Current Cardiology Reviews[JOURNAL]
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200 papers
Unlocking Platelet Mechanisms through Multi-omics Integration: A Brief Review.
Fareed MM, Qasmi M, Khan Z … +4 more , Ali H, Stavrakis S, Förster CY, Shityakov S
Curr Cardiol Rev · 2025 · PMID 39812040 · Full text
Platelets, tiny cell fragments measuring 2-4 μm in diameter without a nucleus, play a crucial role in blood clotting and maintaining vascular integrity. Abnormalities in platelets, whether genetic or acquired, are linked...
Platelets, tiny cell fragments measuring 2-4 μm in diameter without a nucleus, play a crucial role in blood clotting and maintaining vascular integrity. Abnormalities in platelets, whether genetic or acquired, are linked to bleeding disorders, increased risk of blood clots, and cardiovascular diseases. Advanced proteomic techniques offer profound insights into the roles of platelets in hemostasis and their involvement in processes such as inflammation, metastasis, and thrombosis. This knowledge is vital for drug development and identifying diagnostic markers for platelet activation. Platelet activation is an exceptionally rapid process characterized by various posttranslational modifications, including protein breakdown and phosphorylation. By utilizing multiomics technologies and biochemical methods, researchers can thoroughly investigate and define these posttranslational pathways. The absence of a nucleus in platelets significantly simplifies mass spectrometry-based proteomics and metabolomics, as there are fewer proteins to analyze, streamlining the identification process. Additionally, integrating multiomics approaches enables a comprehensive examination of the platelet proteome, lipidome, and metabolome, providing a holistic understanding of platelet biology. This multifaceted analysis is critical for elucidating the complex mechanisms underpinning platelet function and dysfunction. Ultimately, these insights are crucial for advancing therapeutic strategies and improving diagnostic tools for platelet-related disorders and cardiovascular diseases. The integration of multi-omics technologies is paving the way for a deeper understanding of platelet mechanisms, with significant implications for biomedical research and clinical applications.
Molecular and Functional Significance of Growth Differentiation Factor-15: A Review on Cardiovascular-Kidney-Metabolic Biomarker.
Tiwari K, Saravanan A, Anil A … +6 more , Tiwari VK, Shamim MA, Singh S, Dwivedi P, Deora S, Varthya SB
Curr Cardiol Rev · 2025 · PMID 39781722 · Full text
Cardiovascular-kidney-metabolic (CKM) syndrome is the association between obesity, diabetes, CKD (chronic kidney disease), and cardiovascular disease. GDF-15 mainly acts through the GFRAL (Glial cell line-derived neurotr...
Cardiovascular-kidney-metabolic (CKM) syndrome is the association between obesity, diabetes, CKD (chronic kidney disease), and cardiovascular disease. GDF-15 mainly acts through the GFRAL (Glial cell line-derived neurotrophic factor Family Receptor Alpha-Like) receptor. GDF-15 and GDFRAL complex act mainly through RET co-receptors, further activating Ras and phosphatidylinositol-3-kinase (PI3K)/Akt pathways through downstream signaling. GDF-15 decreases cardiac dysfunction and hypertrophy by inducing HIF-α (hypoxia-inducible factor-1α). It causes increased fractional shortening and a significant decrease in ventricular dilation through the induction of the SMAD 2/3. GDF-15 prevents hyperglycemia-induced apoptosis in diabetes mellitus. GDF-15 causes anorexia by influencing the central systems regulating metabolism and appetite. Therefore, targeting GDF-15 can be useful for the treatment of anorexia caused by cancer as well as the prevention of resulting weight loss. GDF-15 has an important role in predicting mortality in acute kidney injury. Its high levels are related to eGFR decline and also have a prognostic role in CKD patients. Growth differentiation factor-15 (GDF-15) is a vital biomarker for diagnosis, treatment, and prognosis of CKM syndrome. Elevated GDF-15 levels can be utilised as a biomarker to determine the suitable metformin dosage. In light chain amyloidosis, a raised level of GDF-15 predicts early death in heart failure and renal disease patients. In vivo, studies using GDF-15 analogs and antibodies against GFRAL to affect metabolic parameters and ventricular dilatation have shown potential for GDF-15-based therapeutic interventions. This review aims to study the role of GDF-15 in CKM syndrome and establish it as a CKM biomarker.
