Using the National Inpatient Sample (2016-2022), we identified adult hospitalizations with cardiogenic shock (ICD-10-CM R57.0) and an Impella procedure code (ICD-10-PCS 5A0221D or 5A0211D), excluding elective admissions, transfers out, postcardiotomy shock, and missing core data. Patients were classified as acute myocardial infarction-cardiogenic shock (AMI-CS) or non-AMI-CS by diagnosis. One-to-one nearest-neighbor propensity-score matching without replacement was performed on 64 covariates using a caliper of 0.2 standard deviations of the logit propensity score, with balance evaluated by absolute standardized mean differences <0.10. Co-primary outcomes were in-hospital all-cause mortality and the Saito composite (death or any major Impella-related complication: bleeding requiring transfusion, acute kidney injury requiring dialysis, stroke, vascular complication, limb ischemia, or access-site infection). Secondary outcomes included individual complications, length of stay, inflation-adjusted charges, and discharge disposition. The final analytic cohort comprised 9866 unweighted Impella-supported CS hospitalizations (7507 AMI-CS; 2359 non-AMI-CS). After 1:1 propensity-score matching, 1917 pairs were retained with excellent postmatch balance (median |standardized mean difference| 0.014; maximum 0.053). In the matched cohort, in-hospital mortality was significantly lower in AMI-CS (43.9%) than in non-AMI-CS (47.4%) (absolute risk difference -3.5%; OR 0.87, 95% CI, 0.76-0.99; P = 0.030), as was the Saito composite (61.1% vs 65.2%; OR 0.84, 95% CI, 0.74-0.96; p=0.010). Within non-AMI-CS, in-hospital mortality varied substantially by etiology, lowest in myocarditis-associated CS (25.0%) and highest in ventricular arrhythmia and pulmonary embolism etiologies. National Impella-supported CS hospitalizations rose progressively in both groups over 2016-2022 (annual percent change +12.0% and +11.1% for AMI-CS and non-AMI-CS, respectively).

Caffeine is among the most widely consumed bioactive compounds worldwide and remains a target of cardiovascular counseling despite heterogeneous evidence across mechanistic, interventional, and epidemiologic studies. At dietary doses, caffeine acts as a competitive antagonist of adenosine receptors, influencing autonomic tone, vascular resistance, and myocardial electrophysiology. Acute exposure can produce increases in blood pressure, alterations in sympathetic activity, and changes in ventricular ectopy, whereas habitual coffee consumption is associated in cohort studies with neutral or modestly favorable cardiovascular outcomes, including lower risks of cardiovascular mortality, heart failure, and stroke at moderate intake levels. Evidence from randomized and observational studies does not support a consistent proarrhythmic effect of habitual coffee consumption, and recent clinical trials challenge recommendations for caffeine restriction in conditions such as atrial fibrillation. Importantly, caffeine exposure is heterogeneous: energy drinks and concentrated caffeine products demonstrate more consistent electrophysiologic and hemodynamic effects, including QTc prolongation and sustained blood pressure elevation, suggesting a distinct risk profile compared with coffee or tea. Genetic variability in caffeine metabolism and differences in exposure patterns further modify individual responses. Overall, current evidence supports a dose-, source-, and patient-specific framework for interpreting caffeine exposure in cardiovascular medicine rather than universal restriction.

BACKGROUND:The optimal blood pressure (BP) target for adults with type 2 diabetes (T2DM) remains a topic of debate. This systematic review and meta-analysis aimed to investigate the efficacy of intensive BP control strategies compared to standard or less intensive approaches in adults with T2DM. METHODS:We comprehensively searched databases for studies comparing intensive vs. less intensive BP targets in individuals with T2DM. In this study, the group with the most intensive target was compared to the group with the least intensive target. Also, studies were analyzed based on current guideline recommendations. Outcomes of interest included major adverse cardiovascular events (MACE), all-cause mortality, cardiovascular mortality, myocardial infarction (MI), stroke, heart failure, retinopathy, neuropathy, nephropathy, and end-stage renal disease. Risk ratios with 95% confidence intervals were calculated. RESULTS:The meta-analysis included 21 studies (16 RCTs) with 290,907 participants (mean age 61.84 years, 55.03% male). Guideline-based analyses showed comparable clinical outcomes between groups with no significant differences. However, the most intensive targets vs. the least intensive targets revealed that the intensive BP control group experienced a significantly lower risk of MACE (RR = 0.75, 0.58; 0.98), nonfatal MI (RR = 0.61, 0.41; 0.91), nonfatal stroke (RR = 0.60, 0.39; 0.92), and total stroke (RR = 0.61, 0.39; 0.95). Other outcomes were similar between groups. Subgroup analysis of RCTs mirrored the overall findings. CONCLUSIONS:In adults with T2DM, intensive BP control reduces the risk of cardiovascular events, such as MACE, stroke, and MI. Additionally, it demonstrates comparable diabetes-related complications to less intensive or standard controls.

