Cause Of Heart Attack Research Articles

Spline Estimator in Nonparametric Ordinal Logistic Regression Model for Predicting Heart Attack Risk

In Indonesia, one of the main causes of death for both young and elderly people is heart attacks, and the main cause of heart attacks is non-communicable diseases such as hypertension. Deaths due to heart attacks caused by non-communicable diseases, namely hypertension, rank first in Indonesia. Therefore, predictions of the risk of having a heart attack caused by hypertension need serious attention. Further, for determining whether a patient is experiencing a heart attack, an effective method of prediction is required. One efficient approach is to use statistical models. This study discusses predicting risk of heart attack via modeling and classifying hypertension risk based on factors that influence it, namely, age, cholesterol levels, and triglyceride levels by using the spline estimator of the Nonparametric Ordinal Logistic Regression (NOLR) model. In this study, we assume an ordinal scale response variable with q categories to have an asymmetric distribution, namely, a multinomial distribution. The data used in this study are secondary data from medical records of cardiac poly patients at the Haji General Hospital in Surabaya, Indonesia. The results show that the proposed model approach has the greatest classification accuracy and sensitivity values compared to NOLR model approach using GAM, and the classical model approach, namely the Parametric Ordinal Logistic Regression (POLR) model. This means that the NOLR model approach is suitable for predicting hypertension and heart attack risks. Also, the NOLR model estimated using the LS-Spline estimator obtained is valid for predicting the risk of heart attack with accuracy value of 85% and sensitivity value of 100%.

Causal relationship between immune cells and risk of myocardial infarction: evidence from a Mendelian randomization study.

Atherosclerotic plaque rupture is a major cause of heart attack. Previous studies have shown that immune cells are involved in the development of atherosclerosis, but different immune cells play different roles. The aim of this study was to investigate the causal relationship between immunological traits and myocardial infarction (MI). To assess the causal association of immunological profiles with myocardial infarction based on publicly available genome-wide studies, we used a two-sample mendelian randomization (MR) approach with inverse variance weighted (IVW) as the main analytical method. Sensitivity analyses were used to assess heterogeneity and horizontal pleiotropy. A two-sample MR analysis was conducted using IVW as the primary method. At a significance level of 0.001, we identified 47 immunophenotypes that have a significant causal relationship with MI. Seven of these were present in B cells, five in cDC, four in T cells at the maturation stage, six in monocytes, five in myeloid cells, 12 in TBNK cells, and eight in Treg cells. Sensitivity analyses were performed to confirm the robustness of the MR results. Our results provide strong evidence that multiple immune cells have a causal effect on the risk of myocardial infarction. This discovery provides a new avenue for the development of therapeutic treatments for myocardial infarction and a new target for drug development.

Delayed ventricular septal rupture complicated with ventricular aneurysm in a case of myocardial infarction with non-obstructive coronary arteries

BackgroundMyocardial infarction with non-obstructive coronary arteries (MINOCA) is a rare cause of heart attack, which may not receive sufficient attention from patients during post-discharge treatment, especially among those with normal coronary angiography results.Case presentationWe present the case of a 65-year-old woman who was readmitted to the hospital with ventricular septal rupture (VSR) complicated by ventricular aneurysm, occurring 2 weeks after myocardial infarction. During the initial admission, coronary angiography revealed normal coronary arteries, leading to a diagnosis of MINOCA. Epicardial coronary vasospasm or coronary embolism was considered as potential causes; however, the patient did not adhere to standardized treatment upon initial discharge. The delayed VSR led to a decline in cardiac function but did not result in severe hemodynamic impairment. Following correction of heart failure with medications, the patient underwent percutaneous VSR repair 19 days after diagnosis and was discharged with a favorable recovery.ConclusionsThe occurrence of delayed VSR complicated with ventricular aneurysm in patients with MINOCA is rare, highlighting the possibility of serious complications in MINOCA cases. Both cardioprotective therapies and cause-targeted therapies are essential in the management of patients with MINOCA.