The Intersection of Heart Failure and Iron Deficiency Anemia: Diagnostic and Therapeutic Approaches.
Thammitage MB, Moussa N, Rezvani A … +9 more , Dhillon DK, Gamarra MLO, Singh K, Hawwa A, Vicente AF, Kaur S, Nemalapuri KS, Poonwassie D, Rai M
Curr Cardiol Rev · 2025 · PMID 39773062 · Full text
Iron deficiency anemia (IDA) is highly prevalent among individuals with heart failure (HF), impacting 40-70% of patients and serving as a significant prognostic indicator. Linked with oxidative metabolism and myocardial...
Iron deficiency anemia (IDA) is highly prevalent among individuals with heart failure (HF), impacting 40-70% of patients and serving as a significant prognostic indicator. Linked with oxidative metabolism and myocardial cell damage, IDA exacerbates HF symptoms, including reduced exercise capacity, diminished quality of life, and heightened cardiovascular morbidity. This review explores the diagnosis, treatment, clinical outcomes, prognostic indicators, and forthcoming challenges associated with IDA in HF patients. Crucially, addressing IDA in HF is critical for enhancing prognosis, including clinical outcomes, quality of life, hospitalizations, and survival rates. While oral iron therapy shows efficacy in reducing mortality and hospitalizations, it falls short in improving exercise capacity and quality of life, often deterring patients due to side effects. In contrast, intravenous (IV) iron therapy is highly effective in enhancing hematological parameters, functional capacity, and reducing HF hospitalizations. Optimizing IV iron dosing based on individual patient characteristics is essential for balancing treatment efficacy and adverse effects. Emphasizing individualized approaches, with IV iron emerging as a superior option, underscores the necessity for ongoing research to refine dosing strategies and explore novel therapies. Compliance remains paramount for positive outcomes with IDA treatment, with oral supplementation being cost-effective and easily accessible. However, parenteral supplementation proves beneficial for patients intolerant to oral therapy. Addressing IDA through tailored interventions, including oral or parenteral supplementation, is pivotal in averting complications and improving outcomes in HF patients. This paper consolidates insights into the diagnosis, treatment, impact, pathophysiology, clinical outcomes, research gaps, and future directions concerning IDA in HF patients, drawing on extensive literature to offer a comprehensive understanding of this critical issue.
Successful use of Proprotein Convertase Subtilisin/Kexin Type 9 Inhibitors in Hypertriglyceridemia-induced Acute Pancreatitis: A Case Report.
Qi R, Liu H, Li X … +1 more , Chen M
Curr Cardiol Rev · 2025 · PMID 39773061 · Full text
INTRODUCTION: Managing hypertriglyceridemia-induced acute pancreatitis (HTG-AP) can be challenging, particularly due to the need for rapid triglyceride reduction to below 500mg/dL (5.645 mmol/L). CASE REPORT: This is a c...
INTRODUCTION: Managing hypertriglyceridemia-induced acute pancreatitis (HTG-AP) can be challenging, particularly due to the need for rapid triglyceride reduction to below 500mg/dL (5.645 mmol/L). CASE REPORT: This is a case describing a 39-year-old female patient who presented to the Emergency Department with acute abdominal pain resulting from severe HTG-AP. However, under conventional therapy with oral lipid-lowering drugs, the triglyceride levels remained uncontrolled. Oral moderate-intensity statins could not only reduce low-density lipoprotein cholesterol (LDLc) by 25%-50%. However, increasing the dose could not further reduce blood lipids while increasing the risk of liver damage. After the administration of proprotein convertase subtilisin/ kexin type 9 inhibitor (PCSK9i), the triglyceride levels were well controlled with no additional side effects, and the symptoms of the patients were completely relieved. CONCLUSION: In cases of unsatisfactory lipid control under conventional therapy, PCSK9i may offer a viable option for managing HTG-AP.
Identifying Biomarkers for Atherosclerosis via Gene Expression and Biological Networking.
Chhotaray S, Jal S
Curr Cardiol Rev · 2025 · PMID 39773060 · Full text
INTRODUCTION: Atherosclerosis is a chronic disease caused by the accumulation of lipids, inflammatory cells, and fibrous elements in arterial walls, leading to plaque formation and cardiovascular conditions like coronary...
