Histologically Validated Myocardial Fibrosis in Relation to Left Ventricular Geometry and Its Function in Aortic Stenosis.

Background and Objectives: The combination of aortic valve stenosis (AS) and ischemic heart disease (IHD) is quite common and is associated with myocardial fibrosis (MF). The purpose of this study was to evaluate the association between the histologically verified left ventricular (LV) MF and its geometry and function in isolated AS and AS within IHD groups. Materials and Methods: In a single-center, prospective trial, 116 patients underwent aortic valve replacement (AVR) with/without concomitant surgery. The study population was divided into groups of isolated AS with/without IHD. Echocardiography was used, and LV measurements and aortic valve parameters were obtained from all patients. Myocardial tissue was procured from all study patients undergoing elective surgery. Results: There were no statistical differences between isolated AS and AS+IHD groups in LV parameters or systolic and diastolic functions during the study periods. The collagen volume fraction was significantly different between the isolated AS and AS+IHD groups and was 7.3 ± 5.6 and 8.3 ± 6.4, respectively. Correlations between MF and left ventricular end-diastolic diameter (LVEDD) (r = 0.59, p = < 0.001), left ventricular mass (LVM) (r = 0.42, p = 0.011), left ventricular ejection fraction (LVEF) (r = -0.67, p < 0.001) and an efficient orifice area (EOA) (r = 0.371, p = 0.028) were detected in isolated AS during the preoperative period; the same was observed for LVEDD (r = 0.45, p = 0.002), LVM (r = 0.36, p = 0.026), LVEF (r = -0.35, p = 0.026) and aortic annulus (r = 0.43, p = 0.018) in the early postoperative period; and LVEDD (r = 0.35, p ≤ 0.05), LVM (r = 0.43, p = 0.007) and EOA (r = 0.496, p = 0.003) in the follow-up period. In the group of AS and IHD, correlations were found only with LV posterior wall thickness (r = 0.322, p = 0.022) in the follow-up period. Conclusions: Histological MF in AS was correlated with LVM and LVEDD in all study periods. No correlations between MF and LV parameters were found in aortic stenosis in the ischemic heart disease group across all study periods.

Early Detection and Control of Risk Factors for Cardiovascular Diseases in the Aral Region: Experience of Uzbekistan.

AIM: To analyze the results of screening of the population older than 40 years for early detection of risk factors for cardiovascular diseases in real clinical practice of family clinics in the Aral Sea region. MATERIAL AND METHODS: The results of screening of the population older than 40 years were analyzed for a total of 2,430 respondents from family clinics of the district (Republic of Uzbekistan, Republic of Karakalpakstan, Ellikkala district) according to the modified WHO PEN protocol. 1,020 of the respondents with blood pressure ≥140/90 mm Hg were included in the study (mean age, 57.68±8.06 years; women, 61.4%; men, 38.6%). Additionally, the following parameters were determined: salt-taste threshold using the R. Henkin method, echocardiography, ultrasonography of the brachiocephalic arteries, blood lipid spectrum, microalbuminuria, serum creatinine and uric acid. Statistical data are presented as mean±SD. The prevalence of signs in the study group was assessed using the Pearson's chi-square test, and the Pearson correlation coefficient was used. RESULTS: Among the patients with elevated blood pressure included in the study, 24 (2.4%) were younger than 40 years, 847 (81%) were 40-65 years old, and 169 (16.6%) were older than 65 years. Low cardiovascular risk was twice more common among women compared to men: 11.3% vs. 5.6% (χ²=8.990; p=0.003); almost 75% fewer patients with ischemic heart disease, 7.4% vs. 28.9% (χ²=14.939; p=0.0001); however, the incidence of type 2 diabetes mellitus was twice higher, 13.7% vs. 7.4% (χ²=9.205; p=0.002); the female group had significantly fewer cases of postinfarction cardiosclerosis (PICS) (χ²=5.313; p=0.021). Among women, there were no tobacco users or regular alcohol drinkers whereas among men these risk factors were identified in 59.4% (χ²=178.848; p=0.0001) and 35% (χ²=82.238; p=0.0001), respectively. 85.6% of the respondents had a high salt-taste threshold, 96% had left ventricular hypertrophy, 76% had microalbuminuria, 21% had proteinuria, and 92% of both men and women had a common carotid artery intima-media thickening >0.9 mm. CONCLUSION: The study showed a broad prevalence of cardiovascular risk factors in the population of hypertensive patients in the Aral region, a high salt-taste threshold, and significant damages to target organs, which differed from other regions of Uzbekistan. Among hypertensive men, there was a significant prevalence of tobacco and alcohol use, and a significantly more frequent detection of ischemic heart disease, PICS and hyperuricemia compared to women; in the female population, the prevalence of type 2 diabetes mellitus was significantly greater.

