As regard the correlations between ejection fraction measured by modified Simpson method as a marker of systolicheartfailure- versus other variables, there was highly significant positive correlation between ejection fraction and dyslipidemia ( r =0.315, p= 0.001), significant positive correlations between ejection fraction and hypertension ( r = 0.251, p = 0.012). Also there was no significant correlation between systolicheartfailure and both HbA1C (r=0132, p=0 .189) and HOMA-IR (r=0.073, p=0.470) respectively. Conclusions: We conclude that in non-diabetic patients with CAD, HbA1c above the cutoff point 5.5% can predict an increasing severity of the coronary artery disease and the number of the affected coronary arteries.
cigarette is of the critical risk factors in developing heartfailure. Evidence showed that smoking heartfailure patients had lower life quality compared to those who did not smoke (23). In preventive part of self-care behaviors, vaccination against Pneumo coccal and influenza was recommended (15) because of exacerbating heartfailure symptoms after being affected by respiratory diseases like influenza and pneumonia (11). Despite the major role of self- care behaviors in preventing problems and serious outcomes of heartfailure patients, the patients' adherence is poor. The results of Ngoc Huyen's study in 2011 also indicated that 50.9 % of heartfailure patients had poor level of self-care (24). The results of Shojaei's survey also implied that only 26 % of the patients had good self-care behaviors, and three fourth of them adhered to these behaviors poorly (22). To boost life quality, decreasing mortality and rehospitalization of heartfailure patients in hospital, the awareness of and adherence to self-care behaviors are necessary. Comprehensive recognition of self-care requirements and adherence to them by the patient hasan effective role in designing and providing self-care plan. So, the present study has been conducted to determine the rate of adherence to self-care behaviors in systolicheartfailure patients hospitalized in Alborz Social Security Hospital of Karaj and Shahryarduring 2012-2013.
Heartfailure is a major health burden, affecting 40 million people globally. One of the main causes of systolicheartfailure is dilated cardiomyopathy (DCM), the leading global indication for heart transplantation. Our understanding of the genetic basis of both DCM and systolicheartfailure has improved in recent years with the application of next-generation sequencing and genome-wide association studies (GWAS). This has enabled rapid sequencing at scale, leading to the discovery of many novel rare variants in DCM and of common variants in both systolicheartfailure and DCM. Identifying rare and common genetic variants contributing to systolicheartfailure has been challenging given its diverse and multiple etiologies. DCM, however, although rarer, is a reasonably specific and well-defined condition, leading to the identification of many rare genetic variants. Truncating variants in titin represent the single largest genetic cause of DCM. Here, we review the progress and challenges in the detection of rare and common variants in DCM and systolicheartfailure, and the particular challenges in accurate and informed variant interpretation, and in understanding the effects of these variants. We also discuss how our increasing genetic knowledge is changing clinical management. Harnessing genetic data and translating it to improve risk stratification and the development of novel therapeutics represents a major challenge and unmet critical need for patients with heartfailure and their families.
infarction (AMI) which showed that the TESI seems to be a superior route of delivery . In this research, the MSC infusion with TESI has a significant benefit to the end points, the infarct size and LVEF, while the MSC in- fusion with intracoronary injection did not. The poten- tial reasons may be that even though coronary intervention performed timely when AMI happens, the myocardium hardly received complete reperfusion due to microcirculation dysfunction which may be a major threshold for MSCs . Moreover, the acute ischemic re- gion in ventricle has abnormal microenvironment which may active apoptosis of MSCs . TESI can selectively deliver the MSCs to the non-infarcted region avoiding the obstacles in coronary artery microcirculation. However, in non-ischemic cardiomyopathy, the coronary perfusion was almost normal so that intracoronary injection may be more efficient. Besides, in chronic ICM, there was no cor- onary microembolisation caused by acute thrombosis and plaque rupture theoretically. In addition, the long-term is- chaemia results in the improvement of coronary artery collateral circulation . Furthermore, with the progress of ICM, the general remodelling and fibrotic substrate may adverse to the survival and functioning of MSCs in the myocardium which could limit the advantage of TESI. It indicated that the optimal route of delivery of MSCs for different heart disease may be various.