INTRODUCTION: Atherosclerosis is a chronic disease caused by the accumulation of lipids, inflammatory cells, and fibrous elements in arterial walls, leading to plaque formation and cardiovascular conditions like coronary artery disease, stroke, and peripheral arterial disease. Factors like hyperlipidemia, hypertension, smoking, and diabetes contribute to its development. Diagnosis relies on imaging and biomarkers, while management includes lifestyle modifications, pharmacotherapy, and surgical interventions. Computational biology is transforming biological knowledge into clinical practice by identifying biomarkers that can predict clinical outcomes. This involves omics data, predictive modeling, and data integration. Statistical analysis-based methods are also being developed to develop and integrate methods for screening, diagnosing, and prognosing atherosclerosis. METHODOLOGY: The present work aimed to uncover critical genes and pathways to enhance the understanding of the mechanism of atherosclerosis. GSE23746 was analyzed to find differentially expressed genes (DEGs) using 19 control samples and 76 atherosclerotic samples. RESULTS: A total of 76 DEGs were identified. Analysed DEGs using Gene Ontology (GO) and Kyoto Encyclopaedia of Genes and Genomes (KEGG) to generate enrichment datasets. A Protein- protein Interaction (PPI) network of DEGs was created utilizing the Search Tool for the Retrieval of Interacting Genes (STRING). CONCLUSION: Ten hub genes, namely EGR1, PTGS2, TNF, NFKBIA, CXCL8, TNFAIP3, CCL3, IL1B, PTPRC, and CD83, were found to be significantly linked to atherosclerosis. Furthermore, the metabolic pathway analysis through KEGG and STRING provides potential targets for therapeutic interventions through HUB genes to diagnose the illness at an early stage, which aids in the reduction of cardiovascular risk. From risk factor profiling to the discovery of novel biomarkers, several components such as phospholipids, ANGPTL3, LCAT, and the proteinencoded OCT-1 gene, play a vital role in crucial processes. These compounds are potential therapeutic targets for early diagnosis of atherosclerotic lesions and future novel biomarkers.
Unlocking the Potential: Phytoestrogens and Cardiovascular Health.
Gulati A, Banker H, Muhammad AA … +2 more , Anamika F, Jain R
Curr Cardiol Rev · 2025 · PMID 39757642 · Full text
Phytoestrogens are plant-derived compounds resembling human estrogen and have recently gained attention due to their potential role in improving cardiovascular health. These compounds exert their effects through various...
Phytoestrogens are plant-derived compounds resembling human estrogen and have recently gained attention due to their potential role in improving cardiovascular health. These compounds exert their effects through various mechanisms, including interactions with estrogen receptors, growth factor receptors, inflammatory mediators, thrombogenic reactions, and apoptotic pathways. This results in cardioprotective effects like modulating endothelial function, decreasing vessel tone, reducing inflammation, altering lipid profiles, and influencing arrhythmogenesis. Recent studies indicate the intricate and multidimensional association between phytoestrogens and cardiovascular disease. Despite the overwhelming evidence that phytoestrogen intake lowers the risk of myocardial infarction (MI), prevents atherosclerosis, improves cardiac function, prevents hypertension, and reduces the risk of arrhythmias, there have been studies that show contradictory outcomes. For this reason, the therapeutic use of phytoestrogens for the treatment of cardiovascular diseases, which appears to be extremely promising, should be handled cautiously, considering the individual variances, dosage, and the specific components of phytoestrogens. This review consolidates findings on the effects of phytoestrogens on the heart and blood vessels, explores the mechanisms behind these interactions, and seeks to determine the best methods for using phytoestrogens as a supplement in managing and preventing cardiovascular disease. By understanding these aspects, we can better evaluate the potential of phytoestrogens in cardiovascular health and develop guidelines for their safe and effective use.
Serum Cortisol and Cardiovascular Disease Risk - A Potential Biomarker.
Oo WJ, Lim CL, Goh MH … +1 more , Koh RY
Curr Cardiol Rev · 2025 · PMID 39754772 · Full text
Cardiovascular disease (CVD), the leading cause of death globally, poses a significant burden on the healthcare sector. Its association with stress and Cushing's Syndrome has driven cortisol, the 'stress hormone,' to be...
