Severity Of Ischemic Heart Disease Research Articles

Breathomics Detect the Cardiovascular Disease: Delusion or Dilution of the Metabolomic Signature.

Volatile organic compounds (VOCs) can be subdivided into exogenous and endogenous categories based on their origin. Analyzing the endogenous VOCs can provide insights into maintaining the internal organs' homeostasis. Despite the ongoing development and the current understanding, studies have suggested a link between cardiovascular metabolic alterations in patients with ischemic heart disease and elevated levels of ethane and isoprene detectable through exhaled breath analysis. Conversely, patients with chronic heart failure exhibit elevated acetone and pentane in their exhaled air. These substances originate from disturbances in the heart tissue, including cellular and subcellular modulations. Hypothetically, ethane levels in the exhaled breath analysis can demonstrate the severity of ischemic heart disease and, consequently, the risk of death in the next 10 years due to cardiovascular disease (CVD). Real-time direct mass spectrometry is the preferred method for assessing VOCs in exhaled breath analysis. The accuracy of this analysis depends on several factors, including the selection of the relevant breath fraction, the type of breath collection container (if used), and the pre-concentration technique.

Correlation of Serum Endocan Level With Apoptosis Indicators and Severity of Atherosclerotic Lesions of Coronary Arteries in Patients With Coronary Heart Disease.

Aim To study the relationship of blood serum concentration of endocan with indexes of apoptosis and clinical and instrumental characteristics of patients with ischemic heart disease (IHD).Material and methods The study included 176 subjects (105 men and 71 women). 150 of them were diagnosed with IHD and 26 were healthy volunteers. Anthropometric measurements, coronary angiography, echocardiography, duplex ultrasound scanning of extracranial parts of the brachiocephalic arteries were performed for all patients. Concentrations of endocan (ng / ml), glucose (mmol / l), and apoptotic markers Bcl-2 (ng / ml), Bax (ng / ml), Bcl-2 / Bax, TRAIL (pg / ml), and p53 (ng / ml) were measured in blood serum. Patients were divided into groups based on their SYNTAX scores: group 1 with moderate atherosclerotic lesions of the coronary arteries (CA) (score < 22, 78 patients); group 2 with severe CA atherosclerosis (score 23-32, 37 patients); and group 3 with extremely severe CA lesions (score >33, 35 patients). The control group consisted of healthy volunteers (26 subjects). All groups were age- and sex-matched. Differences were considered statistically significant at p<0.05.Results A correlation was found between endocan concentration and IHD severity (r=0.32, p<0.001). In group 1, the median endocan concentration was 14.57 ng / ml [8.21; 23.66], in group 2, 19.34 ng / ml [8.425; 26.645], in group 3, 32.13 ng / ml [18.2; 39.12], and in the control group, 6.92 ng / ml [4.62; 9.18]. Correlations of varying strength and significance were observed between the endocan concentration and a number of clinical and instrumental characteristics. Endocan concentrations significantly differed in groups of patients with multifocal atherosclerosis (p<0.01), angina pectoris (p<0.01), a history of myocardial infarction (p<0.001), and obesity (p<0.05) from patients without these signs. Also, a correlation was found between serum endocan concentration and apoptotic markers: TRAIL (r= -0.448, p<0.001); BCL-2 (r= -0.552, p<0.001), Bax (r= -0.519, p<0.001), Bcl-2 / Bax (r= -0.576, p<0.001) and p53 (r= -0.520, p <0.001).Conclusion The study demonstrated a potential role of endocan as a promising biomarker for risk stratification, prognosis and therapeutic monitoring of IHD patients.