Nonobstructive coronary artery disease (CAD) is increasingly recognized as a common cause of ischemic symptoms, especially in women, despite the absence of significant epicardial artery stenosis. This review summarizes the epidemiology and pathophysiology of nonobstructive CAD, encompassing entities such as angina or ischemia with nonobstructive coronary arteries and myocardial infarction with nonobstructive arteries. We discuss diagnostic approaches-including coronary angiography, coronary computed tomography angiography, and functional testing-that can uncover microvascular dysfunction or vasospasm as underlying mechanisms. Evidence-based medical management focuses on aggressive risk factor modification and symptomatic relief, mirroring guideline-directed therapies for obstructive CAD. Key interventions include antiplatelet agents, statins, angiotensin-converting enzyme inhibitors, beta blockers, and lifestyle changes, tailored to patient risk profiles. We highlight findings from recent clinical trials and studies (2020 onward) that inform management, such as the importance of stratified therapy guided by invasive physiology or advanced imaging, and discuss sex-based differences, with women disproportionately affected by nonobstructive CAD. Future directions point toward emerging therapies (eg, PCSK9 inhibitors, anti-inflammatory agents) and advanced imaging or invasive techniques to better characterize disease and personalize treatment.

Cardiovascular disease and chronic kidney disease remain the leading causes of morbidity and mortality in patients with type 2 diabetes, even when conventional risk factors are well managed. Two drug classes have emerged over the past decade that reduce these risks through mechanisms that are largely independent of glucose lowering effect: sodium-glucose cotransporter 2 inhibitors and nonsteroidal mineralocorticoid receptor antagonists. Empagliflozin demonstrated reductions in cardiovascular mortality, heart failure hospitalization, and kidney disease progression in the EMPA-REG OUTCOME trial and was subsequently shown to benefit patients with heart failure across the ejection fraction spectrum in the EMPEROR trials. Finerenone, the first nonsteroidal mineralocorticoid receptor antagonist with phase III cardiorenal outcome data, reduced both cardiovascular and kidney composite endpoints in the FIDELIO-DKD and FIGARO-DKD trials, effects that were confirmed and strengthened in the pooled FIDELITY analysis of over 13,000 patients. These 2 agents target distinct pathophysiological pathways. Sodium-glucose cotransporter 2 inhibition acts primarily through hemodynamic and tubuloglomerular mechanisms, whereas finerenone addresses mineralocorticoid receptor driven inflammation and fibrosis in cardiac and renal tissue. The CONFIDENCE trial, published in 2025, was the first prospective study to test their combination; finerenone plus empagliflozin reduced urinary albumin.

BACKGROUND:Beta-blockers are regarded as one of the primary treatment options for acute coronary syndrome (ACS) patients with reduced left ventricular ejection fraction (LVEF). However, there is ongoing debate about their therapeutic efficacy in patients with non-reduced LVEF (≥ 40%). OBJECTIVE:To determine the impact of long-term beta-blocker administration on major adverse cardiovascular events (MACE) in ACS patients with LVEF ≥ 40%. METHODS:A thorough literature search across four databases was conducted to identify eligible studies comparing beta-blocker therapy with placebo or no medication in addition to standard ACS pharmacotherapy. The outcomes of interest included all-cause mortality and MACE (comprising cardiovascular mortality, recurrent myocardial infarction [Re-MI], stroke, rehospitalization for heart failure, and revascularization). Based on LVEF values, patients were divided into three groups: (1) LVEF > 40%, (2) 40% < LVEF < 50%, and (3) LVEF ≥ 50%, and the random-effects meta-analysis estimated the risk ratios (RRs), hazard ratios (HRs), and 95% confidence intervals (CIs). RESULTS:Five randomized controlled trials (RCTs) and 19 observational studies met the inclusion criteria. Within the RCTs, beta-blocker use was associated with a non-significant 6% reduction in MACE (RR = 0.94, 95%CI = 0.87-1.02, I2 = 19.1%). The pooled analyses of observational studies showed no significant overall impact of beta-blocker use on endpoint outcomes. Subgroup analyses revealed a reduction in MACE (HR = 0.75, 95%CI = 0.59-0.95, I2 = 0%) and Re-MI (HR = 0.45, 95%CI = 0.23-0.89) in patients with LVEF 40%-49%; however, these findings were derived primarily from observational data. Patients with LVEF ≥ 50% did not appear to benefit from long-term beta-blocker use. CONCLUSION:Long-term beta-blocker use did not show a significant benefit in patients with preserved ejection fraction (LVEF ≥ 50%). Observational data suggested a possible reduction in MACE and Re-MI in the LVEF 40%-49% subgroup; however, this finding requires confirmation in dedicated RCTs. Future larger RCTs are needed to clarify the role of beta-blockers in this borderline population.