Cardiovascular disease (CVD), the leading cause of death globally, poses a significant burden on the healthcare sector. Its association with stress and Cushing's Syndrome has driven cortisol, the 'stress hormone,' to be a potential candidate in determining CVD risk. Cortisol synthesis and release through the hypothalamic-pituitary-adrenal (HPA) axis are regulated by several hormones and receptors involved in the pathological cascade towards CVD. Evidence suggests that metabolic syndrome plays a major role in cortisol-mediated CVD risk. On the other hand, non-metabolic features are also implicated when the association between cortisol and CVD risk remains significant upon normalisation of metabolic parameters. Correspondingly, the treatment for hypercortisolism is often found effective in lowering CVD risk. Despite available evidence, several factors continue to hinder the clinical use of cortisol as a risk biomarker for CVD. This review provides an insight into the role of serum cortisol in CVD progression and risk, with emphasis on the mechanistic features and parameters.
Disparities in Peripheral Artery Disease-related Mortality in Chronic Inflammatory Disease in the United States from 1999 to 2020.
Olson A, Pham HN, Ibrahim R … +3 more , Salih M, Singh A, Mamas MA
Curr Cardiol Rev · 2025 · PMID 39660527 · Full text
INTRODUCTION: Peripheral arterial disease (PAD) is a marker of significant atherosclerotic cardiovascular disease and is associated with greater healthcare burden and worse prognosis in individuals with chronic inflammat...
INTRODUCTION: Peripheral arterial disease (PAD) is a marker of significant atherosclerotic cardiovascular disease and is associated with greater healthcare burden and worse prognosis in individuals with chronic inflammatory disease (CID). We aimed to investigate temporal trends and disparities of PAD-related mortality in populations with CID from 1999-2020 across six common CIDs (i.e., chronic viral hepatitis, human immunodeficiency virus, inflammatory bowel disease, psoriasis, rheumatoid arthritis, and systemic lupus erythematosus). METHODS: United States (US) PAD and CID-related mortality and demographic data from 1999- 2020 were extracted from the CDC database through the multiple-cause-of-death files. Ageadjusted mortality rates (AAMR) per 1,000,000 and 95% confidence intervals were standardized to the 2000 US population. The mortality trends were analyzed using Joinpoint Regression. RESULTS: A total of 22,175 PAD-related deaths were recorded in the population with CID between 1999 and 2020. Mortality remained stable during the 22-year period (AAPC -0.04%, p=0.95) with a cumulative AAMR of 4.64. Mortality was highest in rural counties (AAMR 5.27), and among non-Hispanic Black populations (AAMR 7.06). Among the CID subtypes, PAD mortality was highest in populations with RA (AAMR 2.48) and lowest in populations with psoriasis (AAMR 0.11). CONCLUSION: Our findings highlight the disparities of PAD mortality in patients with CID, with the Black population and rural communities disproportionately affected. Further investigation with individual- level data is warranted to identify the contributing factors for the observed disparities.
Atrial Fibrillation Ablation in Heart Failure and Preserved Ejection Fraction: An Observational Study of Risk Factors for Heart Failure Hospitalization.
Qi R, Liu H, Zhu Y … +9 more , Wu N, Wang K, Ding X, Gu Z, Li M, Chen H, Ju W, Li X, Chen M
Curr Cardiol Rev · 2025 · PMID 39660492 · Full text
INTRODUCTION: Long-term heart failure hospitalization (HFH) after radiofrequency catheter ablation (RFCA) in atrial fibrillation (AF) patients with heart failure and preserved ejection fraction (HFpEF) and its risk facto...
INTRODUCTION: Long-term heart failure hospitalization (HFH) after radiofrequency catheter ablation (RFCA) in atrial fibrillation (AF) patients with heart failure and preserved ejection fraction (HFpEF) and its risk factors remain to be investigated. METHODS: AF patients with HFpEF who underwent RFCA from January, 2014 to December, 2018 from three centers were retrospectively included. Patients were assigned to the training and testing cohorts, respectively. In the training cohort, logistic regression analyses were performed to discriminate those with and without HFH. A scoring system was developed accordingly and validated. RESULTS: A total of 417 AF patients with HFpEF receiving RFCA were enrolled. About 35 patients (8.4%) had HFH for 6 years. In the training cohort, the use of diuretics, atrial tachycardia (AT)/AF recurrence, prior HFH, and female sex were independent predictors of HFH in the multivariable analysis. A DAPF score (ranging from 0 to 9.0) was developed. The area under the receiver operating characteristic curve (AUC) of the DAPF score was 0.880 (95% CI, 0.830- 0.929). A DAPF score ≥3.5 could predict HFH with a sensitivity of 81.8% and a specificity of 74.6%. The performance in the testing cohort remained robust (AUC, 0.858; 95% CI, 0.749- 0.967). CONCLUSION: HFH in patients with AF and HFpEF after RFCA is not rare. The DAPF score could predict the risk of HFH in AF patients with HFpEF after RFCA and guide our treatment strategy.
