Myocardial Disease Research Articles

Using machine learning to predict acute myocardial infarction and ischemic heart disease in primary care cardiovascular patients.

Early recognition, which preferably happens in primary care, is the most important tool to combat cardiovascular disease (CVD). This study aims to predict acute myocardial infarction (AMI) and ischemic heart disease (IHD) using Machine Learning (ML) in primary care cardiovascular patients. We compare the ML-models' performance with that of the common SMART algorithm and discuss clinical implications. Patient-level medical record data (n = 13,218) collected between 2011-2021 from 90 GP-practices were used to construct two random forest models (one for AMI and one for IHD) as well as a linear model based on the SMART risk prediction algorithm as a suitable comparator. The data contained patient-level predictors, including demographics, procedures, medications, biometrics, and diagnosis. Temporal cross-validation was used to assess performance. Furthermore, predictors that contributed most to the ML-models' accuracy were identified. The ML-model predicting AMI had an accuracy of 0.97, a sensitivity of 0.67, a specificity of 1.00 and a precision of 0.99. The AUC was 0.96 and the Brier score was 0.03. The IHD-model had similar performance. In both ML-models anticoagulants/antiplatelet use, systolic blood pressure, mean blood glucose, and eGFR contributed most to model accuracy. For both outcomes, the SMART algorithm was substantially outperformed by ML on all metrics. Our findings underline the potential of using ML for CVD prediction purposes in primary care, although the interpretation of predictors can be difficult. Clinicians, patients, and researchers might benefit from transitioning to using ML-models in support of individualized predictions by primary care physicians and subsequent (secondary) prevention.

Seasonal Variation in Sudden Cardiac Death: Insights from a Large United Kingdom Registry

BackgroundSudden cardiac death (SCD) is relatively common and may occur in apparently healthy individuals. The role of seasonal variation as a risk factor for SCD is poorly understood. The aim of this study was to investigate whether SCD exhibits a predilection for specific seasons. MethodsWe reviewed a database of 4751 cases of SCD (mean age 38 ± 17 years) referred to our Center for Cardiac Pathology at St George’s University of London between 2000 and 2018. Clinical information was obtained from referring coroners who were asked to complete a detailed questionnaire. All cases underwent macroscopic and histological evaluation of the heart, by expert cardiac pathologists. ResultsSCD was more common during winter (26%) and rarer during summer (24%), p = 0.161. Significant seasonal variation was not observed among cases of sudden arrhythmic death syndrome (SADS, 2910 cases) in which the heart is structurally normal. In contrast, a significant difference in seasonal distribution among decedents exhibiting cardiac structural abnormalities at the post-mortem examination (n = 1841) was observed. In this subgroup, SCDs occurred more frequently during winter (27 %) compared to summer (22%) (p = 0.007). In cases diagnosed with a myocardial disease (n = 1399), SCD was most common during the winter (27%) and least common during the summer (22%) (p = 0.027). ConclusionsWhile SADS occurs throughout the year with no seasonal variation, SCD due to structural heart disease appears to be more common during the winter. Bio-meteorological factors may be potential triggers of SCD in individuals with an underlying structural cardiac abnormality.

Shock Wave Therapy Alleviates Hypoxia/Reoxygenation-Induced Cardiomyocyte Injury by Inhibiting Both Apoptosis and Ferroptosis.