MODIFIABLE RISK FACTORS AND CORONARY ARTERY DISEASE SEVERITY: INSIGHTS FROM A CASE-CONTROL ANALYSIS

Atherosclerotic coronary disease stands as a leading cause of both mortality and morbidity globally. The well-documented risk factors for coronary artery disease (CAD) include abnormal lipid levels, obesity, smoking, high blood pressure, and diabetes. The established association between these cardiovascular risk factors and ischemic heart disease is widely recognized. However, the correlation between risk factors for ischemic heart disease and the severity of CAD on coronary angiography remains less explored, with varying findings across studies. Our research involved a total of 200 patients aged 30 to 70 years, comprising 100 cases diagnosed with severe CAD and 100 controls with insignificant CAD. Factors contributing to CAD, such as smoking, high sugar levels, high blood pressure, lipid profiles, family history of CAD, and obesity, were assessed in all patients. Statistical analysis, employing the chi-square test, was conducted, and a significant association was considered when the odds ratio value exceeded 1. The mean age in our study population was 51.01 ± 7.76 years, with 159 (79.50%) being male. Among the patients, 99 (49.50%) were obese, 90 (45.0%) were diabetic, 94 (47.0%) were hypertensive, 77 (38.5%) were smokers, 53 (26.5%) had a positive family history, and 17 (8.5%) were dyslipidemic. In evaluating the association of cardiovascular risk factors with CAD severity, smoking (odds ratio 1.73, p-value 0.04), hypertension (odds ratio 1.6, p-value 0.05), diabetes (odds ratio 1.6, p-value 0.05), and obesity (odds ratio 1.98, p-value 0.016) emerged as independent factors significantly linked to the severity of CAD. Our findings underscore the independent roles of smoking, hypertension, diabetes, and obesity as risk factors contributing to the severity of ischemic heart disease.

Frank's sign associated with the severity of ischemic heart disease in patients under 65 years old

Background and objectiveFrank's sign is the diagonal ear fold which has been associated with ischemic heart disease. The objective of this work was to evaluate the relationship of Frank's sign with severity of ischemic heart disease in adults ≤ 65 years old in the northeast of Mexico. Patients and methodsA cross-sectional study was conducted in patients ≤ 65 years old who underwent coronary angiography consecutively over a period of 5 months in 2022. Severe coronary artery disease (CAD) was associated with Frank's sign and other common cardiovascular risks. To determine the association, bivariate and multivariate analysis was performed using logistic regression that included variables with a value of p<0.05. Statistical analysis was performed with SPSS version 22. ResultsWe included 311 patients ≤ 65 years, of whom 80% were men. The median age was 57 years (range 28–65). Frank's sign was positive in 62% of the population. The main clinical characteristics in patients with Frank's sign were type 2 diabetes mellitus (55%), p=0.003, dyslipidemia (53%), p=0.026 and smoking (68%), p=0.002.In the multivariate analysis, the independent variables associated with severe CAD were Frank's Sign OR 3.26; 95% CI (1.98–5.38), p≤0.001, male gender OR 2.28; 95% CI (1.20–4.35), p=0.012, and dyslipidemia OR 1.81; 95% CI (1.11–2.97), p=0.017. ConclusionsThere is an independent association between Frank's sign with the presence of severe CAD in patients ≤ 65 years old, which may be useful for screening and prevention.

Frank's sign associated with the severity of ischemic heart disease in patients under 65 years old

Background and objectiveFrank's sign is the diagonal ear fold which has been associated with ischemic heart disease. The objective of this work was to evaluate the relationship of Frank's sign with severity of ischemic heart disease in adults ≤ 65 years old in the northeast of Mexico. Patients and methodsA cross-sectional study was conducted in patients ≤ 65 years old who underwent coronary angiography consecutively over a period of 5 months in 2022. Severe coronary artery disease (CAD) was associated with Frank's sign and other common cardiovascular risks. To determine the association, bivariate and multivariate analysis was performed using logistic regression that included variables with a value of p<0.05. Statistical analysis was performed with SPSS version 22. ResultsWe included 311 patients ≤ 65 years, of whom 80% were men. The median age was 57 years (range 28–65). Frank's sign was positive in 62% of the population. The main clinical characteristics in patients with Frank's sign were type 2 diabetes mellitus (55%), p=0.003, dyslipidemia (53%), p=0.026 and smoking (68%), p=0.002.In the multivariate analysis, the independent variables associated with severe CAD were Frank's Sign OR 3.26; 95% CI (1.98–5.38), p≤0.001, male gender OR 2.28; 95% CI (1.20–4.35), p=0.012, and dyslipidemia OR 1.81; 95% CI (1.11–2.97), p=0.017. ConclusionsThere is an independent association between Frank's sign with the presence of severe CAD in patients ≤ 65 years old, which may be useful for screening and prevention.