Elevated Perspectives: Unraveling Cardiovascular Dynamics in High-Altitude Realms.
Aggarwal K, Pathan MS, Dhalani M … +5 more , Kaur IP, Anamika F, Gupta V, Jayaraman DK, Jain R
Curr Cardiol Rev · 2025 · PMID 39506447 · Full text
High-altitude regions pose distinctive challenges for cardiovascular health because of decreased oxygen levels, reduced barometric pressure, and colder temperatures. Approximately 82 million people live above 2400 meters...
High-altitude regions pose distinctive challenges for cardiovascular health because of decreased oxygen levels, reduced barometric pressure, and colder temperatures. Approximately 82 million people live above 2400 meters, while over 100 million people visit these heights annually. Individuals ascending rapidly or those with pre-existing cardiovascular conditions are particularly vulnerable to altitude-related illnesses, including Acute Mountain Sickness (AMS) and Chronic Mountain Sickness (CMS). The cardiovascular system struggles to adapt to hypoxic stress, which can lead to arrhythmias, systemic hypertension, and right ventricular failure. Pathophysiologically, high-altitude exposure triggers immediate increases in cardiac output and heart rate, often due to enhanced sympathetic activity. Over time, acclimatisation involves complex changes, such as reduced stroke volume and increased blood volume. The pulmonary vasculature also undergoes significant alterations, including hypoxic pulmonary vasoconstriction and vascular remodelling, contributing to conditions, like pulmonary hypertension and high-altitude pulmonary edema. Genetic adaptations in populations living at high altitudes, such as gene variations linked to hypoxia response, further influence these physiological processes. Regarding cardiovascular disease risk, stable coronary artery disease patients generally do not face significant adverse outcomes at altitudes up to 3500 meters. However, those with unstable angina or recent cardiac interventions should avoid high-altitude exposure to prevent exacerbation. Remarkably, high-altitude living correlates with reduced cardiovascular mortality rates, possibly due to improved air quality and hypoxia-induced adaptations. Additionally, there is a higher incidence of congenital heart disease among children born at high altitudes, highlighting the profound impact of hypoxia on heart development. Understanding these dynamics is crucial for managing risks and improving health outcomes in high-altitude environments.
Diabetic Cardiomyopathy: An Update on Emerging Pathological Mechanisms.
Kakkar C, Sharma V, Mannan A … +8 more , Gupta G, Singh S, Kumar P, Dua K, Kaur A, Singh S, Dhiman S, Singh TG
Curr Cardiol Rev · 2025 · PMID 39501954 · Full text
Diabetic Cardiomyopathy (DCM) is a notable consequence of diabetes mellitus, distinguished by cardiac dysfunction that occurs separately from coronary artery disease or hypertension. A recent study has revealed an intric...
Diabetic Cardiomyopathy (DCM) is a notable consequence of diabetes mellitus, distinguished by cardiac dysfunction that occurs separately from coronary artery disease or hypertension. A recent study has revealed an intricate interaction of pathogenic processes that contribute to DCM. Important aspects involve the dysregulation of glucose metabolism, resulting in heightened oxidative stress and impaired mitochondrial function. In addition, persistent high blood sugar levels stimulate inflammatory pathways, which contribute to the development of heart fibrosis and remodelling. Additionally, changes in the way calcium is managed and the presence of insulin resistance are crucial factors in the formation and advancement of DCM. This may be due to the involvement of many molecular mechanistic pathways such as NLRP3, NF-κB, PKC, and MAPK with their downstream associated signaling pathways. Gaining a comprehensive understanding of these newly identified pathogenic pathways is crucial in order to design precise therapy approaches that can enhance the results for individuals suffering from diabetes. In addition, this review offers an in-depth review of not just pathogenic pathways and molecular mechanistic pathways but also diagnostic methods, treatment options, and clinical trials.
