A 54-year-old female patient with congenital heart disease had a persistent complete left bundle branch block three months after closure by an Amplatzer ventricular septal defect occluder. Nine months later, the patient suffered from chest distress, palpitation, and sweating at daily activities, and her 6-min walk distance decreased significantly (155 m). Her echocardiography showed increased left ventricular end-diastolic diameter with left ventricular ejection fraction of 37%. Her symptoms reduced significantly one week after received cardiac resynchronization therapy. She had no symptoms at daily activities, and her echo showed left ventricular ejection fraction of 46%and 53%. Moreover, left ventricular end-diastolic diameter decreased 6 and 10 months after cardiac resynchronization therapy, and 6-min walk dis-tance remarkably increased. This case demonstrated that persistent complete left bundle branch block for nine months after transcatheter closure with ventricular septal defect Amplatzer occluder could lead to left ventricular enlargement and a significant decrease in left ventricular systolic function. Cardiac resynchronization therapy decreased left ventricular end-diastolic diameter and increased left ventricular ejection fraction, thereby improving the patient’s heart functions.

Coronary fistulae and ventricular septal perforation are very rare clinically, and even less caused by cardiac leiomyosarcoma. A case is reported that a 67-year-old female had cardiac leiomyosarcoma with progressive heart failure and coronary fistulae and ventricular septal perforation. This case was special since all ante-mortem examinations and cardiac surgery failed to detect the presence of any abnormal car-diac mass. Therefore, the malignant cardiac tumors could appear in an invasive form without mass and be one of the causes of the coronary fistulae and ventricular septal perforation.

Chronic heart failure (CHF) is the leading cause of hospitalization for those over the age of 65 and represents a significant clinical and economic burden. About half of hospital re-admissions are related to co-morbidities, polypharmacy and disabilities associated with CHF. Moreover, CHF also has an enormous cost in terms of poor prognosis with an average one year mortality of 33%–35%. While more than half of patients with CHF are over 75 years, most clinical trials have included younger patients with a mean age of 61 years. Inadequate data makes treatment decisions challenging for the providers. Older CHF patients are more often female, have less cardiovascular diseases and associated risk factors, but higher rates of non-cardiovascular conditions and diastolic dysfunction. The prevalence of CHF with reduced ejection fraction, ischemic heart disease, and its risk factors declines with age, whereas the prevalence of non-cardiac co-morbidities, such as chronic renal failure, dementia, anemia and malignancy increases with age. Diabetes and hypertension are among the strongest risk factors as predictors of CHF particularly among women with coronary heart disease. This review paper will focus on the specific consideration for CHF assessment in the older population. Management strategies will be reviewed, including non-pharmacologic, pharmacologic, quality care indicators, quality improvement in care transition and lastly, end-of-life issues. Palliative care should be an integral part of an interdiscipli-nary team approach for a comprehensive care plan over the whole disease trajectory. In addition, frailty contributes valuable prognostic in-sight incremental to existing risk models and assists clinicians in defining optimal care pathways for their patients.

Cognitive damage in heart failure (HF) involves different domains thus interfering with the ability for single patient to self-care and to cope with treatment regimens, modifying symptoms and health behaviours. Many cerebral and functional changes were detected in brain imaging, involving areas of both grey and white matter deputed to cognition. Although various instruments are available to explore cognition, no consensus was obtained on better tools to be used in HF population. Reduction in cerebral blood flow, decreased cardiac output, altera-tions of cerebrovascular reactivity and modification of blood pressure levels are the main features involved in the etiopathogenetic mecha-nisms of cognitive deficit. Several cardiac variables, laboratory parameters, demographic and clinical elements were studied for their possible relation with cognition and should be properly evaluated to define patients at increased risk of impairment. The present review gathers avail-able data pointing out assured information and discussing possible areas of research development.

Background Oxidative stress is a major mechanism underlying the pathogenesis of cardiovascular disease. It can trigger inflammatory cascades which are primarily mediated via nuclear factor-κB (NF-κB). The NF-κB transcription factor family includes several subunits (p50, p52, p65, c-Rel, and Rel B) that respond to myocardial ischemia. It has been proved that persistent myocyte NF-κB p65 activation in heart failure exacerbates cardiac remodeling. Mechods A recombinant adeno-associated virus serotype 9 carrying enhanced green fluorescent protein and anti-NF-κB p65 ribozyme (AAV9-R65-CMV-eGFP) was constructed. The cells were assessed by MTT assay, Annexin V–propidium iodide dual staining to study apoptosis. The expression of P65 and P50 were assessed by Western blot to investigate the under-lying molecular mechanisms. Results After stimulation with H2O2 for 6 h, H9c2 cells viability decreased significantly, a large fraction of cells underwent apoptosis. We observed a rescue of H9c2 cells from H2O2-induced apoptosis in pretreatment with AAV9-R65-CMV-eGFP. Moreover, AAV9-R65-CMV-eGFP decreased H2O2-induced P65 expression. Conclusions AAV9-R65-CMV-eGFP protects H9c2 cells from oxidative stress induced apoptosis through down-regulation of P65 expression. These observations indicate that AAV9-R65-CMV-eGFP has the potential to exert cardioprotective effects against oxidative stress, which might be of great importance to clinical efficacy for cardiovascular disease.