A Lipid-Structured Model of Atherosclerosis with Macrophage Proliferation

Atherosclerotic plaques are fatty deposits that form in the walls of major arteries and are one of the major causes of heart attacks and strokes. Macrophages are the main immune cells in plaques and macrophage dynamics influence whether plaques grow or regress. Macrophage proliferation is a key process in atherosclerosis, particularly in the development of mid-stage plaques, but very few mathematical models include proliferation. In this paper we reframe the lipid-structured model of Ford et al. (J Theor Biol 479:48–63, 2019. https://doi.org/10.1016/j.jtbi.2019.07.003) to account for macrophage proliferation. Proliferation is modelled as a non-local decrease in the lipid structural variable. Steady state analysis indicates that proliferation assists in reducing eventual necrotic core lipid content and spreads the lipid load of the macrophage population amongst the cells. The contribution of plaque macrophages from proliferation relative to recruitment from the bloodstream is also examined. The model suggests that a more proliferative plaque differs from an equivalent (defined as having the same lipid content and cell numbers) recruitment-dominant plaque in the way lipid is distributed amongst the macrophages. The macrophage lipid distribution of an equivalent proliferation-dominant plaque is less skewed and exhibits a local maximum near the endogenous lipid content.

Atherosclerotic changes in the aortic wall in lower monkeys

Atherosclerotic changes in the walls of arterial vessels are currently considered as one of the initial stages in the development of a number of diseases of the cardiovascular system. According to the World Health Organization, atherosclerosis is the main cause of heart attack and stroke. The similarity of pathomorphological changes in atherosclerosis in humans and in lower monkeys of the baboon hamadryad and baboon anubis species allows the use of animals of these species as laboratory models in the study of this disease. The material for morphological studies was obtained during the autopsy of 109 corpses of baboon hamadryad and baboon anubis monkeys (53 males and 56 females) in the period from 2019 to 2022. To analyze the species and age characteristics, all animals were conditionally divided into three age groups: group 1 (n=74) monkeys of both sexes aged 15-20 years; group 2 (n=23) animals of both sexes aged 21-25 years; group 3 (n=12) included animals older than 26 years. The results of the research showed that atherosclerotic changes in the aortic wall in the lower monkeys of the studied species kept in the nursery of the Kurchatov Complex of Medical Primatology of the Kurchatov Institute Research Center are detected from the age of 15. As the age of the animals increases, the changes are more pronounced. A reliable relationship between different age groups has been established. The frequency of atherosclerotic changes increases with increasing age, regardless of the sex of the animals. Morphological changes in the wall of the thoracic aorta in baboons are similar to those in human atherosclerosis.

LARP7 overexpression alleviates aortic senescence and atherosclerosis.

Atherosclerosis, characterized by the accumulation of lipid plaques on the inner walls of arteries, is the leading cause of heart attack, stroke and severe ischemic injuries. Senescent cells have been found to accumulate within atherosclerotic lesions and contribute to the progression of atherosclerosis. In our previous study, we discovered that suppressing Larp7 accelerates senescence by inhibiting Sirt1 activity, resulting in increased atherosclerosis in high-fat diet (HFD) fed and ApoE deficient (ApoEKO) mice. However, there has been no direct evidence demonstrating Larp7 per se could attenuate atherosclerosis. To this end, we generated a tetO-controlled and Cre-activated Larp7 gain-of-function mouse. Through RT-PCR and western blotting, we confirmed Larp7 overexpression in the aortas of HFD-fed ApoEKO; Larp7tetO mice. Larp7 overexpression led to increased Sirt1 activity and decreased cellular senescence signals mediated by p53/p65 in the aortas. Additionally, Larp7 overexpression reduced the presence of p16-positive senescent cells in the aortic lesions. Furthermore, Larp7 overexpression resulted in a decrease in pro-inflammatory macrophages and SASP factors. Consequently, Larp7 overexpression led to a reduction in the area of atherosclerotic lesions in HFD-fed ApoEKO; Larp7tetO mice. In summary, our study provides evidence that Larp7 overexpression holds promise as an approach to inhibit cellular senescence and prevent atherosclerosis.