A novel preliminary metabolomic panel for IHD diagnostics and pathogenesis.

Cardiovascular disease (CVD) represents one of the main causes of mortality worldwide and nearly a half of it is related to ischemic heart disease (IHD). The article represents a comprehensive study on the diagnostics of IHD through the targeted metabolomic profiling and machine learning techniques. A total of 112 subjects were enrolled in the study, consisting of 76 IHD patients and 36 non-CVD subjects. Metabolomic profiling was conducted, involving the quantitative analysis of 87 endogenous metabolites in plasma. A novel regression method of age-adjustment correction of metabolomics data was developed. We identified 36 significantly changed metabolites which included increased cystathionine and dimethylglycine and the decreased ADMA and arginine. Tryptophan catabolism pathways showed significant alterations with increased levels of serotonin, intermediates of the kynurenine pathway and decreased intermediates of indole pathway. Amino acid profiles indicated elevated branched-chain amino acids and increased amino acid ratios. Short-chain acylcarnitines were reduced, while long-chain acylcarnitines were elevated. Based on these metabolites data, machine learning algorithms: logistic regression, support vector machine, decision trees, random forest, and gradient boosting, were used for IHD diagnostic models. Random forest demonstrated the highest accuracy with an AUC of 0.98. The metabolites Norepinephrine; Xanthurenic acid; Anthranilic acid; Serotonin; C6-DC; C14-OH; C16; C16-OH; GSG; Phenylalanine and Methionine were found to be significant and may serve as a novel preliminary panel for IHD diagnostics. Further studies are needed to confirm these findings.

Incidental Detection of Myocardial Ischemia on Whole-Body PET/CT in a Patient With Carcinoma Lung.

ABSTRACT: 18 F-FDG PET/CT being a whole-body technique can detect multiple other critical nononcological findings. Various cardiac disorders identified incidentally on 18 F-FDG have been reported to help in timely management and improve overall patient care. We hereby present one such case where 18 F-FDG PET/CT performed for a workup of carcinoma lung revealed abnormal myocardial FDG uptake in the anteroseptal and apical region, which raised suspicion of myocardial ischemia such as hot spot imaging. On coronary angiography, coronary artery disease was detected and subsequently managed.

The existence of a bidirectional link between ischemic heart disease and fibromyalgia.

STUDY OBJECTIVES: Fibromyalgia (FM) is one of the most common causes of chronic widespread musculoskeletal pain, but also sleep disturbances, cognitive and psychological disorders. It has been suggested that FM may have a correlation with cardiovascular events. In this study, we aimed to assess the association between FM and ischemic heart disease (IHD). METHODS: A population-based cross-sectional study was conducted utilizing data retrieved from the largest medical records database in Israel, Clalit Health Services. Patients were defined as having FM or IHD when there were at least two such documented diagnoses in their medical records. The occurrence of IHD was compared between FM and age- and sex-frequency-matched healthy controls. A logistic regression model was used to estimate this association following an adjustment for conventional cardiovascular risk factors and depression. RESULTS: An overall population of 18 598 FM patients and 36 985 age- and gender-matched controls were included in the study. The proportion of IHD amongst FM patients was increased in comparison to controls (9.2% and 6.2%, respectively; P  < 0.001). Furthermore, FM demonstrated an independent association with IHD on multivariate analysis (odds ratio [OR], 1.43; 95% confidence intervals [CI], 1.33-1.54; P  < 0.0001). Finally, IHD was also found to be independently associated with the diagnosis of FM (OR, 1.40; CI, 1.31-1.51; P  < 0.0001). CONCLUSION: Our data suggest a bidirectional link between FM and IHD even after the adjustment for conventional cardiovascular risk factors. These findings should be considered when treating patients with either FM or IHD, and their routine interactional screening may be of clinical importance.

