Hypertensive disorders of pregnancy (HDP) affect approximately 1 in 7 pregnancies in the United States and are increasingly recognized as early and independent markers of lifetime cardiovascular disease. This review provides an update of the evidence for classification, pathophysiology, and management of HDP with an emphasis on risk stratification, treatment, and the long-term cardiovascular consequences with suggested models for postpartum care transitions. Contemporary evidence supports a mechanistic link between the endothelial dysfunction that occurs in HDP and persistent vascular injury, supporting the observations that the greatest risk for cardiovascular complications occur outside of the traditional postpartum period. Remote blood pressure monitoring programs have emerged as a vital strategy, reducing morbidity and long-term hemodynamic benefit to extended surveillance for patients with HDP. Advances in prediction models to identify patients during pregnancy at risk of developing severe disease include incorporation of biomarkers such as the soluble fms-like tyrosine kinase-1 to placenta growth factor (sFlt-1/PlGF) ratio. However, risk prediction and stratification strategies for long-term consequences of HDP and prevention well after the pregnancy episode remain understudied. HDP presents short- and long-term cardiovascular risk that begins in the immediate postpartum period and persists across the lifespan. These risks, particularly in the long-term, are underrecognized and lack structured stratification tools. This represents a significant gap in care and opportunity to improve care for the pregnant and postpartum population. Closing this care gap requires structured, multidisciplinary, and equity-driven approaches that extend cardiovascular surveillance and prevention well beyond the traditional postpartum window.
Conduction disturbances remain a major complication of transcatheter valve replacement, yet a unified review spanning all three valve positions is lacking. This review examines the anatomical substrates, risk stratification tools, and mitigation strategies for conduction disease after transcatheter aortic (TAVR), mitral (TMVR), and tricuspid (TTVR) valve replacement. The risk of conduction injury is determined by the proximity of the device landing zone to the cardiac conduction system. In TAVR, shorter membranous septum length, noncoronary cusp calcification, self-expanding valve use, and deeper implantation depth are established predictors of permanent pacemaker implantation (PPI). Baseline right bundle branch block is the strongest predictor of high-grade atrioventricular block (HAVB). High implantation strategies can reduce PPI to single-digit rates regardless of valve type. In TTVR, the EVOQUE valve carries a PPI rate of 27.8
The prevalence of aortic stenosis (AS) is increasing as the population ages, particularly among adults over 65 years old [1]. Despite advances in the treatment of severe AS, including transcatheter aortic valve replacement (TAVR), disparities in diagnosis, referral, and treatment persist across sex, racial, and socioeconomic groups. This review summarizes the current evidence regarding disparities in valvular heart disease (VHD) diagnosis and AS treatment, highlights barriers that contribute to inequitable access to valve replacement therapies and examines the potential of system-level interventions to improve equity in care delivery. Persistent disparities in AS care have been documented across multiple stages of the care pathway, including disease recognition, specialist referral, and receipt of aortic valve replacement (AVR). We present findings from a pragmatic randomized quality improvement intervention evaluating electronic provider notifications (EPNs) designed to improve recognition and treatment of severe AS. In a cluster-randomized trial, EPNs significantly increased rates of AVR, improved survival among symptomatic patients, and eliminated observed sex-based disparities within this study [2]. Despite the availability of effective therapies for severe AS, including TAVR, inequities in diagnosis and treatment remain substantial. Findings from the EPN trial suggest that system-level interventions integrated into routine clinical workflows may represent scalable strategies for improving both quality and equity in the delivery of life-saving therapies for severe AS [2].
To summarize research on the interaction between frailty, depression, and their treatment implications in older adults. Frailty predicts later depression and depression predicts later frailty. Body weight predicts depression differently by gender. Underweight predicts depression in Asian countries and among men in Western countries, while obesity predicts depression in Western countries, especially women. Malnutrition, anorexia of aging, and isolation may contribute to both depression and frailty. Frailty decreases effectiveness of antidepressant medication. Frailty and depression are closely related and treatment of both is hampered when they co-occur. Providers may wish to treat frailty first. Possible interventions include encouraging better nutrition, social activities, and physical activity.
