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.

BackgroundCalcific aortic stenosis (AS) is an active process sharing similarities with atherosclerosis and chronic inflammation. The pathophysiology of AS is notable for three cardinal components: inflammation, fibrosis and calcification. Monocytes play a role in each of these processes. The role of circulating monocytes in AS is not clear. The aim of the present study was to study an association between cir-culating apoptotic and non apoptotic CD14+ monocytes and AS features.MethodsWe assessed the number of CD14+ monocytes and apoptotic monocytes in 54 patients with significant AS (aortic valve area 0.74 ± 0.27 cm2) and compared them to 33 patients with similar risk factors and no valvular disease. The level of CD14+ monocytes and apoptotic monocytes was assessed by flow cytometry.ResultsThere was no difference in the risk factor profile and known coronary or peripheral vascular diseases between patients with AS and controls.Pa-tients with AS exhibited increased numbers of CD14+ monocytes as compared to controls (9.9% ± 4.9%vs. 7.7% ± 3.9%,P= 0.03). CD14+ monocyte number was related to age and the presence and severity of AS. In patients with AS, both CD14+ monocytes and apoptotic mono-cytes were inversely related to aortic valve area.ConclusionsPatients with significant AS have increased number of circulating CD14+ monocytes and there is an inverse correlation between monocyte count and aortic valve area. These findings may suggest that inflammation is operative not only in early valve injury phase, but also at later developed stages such as calcification when AS is severe.

Background One of the major challenges in arrhythmogenic right ventricular cardiomyopathy (ARVC) ablation is ventricular tachy-cardia (VT) non-inducibility. The study aimed to assess whether fast rate (≥ 250 beats/min) right ventricular burst stimulation was useful for VT induction in patients with ARVC.Methods Ninety-one consecutive ARVC patients with clinical sustained VT that underwent electro-physiological study were enrolled. The stimulation protocol was implemented at both right ventricular apex and outflow tract as follows: Step A, up to double extra-stimuli; Step B, incremental stimulation with low rate (< 250 beats/min); Step C, burst stimulation with fast rate (≥ 250 beats/min); Step D, repeated all steps above with intravenous infusion of isoproterenol.Results A total of 76 patients had inducible VT (83.5%), among which 49 were induced by Step C, 15 were induced by Step B, 8 and 4 by Step A and D, respectively. Clinical VTs were induced in 60 patients (65.9%). Only two spontaneously ceased ventricular fibrillations were induced by Step C. Multivariate analysis showed that a narrower baseline QRS duration under sinus rhythm was independently associated with VT non-inducibility (OR: 1.1; 95% CI: 1.0–1.1;P = 0.019).ConclusionFast rate (≥ 250 beats/min) right ventricular burst stimulation provides a useful supplemental method for VT induction in ARVC patients.