Background Electroacupuncture pretreatment plays a protective role in myocardial ischemia/reperfusion (I/R) injury and microRNAs (miRNAs) could act on various facets of cardiac function. However, the role of miRNAs in the cardioprotection by electroacupuncture pre-treatment on myocardial I/R injury remains unknown. The purpose of the study was to examine whether miR-214 was involved in cardio-protection by electroacupuncture. Methods Using rat myocardial I/R model, we examined the role of electroacupuncture pretreatment in myocardial I/R injury and analyzed the changes in the expression of miR-214. In addition, I/R was simulated in vitro by performing oxy-gen-glucose deprivation (OGD) on H9c2 cell cultures, and the effect of electroacupuncture pretreatment on I/R injury as well as expressional level of miR-214 were examined in vitro. Furthermore, the miR-214 mimic was transfected into OGD-treated H9c2 cells, we analyzed the cell apoptosis, lactate dehydrogenase (LDH) and creatine kinase (CK) activities, intracellular free Ca2+concentration ([Ca2+]i) as well as the relative protein levels of sodium/calcium exchanger 1(NCX1), BCL2-like 11 (BIM), calmodulin-dependent protein kinase IIδ(CaMKIIδ) and Cyclophilin D (CypD). Results The in vivo results revealed that compared with the I/R group, the electroacupuncture pretreatment group showed significant decreased myocardial infarct size, as well as the increased indices of the cardiac function, including heart rate, mean arterial pressure, left ventricular systolic pressure and maximal rate for left ventricular pressure rising and declining (±dp/dt max). In addition, electroacupuncture pretreatment could inhibit the elevation of LDH and CK activities induced by I/R injury. The quantitative PCR (qPCR) results demonstrated electroacupuncture pretreatment could provide cardioprotection against myocardial I/R injury in rats with miR-214 up-regulation. In the meanwhile, in vitro, electroacupuncture pretreatment protected H9c2 cells from OGD-induced injury. Trans-fection of miR-214 mimic showed protective effects on OGD-induced injury to H9c2 cells by reducing apoptosis, decreasing LDH and CK activities, rescuing the OGD-induced Ca2+and down-regulating elevated protein levels of NCX1, BIM, CaMKIIδand CypD. Conclusions Our findings firstly demonstrated that electroacupuncture pretreatment promotes the expression of miR-214 in myocardial I/R injury and miR-214 contributes to the protective effect of electroacupuncture on myocardial I/R injury.

Background The data on the prognostic values of high sensitivity C-reactive protein (hsCRP) levels in patients with advanced symp-tomatic heart failure (HF) receiving cardiac resynchronization therapy (CRT) are scarce. The aim of present study was to investigate the association of serum hsCRP levels with left ventricle reverse remodeling after six months of CRT as well as long-term outcome. Methods A total of 232 CRT patients were included. The assessment of hsCRP values, clinical status and echocardiographic data were performed at baseline and after six months of CRT. Long-term follow-up included all-cause mortality and hospitalizations for HF. Results During the mean follow-up periods of 31.3 ± 31.5 months, elevated hsCRP (>3 mg/L) prior to CRT was associated with a significant 2.39-fold increase (P=0.006) in the risk of death or HF hospitalizations. At 6-month follow-up, patients who responded to CRT showed significant reductions or maintained low in hsCRP levels (–0.5 ± 4.1 mg/L reduction) compared with non-responders (1.7 ± 6.1 mg/L increase, P=0.018). Com-pared with patients in whom 6-month hsCRP levels were reduced or remained low, patients in whom 6-month hsCRP levels were increased or maintained high experienced a significantly higher risk of subsequent death or HF hospitalizations (Log-rank P<0.001). The echocardio-graphic improvement was also better among patients in whom 6-month hsCRP levels were reduced or remained low compared to those in whom 6-month hsCRP levels were raised or maintained high. Conclusions Our findings demonstrated that measurement of baseline and follow-up hsCRP levels may be useful as prognostic markers for timely potential risk stratification and subsequent appropriate treatment strategies in patients with advanced HF undergoing CRT.

