Current Cardiology Reviews - Volume 21, Issue 6, 2025

Heart failure remains a significant global health challenge, necessitating continuous advancements in management strategies to improve patient outcomes. This review aimed to elucidate the current scenario of heart failure and its management in the modern era, focusing on integrating medical therapy and implantable device interventions. According to guidelines, medical treatment remains the primary method of treating heart failure. Such medications include ACE inhibitors, neprilysin-angiotensin receptor inhibitors, beta-blockers, angiotensin II receptor blockers, mineralocorticoid receptor antagonists, and blockers of sodium-glucose co-transporter-2. These pharmacologic agents have demonstrated efficacy in decreasing mortality and morbidity in patients. The advent of implantable devices has revolutionized treatment, providing substantial benefits in specific patient populations. Cardiac resynchronization therapy has emerged as a pivotal intervention for patients with reduced ejection fraction and dyssynchronous ventricular contraction, effectively enhancing cardiac function and quality of life. Furthermore, left bundle branch area pacing improvements provide fascinating alternatives to traditional cardiac resynchronization therapy. The essential significance of device-based therapies is further highlighted by the function of implanted cardioverter-defibrillators in preventing unexpected cardiac deaths in high-risk patients. Furthermore, integrating remote monitoring technologies and novel device innovations continues to enhance the precision and efficacy of heart failure management. This review comprehensively examines current guidelines and evidence supporting the use of these therapies, addressing their synergistic potential and the practical considerations for their implementation, while synthesizing recent advancements in pharmacologic and device-based interventions.

RAS proteins are critical in cellular signal transduction, influencing cell proliferation, differentiation, and survival. While extensively studied for their role in cancer, RAS gene mutations also contribute significantly to cardiovascular diseases, such as hypertrophic cardiomyopathy, pulmonary valve stenosis, and atrial septal defects. Despite their similar primary structures, RAS proteins exhibit distinct functions in cardiac biology: H-RAS regulates cardiomyocyte size, K-RAS governs proliferation, and N-RAS, less associated with cardiac defects, is understudied in cardiac cells. Congenital RAS mutations, collectively known as RASopathies, include syndromes, like Noonan syndrome and cardio-facio-cutaneous syndrome, which often lead to severe cardiac complications, including heart failure. Genetic testing and imaging advances have improved the diagnosis and management of these conditions. Recent research has shown promise with MEK inhibitors and other targeted therapies, offering potential improvements in managing RAS-related cardiac conditions. This review explores the role of the RAS subfamily in heart disease, highlighting key concepts and potential therapeutic targets. PubMed database was searched using keywords, such as RASopathies, RAS gene mutations, cardiac hypertrophy, cardiovascular disease, RAS/MAPK pathway, congenital heart disease, and more. Relevant literature up to June 2024 was examined and summarized, consisting of data from various clinical trials, meta-analyses, retrospective/prospective cohort studies, and current guidelines.

The health and survival of people with heart failure is a growing concern due to the associated illness and death. Traditional treatments such as medication, surgery, and lifestyle changes have not significantly improved life expectancy, leading to a search for more effective drug options. A drug that can act on oxidative stress and cardiac inflammatory markers while carrying the benefits of existing therapies is needed. Targeting the soluble guanylate cyclase (sGC)-cyclic guanosine monophosphate (cGMP) dependent pathway significantly reduces cardiac myocyte death and improves ejection fraction. In 2021, the USFDA approved Vericiguat, a derivative of pyrazolo[3,4-b]pyridine, to decrease the risk of cardiovascular death and hospitalization. This review provides information on the structure, pharmacokinetics, pharmacodynamics, clinical status, and treatment of Vericiguat in heart failure. Riociguat was the first sGC stimulator used in pulmonary hypertension therapy, but its short half-life required multiple dosing, making it unsuitable for cardiovascular diseases. Vericiguat was developed to address this limitation by decreasing metabolism, and both preclinical and clinical investigations have indicated its minimal pharmacokinetic interactions. This makes it appropriate for long-term use in cardiac patients with multiple comorbidities who require several medications. Vericiguat represents a promising new option for heart failure treatment, potentially improving patient outcomes and quality of life. Its compatibility with other heart failure therapies without significant drug-drug interactions further highlights its potential as a cornerstone treatment. Ongoing studies continue to explore its benefits, suggesting that vericiguat may enable more comprehensive and effective management of heart failure, reducing the burden of this debilitating condition.