Shock wave therapy (SWT) is a new alternative therapy for patients with severe coronary artery disease that improves myocardial ischemic symptoms by delivering low-energy shock wave stimulation to ischaemic myocardium with low-energy pulsed waves. However, the specific mechanism of its protective effect is not fully understood, especially for the protective mechanism in cardiomyocytes after hypoxia/reoxygenation (H/R). We selected a rat H9c2 cardiomyocyte cell line to establish a stable H/R cardiomyocyte injury model by hypoxia/reoxygenation, and then used SWT for therapeutic intervention to explore its cardiomyocyte protective mechanisms. The results showed that SWT significantly increased cell viability and GSH levels while decreasing LDH levels, ROS levels, and MDA levels. SWT also improved mitochondrial morphology and function of cells after H/R. Meanwhile, we found that SWT could increase the expression of GPX4, xCT, and Bcl-2, while decreasing the expression of Bax and cleaved caspase-3, and inhibiting cardiomyocyte apoptosis and ferroptosis. Moreover, this protective effect of SWT on cardiomyocytes could be significantly reversed by knockdown of xCT, a key regulator protein of ferroptosis. In conclusion, our study shows that SWT can attenuate hypoxia-reoxygenation-induced myocardial injury and protect cardiomyocyte function by inhibiting H/R-induced apoptosis and ferroptosis, and this therapy may have important applications in the treatment of clinical myocardial ischemic diseases.

Morbidity and prevalence of diseases of the circulatory system in the adult population of the Kyiv region, including the working-age population.

Aim: To analyze the incidence and prevalence of diseases of the circulatory system in the adult population of the Kyiv oblast region, including the able-bodied population. Material and Methods: Medical history records on cardiovascular diseases were the materials, and statistical methods of medical and social data procession were used in the study. Results: The distribution of cardiovascular diseases in the adult population of the Kyiv oblast region was highlighted. The districts with the lowest and highest rates of myocardial infarction, strokes, ischemic disease and hypertension were found. The trends in relevant morbidity were described. Conclusions: When analyzing data from statistical reporting, it was established that before the start of a full-scale invasion and partial quarantine restrictions due to the spread of SARS-CoV-2, the incidence of diseases in the circulatory system was characterized by significant unevenness across administrative units. However, a specific area with the highest morbidity was not singled out, only in respect of which it would be necessary to carry out measures to improve the provision of medical cardiology care. In general morbidity, areas with the highest levels of morbidity were established, which need to improve the provision of cardiac care, as this is a negative socio-economic factor with the need for intervention measures.

Kiosk 4R-TC-11 - Novel Image Navigator Based Isotropic 3D Late Gadolinium Enhancement Sequence Allows Differentiation of Healthy and Diseased Left Atrial Myocardium

Kiosk 4R-TC-11 - Novel Image Navigator Based Isotropic 3D Late Gadolinium Enhancement Sequence Allows Differentiation of Healthy and Diseased Left Atrial Myocardium

Inter-scanner comparability of Z-scores for native myocardial T1 and T2 mapping

BackgroundCardiovascular Magnetic Resonance (CMR) native T1 and T2 mapping serve as robust, contrast-agent-free diagnostic tools, but hardware- and software-specific sources of variability limit the generalizability of data across CMR platforms, consequently limiting the interpretability of patient-specific parametric data. Z-scores are used to describe the relationship of observed values to the mean results as obtained in a sufficiently large normal sample. They have been successfully used to describe the severity of quantifiable abnormalities in medicine, specifically in children and adolescents. The objective of this study was to observe whether z-scores can improve the comparability of T1 and T2 mapping values across CMR scanners, field strengths, and sequences from different vendors in the same participant rather than different participants (as seen in previous studies). MethodsFifty-one healthy volunteers (26 men/25 women, mean age = 43 ± 13.51) underwent three CMR exams on three different scanners, using a Modified Look-Locker Inversion Recovery (MOLLI) 5-(3)− 3 sequence to quantify myocardial T1. For T2 mapping, a True Fast Imaging with steady-state free precession (TRUFI) sequence was used on a 3 T Skyra™ (Siemens), and a T2 Fast Spin Echo (FSE) sequence was used on 1.5 T Artist™ (GE) and 3.0 T Premier™ (GE) scanners. The averages of basal and mid-ventricular short axis slices were used to derive means and standard deviations of global mapping values. We used intra-class comparisons (ICC), repeated measures ANOVA, and paired Student’s t-tests for statistical analyses. ResultsThere was a significant improvement in intra-subject comparability of T1 (ICC of 0.11 (95% CI= −0.018, −0.332) vs 0.78 (95% CI= 0.650, 0.866)) and T2 (ICC of 0.35 (95% CI= −0.053, 0.652) vs 0.83 (95% CI= 0.726, 0.898)) when using z-scores across all three scanners. While the absolute global T1 and T2 values showed a statistically significant difference between scanners (p < 0.001), no such differences were identified using z-scores (T1z: p = 0.771; T2z: p = 0.985). Furthermore, when images were not corrected for motion, T1 z-scores showed significant inter-scanner variability (p < 0.001), resolved by motion correction. ConclusionEmploying z-scores for reporting myocardial T1 and T2 removes the variation of quantitative mapping results across different MRI systems and field strengths, improving the clinical utility of myocardial tissue characterization in patients with suspected myocardial disease.