Heart Rate Variability and Heart Failure with Reduced Ejection Fraction: A Systematic Review of Literature.
Nagai M, Ewbank H, Nakano Y … +3 more , Scherlag BJ, Po SS, Dasari TW
Curr Cardiol Rev · 2025 · PMID 39492768 · Full text
INTRODUCTION: Autonomic impairment is a hallmark of heart failure with reduced ejection fraction (HFrEF). While there have been studies on general values for each index of heart rate variability (HRV) analysis in HFrEF,...
INTRODUCTION: Autonomic impairment is a hallmark of heart failure with reduced ejection fraction (HFrEF). While there have been studies on general values for each index of heart rate variability (HRV) analysis in HFrEF, a systematic review comprehensively examining representative values in HFrEF is lacking. METHODS: We searched PubMed, Embase, and Cochrane databases to extract studies reporting representative values of HRV metrics in HFrEF. RESULTS: A total of 470 HFrEF patients from 6 studies were included in the review. In general, time and frequency domains were abnormally lower in HFrEF, portending a worse prognosis. In HFrEF, the mean or median value of the standard deviation of NN interval, root mean square successive difference, pNN50, and low-frequency power/high-frequency power were 40 to 121 msec, 19 to 62 msec, 1.3 to 14%, and 1.00 to 1.73, respectively. CONCLUSION: In this systematic review, most HRV metrics were found to be calculated from 24- hour Holter recordings and were lower in HFrEF patients with poor prognosis.
Unveiling the Complexities: Exploring Mechanisms of Anthracyclineinduced Cardiotoxicity.
Tayal R, Mannan A, Singh S … +2 more , Dhiman S, Singh TG
Curr Cardiol Rev · 2025 · PMID 39484769 · Full text
The coexistence of cancer and heart disease, both prominent causes of illness and death, is further exacerbated by the detrimental impact of chemotherapy. Anthracycline-induced cardiotoxicity is an unfortunate side effec...
The coexistence of cancer and heart disease, both prominent causes of illness and death, is further exacerbated by the detrimental impact of chemotherapy. Anthracycline-induced cardiotoxicity is an unfortunate side effect of highly effective therapy in treating different types of cancer; it presents a significant challenge for both clinicians and patients due to the considerable risk of cardiotoxicity. Despite significant progress in understanding these mechanisms, challenges persist in identifying effective preventive and therapeutic strategies, rendering it a subject of continued research even after three decades of intensive global investigation. The molecular targets and signaling pathways explored provide insights for developing targeted therapies, emphasizing the need for continued research to bridge the gap between preclinical understanding and clinical applications. This review provides a comprehensive exploration of the intricate mechanisms underlying anthracycline-induced cardiotoxicity, elucidating the interplay of various signaling pathways leading to adverse cellular events, including cardiotoxicity and death. It highlights the extensive involvement of pathways associated with oxidative stress, inflammation, apoptosis, and cellular stress responses, offering insights into potential and unexplored targets for therapeutic intervention in mitigating anthracycline-induced cardiac complications. A comprehensive understanding of the interplay between anthracyclines and these complexes signaling pathways is crucial for developing strategies to prevent or mitigate the associated cardiotoxicity. Further research is needed to outline the specific contributions of these pathways and identify potential therapeutic targets to improve the safety and efficacy of anthracycline-based cancer treatment. Ultimately, advancements in understanding anthracycline-induced cardiotoxicity mechanisms will facilitate the development of more efficacious preventive and treatment approaches, thereby improving outcomes for cancer patients undergoing anthracycline-based chemotherapy.
Comprehensive Review of Coronary Artery Anatomy Relevant to Cardiac Surgery.
Kesieme EB, Omoregbee B, Ngaage DL … +1 more , Danton MHD
Curr Cardiol Rev · 2025 · PMID 39484768 · Full text
In order to perform safe cardiac surgery, a knowledge of applied coronary artery anatomy and its variants is essential for cardiac surgeons. In normal individuals, the right and the left coronary arteries arise from the...
