with the severity of heart failure in CRT recipients.Patients with lower pre-CRT albumin level face increased risk of all-cause mortality and HF rehospitalization in chronic heart failure patients receiving cardiac resynchronization.
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Objective: To create and validate a scoring system for predicting clinical prognosis in patients with cardiac resynchronization therapy (CRT). Methods: A cohort of 367 consecutive patients received CRT in our hospital from 2010-01 to 2015-12 were enrolled. The endpoint follow-up events were all-cause death including heart transplantation and heart failure re-admission. The patients were randomly categorized into 2 groups: Modeling group, to develop HEAL scoring system,n=300 and Veriifcation group, to validate HEAL model,n=67. HEAL system was established by Cox proportional hazards regression model, discrimination between HEAL and EARRN scoring systems was evaluated by AUC of ROC, HEAL calibration was assessed by Hosmer-Lemeshow test and clinical endpoint evaluation by 2 scoring systems were compared by Kaplan-Meier method. Results: Modeling group analysis indicated that hs-CRP (HR=1.137, 95% CI 1.072-1.205,P10. AUC for risk classification in Modeling group and Verification group were 0.719(95% CI 0.629-0.809) and 0.708 (95% CI 0.539-0.878), HEAL can well distinguish clinical prognosis in patients at different risk levels (log-rank test showed in Modeling groupP<0.001 and in Veriifcation groupP=0.002); Hosmer-Lemeshow test presented good calibration,P=0.952. All 367 patients were respectively evaluated by HEAL and EARRN scoring systems, HEAL had the better discrimination than EARRN as AUC 0.763 (95% CI 0.692-0.833) vs AUC 0.602 (95% CI 0.517-0.687). Conclusion: HEAL scoring system can effectively predict adverse prognosis in CRT patients, it had the better discrimination than EARRN system and was valuable to distinguish high risk patients in clinical practice.
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Objective: To explore the impact of atrial fibrillation (AF) on clinical outcomes in patients with cardiac resynchronization therapy (CRT). Methods: A total of 258 arrhythmia patients who received CRT in our hospital from 2010-01 to 2014-12 were retrospectively enrolled. According to AF occurrence, the patients were divided into 2 groups: AF group,n=42 and Non-AF group,n=216. The end point events were deifned by heart failure (HF) re-admission and all-cause death (including heart transplantation). Survival curve was drawn by Kaplan-Meier method, clinical prognosis was comparedbetween 2 groups with log-rank test and the impact of AF on end point prediction was analyzed by uni- and multivariate Cox proportional-hazards regression models. Results: There were 16.3% (42/258) patients combining AF. The following indexes were statistically different between AF group and Non-AF group: patients' age, the ratios of male gender and left bundle branch block (LBBB), eGFR, blood levels of creatinine, uric acid, big endothelin-1, left atrial diameter and application of amiodarone. With the median of 22 months follow-up study, there were 33/258 (12.8%) patients died, 5 (1.9%) received heart transplantation and 72 (27.9%) with HF re-admission. Survival analysisindicated that HF re-admission rate in AF group was higher than Non-AF group (χ2=6.651,P=0.010), all cause mortality was similar between 2 groups (χ2=0.528,P=0.468). Univariate Cox proportional-hazards regression analysis showed that AF, LBBB, higher blood levels of creatinine, big endothelin-1 and large left atrium were the suspiciousrisk factors for HF re-admission; increased blood levels of creatinine, big endothelin-1 and large left atrium were thesuspiciousrisk factors for all cause death. Multivariate Cox proportional-hazards regression analysis presented that AF was not the independent risk factor for HF re-admission and all-cause death, while largeleft atrium was the independent risk factor for HF re-admission (HR=1.041, 95% CI 1.007-1.075,P=0.018); large left atrium and increased serum creatinine were the independent risk factors for all cause death (HR=1.045, 95% CI 1.001-1.091,P=0.048) and (HR=1.008, 95% CI 1.001-1.015,P=0.035) respectively. Conclusion: AF was associated with the higher rate of HF re-admission in CRT patients; while no clear evidencesupported that AF was the independent risk factor for HF re-admission and all cause death in CRT patients.