Pathophysiological mechanisms underlying increased circulating cardiac troponin in noncardiac surgery: a narrative review.

Assay-specific increases in circulating cardiac troponin are observed in 20-40% of patients after noncardiac surgery, depending on patient age, type of surgery, and comorbidities. Increased cardiac troponin is consistently associated with excess morbidity and mortality after noncardiac surgery. Despite these findings, the underlying mechanisms are unclear. The majority of interventional trials have been designed on the premise that ischaemic cardiac disease drives elevated perioperative cardiac troponin concentrations. We consider data showing that elevated circulating cardiac troponin after surgery could be a nonspecific marker of cardiomyocyte stress. Elevated concentrations of circulating cardiac troponin could reflect coordinated pathological processes underpinning organ injury that are not necessarily caused by ischaemia. Laboratory studies suggest that matching of coronary artery autoregulation and myocardial perfusion-contraction coupling limit the impact of systemic haemodynamic changes in the myocardium, and that type 2 ischaemia might not be the likeliest explanation for cardiac troponin elevation in noncardiac surgery. The perioperative period triggers multiple pathological mechanisms that might cause cardiac troponin to cross the sarcolemma. A two-hit model involving two or more triggers including systemic inflammation, haemodynamic strain, adrenergic stress, and autonomic dysfunction might exacerbate or initiate acute myocardial injury directly in the absence of cell death. Consideration of these diverse mechanisms is pivotal for the design and interpretation of interventional perioperative trials.

Sodium-glucose co-transporter 2 inhibitor canagliflozin modulates myocardial metabolism and inflammation in a swine model for chronic myocardial ischemia.

BACKGROUND: Inflammation and disruption of cardiac metabolism are prevalent in the setting of myocardial ischemia. Canagliflozin, a sodium-glucose costransporter-2 inhibitor, has beneficial effects on the heart, though the precise mechanisms are unknown. This study investigated the effects of canagliflozin therapy on metabolic pathways and inflammation in ischemic myocardial tissue using a swine model of chronic myocardial ischemia. METHODS: Sixteen Yorkshire swine underwent placement of an ameroid constrictor to the left circumflex artery to induce chronic ischemia. Two weeks later, pigs received either no drug (n = 8) or 300 mg canagliflozin (n = 8) daily. Five weeks later, pigs underwent terminal harvest and tissue collection. RESULTS: Canagliflozin treatment was associated with a trend toward decreased expression of fatty acid oxidation inhibitor acetyl-CoA carboxylase and decreased phosphorylated/inactivated acetyl-CoA carboxylase, a promotor of fatty acid oxidation, compared with control ischemic myocardium (P = .08, P = .03). There was also a significant modulation in insulin resistance markers p-IRS1, p-PKCα, and phosphoinositide 3-kinase in ischemic myocardium of the canagliflozin group compared with the control group (all P < .05). Canagliflozin treatment was associated with a significant increase in inflammatory markers interleukin 6, interleukin 17, interferon-gamma, and inducible nitric oxide synthase (all P < .05). There was a trend toward decreased expression of the anti-inflammatory cytokines interleukin 10 (P = .16) and interleukin 4 (P = .31) with canagliflozin treatment. CONCLUSION: The beneficial effects of canagliflozin therapy appear to be associated with inhibition of fatty acid oxidation and enhancement of insulin signaling in ischemic myocardium. Interestingly, canagliflozin appears to increase the levels of several inflammatory markers, but further studies are required to better understand how canagliflozin modulates inflammatory signaling pathways.