We explore the costs and safety of compounded Glucagon-Like Peptide-1 receptor agonist (GLP-1 RA) and dual Glucagon-Like Peptide-1/Glucose-dependent insulinotropic polypeptide receptor agonist (GLP-1/GIP RA) therapy. Compounded products were widely utilized during a period of shortage after the approval for weight loss, but their safety and role today has changed. Since the FDA removed permissions for pharmacies and outsourcing facilities to compound GLP-1 RA and dual GLP-1/GIP RA products, many are still operating inappropriately, and their advertisements can be misleading to consumers. Patients may inadvertently purchase products that are not FDA-approved or regulated. Additionally, several case reports and safety analyses of compounded GLP-1 RA and dual GLP-1/GIP RA products highlight dosing and administration errors as well as sterility concerns. With widespread availability of manufactured GLP-1 RA and dual GLP-1/GIP RA products, compounded products should be reserved for patients who otherwise would not tolerate the commercially available product. Patients and prescribers should verify if pharmacies have accreditation for compounding by the National Association of Boards of Pharmacy or the Pharmacy Compounding Accreditation Board and utilize the FDA’s BeSafeRx to evaluate the safety and legitimacy of pharmacies.
The advancement of cancer therapeutics has seen a rise in cancer therapy-related cardiac dysfunction. Concomitantly, a rise in heart failure has paralleled an expanding role of guideline-directed medical therapy (GDMT). As the two disease processes intersect, a shifting paradigm in both identification and treatment of cardiomyopathy and of heart failure has emerged for patients with cancer therapy-related cardiac dysfunction (CTRCD). For patients at risk for cardiac dysfunction (stage A heart failure [HF]) these cardioprotective strategies including traditional GDMT - most notably beta blockers, angiotensin converting enzyme inhibitors/angiotensin receptor blockers, and more recently sodium-glucose co-transporter 2 inhibitors. Imaging modalities such as strain echocardiography and cardiac MRI are being explored to identify high-risk cohorts who may benefit from early intervention. In patients with asymptomatic cardiac dysfunction (stage B HF), permissive cardiotoxicity leverages the practice of accepting some level of cardiac dysfunction and increased HF risk in exchange for delivering optimal cancer therapy. This practice has been supported by recent randomized controlled trials demonstrating feasibility and safety in patients with asymptomatic left ventricular dysfunction. Unfortunately, patients with more advanced HF (stages C and D) continue to experience poorer outcomes and receive fewer therapies compared to non-cancer counterparts. As the field evolves, there has been increased willingness to provide advanced therapies to carefully selected individuals with prior or active cancer. When taken as a whole, the majority of data indicates that the use of traditional GDMT and adjunct agents in the cardio-oncology population may have cardioprotective effects. This has been most well-studied in patients with cancer who are at risk for developing CTRCD. In patients with asymptomatic CTRCD, there is also data to suggest that the use and optimization of GDMT could help cardio-oncologists more safely practice permissive cardiotoxicity, the concept of allowing some degree of cardiac dysfunction in return for optimal cancer therapy. Areas that remain relatively unstudied include the use of these agents in stage D HF or cardiogenic shock, as well as the use of newer agents. As newer HF therapeutics find a place within the spectrum of GDMT, future studies should investigate the use of these agents in the population of patients with cardiomyopathy, HF, and cancer.
This review discusses the epidemiology and mechanisms of atrial fibrillation (AF) in cardiac amyloidosis (CA), the limitations of current stroke risk assessment models in this population, the utility of advanced imaging to detect atrial thrombus, the role of oral anticoagulation, and the emerging role of left atrial appendage occlusion. Patients with cardiac amyloidosis are at increased risk of developing atrial fibrillation, and the coexistence of these conditions significantly elevates the risk of thromboembolic events, particularly ischemic stroke. Standard stroke risk stratification tools such as CHA₂DS₂-VASc may underestimate this risk in amyloidosis due to disease-specific factors like atrial mechanical dysfunction, impaired hemodynamics and intracardiac thrombus formation in sinus rhythm. A precision medicine approach is required to mitigate stroke risk in this high-risk population.
To evaluate whether “idiopathic ventricular tachycardia” remains an appropriate label in the modern era. We synthesize current literature and review sites of origin, mechanisms, and characteristic ECG signatures, and appraise contemporary diagnostic approaches capable of revealing occult substrate. Tools such as cardiac MRI with late gadolinium enhancement and electroanatomic mapping frequently reveals substrate in patients once considered “idiopathic.” 18F-FDG PET-CT can also detect active myocardial inflammation when CMR is nondiagnostic, and high-density voltage mapping may expose low-voltage scar below imaging resolution. Early genetic signals (e.g., CCR7, PKN2) suggest heritable underpinnings for some “idiopathic” presentations. A substantial fraction of “idiopathic” VT appears to reflect limitations in detection rather than true absence of disease. A pragmatic workup includes history/ECG, ischemia evaluation, CMR (LGE ± T1/T2 mapping), targeted inflammatory imaging when suspicion is high, and consideration of high-density voltage mapping in select cases. Standardized definitions incorporating modern diagnostics and long-term follow-up are needed.
