Beta-blocker therapy in elderly patients with renal dysfunction and heart failure

OBJECTIVE To assess the role of beta-blockers(BB)in patients with chronic kidney disease(CKD)aged≥75 years.METHODS AND RESULTS From January 2008 to July 2014,we included 390 consecutive patients≥75 years of age with ejection fraction≤35%and glomerular filtration rate(GFR)≤60 m L/min per 1.73 m^2.We analyzed the relationship between treatment with BB and mortality or cardiovascular events.The mean age of our population was 82.6±4.1 years.Mean ejection fraction was 27.9%±6.5%.GFR was 60-45 m L/min per 1.73 m^2 in 50.3%of patients,45-30 m L/min per 1.73 m^2 in 37.4%,and<30 m L/min per 1.73 m^2 in 12.3%.At the conclusion of follow-up,67.4%of patients were receiving BB.The median follow-up was28.04(IR:19.41-36.67)months.During the study period,211 patients(54.1%)died and 257(65.9%)had a major cardiovascular event(death or hospitalization for heart failure).BB use was significantly associated with a reduced risk of death(HR=0.51,95%CI:0.35-0.74;P<0.001).Patients receiving BB consistently showed a reduced risk of death across the different stages of CKD:stage IIIa(GFR=30-45 m L/min per 1.73 m^2;HR=0.47,95%CI:0.26-0.86,P<0.0001),stage IIIb(GFR 30-45 m L/min per 1.73 m^2;HR=0.55,95%CI:0.26-1.06,P=0.007),and stages IV and V(GFR<30 m L/min per 1.73 m~2;HR=0.29,95%CI:0.11-0.76;P=0.047).CONCLUSIONS The use of BB in elderly patients with HFr EF and renal impairment was associated with a better prognosis.Use of BB should be encouraged when possible.

Understanding heart failure in the elderly with respect to diastolic dysfunction and role for natriuretic peptides

The current issue of the Journal of Geriatric Cardiology contains an interesting paper by Dr. Yixin Song and colleagues raising important issues in the diagnosis and management of heart failure in elderly patients. Readers of this journal are in all likelihood aware that the epidemic of heart failure is of great impact medically and economically worldwide.

The investigation of the relationship between renal dysfunction and coronary heart disease

Objectives To evaluate the relationship of renal dysfunction,coronary heart disease and percutaneous coronary intervention(PCI).Methods(l)The subjects:There were 376 patients who come from department of cardiology of our hospital in this study undergoing coronary angiography.The patients were divided into two groups? according to coronary angiography:coronary artery disease(group A,n =263),in which 141 patients with renal dysfunction(group A1) and 122 patients with normal renal function(group A2):patients with other kinds of cardiovascular disease but normal coronary angiography(group B.n=113).Before the coronary angiography, all patients were measured the serum creatinine, microalbuminuria,fasting blood-glucose,triglycerides,total cholesterol,high density lipoprotein,low density lipoprotein, blood pressure in fasting 12 hours.(2)The diagnostic criteria for renal dysfunction:male serum creatinine】115 umol/L and/or microalbuminuria】30 mg,female】107 umol/L and/ or】30 mg.Results(1)The differences of renal function indexes in the group A and B:The mean level of microalbuminuria and serum creatinine was higher significantly in group A than that of the group B(43.48±38.93 vs.11.23±7.07 and 101.52±37.22 vs.80.62±17.4 respectively.Conclusions The coronary heart disease patients with renal dysfunction had more severe coronary artery stenosis,The renal dysfunction is a strong and independent risk factors for the coronary heart disease and beeds more revascularization therapy.