Programmatic approach to patients with advanced ischemic cardiomyopathy: Integrating microaxial support into strategies for the modern era.

Patients with advanced ischemic cardiomyopathy manifesting as left ventricular dysfunction exist along a spectrum of severity and risk, and thus decision-making surrounding optimal management is challenging. Treatment pathways can include medical therapy as well as revascularization through percutaneous coronary intervention or coronary artery bypass grafting. Additionally, temporary and durable mechanical circulatory support, as well as heart transplantation, may be optimal for select patients. Given this spectrum of risk and the complexity of treatment pathways, patients may not receive appropriate therapy given their perceived risk, which can lead to sub-satisfactory outcomes. In this review, we discuss the identification of high-risk ischemic cardiomyopathy patients, along with our programmatic approach to patient evaluation and perioperative optimization. We also discuss our strategies for therapeutic decision-making designed to optimize both short- and long-term patient outcomes.

Do Clinical Outcomes and Quality of Life Differ by the Number of Antianginals for Stable Ischemic Heart Disease? Insights from the BARI 2D Trial.

Medical therapy, including antianginal treatment, is the cornerstone in the management of stable ischemic heart disease (SIHD). However, it remains unclear whether combining antianginal agents provides benefits beyond monotherapy in terms of quality of life (QoL) and cardiovascular outcomes. We used data from the Bypass Angioplasty Revascularization Investigation 2 Diabetes (BARI 2D) trial, which compared cardiovascular and QoL outcomes in patients with SIHD and diabetes mellitus randomized to revascularization with intensive medical therapy or intensive medical therapy alone. We categorized patients into 3 groups: ≥2 versus 1 versus 0 antianginals. We compared patient characteristics, QoL metrics, and cardiovascular end points at baseline and at 5 years, creating a multivariable model to adjust for key clinical confounders. Of 2,368 patients, 348 patients (14.7%) were on 0 antianginals, 1,020 patients (43.1%) were on 1 antianginal, and 1,000 patients (42.2%) were on ≥2 antianginals at baseline. The most common antianginal class was ß blockers. At baseline, patients on 0 antianginals had better QoL metrics (self-health score, Duke activity status index, and energy rating) than patients on ≥2 antianginals. However, at the 1-year follow-up, patients taking only 1 antianginal showed greater QoL improvement than those taking 0 antianginal, without any incremental benefit in QoL metrics seen in patients taking ≥2 antianginal agents, even after adjusting for multiple covariates such as age, heart failure, diabetes control, and myocardial jeopardy index. Lastly, at the 5-year follow-up, after adjustment, there were no differences in all-cause mortality, major adverse cardiovascular events, or myocardial infarction between patients taking different numbers of antianginals. Adults on a single antianginal for SIHD and diabetes mellitus had similar or better improvements in QoL than those on 2 or more antianginal agents at 1 year of follow-up. These findings merit further research to better understand the impact of medical therapy intensity on QoL in patients with SIHD and associated co-morbidities.

Pericardial Adipose Tissue Thrombospondin-1 Associates With Antiangiogenesis in Ischemic Heart Disease.