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<p><b>BACKGROUND</b>Dyslipidemia caused by liver injury is a significant risk factor for cardiovascular complications. Previous studies have shown that hydrogen sulfide (H2S) protects against multiple cardiovascular disease states in a similar manner as nitric oxide (NO), and NO/endothelial nitric oxide synthase (eNOS) pathway is the key route of NO production. The purpose of this study was to investigate whether H2S can ameliorate the high blood pressure and plasma lipid profile in Nw-nitro-L-argininemethyl ester (L-NAME)-induced hypertensive rats by NO/eNOS pathway.</p><p><b>METHODS</b>Thirty-six 4-week old Sprague-Dawley (SD) male rats were randomly assigned to 6 groups (n = 6): control group, L-NAME group, control + glibenclamide group, control + NaHS group, L-NAME + NaHS group, and L-NAME + NaHS + glibenclamide group. Measurements were made of plasma triglycerides (TG), low-density lipoprotein (LDL), high-density lipoprotein (HDL), total cholesterol (CHO), glutamic-pyruvic transaminase (ALT) levels after 5 weeks. Then measurements of NO level and proteins expression of eNOS, P-eNOS, AKT, P-AKT were made in liver tissue.</p><p><b>RESULTS</b>After 5 weeks of L-NAME treatment, the blood pressure, plasma TG ((1.22±0.12) mmol/L in L-NAME group vs. (0.68±0.09) mmol/L in control group; P < 0.05) and LDL ((0.54±0.04) mmol/L in L-NAME group vs. (0.28±0.02) mmol/L in control group; P < 0.05) concentration were significantly increased, and the plasma HDL ((0.26±0.02) mmol/L in L-NAME group vs. (0.69±0.07) mmol/L in control group; P < 0.05) concentration significantly decreased. Meanwhile the rats treated with L-NAME exhibit dysfunctional eNOS, diminished NO levels ((1.36±0.09) mmol/g protein in L-NAME group vs. (2.34±0.06) mmol/g protein in control group; P < 0.05) and pathological changes of the liver. H2S therapy can markedly decrease the blood pressure ((37.25±4.46) mmHg at the fifth week; P < 0.05), and ameliorate the plasma TG ((0.59±0.06) mmHg), LDL ((0.32±0.04) mmHg), and HDL ((0.46±0.03) mmHg) concentration in L-NAME + NaHS group (all P < 0.05). H2S therapy can also restore eNOS function and NO bioavailability and attenuate the pathological changes in the liver in L-NAME-induced hypertensive rats.</p><p><b>CONCLUSION</b>H2S protects the L-NAME-induced hypertensive rats against liver injury via NO/ eNOS pathway, therefore decreases the cardiovascular risk.</p>
Subject(s)
Animals , Male , Rats , Cardiovascular Diseases , Metabolism , Hydrogen Sulfide , Therapeutic Uses , Hypertension , Drug Therapy , Liver , Metabolism , NG-Nitroarginine Methyl Ester , Toxicity , Nitric Oxide , Metabolism , Nitric Oxide Synthase Type III , Metabolism , Rats, Sprague-Dawley , Signal TransductionABSTRACT
OBJECTIVE To study the effects of Panax quinquef olium 20S-protopanaxdiol saponins extracted from the leaves of panax qu inque-folium (PQDS) on the hemodynamics and cardial oxygen metabolism in dogs with acute myocardial infarction (AMI).METHODS The paramete rs of hemodynamics and cardial oxygen metabolism were determined by using the mo del of ligation of LAD in the anaesthetized open-chest dogs.RESULTS In dogs treated with PQDS (in a dosage of 10 and 20 mg*kg-1 iv infusion),the myocardial blood flow (MBF) was increased and coronary vascular re sistance (CVR) was decreased significantly.The heart rate (HR) was slowed.The ar terial blood pressure (ABP),left ventricular pressure (LVP),the maximum rise rat e of left ventricular pressure(+dp/dtmax),left ventricular work index (LVW I) and total periphery resistance(TPR) were reduced,whereas the stroke index(SI) and cardiac index (CI) were increased.In addition,the decreasing range of the m aximum decline rate of left ventricular pressure(-dp/dtmax) and the rising range of left ventricular end diastolic pressure (LVEDP) were reduced.Meanwhile the cardiac oxygen consumption,myocardial oxygen utilization rate and cardiac o xygen consumption index were also decreased.CONCLUSION PQDS had protective effects on acute myocardial ischemia including improving heart fu nction,decreasing cardiac oxygen consumption and increasing myocardial blood flo w,etc.