The Study on the Correlation Between Plasma Adiponectin Level and Coronary Heart Disease

Objectives To investigate the relationship between plasma adiponectin level and coronary heart disease （CHD）, and some established cardiovascular risk factors and to probe its probable pathogenesis which adiponectin results in CHD. Methods The levels of plasma adiponectin, fasting plasma insulin （FINS）, C-reactive protein （CRP） and P-selectin were measured by ELISA, plasma ET-1 was measured by radioimmunoassay （RIA） in 75 male patients with CHD and 30 healthy male people. Body mass index （BMI）, waist / hip ratio （WHR） and insulin resistance index （Homa-IR） were calculated respectively. Results （1）The plasma adiponectin levels in CHD group were lower compared with control group[（5.18±2.57）mg / L vs（8.94±2.59）mg / L, P〈 0.001 ], there was no significant difference of plasma adiponectin levels in CHD sub-groups （P 〉 0.05）.（2） Based on multinominal stepwise logistic regression analysis, adiponectin was one of significant and independent risk factors for CHD. （3） Multivariate liner stepwise regression analysis showed that adiponectin had significant correlation with BMI and TG, BMI and TG were independent factors influencing on plasma adiponectin levels. （4） Pearson correlation analysis indicated plasma adiponectin levels were inversely related to FINS levels , Homa-IR, CRP, P-selectin and ET-1. Conclusions （ 1 ）Plasma adiponectin levels are lower in CHD patients compared the control subjects, there are no significant difference of plasma adiponectin levels in patients with SAP, UAP and AMI. （2） Plasma adiponectin levels are relative with CHD. Hypoadiponectinemia is an independent risk factor for CHD. （3）Established cardiovascular risk factors such as BMI and TG have an obvious influence on adiponectin. （4）The probable pathogenesis by which adiponectin involves in CHD is suggested that adiponectin relates to insulin resistance, inflammatory reaction and dysfunction of vessel endothelium.

MULTIPLE ORGAN DYSFUNCTION AFTER HEART VALVE REPLACEMENT

Multiple organ dysfunction (MOD) after valve replacement was studied in a period of 1980-1991. The incidences of MOD involving 2, 3 and 4 organs were 17.1%, 5.6% and 4.3% with corresponding mortalities of 12%, 18.5% and 76.2%. We focused on dysfunction of more than 3 organs, the dreadful complication, which can be divided clinically into three types: acute (type I), deteriorating (type II), and pulmonary infection (type III). In MOD, the function of heart and lung is primarily depressed after surgery. So the predisposing factors of MOD are acute pump failure and hypoxemia, and the possible triggering factor is infection, especially pulmonary infection, which re-endangers the organs recovering from the primary blows. Thus prevention of pulmonary infection is of same importance as treatment of pump failure and hypoxemia.

Signaling Pathways Involved in Cardiac Hypertrophy

Cardiac hypertrophy is the heart＇s response to a variety of extrinsic and intrinsic stimuli that impose increased biomechanical stress. Traditionally, it has been considered a beneficial mechanism; however, sustained hypertrophy has been associated with a significant increase in the risk of cardiovascular disease and mortality. Delineating intracellular signaling pathways involved in the different aspects of cardiac hypertrophy will permit future improvements in potential targets for therapeutic intervention. Generally, there are two types of cardiac hypertrophies, adaptive hypertrophy, including eutrophy （normal growth） and physiological hypertrophy （growth induced by conditioning）, and maladaptive hypertrophy, physical including pathologic or reactive hypertrophy （growth induced by pathologic stimuli） and hypertrophic growth caused by genetic mutations affecting sarcomeric or cytoskeletal proteins. Accumulating observations from animal models and human patients have identified a number of intracellular signaling pathways that characterized as important transducers of the hypertrophic response, including calcineurin/nuclear factor of activated Tcells, phosphoinositide 3-kinases/Akt （PI3Ks/Akt）, G protein-coupled receptors, small G proteins, MAPK, PKCs, Gp130/STAT3, Na＋/H＋ exchanger, peroxisome proliferator-activated receptors, myocyte enhancer factor 2/histone deacetylases, and many others. Furthermore, recent evidence suggests that adaptive cardiac hypertrophy is regulated in large part by the growth hormone/insulin-like growth factors axis via signaling through the PI3K/Akt pathway. In contrast, pathological or reactive hypertrophy is triggered by autocrine and paracrine neurohormonal factors released during biomechanical stress that signal through the Gq/phosphorlipase C pathway, leading to an increase in cytosolic calcium and activation of PKC.