Results: In patients with HF, internality was similar to values obtained by patients with diabetes, men after myocardial infarction, and women after mastectomy; and was lower than in healthy subjects. Powerful others externality was more pronounced in patients with HF as compared to other groups of patients and healthy people. Only women after mastectomy had higher scores of PHLC. In patients with HF, chance externality was similar to values reported in patients with renal failure, men after myocardial infarction, and women after mastectomy; and was less pronounced than in healthy subjects. The majority (77%) of patients with HF were characterized by a high sense of self-efficacy (.the 7th sten score), having the highest sense of self-efficacy among patients with other chronic diseases and healthy controls. Higher internality was accompanied by higher sense of self-efficacy (P , 0.05) in patients with HF. Subjects with high plasma N-terminal pro-B type natriuretic peptide (reflecting the disease severity) had the least pronounced internality (P , 0.05), whereas those with more advance depressive symptoms had the lower sense of self-efficacy (P = , 0.05).
Exercise capacity is reduced in patients with HF and has been shown to outperform traditional markers of heartfailure prognosis (Myers et al. 2002, O’Connor et al. 2012). Treadmill stress test protocols such as the Bruce protocol and Naughton protocol can be used to assess exercise capacity. The Bruce protocol is carried out by walking on a treadmill. The initial speed of the treadmill is set to 2.7 km/h and the incline is set to 10%. After every 3 minutes, the end of one stage, both the speed and inclination of the treadmill is increased. The test is generally stopped when ECG machine shows abnormal changes or when a patient reaches his peak heart rate. Patients’ heart rates and perceived exertion are taken every minute. Blood pressure is taken at the end of each stage. The Naughton protocol is less intense compared to the Bruce protocol. It begins with a two minute warm up with the treadmill set to 1.6 km/h and the incline is set to 0%. The treadmill is subsequently set to 3.2 km/h and does not change for the remainder of the test. The incline increases by 3.5% every two minutes.
In animal models of HF and HF patients reduced myocardial antioxidant activity, increased oxidant damage and markers of oxidative stress increased.  The Thesis that reactive oxygen species (ROS) may contribute to the progression of myocardial failure support by these data. The potential stimuli for production of ROS in HF is Xanthine oxidase (XO) and may be an important target for therapy.  production of superoxide and uric acid (UA) Increased during purine metabolism in HF is associated with an increase in the activity of XO. 25% of patients with HF and reduced ejection fraction have significant hyperuricemia (i.e., serum UA ≥ 9.5 mg/dl). ,
authors (MM, SM) for the presence of heart, pulmonary, and pleural abnormalities. On the postero-anterior view, we also measured the cardiothoracic ratio. This was regarded as abnormal if >0.5. We measured the circu- lating levels of hemoglobin, creatinine, and N-terminal pro-hormone of B-type natriuretic peptide (NT-proBNP). The latter was measured by an electrochemiluminescent sandwich immonoassay using Elecsys 2010 analyser (Roche Diagnostics, Germany) . Medications pre- scribed at the time of hospital discharge were also recorded.