Dilated cardiomyopathy in a green-winged saltator (Saltator similis)

Cardiovascular diseases are rarely reported in birds. Among pet birds, they are most documented in psittacine birds. Dilated cardiomyopathy is a myocardial disease frequently found in poultry but with few reports in both pet and wild birds. An elderly male green-winged saltator (Saltator similis) died suddenly after presenting intermittent clinical signs of dyspnea, weakness, and vocalization changes. A general increase in cardiac size with a bulging apex was observed at necropsy. The heart exhibited an enlarged left ventricular space and flaccid musculature on the cut section. The liver was diffusely enlarged with rounded edges. No other gross lesions were observed. Samples were collected in 10% formalin and routinely processed. Histologically, bundles of myocardial fibers were irregularly arranged, with markedly elongated myofibrils and irregular cell contours. Additionally, multifocal areas of disruption were observed between the myofibrils. Diffuse hepatic congestion of sinusoids and portal veins was observed, and diffuse edema in the interstitium and para bronchi was present in the lungs. The clinical signs observed were nonspecific and can be found in several diseases of the cardiovascular and respiratory systems of birds. The gross and histological findings are compatible with what has been described for dilated cardiomyopathy in birds; however, left ventricular dilatation is uncommon in avian patients. Heart diseases in pet birds are still underdiagnosed, and reports of cardiomyopathies are limited to psittacine birds. To the authors’ knowledge, this is the first report of a dilated cardiomyopathy in a passerine bird.

Kiosk 6R-FA-04 - Clinical Utility for Radiomics Features of Cardiac MR Images for the Diagnosis of Myocardial Diseases

Kiosk 6R-FA-04 - Clinical Utility for Radiomics Features of Cardiac MR Images for the Diagnosis of Myocardial Diseases

PATHOGENESIS OF IMMUNE DYSFUNCTION IN THE SETTING OF METABOLIK SYNDROME IN CORONARY HEAT DISEASE. QUALIFYING SCENTIFYING WORK ON THE RIGHTS OF THE MANUSCRIPT

PATHOGENESIS OF IMMUNE DYSFUNCTION IN THE SETTING OF METABOLIK SYNDROME IN CORONARY HEAT DISEASE. QUALIFYING SCENTIFYING WORK ON THE RIGHTS OF THE MANUSCRIPT

Therapeutic effects of the combination of moderate-intensity endurance training and MitoQ supplementation in rats with isoproterenol-induced myocardial injury: The role of mitochondrial fusion, fission, and mitophagy