Prevalence and correlates of anxiety and depressive symptoms after Spontaneous Coronary Artery Dissection (SCAD): a cross-sectional study.

Spontaneous coronary artery dissection (SCAD) is recognised as a particularly stressful cause of heart attack. However few studies have documented the prevalence of post-SCAD anxiety and depressive symptoms, or identified patients most at risk. This study documents the prevalence and correlates of post-SCAD anxiety and depressive symptoms. 310 (95% women) SCAD survivors were recruited by the Victor Chang Cardiac Research Institute from a database of 433 SCAD survivors. Participants completed an online questionnaire to gather demographic, medical and psychosocial information, including the Generalised Anxiety Disorder-7 (GAD-7) and the Patient Health Questionnaire-9 (PHQ-9). Bivariate and multivariate analyses were undertaken to identify the significant demographic, psychosocial and medical correlates of post-SCAD anxiety and depressive symptoms. Time between SCAD and questionnaire completion varied from 2 months to 18 years (mean = 5.5 years; SD = 3.5 years). Rates of anxiety and depressive symptoms were 20.7% (GAD-7 ≥ 10) and 20.9% (PHQ-9 ≥ 10) respectively, and did not vary by time since event. In bivariate analyses, correlates (p < .05) of anxiety and depressive symptoms were absence of a close confidante, financial strain, mental health diagnosis pre-SCAD, comorbid obesity, not being in paid employment (anxiety only), younger age (depression only), and not knowing another SCAD survivor (depression only). Variables retained in multivariate models were absence of a close confidante, financial strain, not being in paid employment, mental health diagnosis pre-SCAD (depression only), and younger age (depression only). This study demonstrated that over one in four SCAD survivors experience either anxiety or depressive symptoms after SCAD, and identified those who may need additional support in their psychological recovery.

The Role of Inflammation in Atherosclerosis: A Comprehensive Review of Mechanisms and Therapeutic Targets

In this review, we examine the evolving importance of inflammation in atherosclerosis, the root cause of heart attacks, and strokes. We analyze the complex processes by which inflammation drives all phases of atherosclerosis and closely assess possible targets for therapy within the inflammatory pathway. For researchers and health-care professionals seeking insight into the crucial role of inflammation in atherosclerosis and its potential for novel therapeutic approaches, this review offers a valuable resource.

New light on changes in the number and function of blood platelets stimulated by cocoa and its products.

Hyperactivation of blood platelets, one of the causes of heart attack, and other cardiovascular diseases (CVDs), is influenced by various dietary components, including phenolic compounds from vegetables, fruits, teas, wines, cocoa and its products, including chocolate. The present paper sheds new light on the effect of cocoa and its products, especially dark chocolate, on the number and function of blood platelets, and the anti-platelet activity of their constituent phenolic compounds. A review was performed of papers identified in various electronic databases, including PubMed, Science Direct, Scopus, Web of Knowledge, and Google Scholar, with the aim of determining whether their anti-platelet activity may serve as part of a sweet strategy in countering CVDs. Various studies demonstrate that cocoa consumption, especially in the form of dark chocolate, with a high flavanol concentration, has anti-platelet activity and may play a significant role in cardioprotection; they also note that cocoa consumption may be a good strategy in diminishing cardiovascular risk, including hyperactivation of blood platelets.

Cholesterol lowering depletes atherosclerotic lesions of smooth muscle cell-derived fibromyocytes and chondromyocytes.

Drugs that lower plasma apolipoprotein B (ApoB)-containing lipoproteins are central to treating advanced atherosclerosis and provide partial protection against clinical events. Previous research showed that lowering ApoB-containing lipoproteins stops plaque inflammation, but how these drugs affect the heterogeneous population of plaque cells derived from smooth muscle cells (SMCs) is unknown. SMC-derived cells are the main cellular component of atherosclerotic lesions and the source of structural components that determine the size of plaques and their propensity to rupture and trigger thrombosis, the proximate cause of heart attack and stroke. Using lineage tracing and single-cell techniques to investigate the full SMC-derived cellular compartment in progressing and regressing plaques in mice, here we show that lowering ApoB-containing lipoproteins reduces nuclear factor kappa-light-chain-enhancer of activated B cells signaling in SMC-derived fibromyocytes and chondromyocytes and leads to depletion of these abundant cell types from plaques. These results uncover an important mechanism through which cholesterol-lowering drugs can achieve plaque regression.