Severity of ischemic heart disease in relation to atherosclerotic cardiovascular risk score and individual atherosclerotic cardiovascular risk factor

Severity of ischemic heart disease in relation to atherosclerotic cardiovascular risk score and individual atherosclerotic cardiovascular risk factor

Paraoxonase-1, a novel link between periodontitis and ischemic heart disease: A case-control study.

Periodontitis is a chronic inflammatory disease and might be a potential risk factor for ischemic heart disease (IHD). However, the link between periodontitis and atherosclerosis is not yet fully understood. Paraoxonase-1 (PON-1) is a new biomarker representing both anti-atherosclerotic and antioxidant activity, which also acts against dental biofilm formation and periodontitis. The possible contributing role of PON-1 in the relationship between periodontitis and atherosclerosis has not been studied to date. The aim of the present study was to investigate the serum level of PON-1 with regard to the periodontal status in IHD patients. In this case-control study, 67 patients with IHD underwent a periodontal examination and were accordingly allocated to one of the 2 study groups: the case group with chronic periodontitis (n = 36); or the control group with a healthy periodontium (n = 31). Serum PON-1 activity was measured by means of colorimetric analysis. There were no significant differences between the groups in terms of demographic data, cardiac risk factors, initial biochemical test results, cardiac pump function, and the number of grafted vessels. The activity of PON-1 in cardiac patients suffering from periodontitis was significantly lower than in cardiac patients with a healthy periodontal status (53.01 ±7.53 U/mL and 59.11 ±9.95 U/mL, respectively; p = 0.007). This finding suggests that the combination of IHD and periodontitis is associated with lower PON-1 activity. Further studies might be required to assess the possible role of periodontal treatment in increasing PON-1 activity and reducing IHD severity.

Microbiota-related metabolites fueling the understanding of ischemic heart disease.

Up-to-date knowledge of gut microbial taxa associated with ischemic heart disease (IHD). Microbial metabolites for mechanistic dissection of IHD pathology. Microbiome-based therapies in IHD prevention and treatment.

Circadian Variations and Associated Factors in Patients with Ischaemic Heart Disease

Circadian rhythms have been identified in cardiovascular diseases, and cardiovascular risk factors can modify the circadian rhythm. The purpose of this study was to describe the onset of ischaemic heart disease symptomatology in relation to the date and time, the day of the week of presentation, the season, AMI location and severity and the level of influence of individual patient characteristics in a retrospective cross-sectional study involving 244 ischaemic heart disease patients from the intensive care unit of La Ribera Hospital (Spain). The onset of pain was more frequent in the morning, the season with the highest frequency of ischaemic events was winter, and the lowest incidence was during weekends. Regarding the severity of ischaemic heart disease, the circadian rhythm variables of weekdays vs. weekends and seasons did not show a significant association. The length of hospital stay was associated with the onset of pain in the afternoon. The onset of pain at night was associated with the subendocardial location of the infarction. In conclusion, living in a Mediterranean country, the Spanish population showed a circadian pattern of AMI, where the onset of pain has an influence on AMI location and on the length of hospital stay and is the same in patients with different individual risk factors.