IntroductionMitochondrial dysfunction causes myocardial disease. This study investigated the effects of MitoQ alone and in combination with moderate-intensity endurance training (EX) on cardiac function and content and mRNA expression of several proteins involved in mitochondrial quality control in isoproterenol (ISO)-induced heart injuries MethodsSeven groups of CTL, ISO, ISO-EX, ISO-MitoQ-125, ISO-MitoQ-250, ISO-EX+MitoQ-125, and ISO-EX+MitoQ-250 were assigned. Rats were trained on a treadmill, and the MitoQ groups received MitoQ in drinking water for 8 weeks, starting one week after the induction of heart injury. Arterial pressure and cardiac function indices, mRNA expression, protein content, oxidant and antioxidant markers, fibrosis, and histopathological changes were assessed by physiograph, Real-Time PCR, immunofluorescence, calorimetry, Masson’s trichrome, and H&E staining, respectively. ResultsThe impacts of MitoQ-125, EX+MitoQ-125, and EX+MitoQ-250 on arterial pressure and left ventricular systolic pressure were higher than MitoQ-250 or EX alone. ± dp/dt max were higher in ISO-EX+MitoQ-125 and ISO-EX+MitoQ-250 than ISO-MitoQ-125 and ISO-MitoQ-250 groups, respectively. Histopathological scores and fibrosis decreased in ISO-EX, ISO-MitoQ-125, ISO-EX+MitoQ-125, and ISO-EX+MitoQ-250 groups. The restoration of MFN2, PINK-1, and FIS-1 changes was higher in ISO-EX+MitoQ-125 and ISO-EX+MitoQ-250 than ISO-EX, ISO-MitoQ-125 and ISO-MitoQ-250 groups. The expression of MFN2 and PINK-1 was lower in ISO-MitoQ-125 and ISO-EX+MitoQ-125 than ISO and CTL groups. The expression of FIS-1 in ISO-EX and ISO-EX+MitoQ-250 increased compared to CTL and ISO groups. MDA decreased in ISO-MitoQ-125 and ISO-EX+MitoQ-125 groups. ConclusionExercise and MitoQ combination have additive effects on cardiac function by modulating cardiac mitochondria quality. This study provided a possible therapy to treat heart injuries.

Using geographic rescue time contours, point-of-care strategies, and spatial care paths to prepare island communities for global warming, rising oceans, and weather disasters

ObjectivesTo perform geographic contour analysis of sea and land ambulance rescue times in an archipelago subject to super typhoons; to design point-of-care testing strategies for medical emergencies and weather disasters made more intense by global warming and rising oceans; and to assess needs for prehospital testing on spatial care paths that accelerate decision making, increase efficiency, improve outcomes, and enhance standards of care in island nations.MethodsWe performed needs assessments, inspected healthcare facilities, and collected ambulance rescue times from professionals in the Bantayan Archipelago, Philippines. We mapped sea/land ambulance rescue routes and time contours. To reveal gaps, we statistically compared the fastest and slowest patient rescue times from islands/islets and barangays to the District Hospital on Bantayan Island. We developed spatial care paths (the fastest routes to care) for acute myocardial infarction, community care, and infectious diseases. We generated a compendium of prehospital diagnostic testing and integrated outcomes evidence, diagnostic needs, and public health goals to recommend point-of-care strategies that build geographic health resilience.ResultsWe observed limited access to COVID-19 assays, absence of blood gas/pH testing for critical care support, and spatial gaps in land and airborne rescues that worsened during inclement weather and sea swells. Mean paired differences (slowest-fastest) in ambulance rescue times to the District Hospital for both islands and barangays were significant (P < 0.0001). Spatial care path analysis showed where point-of-care cardiac troponin testing should be implemented for expedited care of acute myocardial infarction. Geospatial strengths comprised distributed primary care that can be facilitated by point-of-care testing, logical interisland transfers for which decision making and triage could be accelerated with onboard diagnostics, and healthcare networks amenable to medical advances in prehospital testing that accelerate treatment.ConclusionsPoint-of-care testing should be positioned upstream close to homes and island populations that have prolonged rescue time contours. Geospatially optimized point-of-need diagnostics and distributed prehospital testing have high potential to improve outcomes. These improvements will potentially decrease disparities in mortality among archipelago versus urban dwellers, help improve island public health, and enhance resilience for increasingly adverse and frequent climate change weather disasters that impact vulnerable coastal areas. [350 words].