Cardiovascular disease is the leading cause of pregnancy-related mortality, with pregnancy-related cardiovascular issues extending into the postpartum period. Recent studies suggest hyperandrogenism alters sex hormone levels, contributing to gestational cardiovascular disease CVD. Most of the factors behind the onset of CVD in postpartum women remain unknown. Animal studies mimic adverse pregnancy outcomes to explore molecular causes of severe prenatal cardiac events and their role in postpartum cardiovascular disease development. This review will be focused on summarising human and animal research that shows how undesirable pregnancy outcomes, such as obesity in the mother and gestational diabetes (GD), have an impact on postpartum cardiovascular disease and prenatal cardiometabolic dysfunction. We will highlight the adverse effects of gestational hyperandrogenism as a potential biomarker for cardiovascular dysfunction in pregnant women and new mothers. Investigative cardiovascular (CV) risk variables in the early postpartum phase following pregnancy that were impacted by GD was the aim of this study. Current research strongly implies that women with GDM have a higher risk of developing CVD. Finding appropriate, reliable indicators of CVD and specific treatment modalities that can control obesity, diabetes, and metabolic syndrome are critical to reducing the burden of CVD on impacted women. GD and hypertensive disorders are two pregnancy-related illnesses that raise the risk of CVD in the long run. Despite a lack of awareness, early screening, lifelong monitoring, and continuous research to enhance detection and prevention are essential.

Cardiovascular disease (CVD) Continues to be the leading cause of mortality worldwide, underscoring the critical need for effective prevention and management strategies. The ability to predict cardiovascular risk accurately and cost-effectively is central to improving patient outcomes and reducing the global burden of CVD. While useful, traditional tools used for risk assessment are often limited in their scope and fail to adequately account for atypical presentations and complex patient profiles. These limitations highlight the necessity for more advanced approaches, particularly integrating artificial intelligence (AI) into cardiovascular risk prediction. Our review explores the transformative role of AI in enhancing the accuracy, efficiency, and accessibility of cardiovascular risk prediction models. The implementation of AI-driven risk assessment tools has shown promising results, not only in improving CVD mortality rates but also in enhancing quality of life (QOL) markers and reducing healthcare costs. Machine learning (ML) algorithms predicted 2-year survival rates after MI with improved accuracy compared to traditional models. Deep learning (DL) forecasted hypertension risk with a 91.7% accuracy based on electronic health records. Furthermore, AI-driven ECG (Electrocardiography) analysis has demonstrated high precision in identifying left ventricular systolic dysfunction, even with noisy single-lead data from wearable devices. These tools enable more personalized treatment strategies, foster greater patient engagement, and support informed decision-making by healthcare providers. Unfortunately, the widespread adoption of AI in CVD risk assessment remains a challenge, largely due to a lack of education and acceptance among healthcare professionals. To overcome these barriers, it is crucial to promote broader education on the benefits and applications of AI in cardiovascular risk prediction. By fostering a greater understanding and acceptance of these technologies, we can accelerate their integration into clinical practice, ultimately aiming to mitigate the global impact of CVD.

