Ischemic Arrhythmias Research Articles

Soluble epoxide hydrolase inhibitors, t-AUCB, regulated microRNA-1 and its target genes in myocardial infarction mice.

PurposeSoluble epoxide hydrolase inhibitors (sEHIs) had been demonstrated to produce cardioprotective effects against ischemia-induced lethal arrhythmias, but the exact mechanisms remain unknown. The present study was designed to investigate whether the beneficial effects of sEHIs are related to regulation of microRNA-1, which was a proarrhythmic factor in the ischemic heart.MethodsA mousemyocardial infarction (MI) model was established by ligating the coronary artery. sEHI t-AUCB (0.2, 1, 5 mg/L in drinking-water) was administered daily seven days before MI. The incidence of arrhythmias was assessed by in vivo electrophysiologic studies. miR-1, KCNJ2 (encoding the K+ channel subunit Kir2.1), and GJA1 (encoding connexin 43 [Cx43]) mRNA were measured by real-time PCR; Kir2.1 and Cx43 protein were assessed by western blotting and immunohistochemistry.ResultsWe demonstrated that sEHIs reduced the myocardium infarct size and incidence of inducible arrhythmias in MI mice. Up-regulation of miR-1 and down-regulation of KCNJ2/Kir2.1 and GJA1/Cx43 mRNA/protein were observed in ischemic myocaridum, whereas administration of sEHIs produced an opposite effect. In addition, miR-1 overexpression inhibited expression of the target mRNA and their corresponding proteins, whereas t-AUCB reversed the effects. Our results further revealed that PI3K/Akt signaling pathway might participate in the negatively regulation of miR-1 by sEHi.ConclusionsWe conclude that sEHIs can repress miR-1, thus stimulate expression of KCNJ2/Kir2.1 and GJA1/Cx43 mRNA/protein in MI mice, suggesting a possible mechanism for its potential therapeutic application in ischemic arrhythmias.

The Effect of Velvet Antler Proteins on Cardiac Microvascular Endothelial Cells Challenged with Ischemia-Hypoxia.

Velvet antler (VA) is a precious traditional Chinese medicine that is capable of repeated regeneration. Based on the Chinese medicine theory of coordination the heart and kidneys, VA has been employed to treat heart diseases, including ischemic heart disease, heart failure, and arrhythmia. We examined the effects of VA proteins on primary cardiac microvascular endothelial cells (CMECs) that were subjected to ischemia-hypoxia (IH) to investigate their effects on and mechanism of action in the treatment of ischemic heart disease. Velvet antler proteins (VA-pro) were extracted with water as the solvent, the ultrasonic wave method, and freeze-drying technology; then it was analyzed by Nano LC-MS/MS. In addition, the role of VA-pro in cell viability, proliferation, apoptosis, and mitochondrial membrane potential (MMP) were evaluated by the MTS assay, the EdU assay, the Annexin V-FITC/PI double-staining assay, and the JC-1 assay, respectively. Cell migration were evaluated by the scratch assay and the Transwell assay. The expression of apoptosis-associate proteins, Akt and p-Akt, and tube formation in Matrigel of CMECs were also detected. In total, 386 VA-pro were identified. Our results showed that IH significantly reduced the viability of the CMECs (P < 0.001) and suppressed copies of DNA to hold back CMEC proliferation (P < 0.001). The OD of control group was 1.81 ± 0.08 and IH group OD was 1.25 ± 0.03. After suffering with IH for 46 h, CMECs were 75% less likely to migrate (P < 0.001), and its tubule formation ability and MMP were also decreased (P < 0.001). VA-pro treatment resulted in an improvement in CMECs’ viability and proliferation (P < 0.001). Such as, the OD of 0.5, 1, and 2 mg/ml rose to 1.56 ± 0.5, 1.74 ± 0.1 and 1.65 ± 0.1, respectively. Similarly, CMECs’ migration (for the scratch assay P < 0.001, for the Transwell assay P < 0.05) and tubule formation (P < 0.05) ability were better after treated with VA-pro. At the same time, the stability of MMP was retained preferably (P < 0.001). 50% apoptosis was induced after CMECs were cultured in IH conditions (P < 0.001), while VA-pro decreased the number of apoptotic cells (P < 0.001). All above results showed that 1 mg/ml VA-pro produced maximum results. Furthermore, the expression of pro-apoptosis proteins was higher, but the expression of anti-apoptosis proteins was lower in the IH group (P < 0.05); VA-pro reversed these changes (P < 0.001). These findings suggest that VA-pro ameliorate CMEC injuries induced by IH via regulating the PI3K/Akt signaling pathway.