Accumulation of ectopic pericardial adipose tissue has been associated with cardiovascular complications which, in part, may relate to adipose-derived factors that regulate vascular responses and angiogenesis. We sought to characterize adipose tissue microvascular angiogenic capacity in subjects who underwent elective cardiac surgeries including aortic, valvular, and coronary artery bypass grafting. Pericardial adipose tissue was collected intraoperatively and examined for angiogenic capacity. Capillary sprouting was significantly blunted (twofold, p <0.001) in subjects with coronary artery disease (CAD) (age 60 ± 9 years, body mass index [BMI] 32 ± 4 kg/m2, low-density lipoprotein cholesterol [LDL-C] 95 ± 46 mg/100 ml, n = 29) compared with age-, BMI-, and LDL-C matched subjects without angiographic obstructive CAD (age 59 ± 10 y, BMI 35 ± 9 kg/m2, LDL-C 101 ± 40 mg/100 ml, n = 12). For potential mechanistic insight, we performed mRNA expression analyses using quantitative real-time polymerase chain reaction and observed no significant differences in pericardial fat gene expression of proangiogenic mediators vascular endothelial growth factor-A (VEGF-A), fibroblast growth factor-2 (FGF-2), and angiopoietin-1 (angpt1), or anti-angiogenic factors soluble fms-like tyrosine kinase-1 (sFlt-1) and endostatin. In contrast, mRNA expression of anti-angiogenic thrombospondin-1 (TSP-1) was significantly upregulated (twofold, p = 0.008) in CAD compared with non-CAD subjects, which was confirmed by protein western-immunoblot analysis. TSP-1 gene knockdown using short hairpin RNA lentiviral delivery significantly improved angiogenic deficiency in CAD (p <0.05). In conclusion, pericardial fat in subjects with CAD may be associated with an antiangiogenic profile linked to functional defects in vascularization capacity. Local paracrine actions of TSP-1 in adipose depots surrounding the heart may play a role in mechanisms of ischemic heart disease.

Relationship between dynamic electrocardiogram and CRP, IL-6, ET-1 expression in myocardial ischemia patients with coronary heart disease.

This study aimed to observe the relationship between dynamic electrocardiogram and CRP, IL-6, and ET-1 expression in individuals with myocardial ischemia and Coronary Heart Disease (CHD). For this purpose, from January 2021 to December 2022, 80 patients with CHD were admitted to the hospital to determine the presence of myocardial ischemia according to coronary angiography. The individuals were separated into a myocardial ischemia group and a no myocardial ischemia group. Dynamic electrocardiogram (DCG), serum CRP, IL-6, and ET-1 were used in the two groups, respectively. The association between dynamic electrocardiogram indexes and serum CRP, IL-6, and ET-1 levels was discovered using a Pearson correlation analysis. Results showed that the SDNN, SDANNI, rMSSD and PNN50 of Patients with Myocardial Ischemia (PWMI) were lower than individuals with CHD without myocardial ischemia (P<0.05). CRP and IL-6 were negatively correlated with SDNN, SDANNI, rMSSD and PNN50 (P<0.001). ET-1 had a bad relationship with rMSSD and PNN50 (P<0.001). Correlation heat map analysis showed that the color difference of IL-6 was the most obvious between PWMI and Patients Without Myocardial Ischemia (POMI), and IL-6 was more strongly correlated with dynamic electrocardiogram-related indexes of myocardial ischemia. In individuals with CHD myocardial ischemia, there is a negative connection between the DCG index and the production of the inflammatory cytokines CRP, IL-6, and ET-1. In conclusion, CRP, IL-6, and ET-1 levels should be monitored in patients with decreased heart rate variability, so as to further determine the level of micro-inflammation and endothelial function.

Non-peptide orphanin receptor antagonist activity in rat myocardial ischemia-induced cardiac arrhythmias.

One of the causes of sudden cardiac death is arrhythmia after acute myocardial ischemia. After ischemia, endogenous orphanin (N/OFQ) plays a role in the development of arrhythmias. It is discussed in this paper how nonpeptide orphanin receptor (ORL1) antagonists such as J-113397, SB-612111 and compound-24 (C-24) affect arrhythmia in rats following acute myocardial ischemia and what the optimal concentrations for these antagonists are. The electrocardiogram of the rat was recorded as part of the experiment. The concentrations of tumor necrosis factor-α (TNF-α) and interleukin-1ß (IL-1ß) in the myocardium were measured following euthanasia. Following the use of three antagonists, we found the lowest inflammatory factor concentrations and the smallest number of ischemic arrhythmia episodes. All of them had a small impact on cardiac function. LF/HF values were significantly reduced in all three antagonist groups, suggesting that they are involved in the regulation of sympathetic nerves. In conclusion, pretreatment with the three antagonist groups can effectively reduce the concentration of TNF-α and IL-1ß, and the occurrence of arrhythmias after ischemia can also be significantly reduced. Inflammation and sympathetic activity may be related to the mechanism of action of antagonists.