Human macrophages are immunoprofiled by pericardial fluid small extracellular vesicles modulating lipid metabolism mechanisms

Abstract Background The incidence and severity of ischemic heart disease (IHD) is exacerbated by coronary artery disease (CAD). Monocytes and macrophages are central to atherosclerosis. Endogenous small extracellular vesicles (sEVs) can shuttle microRNAs and other molecular cargos from cell to cell, mediating expressional and functional response in the recipient cells. Recent evidence supports a role for sEVs in modulating macrophage phenotype. The pericardial fluid (PF) is in direct contact with the epicardium and contain sEVs. We recently showed that human PF-sEVs are capable to modulate cardiovascular cells via microRNA shuttling. Purpose This study sought to investigate whether PF-sEVs regulate macrophages, contributing to a specific immunophenotype in CAD patients. Methods PF was collected from either CAD patients undergoing coronary bypass surgery (CABG) or non-atherosclerotic patients operated for mitral valve repair (non-CAD control group). sEVs were isolated using size exclusion chromatography and characterised for size (Nanosight tracking analysis; NTA), tetrasapanin content (by Nanoview chips), microRNA content by RNA seq and proteomic analysis. Monocytes from healthy donors were isolated from buffy coats and differentiated into macrophages following established protocols. Macrophages were incubated with either CAD-sEVs or non-CAD sEVs for 24h at 37oC. The cells were collected and processed for mRNA analyses (qRT-PCR) and flow cytometry. Human PF-cells were isolated and analysed to be compared with the in vitro setting. Further bioinformatics were employed to understand functional pathways and validated in PF from patients. Results Exposure to CAD-sEVs induces a proinflammatory profile of human macrophages. CAD-sEVs treated macrophages showed a CD36+low, CD206+low CD40+high profile. While non-CAD-sEVs did not statistically differ from PBS nor untouched groups, CAD-sEVs increased the mRNA level of IL1a, IL1b, TNFa and decreased MRC1. Proteomics revealed that PF-sEVs from CAD patients carried higher amounts of pro-inflammatory molecules (ICAM-1 and IL18) compared to NonCAD control. Bioinformatics analysis showed that 861 miRNAs were decreased in the PF-sEVs from CAD patients compared to non-CAD. miRNA targets prediction and pathway analyses reported that clusters of deregulated miRNAs could regulate CD36 and SRB1 which were shown to be decreased in CAD-sEVs treated macrophages. Human PF-cells revealed a reduced expression of CD36 on PF-macrophages. Conclusions We demonstrate, for the first time, that sEVs isolated from the PF of CAD patients induce a proinflammatory profile of human macrophages and that target crucial lipid metabolism pathways. These clinically relevant results could drive to decipher improved therapeutics able modulate the epicardial/myocardial immune response in CAD patients. Funding Acknowledgement Type of funding sources: Public grant(s) – National budget only. Main funding source(s): British Heart Fundation

Association of Severity of Coronary Artery Disease with Left Ventricular Diastolic Dysfunction among Diabetics with Stable Ischaemic Heart Disease: A Cross-sectional Study from Odisha, India

Introduction: Ischaemic Heart Disease (IHD) is one of the most common co-morbidity among Indian population, so is Diabetes Mellitus (DM). IHD is associated not only with systolic, but also with Diastolic Dysfunction (DDFx) of Left Ventricle (LV). However, there is scarcity of data correlating the severity of Coronary Artery Disease (CAD) with LV DDFx. Aim: To assess the severity of CAD in diabetic stable IHD patients with normal LV systolic function (LV Ejection fraction ≥50%) and it’s association with degree of DDFx. Materials and Methods: A prospective cross-sectional study was conducted over a period of one year, in a tertiary care hospital of Odisha, India among diabetic stable IHD patients. Grades of DDFx were assessed among the study population, using Transthoracic Echocardiography (TTE). Subsequently, severity of CAD was assessed, using invasive Coronary Angiography (CAG) using The SYNergy between percutaneous coronary intervention with TAXus and cardiac surgery (SYNTAX) score. Next, grades of DDFx were correlated with severity of IHD. Results: Among a total of 93 diabetic stable IHD patients with normal LV ejection fraction, 76.3% were males and the mean age was 60.7±8.9 years. Majority presented with chronic stable angina (59, 63.4%). Hypertension (50, 53.7%), followed by dyslipidaemia (36, 38.7%) and renal dysfunction (19, 20.4%) were the most common co-morbidities. Majority of patients had grade I (39.8%), followed by grade II (17.2%), and grade III (9.7%) DDFx. On invasive CAG, 39.8% had a SYNTAX score of ≤ 22, 36.6% had a score of 23-32, and 23.6% had a score of ≥33. Grades of DDFx were found to be significantly higher among the patients with greater SYNTAX score. Conclusion: Among diabetic stable IHD patients, greater the severity of CAD on CAG, higher were the grades of DDFx