Prévalence du syndrome exfoliatif et profil cardiovasculaire des patients programmés pour chirurgie de cataracte

To study the prevalence of exfoliation syndrome (XFS) and its association with cardiovascular disease in patients scheduled for cataract surgery. This is a retrospective, single center, descriptive study of 260patients admitted to a tertiary teaching hospital in Rabat, Morocco, between January 2015and March 2016and scheduled for cataract surgery. All patients had a preoperative cardiovascular exam, an electrocardiogram and, if needed, echocardiography. Statistical analysis was performed using SPSS software. Results with a P-value<0.05were considered statistically significant. This study included 246patients: 146women (59.3%) and 100men (40.7%). The mean age (years) was 67.6±10.1. The percentage of XFS increased with age (P=0.02). Sixty-two percent of patients with cardiovascular disease also had exfoliation syndrome (P<0.001). Patients with XFS had hypertension in 46.5% of cases. 14subjects (19.7%) had ischemic heart disease and XFS. Using multivariate logistic regression and after adjusting for age, diabetes mellitus, hypertension, ischemic heart disease and arrhythmias, smoking was the only factor associated with exfoliation syndrome (P=0.01, odds ratio=5.2, confidence interval 95%=1.35-20.15). Exfoliation syndrome is a common condition in the aging cataract population. Ischemic heart disease and hypertension are frequently associated with XFS. Smoking could be another factor associated with this syndrome.

Effectiveness and safety of concurrent beta-blockers and inhaled bronchodilators in COPD with cardiovascular comorbidities.

Chronic obstructive pulmonary disease (COPD) is the most common chronic respiratory disease and its prevalence is increasing worldwide, in both industrialised and developing countries. Its prevalence is ∼5% in the general population and it is the fourth leading cause of death worldwide. COPD is strongly associated with cardiovascular diseases; in fact, ∼64% of people suffering from COPD are treated for a concomitant cardiovascular disease and approximately one in three COPD patients die as a consequence of cardiovascular diseases.Inhaled bronchodilators might have adverse cardiovascular effects, including ischaemic events and arrhythmias, and beta-blockers might adversely influence the respiratory symptoms and the response to bronchodilators. For these reasons, it is important to know the safety profiles and the possible interactions between these two classes of drug, in order to prescribe them with greater awareness.In this article, we review the literature about the epidemiology of COPD, its association with cardiovascular diseases, and the safety of concurrent use of inhaled bronchodilators and beta-blockers, as a tool for improving the approach to complex therapies in clinical practice.

P805Increased threshold of calcium alternans caused by proinflammatory cytokine: possible mechanism of ischemic ventricular arrhythmia

P805Increased threshold of calcium alternans caused by proinflammatory cytokine: possible mechanism of ischemic ventricular arrhythmia

Cardiac disease and advanced age increase the mortality risk following surgery for periprosthetic femoral fractures.