In order to perform safe cardiac surgery, a knowledge of applied coronary artery anatomy and its variants is essential for cardiac surgeons. In normal individuals, the right and the left coronary arteries arise from the corresponding sinuses of Valsalva within the aortic root. From the cardiac surgical perspective, the coronary artery is divided into the left main coronary artery, its branches (the left anterior descending artery and the circumflex artery), and the right coronary artery. With high-risk cardiac surgeries, including redo procedures, becoming increasingly performed, abnormal courses and variations of the coronary arteries, if not recognized, can predispose the patient to avoidable coronary injuries, resulting in adverse outcomes of cardiac surgical procedures. We aim to describe normal and applied coronary anatomy, common coronary artery variants previously reported, and their clinical relevance to both adult and paediatric cardiac surgery.
Targeting Wnt Pathways with Small Molecules as New Approach in Cardiovascular Disease.
Mousavi SM, Jalali-Zefrei F, Shourmij M … +5 more , Tabaghi S, Davari A, Khalili SB, Farzipour S, Salari A
Curr Cardiol Rev · 2025 · PMID 39482911 · Full text
The increasing incidences of morbidity and mortality associated with cardiovascular diseases represent significant difficulties for clinical treatment and have a major impact on patient health. Wnt signaling pathways are...
The increasing incidences of morbidity and mortality associated with cardiovascular diseases represent significant difficulties for clinical treatment and have a major impact on patient health. Wnt signaling pathways are highly conserved and are well known for their regulatory roles in embryonic development, tissue regeneration, and adult tissue homeostasis. Wnt signaling is classified into two distinct pathways: canonical Wnt/β-catenin signaling and noncanonical pathways, including planar cell polarity and Wnt/Ca pathways. A growing body of experimental evidence suggests the involvement of both canonical and non-canonical Wnt signaling pathways in the development of cardiovascular diseases, including myocardial hypertrophy, arrhythmias, diabetic cardiomyopathy, arrhythmogenic cardiomyopathy, and myocardial infarction. Thus, to enhance patient quality of life, diagnosing and treating cardiac illnesses may require a thorough understanding of the molecular functions played by the Wnt pathway in these disorders. Many small-molecule inhibitors specifically target various components within the Wnt signaling pathways, such as Frizzled, Disheveled, Porcupine, and Tankyrase. This study aims to present an overview of the latest findings regarding the functions of Wnt signaling in human cardiac disorders and possible inhibitors of Wnt, which could lead to novel approaches for treating cardiac ailments.
Insulin Resistance, Hyperinsulinemia and Atherosclerosis: Insights into Pathophysiological Aspects and Future Therapeutic Prospects.
Papaetis GS, Sacharidou A, Michaelides IC … +2 more , Mikellidis KC, Karvounaris SA
Curr Cardiol Rev · 2025 · PMID 39415589 · Full text
Insulin resistance describes the lack of activity of a known quantity of insulin (exogenous or endogenous) to promote the uptake of glucose and its utilization in an individual, as much as it does in metabolically normal...
Insulin resistance describes the lack of activity of a known quantity of insulin (exogenous or endogenous) to promote the uptake of glucose and its utilization in an individual, as much as it does in metabolically normal individuals. On the cellular level, it suggests insufficient power of the insulin pathway (from the insulin receptor downstream to its final substrates) that is essential for multiple mitogenic and metabolic aspects of cellular homeostasis. Atherosclerosis is a slow, complex, and multifactorial pathobiological process in medium to large arteries and involves several tissues and cell types (immune, vascular, and metabolic cells). Inflammatory responses and immunoregulation are key players in its development and progression. This paper examines the possible pathophysiological mechanisms that govern the connection of insulin resistance, hyperinsulinemia, and the closely associated cardiometabolic syndrome with atherosclerosis, after exploring thoroughly both and (preclinical and clinical) evidence. It also discusses the importance of visualizing and developing novel therapeutic strategies and targets for treatment, to face this metabolic state through its genesis.
Non-rodent Models of Atherosclerosis: Repurposing of Existing Drugs and Search for Novel Treatment Strategies.
Dabravolski SA, Khotina VA, Popov MA … +3 more , Glanz VY, Sukhorukov VN, Orekhov AN
Curr Cardiol Rev · 2025 · PMID 39364866 · Full text
Atherosclerosis and associated cardiovascular diseases are the leading causes of illness and mortality worldwide. The development of atherosclerosis is a complex process involving oxidative stress, surplus lipid depositi...