This review focuses on the cardiovascular toxicities linked to both traditional chemotherapy and newer targeted cancer therapies. The objective is to examine the mechanisms behind these toxicities, their clinical implications, and current strategies for detection, prevention, and management. The paper aims to inform ongoing clinical decision-making and highlight areas where evolving evidence can enhance the safety and effectiveness of cancer care. Cardiotoxicity is no longer confined to legacy agents like anthracyclines. New classes of therapies, including HER2-targeted treatments, tyrosine kinase inhibitors, VEGF inhibitors, and antibody-drug conjugates, have been linked to unique cardiac side effects ranging from hypertension and arrhythmias to heart failure. Off-target interactions, cumulative drug exposure, and individual patient susceptibility often influence these effects. Additionally, radiation therapy, particularly in the thoracic region, continues to contribute to late-onset cardiovascular disease. Advances in cardiac imaging, strain-based assessment, biomarker profiling, and clinical risk models may help identify high-risk individuals earlier and more accurately. Cardiotoxicity remains a significant concern in delivering effective care to patients with cancer, impacting both short-term treatment outcomes and long-term survivorship. While traditional agents have well-characterized risks, modern therapies require refined monitoring strategies. Future care will depend on personalized approaches, early identification tools, and interdisciplinary collaboration to optimize cardiovascular health without compromising cancer outcomes.
Artificial intelligence (AI) enabled behavioral health coaching has emerged as a potential solution for managing obesity and related complications. This review aims to evaluate the effectiveness, engagement, and ethical implications of AI-enabled behavioral coaching platforms in the management of obesity. Our search identified 21 relevant studies. Of these, 8 were randomized controlled trials and 13 were observational studies (including pretest-protest, longitudinal, retrospective cohort and single-arm intervention studies). AI-based platforms were associated with clinically significant weight loss (ranging from − 0.8 kg to − 13.9
Not applicable. Pulsed field ablation (PFA) has been increasingly adopted for catheter ablation of atrial fibrillation, owing to its increased procedural efficiency when compared to radiofrequency ablation. Due to its non-thermal and relatively tissue-selective mechanism of action, PFA does not carry many of the traditional risks associated with thermal ablation,but real-world experience has shown that other non-traditional, PFA-specific ablation risks can occur. Among these, hemolysis, coronary artery involvement (spasm and fibrosis), and profound vagal responses have been increasingly reported when using this technology. Herein, we will review the current understanding of the pathophysiology, clinical implications, and prevention or treatment strategies for these PFA-specific ablation risks.
Obesity increases the risk of multiple cardiovascular diseases. This paper reviewed the influence of sex on obesity treatment responses, emphasizing cardiovascular disease risk factor reduction and outcomes. The prevalence of obesity, defined as a BMI ≥ 30 kg/m2, in U.S. adults is 40.3
This article summarizes the relationship between obesity and HIV, including independent risk factors, causes, contributors, and associated outcomes. Recent studies have identified the factors that contribute to the increasing rates of obesity in PLWH. Intrinsic factors play a role, including elevated visceral adiposity and increased inflammation. Difficulty with food access and socioeconomic challenges disproportionally affect PLWH, thus contributing to increased weight gain. Structural factors play a significant role in this food access inequity. In addition, antiretroviral therapy contributes to weight gain. The exact relationship between specific medications and obesity remains unclear. As a result of the increase in obesity, PLWH experience a high rate of negative outcomes, such as diabetes, cardiovascular disease, and nonalcoholic fatty liver. These outcomes are disproportionately high in PLWH compared to the general population. Several risk factors, including sociodemographic factors, intrinsic viral factors, and treatment effects, contribute to overweight and obesity among PLWH.