Periprosthetic fracture is a significant complication of total hip and knee arthroplasty. This study aimed to describe the survival of patients sustaining periprosthetic femoral fractures and compare this with that of the general population, as well as to identify the factors that influence survival. A total of 151 patients (women: men 116:35, mean age 74.6 years, standard deviation 11.5) that sustained a periprosthetic fracture between January 2005 and October 2012 were retrospectively analysed. Epidemiological data, comorbidities, type of surgical management, type of implant, and mortality data were studied. The mean survival time was 77 months (95% confidence interval 71 to 84; numbers at risk: 73) and was lower than that of the general population. The risk analyses showed that previous cardiac disease, particularly ischaemic heart disease, cardiac arrhythmias, and heart failure, age over 75 years and American Society of Anesthesiologists (ASA) scores above 3 were associated with a significantly higher mortality. Periprosthetic fractures carry a high risk of post-operative mortality. Our data demonstrate that advanced age (> 75 years) and previous cardiac disease are associated with a significantly higher risk of mortality. The ASA score is an appropriate instrument for risk stratification. Pre-operative cardiac status should be optimised before surgery. Cite this article: Bone Joint J 2017;99-B:921-6.

Early regional wall distension is strongly associated with vulnerability to ventricular fibrillation but not arrhythmia triggers following coronary occlusion in vivo

Wall stress may favor ischemic ventricular arrhythmias, yet its association with ventricular fibrillation (VF) or ventricular ectopy has been inconsistent among studies and its potential arrhythmogenicity across the cardiac cycle is unclear. In 91 open-chest pigs undergoing 40–50 min left anterior descending artery occlusion, we assessed the association between diastolic or systolic distension of the ischemic area and the incidence of ventricular premature beats (VPBs) and VF. End-diastolic segment length (EDL) and systolic bulging ([maximum systolic length–EDL] × 100/EDL) were measured by ultrasonic crystals. Fifteen minutes after occlusion, EDL increased to 112.7 ± 5.6% of baseline (P < 0.001) and systolic bulging averaged 3.4 ± 2.2%. Median VPB number was 52 (IQR, 16–110), 2 (0–7) in phase Ia and 49 (13–94) in phase Ib. VF occurred in 26 animals (28.6%), the first episode appearing 24 ± 6 min after occlusion. EDL increase was associated with subsequent VF (115.9 ± 5.7 and 111.4 ± 5.1% in animals with and without VF, P < 0.001) and with the number of VF episodes (P = 0.001) but not with VPB number, overall (r = 0.028, P = 0.801) or in phases Ia or Ib. Systolic bulging was related neither to VF occurrence (3.2 ± 2.2 and 3.5 ± 2.2%, respectively, P = 0.561) nor to VBP number (r = 0.095, P = 0.397). EDL increase predicted VF after adjusting for ischemic area size and K+ levels (odds ratio for 1% increase: 1.17, 95%CI 1.06–1.29, P = 0.001). Thus, diastolic regional ventricular distension predicts VF occurrence after coronary occlusion whereas neither diastolic nor systolic distension is associated with ventricular ectopy, which suggests that distension favors VF by acting on the arrhythmic substrate but not on arrhythmia triggers.

Safety and tolerability of oral hypoglycemic therapies in type 2 diabetes mellitus patients at high cardiovascular risk

Oral hypoglycemic drugs for type 2 diabetes aim at preventing the metabolic effects of hyperglycemia and cardiovascular (CV) events. The evidence of the possible CV risk related to the prescription of some antidiabetic drugs prompted regulatory agencies to require safety studies. This review provides an updated analysis of CV safety profiles for antidiabetic drugs used for the treatment of patients with high CV risk.The most recent studies analyze different aspects of CV morbidity, such as ischemic events, heart failure and arrhythmia, and their interactions with hyperglycemia. The endpoints include major adverse cardiovascular events (CV mortality, myocardial infarction, stroke) and hospitalization for heart failure. There is extra-and intra-class variability of CV risk among different oral hypoglycemic drugs, including sulfonylureas, metformin, glitazones, glucagon-like peptide-1 analogues, dipeptidyl peptidase-4 inhibitors and sodium-glucose cotransporter 2 inhibitors. Different treatment settings, selectivity towards pharmacological targets and hypoglycemia-related effects may explain the discrepancies observed.This review may guide cardiologists and diabetologists, in collaboration with general practitioners, to make the most appropriate therapeutic decision fitting the characteristics of the individual diabetic patient.