Atherosclerosis and associated cardiovascular diseases are the leading causes of illness and mortality worldwide. The development of atherosclerosis is a complex process involving oxidative stress, surplus lipid deposition and retention, endothelial dysfunction, and chronic inflammation. Developing novel anti-atherogenic and repurposing existing drugs requires the use of suitable animal models to characterise the fundamental mechanisms underlying atherosclerosis initiation and progression and to evaluate potential therapeutic effects. Commonly used rodent models, however, are not always appropriate, and other models may be required to translate these discoveries into valuable preventive and treatment agents for human applications. Recent advances in gene-editing tools for large animals have allowed the creation of animals that develop atherosclerosis faster and more similarly to humans in terms of lesion localisation and histopathology. In this review, we discuss the major advantages and drawbacks of the main non-rodent animal models of atherosclerosis, particularly rabbits, pigs, zebrafish, and non-human primates. Moreover, we review the application of recently invented novel therapeutic methods and agents, and repurposed existing drugs (such as antidiabetic and anticancer) for atherosclerosis treatment, the efficacy of which is verified on non-rodent animal models of atherosclerosis. In total, the proper selection of a suitable animal model of atherosclerosis facilitates reproducible and rigorous translational research in repurposing of existing drugs, discovering new therapeutic strategies, and validating novel anti-atherosclerotic drugs.
Young Hearts under Attack: The Alarming Increase in Heart Problems among Indian Youth.
Paul P, Kamal R, Awasthi A
Curr Cardiol Rev · 2025 · PMID 39328134 · Full text
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A Contemporary Review on Heart Failure with Preserved Ejection Fraction: Epidemiology, Diagnosis, and Management.
Shahid M, Ibrahim R, Olagunju A … +2 more , Mookadam M, Mookadam F
Curr Cardiol Rev · 2025 · PMID 39301908 · Full text
Heart failure with preserved ejection fraction (HFpEF) includes almost half of heart failure cases typified by a specific clinical syndrome. Despite diagnostic and management advances, HFpEF still presents a diagnostic c...
Heart failure with preserved ejection fraction (HFpEF) includes almost half of heart failure cases typified by a specific clinical syndrome. Despite diagnostic and management advances, HFpEF still presents a diagnostic challenge and a paucity of therapies specifically aimed at enhancing survival and improving quality of life is still lacking. This review elucidates the diagnostic complexity of HFpEF, highlighting the use of both subjective and objective criteria within algorithmic frameworks. It also examines the significant impact of comorbidities on the progression of HFpEF. Additionally, we explore the latest evidence on targeting these comorbidities therapeutically, although the benefits to mortality are still limited.
Importance of Zinc Homeostasis for Normal Cardiac Rhythm.
Kokhabi P, Mollazadeh R, Hejazi SF … +2 more , Nezhad AH, Pazoki-Toroudi H
Curr Cardiol Rev · 2025 · PMID 39301907 · Full text
Current arrhythmia therapies such as ion channel blockers, catheter ablation, or implantable cardioverter defibrillators have limitations and side effects, and given the proarrhythmic risk associated with conventional, i...
Current arrhythmia therapies such as ion channel blockers, catheter ablation, or implantable cardioverter defibrillators have limitations and side effects, and given the proarrhythmic risk associated with conventional, ion channel-targeted anti-arrhythmic drug therapies, a new approach to arrhythmias may be warranted. Measuring and adjusting the level of specific ions that impact heart rhythm can be a simple and low-complication strategy for preventing or treating specific arrhythmias. In addition, new medicines targeting these ions may effectively treat arrhythmias. Numerous studies have shown that intracellular and extracellular zinc concentrations impact the heart's electrical activity. Zinc has been observed to affect cardiac rhythm through a range of mechanisms. These mechanisms encompass the modulation of sodium, calcium, and potassium ion channels, as well as the influence on beta-adrenergic receptors and the enzyme adenylate cyclase. Moreover, zinc can either counteract or induce oxidative stress, hinder calmodulin or the enzyme Ca ()/calmodulin-dependent protein kinase II (CaMKII), regulate cellular ATP levels, affect the processes of aging and autophagy, influence calcium ryanodine receptors, and control cellular inflammation. Additionally, zinc has been implicated in the modulation of circadian rhythm. In all the aforementioned cases, the effect of zinc on heart rhythm is largely influenced by its intracellular and extracellular concentrations. Optimal zinc levels are essential for maintaining a normal heart rhythm, while imbalances-whether deficiencies or excesses-can disrupt electrical activity and contribute to arrhythmias.
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