Development of a Novel Atherosclerotic Heart Disease Biomarker Program

Background: Atherosclerotic cardiovascular disease (ASCVD) is the leading cause of heart attack, stroke, and sudden death worldwide. Clinical risk scores help estimate the likelihood of adverse cardiac events to guide preventative strategies. Current risk scores for atherosclerotic events like heart attack and stroke use known cardiovascular risk factors including smoking, diabetes, lipid levels, and blood pressure. However, these scores underestimate risk in certain patient populations and do not predict the atherosclerotic disease in individual patients that leads to subsequent events. Our aim is to design a novel biomarker-enabled model to predict the presence and burden of coronary artery atherosclerosis in patients with diabetes, to ultimately help personalize preventive therapies that target disease burden, not just risk factors, for more effective prevention of ASCVD events.&#x0D; Methods: Patients with diabetes have been prospectively enrolled in a health plans-based screening program with co-enrollment in the Indiana Biobank, which includes coronary CT angiography, an AI-based quantitation of atherosclerosis, and biobanking of DNA, plasma, and serum. We identified candidate biomarkers based on current literature and determined which could be impactful based on cost, efficacy, and feasibility of implementation guided by interviews with potential collaborating entities.&#x0D; Results: We have identified polygenic risk scores, non-coding RNAs and candidate blood biomarkers with predictive potential for atherosclerotic heart disease. Subsequent work will entail i) direct assays of banked biospecimens for the selected minimally invasive biomarkers and ii) computational analysis to assess incremental predictive value for disease burden over clinically available risk scores.&#x0D; Conclusions and Potential Impact: We are progressing towards the development of a novel mode to predict patient-specific burden of coronary atherosclerotic disease burden in patients with diabetes. We expect that a multidimensional approach including contemporary biomarkers will improve predictive value of atherosclerotic heart disease burden, affording more tailored treatment to prevent ASCVD events.

Lasso regression and random forest analysis on variables contributing to myocardial infarction

Heart attack is a dangerous medical emergency that affects millions of people worldwide, and many factors may lead to its onset, such as high blood pressure and cholesterol. Since the cause of heart attack is very multivariate, it is imperative to understand which factors contribute more than others to achieve better clinical outcomes for heart attack patients. This paper collects data from a dataset that contains 1319 samples of eight variables that have been associated with causing increased likelihood of heart attack and aims to investigate which of the eight variables contribute to heart attack more than others. Lasso regression is applied to eliminate least relevant predicting variables in the dataset, and Random Forest model is applied to the remaining predictors to rank their relative importance to the output. It is found that the predictors troponin and KCM are the strongest contributing risk factors to the output heart attack. The finding may prove to be helpful for physicians’ heart attack diagnosis process in the future.

Non-clinical evaluation of YN001-a promising drug for atherosclerotic therapy by targeted delivery system