The IK1/Kir2.1 channel agonist zacopride prevents and cures acute ischemic arrhythmias in the rat.

Arrhythmogenesis in acute myocardial infarction (MI) is associated with depolarization of resting membraine potential (RMP) and decrease of inward rectifier potassium current (IK1) in cardiomyocytes. However, clinical anti-arrhythmic agents that primarily act on RMP by enhancing the IK1 channel are not currently available. We hypothesized that zacopride, a selective and moderate agonist of the IK1/Kir2.1 channels, prevents and cures acute ischemic arrhythmias. To test this viewpoint, adult Sprague-Dawley (SD) rats were subjected to MI by ligating the left main coronary artery. The antiarrhythmic effects of zacopride (i.v. infusion) were observed in the settings of pre-treatment (zacopride given 3 min prior to coronary occlusion), post-treatment (zacopride given 3 min after coronary occlusion) and therapeutic treatment (zacopride given 30 s after the onset of the first sustained ventricular tachycardia (VT)/ventricular fibrillation (VF) post MI). In all the three treatment modes, zacopride (15 μg/kg) inhibited MI-induced ventricular tachyarrhythmias, as shown by significant decreases in the premature ventricular contraction (PVC) and the duration and incidence of VT or VF. In Langendorff perfused rat hearts, the antiarrhythmic effect of 1 μmol/L zacopride were reversed by 1 μmol/L BaCl2, a blocker of IK1 channel. Patch clamp results in freshly isolated rat ventricular myocytes indicated that zacopride activated the IK1 channel and thereby reversed hypoxia-induced RMP depolarization and action potential duration (APD) prolongation. In addition, zacopride (1 μmol/L) suppressed hypoxia- or isoproterenol- induced delayed afterdepolarizations (DADs). In Kir2.x transfected Chinese hamster ovary (CHO) cells, zacopride activated the Kir2.1 homomeric channel but not the Kir2.2 or Kir2.3 channels. These results support our hypothesis that moderately enhancing IK1/Kir2.1 currents as by zacopride rescues ischemia- and hypoxia- induced RMP depolarization, and thereby prevents and cures acute ischemic arrhythmias. This study brings a new viewpoint to antiarrhythmic theories and provides a promising target for the treatment of acute ischemic arrhythmias.

Roles of autophagy in cardiovascular diseases: research progression

The morbidity and mortality of cardiovascular diseases(CVD)are still high in our country, they severely threaten peopleS health and quality of life.A dysregulated or reduced autophagy is associated with ischemic heart disease, cardiac hypertrophy, heart failure and arrhythmia.Autophagy is a key regulator in CVD development, and is essential for maintenance of heart function and improvement of prognosis.Thus, modulating autophagy represents an attractive future therapeutic target for treating cardiovascular disease.This article reviewed the research progression about effects of autophagy on ischemic heart disease, cardiac hypertrophy, heart failure and arrhythmia. Key words: Cardiovascular diseases; Autophagy

Rat Models of Ventricular Fibrillation Following Acute Myocardial Infarction.

A number of animal models have been designed in order to unravel the underlying mechanisms of acute ischemia-induced arrhythmias and to test compounds and interventions for antiarrhythmic therapy. This is important as acute myocardial infarction (AMI) continues to be the major cause of sudden cardiac death, and we are yet to discover safe and effective treatments of the lethal arrhythmias occurring in the acute setting. Animal models therefore continue to be relevant for our understanding and treatment of acute ischemic arrhythmias. This review discusses the applicability of the rat as a model for ventricular arrhythmias occurring during the acute phase of AMI. It provides a description of models developed, advantages and disadvantages of rats, as well as an overview of the most important interventions investigated and the relevance for human pathophysiology.