Numerous studies have attempted to understand the fac- tors that contribute to loss of pulmonary function in HF. Heart size has been found to be a significant factor accounting for loss of lung volume (Olson et al. 2007). We hypothesized that airway structure would also change with the development of HF and increased EVLW. Specif- ically, we hypothesized that HF (associated with increased pulmonary wedge pressure) leading to vascular engorge- ment of the bronchial circulation within the bronchiole walls would cause thickening of the airway walls and a subsequent decrease in luminal areas. Previous work has suggested that the bronchial circulation is contained within the airway wall, and its modulation can improve exercise capacity in individuals with HF (Cabanes et al. 1989; King et al. 2002). Interestingly, we found that HF patients maintained airway wall thickness and luminal areas similar to control subjects, at least through six air- way generations from the trachea (Figs 2 and 3).The lack of change in the wall thickness suggests that the bronchial circulation is not expanded in this population. Previous studies in humans and animals after rapid fluid loading have shown increased wall thicknesses and decreased luminal areas, especially in smaller airways (Michel et al. 1986, 1987; Brown et al. 1995; King et al. 2002). How- ever, one study found changes in respiratory bronchioles and bronchioles, but not in bronchi after rapid fluid loading in dogs, and a study in humans found changes in airway wall thickness and luminal areas in only some
Background: Chronic obstructive pulmonary disease (COPD) is an important differential diagnosis in heartfailure (HF). However, routine use of spirometry in outpatient HF clinics is not implemented. The aim of the present study was to determine the prevalence of both airflow obstruction and non obstructive lung function impairment in patients with HF and to examine the effect of optimal medical treatment for HF on lung function parameters. Methods: Consecutive patients with HF (ejection fraction (EF) < 45%) and New York Heart Association (NYHA) functional class II-IV at 10 different outpatient heartfailure clinics were examined with spirometry at their first visit and after optimal medical treatment for HF was achieved. airflow obstruction was classified and graded according to the GOLD 2011 revision.
Continuous variables with a normal distribution are expressed as mean ± standard deviation (SD). To com- pare numerical data between two groups, paired and unpaired Student t-test was used when appropriate. Nominal variables were compared using either the χ 2 or Fischer tests when appropriate. Univariate analysis of the predictive factors of cardiovascular event was performed using respectively log rank and cox methods for qualitative and quantitative variables. Kaplan Meier curve and log mantel cox method were used to illus- trate prognosis of high and low level of systolic BP and VBP. Variables from the univariate analysis with P < 0.1 were included in the multivariable stepwise analysis to identify independent predictors of events. Two-tailed P-values <0.05 were considered statistically significant.
chronic renal disease, valvular heart disease, glycosylated hemoglobin and Hs-CRP were closely associated with SHF morbidity, however, ADRB1 and GRK5 variants did not present significantly independently associated with the risk of SHF morbidity (see Table 2). Furthermore GRK5 and ADRB1 polymorphisms did not present sig- nificantly difference between non-SHF group and SHF group (see Table 3). Importantly, the two functional β- adrenergic receptor signaling polymorphisms in our population showed not significantly different of genotype frequency distribution and allele frequency distribution between non-SHF group and SHF group, thus this study suggested that GRK5 and ADRB1 polymorphisms did not induce the risk of SHF morbidity.
Recent studies have indicated that more than half patients diagnosed with HF even though ejection fraction (EF) is normal or near normal  . This clinical condition is termed as “heartfailure with normal ejection fraction” (HFnEF) or “diastolic heartfailure” (DHF). It is characterized by the evidence of diastolic dysfunction (e.g., impaired LV relaxation, abnormal left ventricular filling and elevated filling pressure). There has been substantial progress in the treatment of systolicheartfailure (SHF). However, very little progress has been made in the management of DHF. The mortality due to DHF is 8% to 9% per year which is about the half of the SHF but the morbidity, hospitalisation rates and healthcare costs per patient are almost similar to those of SHF .
The ultimate treatment for heartfailure with reduced systolic function is a left ventricular assist device or heart transplantation, which is practically never utilized in heartfailure with normal systolic function, except for specific cases of restrictive or hypertrophic obstructive cardiomyopathy. It is likely that, at some point in time, left ventricular dilata- tion and remodeling reaches a critical limit and becomes the driving force of the downward spiral of terminal heartfailure. The angiotensin-converting enzyme inhibitors and beta-blockers work in systolicheartfailure because they slow down and partially reverse left ventricular remodeling. Without such remodeling, as in heartfailure with preserved systolic function, they do not have a substrate to work on. All clinical trials testing drugs used successfully in reduced ejection fraction failed to demonstrate their benefit in the subset with preserved systolic function. The difference in morbidity and mortality between heartfailure with preserved and reduced ejection fraction measures the contribution of the low output syndrome, together with electric instability created by left ventricular remodeling, to the natural course of heartfailure.