This review examines the recent advances in transthyretin amyloid cardiomyopathy (ATTR-CM), focusing on evolving diagnostic strategies and emerging therapeutic interventions. We sought to analyze the current state of diagnostic modalities, evaluate newly approved disease-modifying therapies, and discuss the impact of these developments on patient outcomes and clinical practice patterns. The incidence of ATTR-CM has increased dramatically due to improved recognition particularly among women and non-invasive diagnostics with bone scintigraphy utilization. Diagnostic advances include refined clinical scoring systems such as ATTR-CM and T-AMYLO as well as more widespread use of MRI. The therapeutic landscape has expanded significantly with FDA approval of three disease-modifying agents: tafamidis (TTR stabilizer), acoramidis (TTR stabilizer achieving > 90
Glucagon-like peptide 1 (GLP-1) receptor agonists (RA) have transformed obesity and type 2 diabetes (T2D) management. Tirzepatide, the first dual GLP-1/glucose-dependent insulinotropic polypeptide (GIP) RA approved for both conditions, has paved the way for next-generation incretin-based therapies. Among these, triple agonists targeting GLP-1, GIP, and glucagon receptors represent a promising next step. This review outlines the rationale for their development and summarizes clinical trial data, focusing on retatrutide, the most advanced candidate. Retatrutide is the first triple agonist (acting on GLP-1/GIP/glucagon receptors) with published phase 2 data in people with obesity as well as in people with T2D. Retatrutide achieved up to 24.2
In this review, we discuss the prevalence and reasons for such disparities, as well as the social determinants of health that compound such disparities and their effect on adverse cardiovascular outcomes. We also discuss factors contributing to these disparities and how to address them. Cardiovascular mortality has increased in the United States (US) since 2015 after 5 decades of decline, with a higher rate of increase in certain racial/ethnic groups compared to non-Hispanic Whites. (Tsao et al., Circulation. 2023;147:e93–621) There has also been a concomitant worsening of cardiovascular risk factor profiles in US adults (i.e., rising rates of hypertension, obesity, diabetes, and dyslipidemia). Despite recommendations for lipid screening by various health agencies and guidelines, screening rates remain suboptimal among non-Hispanic Black and Hispanic adults, especially in women. Significant disparities exist in lipid-lowering therapy (LLT) prescribing, initiation, dosing, and adherence. Several factors influence racial and gender disparities, including social determinants of health, clinician factors, and lack of culturally inclusive initiatives. Although lipid management has improved over decades, racial and gender disparities still persist. In this review, we offer a few strategies to mitigate these disparities and discuss a toolkit that can be implemented to ensure equitable cardiovascular preventive care in all racial groups and sexes. Central Illustration: Strategies to address racial and ethnic disparities in atherosclerotic cardiovascular disease. The upper section of the figure presents various risk factors for atherosclerotic cardiovascular disease within vulnerable racial and ethnic populations. The lower segment of the figure shows strategies aimed at mitigating these racial/ethnic disparities in preventive therapies.
In this review, we summarize sex-based variations in Lipoprotein (a) [Lp(a)] levels, describe their influence on atherosclerotic cardiovascular disease (ASCVD) risk over the course of a woman’s lifetime, and examine the implications for tailored prevention and treatment. Factors unique to women include endogenous and exogenous hormonal influences on Lp(a); Lp(a) variations related to the menstrual cycle, fertility treatment, and menopause both natural and surgical; and response to therapies such as proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors. Lp(a) is a genetically determined lipoprotein that has been recognized as a causal risk factor for ASCVD in both men and women. Emerging evidence suggests that elevated Lp(a) confers risk with sex-based differences that have important implications for women, specifically, and may be relevant to risk stratification and personalized treatment approaches.
Rates of stroke in the United States either continue to decline or appear to have plateaued over time. However, due to changing demographics, namely the aging population and growing diversification by race and ethnicity, healthcare disparities persist and may widen with regards to stroke prevalence among diverse racial and ethnic communities. This review focuses on updated data and trends regarding racial/ethnic disparities in stroke and stroke outcomes. Black Americans continue to have higher risk for incident stroke, with poorer functional and cognitive outcomes and more difficulty with self-care, mobility, and return to household activities. Disparities in stroke risk for Hispanic Americans are present but vary by region in the United States and Hispanic country of origin/subpopulation. For example, stroke disparities for Mexican Americans in South Texas may be narrowing over time but the population continues to have worse functional and cognitive outcomes, compared to non-Hispanic White stroke survivors. Differences in stroke mortality are present, but may be modified by stroke type (ischemic, hemorrhagic) and according to long-term follow up of mortality outcomes, especially among Black Americans with worse survival rates after stroke. Racial/ethnic stroke and stroke outcome disparities are modified by sex and social determinants of health, specifically factors related to socioeconomic status, education, and healthcare access and quality. Disparities by race and ethnicity are identified for stroke incidence, mortality, functional outcomes, and cognitive outcomes. Research must expand to broaden understanding of the role of social determinants of health in driving or exacerbating racial and ethnic stroke disparities.
This review article outlines the racial disparities in air pollution that contribute to the cardiovascular disease morbidity and mortality gap in minoritized racial and ethnic groups. It offers a compelling framework to address this gap through greenification, emphasizing the need for immediate action. Although medical advancements have reduced cardiovascular-related mortality, racial disparities persist. Air pollution increases cardiovascular risk and disproportionately affects racial and ethnic minority groups and individuals with adverse social determinants of health. Greenification is the creation of environmentally conscious processes in areas with significant pollution, such as green spaces in urban areas. Green spaces in urban areas created to reduce disparities can aid in addressing communities disproportionately affected by air pollution. Greenification can be utilized to help mitigate the gap of cardiovascular mortality in racial and ethnic minority groups and individuals with poor social determinants of health.