Renal sympathetic stimulation and ablation affect ventricular arrhythmia by modulating autonomic activity in a cesium-induced long QT canine model

Our previous studies showed that renal sympathetic stimulation (RS) may facilitate ischemic ventricular arrhythmia (VA) by increasing left stellate ganglion (LSG) nerve activity, whereas renal sympathetic ablation (RA) may suppress VA. The purpose of this study was to investigate whether renal sympathetic interventions also can affect VA by modulating LSG activity in a cesium-induced long QT canine model. Twenty-four dogs were randomly divided into RS group (n = 8), RA group (n = 8), or control group (n = 8). Serum norepinephrine, LSG function, and LSG neural activity were measured before and 3 hours after RS or RA. Increasing doses of cesium chloride then were administered until a "threshold dose" produced sustained ventricular tachycardia or ventricular fibrillation. Early afterdepolarization amplitude, VA prevalence, and tachycardia threshold dose were compared among these groups. Nerve growth factor and c-fos protein expressed in the LSG also were examined. Serum norepinephrine, LSG function, and LSG neural activity were all significantly increased after 3 hours of RS and all were decreased 3 hours after RA. In addition, RS significantly decreased the tachycardia threshold dose, increased the early afterdepolarization amplitude, facilitated the incidence of VAs, and increased the expression of nerve growth factor and c-fos protein. In contrast, RA induced the opposite effects. RS promotes, whereas RA suppresses, the incidence of VAs in a canine model of cesium-induced long QT. Modulation of LSG neural activity by RS and RA may be responsible for these different effects.

Abstract 162: Processes of Care that are Associated With Reduced Risk of Recurrent Vascular Events Among Patients With a Transient Ischemic Attack and Minor Stroke

Background: Interventions that emphasize early evaluation and management of patients with TIA and minor stroke have demonstrated reductions in recurrent vascular events. Objective: To identify processes of care that were associated with reduced risk of recurrent vascular events after TIA or minor stroke. Methods: We identified patients with a TIA or minor stroke cared for in a Department of Veterans Affairs (VA) Emergency Department or inpatient ward (fiscal year 2011). Recurrent vascular events included ischemic stroke, myocardial infarction, heart failure, arrhythmia or death within 90-days and 1-year of discharge. 32 processes of care were examined. Defect-free care was assessed for a set of 6 processes (brain imaging, carotid artery imaging, hypertension management, high or moderate potency statin, antithrombotics, and anticoagulation for atrial fibrillation); patients who received all processes for which they were eligible passed the defect-free measure. Multivariable logistic regression with a random facility effect was used to model recurrent events. Clinically important potential confounders were forced into all models; other significant covariates were identified by backward selection. Results: Among 8107 patients, 14.0% had a recurrent vascular event within 90-days; 26.5% within 1-year. Three processes were associated with lower 90-day events after adjustment for 24 covariates: carotid artery imaging (adjusted OR, 0.74 [95%CI, 0.65-0.85], lipid measurement (0.80 [0.68-0.94]), and anticoagulation quality for atrial fibrillation (0.56 [0.35-0.88]). Three processes were associated with reduced 1-year events: carotid artery imaging (0.80 [0.71-0.89]), lipid measurement (0.85 [0.75-0.97]), and timely carotid stenosis intervention (0.49 [0.26-0.94]). The defect-free care rate, observed in 17.4%, was also associated with a reduction in recurrent vascular event risk both within 90-days (0.78 [0.65-0.93]) and 1-year (0.82 [0.71-0.94]). Conclusions: The delivery of a comprehensive set of clinical processes was associated with clinically meaningful reductions in short and longer-term risk of recurrent vascular events. Widespread implementation of these processes should be strongly considered.

Znaczenie wskaźnika neutrofilowo-limfocytowego w chorobach układu sercowo-naczyniowego