The pathology of type 2 diabetes mellitus and relevant treatments

The prevalence rates of Type 2 Diabetes Mellitus (T2DM) continue to rise globally making it an urgent health concern warranting comprehensive examination closely scrutinizing pathophysiology causes symptoms management techniques as well as anticipated methods addressing how best to prevent or cure resulting complications. We know that T2DM is characterized by defective insulin secretion and tissues not responding adequately to treatment- a condition exclusively termed Insulin Resistance - which could influence both genetic predisposition or environmental factors like obesity or sedentary lifestyles. Increased morbidity indicators ranging from myocardial infarction peripheral vascular disease and stroke alike make timely diagnosis imperative. Lifestyle modifications offer optimal intervention possibilities for both preventing onset or long-standing concerns. A concentration on bolstering insulin sensitivity while halting progressive pancreatic cell failure that common among T2DM patients is to enhance comprehensive and effective treatment plans. From the diversity of T2DM established in terms of its symptoms points to the need for targeted preventive procedures designed towards reducing cases in the future.

Assessment of biomarkers and clinical parameters as predictors of survival in patients with chagasic heart failure.

Chagas disease, endemic in Latin America and spreading globally due to emigration, has a significant health burden, particularly in relation to chagasic heart failure (HF). Chagasic cardiomyopathy (CCM) is characterized by chronic inflammatory myocardial disease. This study aimed to identify inflammatory parameters and biomarkers that could aid in the management of patients with chagasic HF. A cohort study was conducted at a tertiary cardiology single-center over a mean follow-up period of 2.4 years. The study included patients with HF secondary to CCM enrolled between October 2013 and July 2017. Various clinical parameters, echocardiography findings, parasitemia status, brain natriuretic peptide (BNP) and troponin T (TnT) levels, and inflammatory biomarkers (IL-6, IL-10, IL-12p70, IL-17A, adiponectin, and IFN-γ) were assessed. The study encompassed a cohort of 103 patients, with a median age of 53 years and 70% being male. The left ventricular ejection fraction (LVEF) was 28%, with 40% of patients classified as NYHA II functional class. The median BNP level was 291 pg/ml. The observed mortality rate during the study period was 38.8%. Predictors of lower survival were identified as elevated levels of BNP, TnT, reduced LVEF, and increased adiponectin (thresholds: BNP > 309 pg/ml, TnT > 27.5 ng/ml, LVEF < 25.5%, adiponectin > 38 μg/mL). Notably, there was no evidence indicating a relationship between parasitemia and the inflammatory parameters with lower survival in these patients, including INF-γ, IL-6, IL-10, IL12-(p70), and IL17a. Despite the presence of a chronic inflammatory process, the evaluated inflammatory biomarkers in this cohort were not predictive of survival in patients with chagasic HF with reduced ejection fraction (HFrEF). However, reduced LVEF, elevated BNP, adiponectin levels, and troponin T were identified as predictors of lower survival in these patients.

Implications for neutrophils in cardiac arrhythmias.

Cardiac arrhythmias commonly occur as a result of aberrant electrical impulse formation or conduction in the myocardium. Frequently discussed triggers include underlying heart diseases such as myocardial ischemia, electrolyte imbalances, or genetic anomalies of ion channels involved in the tightly regulated cardiac action potential. Recently, the role of innate immune cells in the onset of arrhythmic events has been highlighted in numerous studies, correlating leukocyte expansion in the myocardium to increased arrhythmic burden. Here, we aim to call attention to the role of neutrophils in the pathogenesis of cardiac arrhythmias and their expansion during myocardial ischemia and infectious disease manifestation. In addition, we will elucidate molecular mechanisms associated with neutrophil activation and discuss their involvement as direct mediators of arrhythmogenicity.