Risk of Ischemic Heart Disease in Chronic Obstructive Pulmonary Disease: A Nationwide Cohort Study.

BACKGROUND: Subjects with chronic obstructive pulmonary disease (COPD) have a higher risk of ischemic heart disease (IHD) than individuals without COPD; however, longitudinal evidence is lacking. Therefore, we aimed to estimate the risk of IHD between COPD and control cohorts using a longitudinal nationwide database. METHODS: We used 2009-2017 data from the Korean National Health Insurance Service National Sample Cohort (NHIS-NSC). Adult participants at least 20 years of age who underwent health examinations and without a history of COPD or IHD were included (n = 540,976). Participants were followed from January 1, 2009, until death, development of IHD, or December 31, 2019, whichever came first. RESULTS: At baseline, there were 3,421 participants with incident COPD and 537,555 participants without COPD. During a median of 8.0 years (5.3-9.1 years) of follow-up, 2.51% of the participants with COPD (n = 86) and 0.77% of the participants without COPD (n = 4,128) developed IHD, with an incidence of 52.24 and 10.91 per 10,000 person-years, respectively. Participants with COPD had a higher risk of IHD (adjusted hazard ratio, 1.55; 95% confidence interval, 1.25-1.93) than subjects without COPD. Demographics such as age, sex, body mass index, and personal health behaviors including smoking status and physical activity did not show significant interaction with the relationship between COPD and IHD (P for interaction > 0.05 for all). CONCLUSION: The results indicate that COPD is associated with the development of IHD independent of demographic characteristics and health-related behaviors. Based on these results, clinicians should closely monitor the onset of IHD in subjects with COPD.

Aortic stiffness effectively risk stratifies diabetic patients with suspected myocardial ischemia undergoing vasodilatory stress perfusion cardiac magnetic resonance.

BACKGROUND AND AIMS: Cardiovascular magnetic resonance (CMR) comprehensively assesses aortic stiffness and myocardial ischemia in a single examination. Aortic stiffness represents a subclinical marker of cardiovascular risk in the general population, including patients with diabetes mellitus. However, there is no prognostic data regarding aortic stiffness in patients with diabetes mellitus undergoing stress perfusion CMR. METHODS: Consecutive patients with diabetes mellitus with suspected myocardial ischemia referred for adenosine stress perfusion CMR with aortic pulse wave velocity (PWV) during 2010-2013 were studied. The primary outcome was major adverse cardiovascular events (MACE), defined as the composite of cardiac mortality, nonfatal myocardial infarction (MI), hospitalization for heart failure, coronary revascularization (> 90 days post-CMR), and ischemic stroke. The secondary outcome was hard cardiac events, defined as the composite of cardiac mortality and nonfatal MI. RESULTS: A total of 424 patients (median follow-up 7.2 years) were included. The mean PWV was 12.16 ± 6.28 m/s. MACE and hard cardiac events occurred in 26.8% and 9.4% of patients, respectively. Patients with elevated PWV (> 12.16 m/s) had a significantly higher incidence of MACE (HR 2.14 [95%CI 1.48, 3.09], p < 0.001) and hard cardiac events (HR 2.69 [95%CI 1.42, 5.10], p = 0.002) compared to those with non-elevated PWV. Multivariable analysis demonstrated that PWV independently predicts MACE (p = 0.003) and hard cardiac events (p = 0.01). Addition of PWV provided incremental prognostic value beyond clinical data, left ventricular mass index, myocardial ischemia, and late gadolinium enhancement in predicting MACE (incremental χ² 7.54, p = 0.006) and hard cardiac events (incremental χ² 5.99, p = 0.01). CONCLUSIONS: Aortic stiffness measured by CMR independently predicts MACE and hard cardiac events and confers significant incremental prognostic value in patients with diabetes mellitus with suspected myocardial ischemia. Aortic stiffness measurement could potentially be considered as part of a stress perfusion CMR protocol to enhance risk prediction in patients with diabetes mellitus.