Abstract Background Atherosclerosis (AS) is a systemic disease and the common cause of heart attacks, strokes and peripheral vascular disease collectively referred to as cardiovascular diseases (CVD). In AS plaques, CD44 is upregulated and functionally activated on vascular endothelial cells, smooth muscle cells, and macrophages. YN001 is a liposome encapsulated Rosuvastatin calcium which was initially approved for the reduction of cholesterol levels and slowing the progression of atherosclerosis. YN001 is being developed for the treatment of AS by targeted enrichment of Rosuvastatin in the local atherosclerotic plaques by CD44 active targeting ability of HPD, one of the components of liposome. Purpose Investigating pharmacology, PK and toxicity of YN001 to evaluate its clinical use potential for AS patients. Results As expected, YN001 could bind to CD44 with KD as 485.5pm while there’s no binding affinity of non-targeted liposome (encapsulate Rosuvastatin without HPD). In stimulated human macrophages in which CD44 was overexpressed, YN001 showed enhanced uptake and higher cholesterol effluxion ability than Rosuvastatin, meanwhile more MCP-1 reduction was also observed. In ApoE AS mice model, single YN001 administration showed much higher drug concentrations in the plaque of aortas compared to Rosuvastatin (oral or iv) or non-targeted liposome which demonstrated targeted enrichment ability by HPD. With repeat treatment of YN001 at 5mg/kg in AS mice model, atherosclerotic plaque weight decreasing and plaque area reduction were observed, following MCP-1 reduction. YN001 may down-regulate the expression of inflammatory signaling pathways, such as chemokine-related signaling pathway to reduce the inflammatory response of atherosclerotic plaques to decrease plaque levels. In pharmacokinetic studies in rats and dogs, YN001 had much higher exposure in plasma and prolonged existence compared to Rosuvastatin i.v administration. A comprehensive safety evaluation package was performed in rats and dogs including safety pharmacology, general toxicity, genotoxicity, immunotoxicity and local tolerance. Results showed YN001 has promising safety with NOAEL as 40mg/kg in both or rats and dogs. Conclusion YN001 demonstrated excellent efficacy in AS model, a favorable pharmacokinetic and safety profiles in rats and dogs. These support its FDA IND approval and phase I study is ongoing to investigate further character in clinical.Efficacy and pharmacokinetics resultsSafety evaluation

The inflammatory oxidant peroxynitrous acid modulates the structure and function of the recombinant human V3 isoform of the extracellular matrix proteoglycan versican

Continued oxidant production during chronic inflammation generates host tissue damage, with this being associated with pathologies including atherosclerosis. Atherosclerotic plaques contain modified proteins that may contribute to disease development, including plaque rupture, the major cause of heart attacks and strokes. Versican, a large extracellular matrix (ECM) chondroitin-sulfate proteoglycan, accumulates during atherogenesis, where it interacts with other ECM proteins, receptors and hyaluronan, and promotes inflammation. As activated leukocytes produce oxidants including peroxynitrite/peroxynitrous acid (ONOO−/ONOOH) at sites of inflammation, we hypothesized that versican is an oxidant target, with this resulting in structural and functional changes that may exacerbate plaque development. The recombinant human V3 isoform of versican becomes aggregated on exposure to ONOO−/ONOOH. Both reagent ONOO−/ONOOH and SIN-1 (a thermal source of ONOO−/ONOOH) modified Tyr, Trp and Met residues. ONOO−/ONOOH mainly favors nitration of Tyr, whereas SIN-1 mostly induced hydroxylation of Tyr, and oxidation of Trp and Met. Peptide mass mapping indicated 26 sites with modifications (15 Tyr, 5 Trp, 6 Met), with the extent of modification quantified at 16. Multiple modifications, including the most extensively nitrated residue (Tyr161), are within the hyaluronan-binding region, and associated with decreased hyaluronan binding. ONOO−/ONOOH modification also resulted in decreased cell adhesion and increased proliferation of human coronary artery smooth muscle cells. Evidence is also presented for colocalization of versican and 3-nitrotyrosine epitopes in advanced (type II-III) human atherosclerotic plaques. In conclusion, versican is readily modified by ONOO−/ONOOH, resulting in chemical and structural modifications that affect protein function, including hyaluronan binding and cell interactions.

Enhancing the biopharmaceutical attributes of atorvastatin calcium using polymeric and lipid-polymer hybrid nanoparticles: An approach for atherosclerosis treatment