In the modern world, Polycystic Ovary Syndrome (PCOS) is thought to be the most prevalent endocrine condition affecting women. Compared to their normal counterparts, PCOS patients have higher rates of morbidity and death because they are more susceptible to these anomalies from an early age. Cardiovascular disease (CVD) and PCOS are prevalent in women. PCOS often results from a combination of hereditary and environmental causes. Insulin resistance (IR) is considered the primary cause of several metabolic risk factors, such as Type 2 Diabetes Mellitus (T2DM), Metabolic Syndrome (MetS), dyslipidemia, obesity, and hypertension (HTN). Additionally, patients with PCOS may also have elevated levels of non-traditional factors, including C-reactive protein (CRP), carotid intima-media thickness (IMT), coronary artery calcification (CAC), as well as endothelial dysfunction, which raises the likelihood of complications from CVD. This review utilizes statistics and data mostly sourced from research in India, offering insight into the nation's distinct PCOS prevalence and related cardiovascular risks. To lessen the impact of PCOS in the modern world, prompt identification and effective management of these warning signs with food, lifestyle changes, and/or medication are crucial. The research that examined the potential impact of PCOS on the most prevalent CVD-hypertension, insulin resistance, obesity, malignancy, diabetes mellitus, and dyslipidemia-is reviewed in this study. Measuring subclinical atherosclerosis, such as coronary artery calcium or carotid plaque, might help inform shared decision-making over the start of statin therapy when CVD risk is unknown.

Stroke and heart disease are two of the leading causes of the global disease burden. However, modern research has gradually revealed a potential causal link between these two conditions. Most studies have focused on the direct role of arrhythmias in stroke. However, clinical evidence suggests that the incidence of arrhythmias increases after stroke in patients without a history of arrhythmia, and cardiac disease after stroke has become the second leading cause of death after stroke. This article focuses on arrhythmias after stroke and reviews brain-heart crosstalk after stroke. This article examines the potential mechanisms of brain-heart interactions after stroke, including increased catecholamines due to autonomic imbalance, gut microbial dysbiosis, immune response, and systemic inflammation. In addition, this article discusses the impact of arrhythmia on stroke severity and the role of brain injury sites in brain-heart interactions. To address these mechanisms, we propose that post-stroke arrhythmia is a type of stroke-induced disease distinct from primary arrhythmia. We aimed to identify new therapeutic targets and treatments, both pharmacological and non-pharmacological, to achieve targeted treatment and provide guidance for future clinical prevention and treatment.

Cancer immunotherapy is based on immune checkpoint inhibitors (ICIs) and has brought a revolution in oncology with promising treatment possibilities for diverse cancers. Yet, immune-related adverse events (irAEs) frequently limit the clinical efficacy of ICIs, with cardiotoxicity representing a significant salient consequence. These ICI side-effects underscore the need for well-established models for the assessment of cardiac risk. This review proposes a risk evaluation strategy that uses biomarkers, non-invasive imaging, and individual patient data. The goal is to elucidate the mechanism through which immune-related adverse events affecting the heart might arise, and the need for predictive tools to better tailor treatment regimens to increase both safety and efficacy. Biomarkers play a vital role in the detection and prevention of heart-related side effects,  which means adequate intervention while preserving therapeutic outcomes. Moreover, the study discusses the acknowledgement of novel treatment regimens and the ability of integration of artificial intelligence (AI) and machine learning (ML) to improve the assessment of risk. AI/ML tools are experts at synthesizing heterogeneous datasets to reveal patterns and risk factors, providing clinicians with powerful capabilities to enhance safety and efficacy. This paper aims to develop sound risk assessment models to enhance both the safety and efficacy of cancer immunotherapies by exploring various strategies and interactions in immunotherapy.

Recent advancements have emerged in understanding the epidemiology and optimal therapeutic options for left ventricular thrombi (LVT). With early percutaneous interventions in acute myocardial infarction, the prevalence of LVT has decreased. However, the best strategies for prevention, risk stratification, and management remain unclear, especially among non-ischemic cardiomyopathy disorders. This review outlines these advancements and provides an overview of the diagnostic and therapeutic implications of LVT in ischemic and non-ischemic cardiomyopathies. Significant gaps in the current evidence persist, particularly regarding the optimal timing for LVT screening and the need for prophylactic anticoagulation, highlighting opportunities for prospective cohort studies. Furthermore, a better understanding of the unique risk factors that contribute to increased LVT risk would lead to more comprehensive algorithms that may quantify the risk of LVT development, aiding in developing preventive strategies targeted at reducing rates of LVT. Until more definitive evidence is available, clinicians should custom LVT screening, preventive measures, and management strategies based on individual patient risk factors.