Human pericardial fluid exosomes regulate macrophage immunophenotype: new prospective for cardiovascular myocardium-epicardium crosstalk in coronary artery disease

Abstract Background The incidence and severity of ischemic heart disease (IHD) is exacerbated by coronary artery disease (CAD). Monocytes and macrophages are central to atherosclerosis. Endogenous small extracellular vesicles (sEVs) can shuttle microRNAs and other molecular cargos from cell to cell, mediating expressional and functional response in the recipient cells. Recent evidence supports a role for sEVs in modulating macrophage phenotype. The pericardial fluid (PF) is in direct contact with the epicardium and contain sEVs of myocardial origin (C. Beltrami et.al 2017). We recently showed that human PF-sEVs are capable to modulate cardiovascular cells via microRNA shuttling (C.Beltrami et.al. 2017). Moreover, epicardial cells reportedly cross-talk with the myocardium to regulate immune response to IHD (V.Ramjee et.al 2017). Purpose This study sought to investigate whether PF-sEVs regulate macrophages, contributing to a specific immunophenotypes in CAD patients. Methods PF was collected from either CAD patients undergoing coronary bypass surgery (CABG) or non-atherosclerotic patients operated for mitral valve repair (non-CAD control group). sEVs were isolated using size exclusion chromatography and characterised for size (Nanosight tracking analysis; NTA) and microRNA content (Exiqon miR-array). Monocytes from healthy donors were isolated from buffy coats and differentiated into macrophages following established protocols. Macrophages were incubated with either CAD-sEVs or non-CAD sEVs for 24h at 37oC. PBS and sEV-free serum were used as negative controls and LPS as a proinflammatory control. The cells were collected and processed for mRNA analyses (qRT-PCR) and Flow cytometry (FACS). Results Twenty-four-hour exposure to CAD-sEVs induces a proinflammatory profile of human macrophages. While non-CAD-sEVs did not statistically differ from PBS nor Exo-free groups, CAD-sEVs increased the mRNA level of IL1a, NOS3, TNFa, CCL2 and IL6 (comparison to both non-CAD and negative controls). These data were not associated with changes in apoptosis. Bioinformatics analysis showed that 11 miRNAs where consistently increased, and 67 miRNAs decreased in the PF-sEVs from all CAD patients compared to non-CAD. miRNA targets prediction and pathway analyses (R-Project) revealed that the deregulated miRNAs could regulate macrophage motility and cytokine signalling. Conclusions We demonstrate, for the first time, that sEVs isolated from the PF of CAD patients induce a proinflammatory profile of human macrophages. These clinically relevant results could drive to decipher improved therapeutics able to modulate the epicardial/myocardial immune response in CAD patients. Funding Acknowledgement Type of funding sources: Public Institution(s). Main funding source(s): Biritish Heart Fundation grant to Prof. Costanza Emanueli

Hyperlipidemia and male infertility

ABSTRACT Hyperlipidemia is a common disease affecting 25% of adults in developed nations. Approximately 50% of the middle-aged adult population have been reported to have total cholesterol level above the normal range. Worldwide, the incidence of dyslipidaemia is increasing in both low and high income countries. It is a major risk factor for the prevalence and severity of ischemic heart disease. Less recognized but growing in importance are the effects of dyslipidaemia on reproductive functions. A growing evidence has linked dyslipidaemia and abnormal lipid metabolism with alteration of male fertility. The purpose of this review is to summarize the data gathered from both experimental animal models and human studies on the effects of hyperlipidemia on semen parameters, spermatogenesis, male reproductive organs, hormones and fertility.