Atherosclerosis is associated with inflammation in the arteries, a significant cause of heart attacks and strokes. Although statin therapy can reduce the chances of atherosclerotic plaque formation, they need to be administered in high doses due to low systemic bioavailability and encountered with side effects. To overcome these challenges, we developed nanoparticles using biocompatible and biodegradable lipids and polymers for improving systemic drug absorption and therapeutic response. The polymeric nanoparticles were prepared using PLGA and PVA, while hybrid nanoparticles were prepared using PLGA and Phospholipon 90 G. Both nanoparticles were systematically optimized by I-optimal response surface design. The optimum formulation composition exhibited particle size of less than 250 nm, polydispersity index of less than 0.3, entrapment efficiency of more than 70%, and sustained drug release up to 6 h. In vivo pharmacokinetic evaluation in rats indicated multi-fold improvement in the extent of drug absorption (Cmax and AUCtotal) for atorvastatin from the nanoparticles vis-à-vis the pure drug suspension. In vivo pharmacodynamic studies also indicated the excellent ability of nanoparticles to lower the elevated levels of lipids (total cholesterol, triglycerides, and low-density lipoproteins) and increase the level of high-density lipoproteins as compared to that of the pure drug suspension.

Hydrodynamic theory of atherosclerosis formation in humans - «Reaction to spasm». Cylindrical cholesterol plaque is the cause of heart attack and stroke.

An analysis of scientific literature, photo and video materials showed that plaques in humans are completely different from plaques in animals and the «contemporary official description» of AS. They differ in appearance, lack of inflammation of the walls of the artery, clinical manifestations, complications. It has also been found that «true» plaque has nothing to do with the first four types of atherosclerosis in humans. It was necessary to understand how in the lumen of a healthy artery a strong, elastic, yellow, homogeneous plaque in the form of a hollow cylinder - a «cylindrical plaque» - appears very quickly? As a result, the «Hydrodynamic Theory» was proposed, which answers all the complex questions related to the appearance, aging and destruction of «true» plaques in humans. It describes the etiology, pathogenesis, clinical manifestations, classification, complications, methods of treatment and prevention of «cylindrical» plaques that cause heart attacks and strokes in humans.

TRIM59 attenuates ox-LDL-induced endothelial cell inflammation, apoptosis, and monocyte adhesion through AnxA2.

Atherosclerosis (AS), a chronic inflammatory vascular disease, is a cause of heart attack and ischemic stroke. Tripartite motif-containing protein 59 (TRIM59), a member of the tripartite motif family, has been reported to be involved in inflammatory diseases. This study was to investigate the role of TRIM59 in oxidized low-density lipoprotein (ox-LDL)-induced endothelial cells and examine the mechanism of TRIM59. To simulate a cellular model of AS in vitro, varying concentrations of ox-LDL (i.e., 20, 40, 60, 80, and 100 µg/mL) were used to treat the human umbilical vein endothelial cells (HUVECs) for 24 h. The messenger ribonucleic acid (RNA) and protein levels of TRIM59, lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1), and annexin 2 (AnxA2) were examined by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blot. The transfection efficacy of overexpression (Ov)-TRIM59 and small-interfering RNA-AnxA2 was examined by RT-qPCR and western blot. Cell counting kit-8 assays, lactate dehydrogenase (LDH) assays, enzyme-linked immunosorbent assays, and terminal-deoxynucleotidyl transferase mediated nick end labeling staining were used to examine viability, LDH expression, inflammation, and apoptosis in HUVECs. The protein levels of B-cell lymphoma 2, Bcl-2-associated X (BAX), cleaved caspase3, intercellular adhesion molecule 1, and vascular cell adhesion molecule 1 were assessed by western blot. Additionally, the adhesion of THP-1 to ox-LDL-induced HUVECs was detected using monocyte adhesion assays and the binding of TRIM59 and AnxA2 was verified by co-immunoprecipitation. This study showed that TRIM59 expression was decreased in the ox-LDL-induced HUVECs while LOX-1 expression was increased. After transfection with Ov-TRIM59, TRIM59 in ox-LDL-induced HUVECs was increased, and TRIM59 overexpression alleviated the viability damage, inflammation, and apoptosis of the ox-LDL-induced HUVECs. In addition, THP-1 adhesion to the ox-LDL-induced HUVECs was also suppressed by TRIM59 overexpression. This study also showed that TRIM59 could bind to AnxA2 and promote AnxA2 expression in ox-LDL-stimulated HUVECs. Moreover, the rescue experiments revealed that TRIM59 suppressed the viability damage, inflammation, apoptosis, and monocyte adhesion of the ox-LDL-induced HUVECs via AnxA2. TRIM59 protected against ox-LDL-induced AS by binding to AnxA2.