Ginsenoside Rb2 inhibits p300-mediated SF3A2 acetylation at lysine 10 to promote Fscn1 alternative splicing against myocardial ischemic/reperfusion injury

IntroductionGinsenosides (GS) derived from Panax ginseng can regulate protein acetylation to promote mitochondrial function for protecting cardiomyocytes. However, the potential mechanisms of GS for regulating acetylation modification are not yet clear. ObjectivesThis study aimed to explore the potential mechanisms of GS in regulating protein acetylation and identify ginsenoside monomer for fighting myocardial ischemia-related diseases. MethodsThe 4D-lable free acetylomic analysis was employed to gain the acetylated proteins regulated by GS pretreatment. The co-immunoprecipitation assay, immunofluorescent staining, and mitochondrial respiration measurement were performed to detect the effect of GS or ginsenoside monomer on acetylated protein level and mitochondrial function. RNA sequencing, site-specific mutation, and shRNA interference were used to explore the downstream targets of acetylation modificationby GS. Cellular thermal shift assay and surface plasmon resonance were used for identifying the binding of ginsenoside with target protein. ResultsIn the cardiomyocytes of normal, oxygen glucose deprivation and/or reperfusion conditions, the acetylomic analysis identified that the acetylated levels of spliceosome proteins were inhibited by GS pretreatment and SF3A2 acetylation at lysine 10 (K10) was significantly decreased as a potential target of GS. Ginsenoside Rb2 was identified as one of the active ginsenoside monomers for reducing the acetylation of SF3A2 (K10), which enhanced mitochondrial respiration against myocardial ischemic injury in in vivo and in vitro experiments. RNA-seq analysis showed that ginsenoside Rb2 promoted alternative splicing of mitochondrial function-related genes and the level of fascin actin-bundling protein 1 (Fscn1) was obviously upregulated, which was dependent on SF3A2 acetylation. Critically, thermodynamic, kinetic and enzymatic experiments demonstrated that ginsenoside Rb2 directly interacted with p300 for inhibiting its activity. ConclusionThese findings provide a novel mechanism underlying cardiomyocyte protection of ginsenoside Rb2 by inhibiting p300-mediated SF3A2 acteylation for promoting Fscn1 expression, which might be a promising approach for the prevention and treatment of myocardial ischemic diseases.

Review of the potential pharmacological role of erucic acid: a monounsaturated omega-9 fatty acid.

This comprehensive review aims to provide an overview of the pharmacological properties of erucic acid (EA) and highlight areas that require further research. EA is an omega-9 fatty acid found in certain vegetable oil, such as rapeseed oil has demonstrated favourable effects in rodents, including ameliorating myocardial lipidosis (fat accumulation in the heart muscle), congestive heart disease, hepatic steatosis (fat accumulation in the liver), and memory impairments. These findings have prompted regulatory bodies to establish limits on EA content in food oils. The studies were performed on rodents and led to caution on ingesting the EA at high levels. Moreover, EA is frequently utilized as a nutritional supplement for the treatment of adrenoleukodystrophy, myocardial disease, and memory improvement. The review of the article indicated that EA improves cognitive function, has a part in Huntington's disease, interacts with peroxisome proliferator-activated receptors, inhibits elastase and thrombin, has anti-inflammatory, antioxidant, and anti-tumour properties, and inhibits influenza A virus. This article elucidates the pharmacological effects of EA, an omega-9 fatty acid.

Dynamic and Label-Free Sensing of Cardiomyocyte Responses to Nanosized Vesicles for Cardiac Oxidative Stress Injury Therapy.

Cardiac oxidative stress is a significant phenotype of myocardial infarction disease, a leading cause of global health threat. There is an urgent need to develop innovative therapies. Nanosized extracellular vesicle (nEV)-based therapy shows promise, yet real-time monitoring of cardiomyocyte responses to nEVs remains a challenge. In this study, a dynamic and label-free cardiomyocyte biosensing system using microelectrode arrays (MEAs) was constructed. Cardiomyocytes were cultured on MEA devices for electrophysiological signal detection and treated with nEVs from E. coli, gardenia, HEK293 cells, and mesenchymal stem cells (MSC), respectively. E. coli-nEVs and gardenia-nEVs induced severe paroxysmal fibrillation, revealing distinct biochemical communication compared to MSC-nEVs. Principal component analysis identified variations and correlations between nEV types. MSC-nEVs enhanced recovery without inducing arrhythmias in a H2O2-induced oxidative stress injury model. This study establishes a fundamental platform for assessing biochemical communication between nEVs and cardiomyocytes, offering new avenues for understanding nEVs' functions in the cardiovascular system.