Sudden Death from Ischemic Heart Disease While Driving: Cardiac Pathology, Clinical Characteristics, and Countermeasures.

BackgroundSudden death from ischemic heart disease while driving is an important cause of traffic accidents. This study discusses causes of traffic accidents in relation to risk factors for acute myocardial infarction such as hypertension and overwork and provides references for the early prevention and regulation of drivers’ health conditions.Material/MethodsData on 21 cases of sudden death by ischemic heart disease while driving from January 2015 to December 2019 were collected. Age, symptoms, and cardiac pathological changes of patients were summarized by systematic anatomical and medical history data.ResultsPatients were 21 men with an average age of 47±7.27 years (most aged 40 to 60 years), and the average weight of their hearts was 439.45±76.3 g. Twelve patients had a history of hypertension, 8 had previous myocardial infarction, and 4 had fatty liver. All had at least 1 severe narrowing of a major coronary artery. Twelve patients died within a short period; 9 died more than 12 h after myocardial infarction onset. Ten patients had worked more than 80 h of overtime per month, 4 patients, more than 45 h, and 7 patients, less than 45 h.ConclusionsRegular physical examination and information about ischemic heart disease should be emphasized for men aged 40 to 60 years who drive frequently, especially for those with hypertension, overwork, or previous myocardial infarction. Incorporating objective evaluation criteria for the severity of ischemic heart disease and overwork into health condition-related driving regulations is needed.

Abstract 358: Hypoxia and Hyperglycemia Induces M 6 A Mrna Methylation in Major Heart Cells

Background: According to American heart association, over 70 % diabetic patients die from heart and stroke related diseases. The term “diabetic heart diseases” includes coronary heart disease, heart failure and diabetic cardiomyopathy in diabetic patients. Epigenetic and epitranscriptomic modifications play critical roles in progress of diabetic heart disease. Recent evidences indicated that m 6 A methylation involved in ischemic cardiomyopathy. But, the role of m 6 A mRNA methylation in cardiovascular diseases along with diabetic co-morbidity factors has not been studied in details. Thus, here we hypothesize that alterations in m 6 A mRNA methylation under hypoxic and hyperglycemic conditions contributes to severity of ischemic heart disease. Method and Results: To address our hypothesis, we have determined the levels of m 6 A mRNA methylation in NRVM, NRVF and HUVEC, HMVE and mouse primary endothelial cells under hypoxic and hyperglycemic conditions. We also examined the m 6 A levels in mice hearts post 5 days of MI. m 6 A mRNA methylation was significantly upregulated both in human and mouse ischemic hearts. Furthermore, hypoxia and hyperglycemia significantly induced m 6 A methylation in neonatal rat cardiomyocytes, fibroblasts, and mouse primary endothelial cells (isolated from WT and db/db mice). Next, we measured the methylation machinery both at RNA and protein levels. Interestingly, in corroboration with our methylation data, the expression of both m 6 A writers (Mettl3 and WTAP) and Readers (YTHDF2) was significantly increased. To determine the target transcripts which were highly methylated post-ischemia, we performed deep sequencing of methylated RNA after their immunoprecipitation using MeRIP-sequencing protocol. Our MeRIP-seq data has suggested a differentially m 6 A methylated targets both in-vitro and in-vivo ischemic sample. Conclusion: Over all, for the first time our data showed that hypoxia and hyperglycemia alters m 6 A mRNA methylation which may contribute to enhance the severity of cardiovascular diseases under hyperglycemic conditions. Further understanding of the mechanisms, may present a novel approach to potentially regulate m 6 A methylation, which may help in preventing/reducing heart failure in diabetic patients.