Vessels Segmentation in Angiograms Using Convolutional Neural Network: A Deep Learning Based Approach

Coronary artery disease (CAD) has become a significant cause of heart attack, especially among those 40 years old or younger. There is a need to develop new technologies and methods to deal with this disease. Many researchers have proposed image processing-based solutions for CAD diagnosis, but achieving highly accurate results for angiogram segmentation is still a challenge. Several different types of angiograms are adopted for CAD diagnosis. This paper proposes an approach for image segmentation using Convolution Neural Networks (CNN) for diagnosing coronary artery disease to achieve state-of-the-art results. We have collected the 2D X-ray images from the hospital, and the proposed model has been applied to them. Image augmentation has been performed in this research as it’s the most significant task required to be initiated to increase the dataset’s size. Also, the images have been enhanced using noise removal techniques before being fed to the CNN model for segmentation to achieve high accuracy. As the output, different settings of the network architecture undoubtedly have achieved different accuracy, among which the highest accuracy of the model is 97.61%. Compared with the other models, these results have proven to be superior to this proposed method in achieving state-of-the-art results.

Metabolomic Profiling in Atherosclerotic Lesions and the Effect of Heavy Metals on the Course of Disease: A Literature Review

Introduction: In the developed metallurgical industry, maximum permissible concentrations of heavy metals in the work environment are often exceeded, and the elevated exposure levels have a detrimental effect on workers’ health. Heavy metals cause oxidative stress, which is key factor in the development of atherosclerotic lesions. Atherosclerosis, in its turn, is the primary cause of heart attacks and stroke, which account for 85 % of all deaths from cardiovascular diseases. Objective: To study molecular mechanisms of atherosclerosis and the impact of heavy metals on the disease course. Methods: We applied methods of information analysis based on the review and generalization of published up-to-date research data on the pathogenesis and effects of heavy metals on the course of atherosclerosis found in NLM, Scopus, CyberLeninka, Google Scholar, and eLibrary abstract and citation databases, as well as on information portals, as of January 2022. More than 400 papers were analyzed and 66 full-text articles were found eligible for inclusion in this review. Results: We established the relationship between the exposure to heavy metals and the molecular mechanisms of atherosclerosis and compared the main stages of the disease development with the respective blood metabolomic profiles. Conclusions: Our literature review has revealed problems in the regulatory framework and practical assessment of the contribution of heavy metal exposures to the course of atherosclerotic lesions. So far, the effect of heavy metals only on isolated processes of the pathogenesis of atherosclerosis has been established, such as a change in permeability and destruction of vascular membranes, increased oxidative stress, inflammation, proliferation of smooth muscle cells, changes in blood rheological properties, and an increased risk of thrombosis. The observed patterns in the change in concentrations of some blood metabolites and the potential adverse vascular effect of heavy metals will help develop new methods for detecting atherosclerosis and include industrial workers in the group at risk of the disease for its early diagnosis.

Deep learning models on Heart Disease Estimation - A review

Heart disease, also known as cardiovascular disease (CVD), is the foremost among all widespread diseases in the people community. Any disorder that affects the heart's function is typically called heart disease. Narrowing or blockage of the coronary arteries, which supply blood to the heart, is the most common cause of heart failure. Coronary Artery Disease (CAD) is a common form of heart disease and the leading cause of heart attacks. Nowadays, there is no age limit for people to get affected by this disease. There are so many diagnosis methods available where most are costly, the risk involved, and technical experts are needed to perform the disease diagnosis. Clinical research has pointed out different factors that increase the risk of CAD and heart attack. These factors can be categorized into two types, i.e., risk factors that cannot be changed and those that can be changed. Sex, age and family history are those factors that cannot be altered. In contrast, factors related to a subject's lifestyle, e.g., smoking, high cholesterol, high blood pressure and physical inactivity, can be changed. This paper reviews various deep learning techniques involving heart disease prognostic and their accuracy in predicting that they can be treated in advance to prevent fatalities.