Overactivation of the renin angiotensin-II aldosterone system (RAAS) occurs in diabetic cardiomyopathy resulting in cardiac insulin resistance and a cascade of abnormalities mediated by angiotensin II and aldoster- one (Figure 1). Aldosterone plays an important role in promoting fibrosis by stimulating fibroblast proliferation and collagen synthesis, triggering proinflammatory fac- tors leading to activation of matrix metalloproteinases (MMPs), and increasing transforming growth factor-β (TGF-β) . Aldosterone antagonism has been shown to improve symptoms and outcomes in advanced systolicheartfailure and after acute myocardial infarction (AMI). Attenuation of the excessive ECM turnover by aldosterone antagonism was suggested as one of the mechanisms underlying its beneficial effects in systolicheartfailure [10,11]. The beneficial effects of aldosterone antagonism on myocardial fibrosis may help to explain the impressive improvement in patient outcomes in systolicheartfailure and after AMI despite only modest improvement in left ventricular (LV) ejection fraction.
Background: Noninvasive assessment of diastolic filling by Doppler echocardiography provides important information about left ventricular (LV) status in selected subsets of patients. This study was designed to assess whether the lateral mitral annular velocity as assessed by tissue Doppler imaging is associated with invasive measures of diastolic LV performance in patients with diastolic and systolicheartfailure. Aim of the study was to compare the diagnostic accuracy of lateral mitral annular E/E′ as an estimate of LV filling pressure with invasive LVEDP measurement in subjects with systolic or purely diastolic heartfailure.
Lim et al.  have demonstrated a strong predictive value of longitudinal speckle tracking strain for predicting response to CRT in both ischemic and non-ischaemic patients, as mentioned previously. Donal et al.  as- sessed longitudinal and radial dyssynchrony in ischemic and non-ischaemic chronic systolicheartfailure in 95 consecutive patients and suggested that the profile of dyssynchrony is influenced by the underlying cause of HF, and that assessment of radial, instead of longitudinal, deformation might be relevant for CRT selection of pa- tients with ischaemic aetiology. The two different aetiologies resulted in different electromechanical correlates. Electrical and mechanical dyssynchrony correlated homogeneously in patients with non-ischaemic heartfailure considering radial and longitudinal strain. In ischaemic heartfailure radial dyssynchrony was the best mechani- cal index that correlated with QRS duration.
Patients with systolic left ventricular dysfunction die progressively from congestive heartfailure or die suddenly from cardiac arrhythmias. Myo- cardial hypertrophy is an early event in most forms of heartfailure, but the majority of patients with myocardial hypertrophy do not develop heartfailure. Developing improved therapies for targeting the cell signaling pathways that enable this deadly transition from early myocardial insult to heartfailure and sudden death is a key goal for improving public health. In this issue of the JCI, Ling and colleagues provide new evidence that acti- vation of the multifunctional Ca 2+ /calmodulin–dependent kinase IIδ is a
Data are presented as medians (lower quartile – upper quartile), numbers (percentages), and means with stand- ard deviations (range), as appropriate. Inter-observer vari- ability of echocardiographic parameters was determined by the intra-class correlation coefficient, Pearson’s correl- ation coefficient and Bland-Altman plots . Reliability analyses using kappa statistics were performed to deter- mine consistency between observers regarding the pres- ence or absence of diastolic or systolic dysfunction. The kappa value for agreement was interpreted as follows: poor <0.20, fair, 0.21 – 0.40; moderate, 0.41 – 0.60; good, 0.61 – 0.80; and very good, 0–81 – 1.0 . Intra-observer repeatability was calculated using intra-class correlation coefficient. All probability values are two-tailed and sig- nificance was set at p < 0.05. All statistical analyses were performed using IBM SPSS v22.0 (IBM Corp, Armonk, NY, USA).