Choroby ukladu sercowo-naczyniowego (CVD) wciąz są najczestszą przyczyną umieralności. Istotną role w rozwoju tych chorob odgrywa stan zapalny niskiego stopnia. Jednym z wyznacznikow takiego stanu jest wskaźnik neutrofilowo-limfocytowy (NLR). Określa sie go jako iloraz liczby granulocytow obojetnochlonnych i limfocytow. Prawidlowa wartośc NLR pozostaje nieznana. Wartości prawidlowe i patologiczne zalezą od jednostki chorobowej. Udowodniono istotne znaczenie NLR w niektorych CVD, takich jak choroba niedokrwienna serca, zaburzenia rytmu serca, nadciśnienie tetnicze. W tych jednostkach chorobowych NLR stanowi istotny czynnik predykcyjny miedzy innymi gorszego rokowania, krotszego czasu przezycia oraz wystąpienia groźnych dla zycia zaburzen rytmu. Szerokie rozpowszechnienie CVD, takze w populacji osob mlodych, jest przyczyną poszukiwania nowych, tanich i latwo dostepnych metod wykrywania tych chorob.

Soluble epoxide hydrolase inhibitors might prevent ischemic arrhythmias via microRNA-1 repression in primary neonatal mouse ventricular myocytes.

Ischemic arrhythmias are the main causes of sudden cardiac death. It has been reported that soluble epoxide hydrolase inhibitors (sEHis) could prevent arrhythmias; however, the underlying molecular mechanisms remain unclear. In recent years, the proarrhythmic role of microRNA-1 (miR-1) has been investigated. This study aimed to elucidate whether sEHis prevented ischemic arrhythmias by suppressing miR-1. The primary neonatal mouse ventricular myocyte model of miR-1 overexpression was established by incubating with agonist microONTM mmu-miR-1a-3p agomir (DAEDstainTM Dye) (agomiR-1). The sEHi, trans-4-[4-(3-adamantan-1-yl-ureido)-cyclohexyloxy]-benzoic acid (t-AUCB), was administered following miR-1 overexpression. Quantitative real-time PCR (qPCR) and western blotting were used to test alterations in the expression of miR-1 and its target mRNAs GJA1 and KCNJ2 and their respective encoded proteins connexin 43 (Cx43) and the K+ channel subunit (Kir2.1). The whole-cell patch-clamp technique was used to record the alterations of the inward rectifying K+ current (IK1). Compared with the control group, miR-1 levels were significantly increased in the agomiR-1 group (p < 0.05), which suggested the successful construction of the miR-1 overexpression model. Compared with the control group, the levels of GJA1 and KCNJ2 mRNAs and Cx43 and Kir2.1 proteins in the agomiR-1 group were significantly decreased, and IK1 was significantly impaired (all p < 0.05). The miR-1 levels were dose-dependently decreased by t-AUCB, whereas t-AUCB dose-dependently increased the levels of GJA1 and KCNJ2 mRNAs and Cx43 and Kir2.1 proteins. Furthermore, t-AUCB restored the impaired IK1 (all p < 0.05). In conclusion, the sEHi t-AUCB has the ability to down-regulate proarrhythmic miR-1 and up-regulate its target genes and proteins, eventually restoring IK1.

Prospective randomized study of the effect of nebivolol on the incidence of late invasive mechanical ventilation in ischemic heart disease patients with acute exacerbation of chronic obstructive pulmonary disease