Multidisciplinary approach in cardiomyopathies: From genetics to advanced imaging.

Cardiomyopathies are myocardial diseases characterized by mechanical and electrical dysfunction of the heart muscle which could lead to heart failure and life-threatening arrhythmias. Certainly, an accurate anamnesis, a meticulous physical examination, and an ECG are cornerstones in raising the diagnostic suspicion. However, cardiovascular imaging techniques are indispensable to diagnose a specific cardiomyopathy, to stratify the risk related to the disease and even to track the response to the therapy. Echocardiography is often the first exam that the patient undergoes, because of its non-invasiveness, wide availability, and cost-effectiveness. Cardiac magnetic resonance imaging allows to integrate and implement the information obtained with the echography. Furthermore, cardiomyopathies' genetic basis has been investigated over the years and the list of genetic mutations deemed potentially pathogenic is expected to grow further. The aim of this review is to show echocardiographic, cardiac magnetic resonance imaging, and genetic features of several cardiomyopathies: dilated cardiomyopathy (DMC), hypertrophic cardiomyopathy (HCM), arrhythmogenic cardiomyopathy (ACM), left ventricular noncompaction cardiomyopathy (LVNC), myocarditis, and takotsubo cardiomyopathy.

Multi-proteomic Biomarker Risk Scores for Predicting Risk and Guiding Therapy in Patients with Coronary Artery Disease.

Patients with established coronary artery disease (CAD) are at high residual risk for adverse events, despite guideline-based treatments. Herein, we aimed to determine whether risk scores based on multiple circulating biomarkers that represent activation of various pathophysiologically important pathways involved in atherosclerosis and myocardial dysfunction help identify those at greatest residual risk. Numerous circulating proteins, representing dysregulation of the pathways involved in the development and stability of coronary and myocardial diseases, have been identified. When aggregated together, biomarker risk scores (BRS) more accurately stratify patients with established CAD that may help target interventions in those individuals who are at elevated risk. Moreover, intensification of guideline-based therapies has been associated with parallel improvements in both BRS and outcomes, indicating that these risk scores may be employed clinically to target therapy. Multi-protein BRS are predictive of risk, independent of, and in addition to traditional risk factor assessments in patients with CAD. Those with elevated risk may benefit from optimization of therapies, and improvements in the BRS will identify those with improved outcomes.

Comprehensive review on gene mutations contributing to dilated cardiomyopathy.

Dilated cardiomyopathy (DCM) is one of the most common primary myocardial diseases. However, to this day, it remains an enigmatic cardiovascular disease (CVD) characterized by ventricular dilatation, which leads to myocardial contractile dysfunction. It is the most common cause of chronic congestive heart failure and the most frequent indication for heart transplantation in young individuals. Genetics and various other factors play significant roles in the progression of dilated cardiomyopathy, and variants in more than 50 genes have been associated with the disease. However, the etiology of a large number of cases remains elusive. Numerous studies have been conducted on the genetic causes of dilated cardiomyopathy. These genetic studies suggest that mutations in genes for fibronectin, cytoskeletal proteins, and myosin in cardiomyocytes play a key role in the development of DCM. In this review, we provide a comprehensive description of the genetic basis, mechanisms, and research advances in genes that have been strongly associated with DCM based on evidence-based medicine. We also emphasize the important role of gene sequencing in therapy for potential early diagnosis and improved clinical management of DCM.