A full-width half-maximum method to assess retinal vascular structural changes in patients with ischemic heart disease and microvascular angina

Chest pain patients without obstructive ischemic heart disease (IHD) have increased attention in the clinical practice as carrying higher cardiovascular (CV) risk and impaired life quality. Retinal vasculature is a novel but reliable risk factor of atherosclerosis and systemic vascular diseases. However, the association of retinal blood vessels and unobstructed IHD, as known as microvascular angina (MA) is poorly understood. This study compared retinal vascular structures of obstructive IHD and MA using spectral domain optical coherence tomography (SD-OCT) and full-width half-maximum (FWHM) methods to provide new risk predictive evidence of MA. Fundus vessels of 120 IHD patients, including 91epicardial IHD and 29 MA patients, and 66 control subjects were evaluated. Significant differences in the retinal arterial lumen diameter (RALD), retinal arterial outer diameter (RAOD), and arteriovenous ratio (AVR) have been found (P < 0.05). The severity of IHD was negatively correlated with diameters of RAOD, RALD and AVR (P < 0.05). In conclusion, there were significant differences in the retinal vascular structure between IHD patients and patients with MA. Thus, assessment of retinal vascular structure is suggested to evaluate CV risk of IHD patients, despite having no obstructive IHD.

Severity of ischemic heart disease and presenting rhythm in patients with out-of-hospital cardiac arrest

IntroductionIschemic heart disease (IHD) is associated with a shockable rhythm in out-of-hospital cardiac arrest (OHCA). However, the impact of IHD severity on first recorded rhythm is unknown. We hypothesized that the strength of the association between IHD and shockable rhythm increases with increasing IHD severity. MethodsOHCA patients were identified in the Danish Cardiac Arrest Registry (2001–2014). Population-based registries were used to identify chronic diseases, drug prescriptions and cardiac procedures such as coronary angiography (CAG), percutaneous coronary intervention (PCI), and coronary artery bypass grafting (CABG). Severity of IHD was categorized as 1) No diagnosis of IHD, 2) IHD without previous CAG, PCI or CABG, 3) IHD with CAG, 4) IHD with PCI, and 5) IHD with CABG. Adjusted odds ratios (ORs) for a shockable rhythm was computed using multivariable logistic regression. ResultsOf 34,749 patients with OHCA, 6325 (18.2%) patients had a diagnosis of IHD. The prevalence of a shockable rhythm was higher for patients with a previous diagnosis of IHD (25.6%) and for those with previous CAG (33.3%), PCI (36.4%) or CABG (34.0%) when compared to patients without IHD (21.2%). IHD was associated with shockable rhythm (OR = 1.69, 95%CI 1.55–1.85) when compared to patients without IHD. The association with shockable rhythm was higher for patients with a history of CAG (OR = 1.92, 95%CI 1.67–2.20) and PCI (OR = 1.93, 95%CI 1.67–2.23), but similar in patients with CABG (OR = 1.69, 95%CI 1.37–2.10). ConclusionIHD was associated with a shockable rhythm, with a moderate increase in the association in patients with a CAG or PCI procedure.

Role of ATP Sensitive Potassium Channel in Exercise-Training Mediated Adaptations in Ventricular Repolarization