Background Chronic obstructive pulmonary disease (COPD) is the third leading cause of death in the USA and acute exacerbations result in more than 800 000 hospitalizations annually. The combination of COPD treatment often coexists with treatment for congestive heart failure or ischemic heart disease (IHD) and present complex therapeutic challenges. β2-Agonists, which are frequently used in the treatment of COPD, have the potential for adverse cardiovascular effects including ischemic events and arrhythmias. β-Blocker therapy improves symptoms and survival among patients with IHD and congestive heart failure, but is frequently withheld in patients with COPD. During an acute exacerbation of chronic obstructive pulmonary disease (AECOPD), patients may be particularly vulnerable to develop acute cardiac events due to increased use in β2-agonists, tachycardia, and hypoxemia. The addition of a cardioselective β-blocker, especially nebivolol, may have a cardioprotective effect in this population, blunting the cardiac toxicity of the β2-agonists. We evaluated the association of the cardioselective β-blocker nebivolol treatment with the incidence of late invasive ventilation among patients with IHD who were hospitalized for an AECOPD. Hypothesizing that the nebivolol as a highly selective β-blocker is not deleterious and is safe in the setting of AECOPD, we also compared the outcomes with patients who are not treated with nebivolol in the setting of AECOPD. Objective The aim of the paper was to study the incidence of late invasive mechanical ventilation among a group of ischemic heart disease patients with AECOPD who received oral nebivolol and compare the results with another group of patients with the same diagnosis who did not receive it. Patients and methods This study was conducted on 90 adult patients of both sexes, who were admitted to the Critical Care Medicine Department of Alexandria Main University Hospital after fulfilling the inclusion and exclusion criteria and obtaining an informed consent from patients’ relatives, and from the local ethics committee. Patients were subjected to full routine examination and categorized into two groups; each group comprised 45 patients using the sealed-envelop technique as a method for randomization of participants in both groups. Group I, patients who received oral nebivolol tablets on the first and/or second day of admission. Group II, patients who did not receive oral nebivolol tablets on the first and/or second day of admission. Results In comparing the patients in both groups, there was no statistically significant difference between them with regard to age, sex, comorbidities, and Acute Physiology and Chronic Health Evaluation II score on admission. Incidence of late invasive ventilation was the same between the case and the control groups. There was no significant difference in causes of intubation between both groups. There was no statistically significant reduction in the duration of invasive ventilation, ICU and hospital stay between both studied groups. Acute ischemic events showed no statistically significant reduction between case and control groups. Regarding in-hospital and 28-day mortality, there was no statistically significant difference between both studied groups. Conclusion Our results suggest that among the studied population of patients with AECOPD with underlying coronary artery disease, using oral nebivolol tablet seems to be safe as it does not cause worsening of the clinical condition of the patients regarding the incidence of late invasive mechanical ventilation or incidence of acute ischemic events. In addition, it does not affect the duration of ICU or hospital stay and showed no effect on in hospital or 28-day mortality.

&lt;b&gt;A Single-Center Experience with Japanese Patients with Severe Ischemic Heart Failure and Arrhythmia Receiving Amiodarone &lt;/b&gt;

&lt;b&gt;A Single-Center Experience with Japanese Patients with Severe Ischemic Heart Failure and Arrhythmia Receiving Amiodarone &lt;/b&gt;

The Relationship between High Sensitive C-reaction Protein (hs-CRP) and Diastolic Heart Function in Diabetes Mellitus Type II

Among several inflammatory markers, high sensitive C-reaction protein (hs-CRP) is outstandingly observed in diabetic individuals. Serum hs-CRP is the main marker of inflammation whose levels independently predict the risk of cardiovascular events, and it has a prognostic value in heart patients. On the other hand, diabetes can lead to diastolic dysfunction of the heart. Diastolic dysfunction can cause symptoms of exertional dyspnea, which restricts the patient's activity. It is likely to predict diastolic dysfunction by screening through hs-CRP. The present investigation was a case-control study that was carried out on 52 patient diagnosed with diabetes mellitus type II. After the demographic data were recorded, and following the collection of data on the patients' history, physical examination, and para-clinical measures, individuals who had factors interfering with level of serum hs-CRP (kidney and liver diseases, inflammatory and infectious diseases, peripheral vascular disease, cerebrovascular disease, connective tissue disease, malignant tumor, trauma, consumption of statins, aspirin, ACEI, and fibrates) and diastolic dysfunction (ischemic heart disease, cardiomyopathies, pericardial disease, arrhythmias and valvular disease) were crossed out of the study. Serum hs-CRP was measured by nephelometry method. According to the results of tissue Doppler echocardiography, these patients are divided into two groups: one with diastolic dysfunction and the other without diastolic dysfunction. The serum hs-CRP levels of these patients were compared with each other. Among the participants, 30.8% were men and 69.2% were women, 36 individuals (69.2%) had diastolic dysfunction while 16 (30.8%) did not. There was a high level of correlation between the level of serumhs-CRP and diastolic dysfunction (p = 0.02, t = 2.36). The results of the present study indicated that there is a correlation between level of serum hs-CRP and diastolic dysfunction, such that the more the level of hs-CRP, the higher probability of diastolic dysfunction existence will be.