MicroRNA-30d-5p-A Potential New Therapeutic Target for Prevention of Ischemic Cardiomyopathy after Myocardial Infarction.

(1) Background and Objective: MicroRNAs (miRs) are biomarkers for assessing the extent of cardiac remodeling after myocardial infarction (MI) and important predictors of clinical outcome in heart failure. Overexpression of miR-30d-5p appears to have a cardioprotective effect. The aim of the present study was to demonstrate whether miR-30d-5p could be used as a potential therapeutic target to improve post-MI adverse remodeling. (2) Methods and Results: MiR profiling was performed by next-generation sequencing to assess different expression patterns in ischemic vs. healthy myocardium in a rat model of MI. MiR-30d-5p was significantly downregulated (p < 0.001) in ischemic myocardium and was selected as a promising target. A mimic of miR-30d-5p was administered in the treatment group, whereas the control group received non-functional, scrambled siRNA. To measure the effect of miR-30d-5p on infarct area size of the left ventricle, the rats were randomized and treated with miR-30d-5p or scrambled siRNA. Histological planimetry was performed 72 h and 6 weeks after induction of MI. Infarct area was significantly reduced at 72 h and at 6 weeks by using miR-30d-5p (72 h: 22.89 ± 7.66% vs. 35.96 ± 9.27%, p = 0.0136; 6 weeks: 6.93 ± 4.58% vs. 12.48 ± 7.09%, p = 0.0172). To gain insight into infarct healing, scratch assays were used to obtain information on cell migration in human umbilical vein endothelial cells (HUVECs). Gap closure was significantly faster in the mimic-treated cells 20 h post-scratching (12.4% more than the scrambled control after 20 h; p = 0.013). To analyze the anti-apoptotic quality of miR-30d-5p, the ratio between phosphorylated p53 and total p53 was evaluated in human cardiomyocytes using ELISA. Under the influence of the miR-30d-5p mimic, cardiomyocytes demonstrated a decreased pp53/total p53 ratio (0.66 ± 0.08 vs. 0.81 ± 0.17), showing a distinct tendency (p = 0.055) to decrease the apoptosis rate compared to the control group. (3) Conclusion: Using a mimic of miR-30d-5p underlines the cardioprotective effect of miR-30d-5p in MI and could reduce the risk for development of ischemic cardiomyopathy.

Effect of atrial fibrillation on plasma galectin-3 and soluble CD40 ligand levels in patients with ischemic cardiomyopathy.

OBJECTIVE: To reveal the significance of plasma galectin-3 and soluble CD40 ligand (sCD40L) levels in patients with ischemic cardiomyopathy (ICM) combined with atrial fibrillation. METHODS: In this case-control study, the case group comprised 60 patients with ICM combined with atrial fibrillation and the control group comprised patients with ICM without atrial fibrillation. Plasma galectin-3 and sCD40L levels, left atrial diameter (LAD), left ventricular ejection fraction (LVEF), and left ventricular diameter (LVD) were compared. RESULTS: The plasma galectin-3 and sCD40L levels, LAD, and LVD were higher and the LVEF was lower in the case than control group. In the case group, the plasma galectin-3 and sCD40L levels were positively correlated with the LAD and LVD but negatively correlated with the LVEF. The area under the receiver operating characteristic curve of the plasma galectin-3 and sCD40L levels in the diagnosis of ICM combined with atrial fibrillation was 0.857 (95% confidence interval, 0.792-0.923) and 0.724 (95% confidence interval, 0.634-0.814), respectively. CONCLUSION: The plasma galectin-3 and sCD40L levels are significantly elevated in patients with ICM combined with atrial fibrillation. Although both may have predictive value in the diagnosis of ICM combined with atrial fibrillation, galectin-3 may have the higher predictive value.