Regular exercise-training is known to reduce the incidences and severity of ischemic heart disease, but the mechanistic nature is unknown. We showed that regular exercise shortened the left ventricular action potential duration (APD) at high heart rate (HR), which would prevent Ca2+ overload and/or inadequate filling under conditions of metabolic stress. Here we test the hypothesis that exercise-training induced APD shortening at high HR is due to the up-regulation of ATP sensitive potassium channel (KATP). Female and male Sprague-Dawley rats were randomly assigned to voluntary wheel running or control groups. After 6-8 weeks training, cardiac myocytes were isolated from the apex and base regions of the left ventricle with collagenase–protease dispersion technique. APD was measured with glass micro-electrode, current-voltage relationship was recorded with discontinuous single electrode voltage clamp, and the expression level of KATP channel pore-forming subunit Kir6.2 and regulatory subunits SUR2A were determined by Western blots. At 1Hz, KATP activator pinacidil (100 µM) shortened APD in myocytes from both sexes and, the shortening was significantly greater in exercise-trained compared to sedentary groups. The KATP inhibitor glibenclamide (2 µM) prolonged the 10Hz APD more in exercise-trained than control rats. Regular exercise enhanced KATP outward current density in apex myocytes from both sexes; in base, trained females exhibited larger KATP inward current than controls. In both sexes, Kir6.2 expression was elevated by wheel-running in apex but not base region. Exercise-training increased SUR2A density in base region of both sexes, and eliminated its reginal difference in females. In conclusion, exercise-training induced APD shortening under energy demanding conditions (e.g. high HR) is caused at least in part by KATP up-regulation, an adaptation that reduces energy requirements for ion homeostasis and maintains a diastolic interval adequate for myocardial relaxation.

Beta-Adrenergic and ATP Sensitive Potassium Channel Effects on Ventricular Action Potential Duration: Alterations with Exercise Training

Regular exercise-training is known to reduce the incidences and severity of ischemic heart disease, but the mechanistic nature is unknown. Recently, we showed that regular exercise prolongs the left ventricular action potential duration (APD) at resting heart rate (HR) while shortening it at high HR. These adaptations enhance cardiac contractility at rest while preventing Ca2+ overload and/or inadequate filling during exercise. Here we test the hypothesis that exercise-training induced changes in the APD are due to a reduced responsiveness to β-adrenergic regulation, and increased ATP sensitive potassium channel (KATP) function. Female and male Sprague-Dawley rats were randomly assigned to voluntary wheel running or control groups. After 6-8 weeks training, cardiac myocytes were isolated from the apex and base regions of the left ventricle with collagenase–protease dispersion technique. APD were measured with glass micro-electrode at 1 or 10 Hz stimulation. At 1 Hz, the non-selective β agonist Isoproterenol shortened the APD an effect largely reversed by selective β1-AR blocker Atenolol (0.1 μM), but not selective β2-AR antagonist ICI 118,551 (0.1 μM). Wheel running shifted the Isoproterenol dose-response curve (0.01-100 nM) rightward compared to controls, with LogIC50 decreased by exercise-training in both male and female rats by ∼ one log unit. The addition of KATP inhibitor glibenclamide (2 µM) prolonged APD at 10 Hz, with a greater prolongation observed in myocytes from exercise-trained rats. In conclusion, the exercise program down regulated the β1-AR to isoproterenol an adaptation that would contribute to prolonged action potential in non-stressed hearts where the activation of the sympathetic nervous system is low, while the exercise-training induced decline in the APD under energy demanding conditions (e.g. high HR) seems caused at least in part by increased KATP repolarizing current.

Evaluation of the relationship between concentration of endothelin-1 and magnesium in the blood and the severity of ischemic heart disease

Aim. To study the relationship between concentrations of endothelin-1 and magnesium in blood depending on functional class and old myocardial infarction in patients with stable angina.Methods. The study included 58 patients with ischemic heart disease, II and III functional class stable angina. 19 of these patients suffered a myocardial infarction in the past. The control group consisted of 25 healthy volunteers. Endothelin-1 level in blood serum was determined by enzyme immunoassay, the concentration of magnesium by colorimetric method.Results.Endothelin-1 level in the general group of patients with stable angina was 1.28±0.23 fmol/ml and was significantly higher than that of control group (0.52±0.13 fmol/ml, pConclusion. In patients with II-III functional class stable angina statistically significant increase in level of endothelin-1 and a decrease in the concentration of magnesium in blood serum compared with the control group was revealed; a negative correlation between endothelin-1 and magnesium levels in the blood, which is characterized by increasing the degree of correlation depending on the severity of the ischemic heart disease clinical form was established.