The Relationship between High Sensitive C-reaction Protein (hs-CRP) and Diastolic Heart Function in Diabetes Mellitus Type II

Among several inflammatory markers, high sensitive C-reaction protein (hs-CRP) is outstandingly observed in diabetic individuals. Serum hs-CRP is the main marker of inflammation whose levels independently predict the risk of cardiovascular events, and it has a prognostic value in heart patients. On the other hand, diabetes can lead to diastolic dysfunction of the heart. Diastolic dysfunction can cause symptoms of exertional dyspnea, which restricts the patient's activity. It is likely to predict diastolic dysfunction by screening through hs-CRP. The present investigation was a case-control study that was carried out on 52 patient diagnosed with diabetes mellitus type II. After the demographic data were recorded, and following the collection of data on the patients' history, physical examination, and para-clinical measures, individuals who had factors interfering with level of serum hs-CRP (kidney and liver diseases, inflammatory and infectious diseases, peripheral vascular disease, cerebrovascular disease, connective tissue disease, malignant tumor, trauma, consumption of statins, aspirin, ACEI, and fibrates) and diastolic dysfunction (ischemic heart disease, cardiomyopathies, pericardial disease, arrhythmias and valvular disease) were crossed out of the study. Serum hs-CRP was measured by nephelometry method. According to the results of tissue Doppler echocardiography, these patients are divided into two groups: one with diastolic dysfunction and the other without diastolic dysfunction. The serum hs-CRP levels of these patients were compared with each other. Among the participants, 30.8% were men and 69.2% were women, 36 individuals (69.2%) had diastolic dysfunction while 16 (30.8%) did not. There was a high level of correlation between the level of serumhs-CRP and diastolic dysfunction (p = 0.02, t = 2.36). The results of the present study indicated that there is a correlation between level of serum hs-CRP and diastolic dysfunction, such that the more the level of hs-CRP, the higher probability of diastolic dysfunction existence will be.

The Relationship between High Sensitive C-reaction Protein (hs-CRP) and Diastolic Heart Function in Diabetes Mellitus Type II

Among several inflammatory markers, high sensitive C-reaction protein (hs-CRP) is outstandingly observed in diabetic individuals. Serum hs-CRP is the main marker of inflammation whose levels independently predict the risk of cardiovascular events, and it has a prognostic value in heart patients. On the other hand, diabetes can lead to diastolic dysfunction of the heart. Diastolic dysfunction can cause symptoms of exertional dyspnea, which restricts the patient's activity. It is likely to predict diastolic dysfunction by screening through hs-CRP. The present investigation was a case-control study that was carried out on 52 patient diagnosed with diabetes mellitus type II. After the demographic data were recorded, and following the collection of data on the patients' history, physical examination, and para-clinical measures, individuals who had factors interfering with level of serum hs-CRP (kidney and liver diseases, inflammatory and infectious diseases, peripheral vascular disease, cerebrovascular disease, connective tissue disease, malignant tumor, trauma, consumption of statins, aspirin, ACEI, and fibrates) and diastolic dysfunction (ischemic heart disease, cardiomyopathies, pericardial disease, arrhythmias and valvular disease) were crossed out of the study. Serum hs-CRP was measured by nephelometry method. According to the results of tissue Doppler echocardiography, these patients are divided into two groups: one with diastolic dysfunction and the other without diastolic dysfunction. The serum hs-CRP levels of these patients were compared with each other. Among the participants, 30.8% were men and 69.2% were women, 36 individuals (69.2%) had diastolic dysfunction while 16 (30.8%) did not. There was a high level of correlation between the level of serumhs-CRP and diastolic dysfunction (p = 0.02, t = 2.36). The results of the present study indicated that there is a correlation between level of serum hs-CRP and diastolic dysfunction, such that the more the level of hs-CRP, the higher probability of diastolic dysfunction existence will be.