Objective To examine the effects of exogenously administered intermedin (IMD,adrenomedullin-2) on arterial blood pressure,cardiac function and the cardiovascular IMD receptor system in spontaneously hypertensive rats (SHRs) as well as to investigate the associated mechanisms.Methods Thirteen week-old male rats were divided in Wistar Kyoto (WKY) group (n =12),SHR group (n =12),IMD group (SHRs infused with IMD 1-47 500 ng/kg per hour,n =12),and ADM group (SHRs infused with adrenomedullin 500 ng/kg per hour,n =12).Results A two-week continuous administration of low dose IMD 1-47 via mini-osmotic pumps markedly reduced blood pressure,the maximal rates of increase and decrease of left-ventricle pressure development (LV ± dp/dtmax),left ventricular systolic pressure and heart rate in SHRs.Furthermore,IMD also inhibited protein over-expression of cardiovascular IMD receptors,myocardial Receptor Activity-Modifying Proteins (RAMP1 and RAMP2),aortic RAMP1,RAMP2,RAMP3,and calcitonin receptor-like receptor (CRLR);suppressed up-regulation of aortic RAMP1,RAMP2,RAMP3 and CRLR gene expression; and markedly elevated the mRNA abundance of myocardial atrial natriuretic peptide (ANP) and myocardial brain natriuretic peptide (BNP).Additionally,IMD 1-47 administration in SHRs increased aortic cAMP concentration and reduced myocardial cAMP concentration.Conclusion These findings support the speculation that IMD,as a cardiovascular active peptide,is involved in blood pressure reduction and cardiac function amelioration during hypertension.The mechanism underlying this effect may involve IMD binding of a receptor complex formed by RAMPs and CRLR,and consequential regulation of cAMP levels and other cardiovascular active factors,such as ANP and BNP.

Objective To assess the effect of altitude hypoxia on the elderly patients with coronary artery disease (CAD). Methods Three subject groups were surveyed during their train trip on the highest railroad--the Qinghai-Tibet Railway: 22 elderly individuals with documented CAD, 20 healthy elderly controls, and 20 healthy young controls, all of whom from Beijing near the sea level (76 m). Survey questions addressed clinical features of their healthy conditions and aspects of their coronary disease. The baseline study was performed at Xining at an altitude of 2261 m, and then during acute exposure to altitudes of 2808 m, 4768m, 5072 m and 4257 m by train for 24 hours. Resting pulse rate, blood pressure, oxygen saturation, electrocardiograph (ECG), and cardiac work estimated by the heart rate-blood pressure double product were obtained five times in each subject at different altitudes. Results On arrival to altitudes between 4768 m and 5072 m, the older passengers, especially those with preexisting coronary disease, had higher HR, higher BP, and lower SaO2, as well as more frequent abnormalities on ECG, as compared to the younger healthy subjects. As compared with the healthy elderly controls, incomplete right bundle branch block, left ventricular hypertrophy, and ST segment depression were more frequently seen in the elderly coronary patients (P<0.01). Cardiac work in group 1 was increased by 13% 12 hours after arrival to altitudes between 2808 m and 5072 m. Oxygen saturation decreased significantly with the altitude increasing by train ascent but improved after inhalation of oxygen. Most of the older subjects tolerated their sojourn at high altitude well except one who developed angina repeatedly with a significant ST segment depression. Conclusions Coronary events and ECG signs of myocardial ischemia are rare in elderly individuals with CAD who travel from sea level to moderate altitudes of 1500m to 2800 m. Patients with CAD who are well compensated at sea level generally tolerate this moderate altitude well. However, it would be prudent for patients with CAD going to altitude above 3000 m. The patients should consult their physician before undertaking a trip to such altitude.

Background and objective Pre-operative assessment of mitral valve(MV)anatomy is essential to surgical design in patientsundergoing MV repair.Although 2-dimensional(2D)echocardiography provides precise information regarding MV anatomy,RT-3DTEE could increase the understanding of MV apparatus and individual scallop identification.We aimed to investigate the value of RT-3DTEE in MV repair. Methods RT-3DTEE was performed in six patients with mitral valve prolapse(MVP) by using Philips IE33with X7-2t probe.Preoperative RT-3DTEE studies were compared with surgical findings in patients undergoing surgical mitral valverepair,and quantitative evaluation was performed by QLab 6.0 software before and after surgicalmitralvalve repair.Results RT-3DTEE could display dynamic morphology of MV,the location of prolapse,and spatial relation to the surrounding tissue.It couldprovide surgical views of the valves and the valvular apparatus.These resuIts were consistent with surgical findings.The quantitativeevahuation before and after surgical MV repair indicated that anterolateral to posteromedial diameter of annalus.anterior to posteriordiameter of annulus,perimeter of annullus.,and area of annalus in projectionplane were significantlv smaller after operation comparedwith those before operation(P＜0.05).The length of posterior leaflet,,the area of anterior and posterior leaflet,the maximal prolapseheight,the volume of leaflet prolapse and the length of coaptation in projection planewere significantly reduced after operation(P＜0.05).Conclusion RT-3DTEE is a unique new medality for rapid and accurate evaluation of mitral valve prolapse and miwal valverepair.