We evaluated the efficacy and safety of baxdrostat in adults with uncontrolled or resistant hypertension. We searched PubMed, Scopus, Web of Science, and Cochrane CENTRAL from inception to January 2026. We included randomized controlled trials that involved hypertension patients with resistance type and compared baxdrostat versus placebo. The primary outcomes were the changes in mean seated systolic blood pressure and diastolic blood pressure. Secondary outcomes included changes in estimated glomerular filtration rate (eGFR), serum potassium, and serum aldosterone. Three randomized controlled trials were finally included, comprising 1264 patients were followed for 12-24 weeks. Compared with placebo, baxdrostat reduced seated systolic blood pressure by 8.62 mm Hg [mean difference (MD) = -8.62, 95% confidence interval (CI), -10.55 to -6.70, P < 0.001] and seated diastolic blood pressure by 3.55 mm Hg (MD = -3.55, 95% CI, -4.81 to -2.28, P < 0.001). Baxdrostat lowered serum aldosterone by 4.03 ng/dL, reduced eGFR by 5.49 mL/min/1.73 m2, and increased serum potassium by 0.39 mmol/L. However, baxdrostat was associated with higher adverse events compared with the placebo. Baxdrostat lowers blood pressure and aldosterone levels in uncontrolled and resistant hypertension but increases potassium and modestly reduces eGFR, supporting careful laboratory monitoring and longer trials to evaluate long-term clinical outcomes.

Atrial fibrillation is a common cause of suboptimal cardiac resynchronization therapy (CRT) delivery because intrinsic atrioventricular conduction reduces effective biventricular capture. We performed an updated systematic review and meta-analysis evaluating atrioventricular junction ablation (AVJA) versus no AVJA or pharmacological rate control in CRT recipients with atrial fibrillation. PubMed, Scopus, and Cochrane Library were searched through February 16, 2026. Sixteen studies were included, comprising 14 observational cohorts and 2 randomized trials. AVJA significantly increased biventricular pacing (mean difference 8.80 percentage points, 95% confidence interval [CI] 5.99-11.61). All-cause mortality (risk ratio [RR] 0.74, 95% CI 0.51-1.10), cardiovascular mortality (RR 0.79, 95% CI 0.49-1.27), and heart failure hospitalization (RR 0.73, 95% CI 0.18-2.97) were directionally favorable but not statistically significant. Remodeling, functional, quality-of-life, and clinical responder outcomes were modest or neutral. Contemporary device-therapy data suggested fewer inappropriate shocks and ventricular arrhythmia-related therapies with AVJA, although reporting heterogeneity precluded formal pooling. AVJA remains a dependable CRT-optimization strategy for selected patients with atrial fibrillation, especially when biventricular pacing is inadequate, but contemporary evidence supports a more measured interpretation of downstream clinical benefit.

Retatrutide is a first-in-class, unimolecular triple hormone receptor agonist targeting glucose-dependent insulinotropic polypeptide, glucagon-like peptide-1, and glucagon receptors. By synergizing incretin-mediated central satiety with glucagon-driven thermogenesis, retatrutide circumvents the compensatory metabolic resistance that often limits traditional weight-loss therapies. Phase 2 clinical data demonstrate that a 12-mg maximal weekly dose yields a 24.2% reduction in total body weight at 48 weeks, with 63% of participants achieving a total body weight loss of ≥20%. In patients with type 2 diabetes, retatrutide achieved an absolute HbA1c reduction of 2.02%, with 27% of participants reaching normoglycemia (HbA1c < 5.7%). Beyond global weight reduction, dual-energy X-ray absorptiometry substudies confirm a 23.2% reduction in fat mass, comparable to bariatric surgery. Retatrutide demonstrates potent efficacy in resolving metabolic dysfunction-associated steatotic liver disease, achieving an 82.4% relative reduction in hepatic fat and normalization of liver fat in 86% of patients. These metabolic improvements are accompanied by systemic hemodynamic unloading, including an 8.79 mm Hg reduction in systolic blood pressure and significant attenuation of the urine albumin-to-creatinine ratio. The safety profile is consistent with established incretins: clinicians must monitor for a dose-dependent chronotropic effect. De-escalation of concurrent antihypertensive therapies may also be required.

Hypertrophic cardiomyopathy (HCM) is a common inherited cardiac disorder characterized by maladaptive myocardial hypertrophy, fibrosis, and an increased risk of arrhythmias and sudden cardiac death. Although HCM arises from mutations in sarcomeric proteins, accumulating evidence indicates that downstream calcium-dependent signaling pathways drive pathological remodeling. Among these, the calcineurin-nuclear factor of activated T cells (NFAT) axis has emerged as a central mediator linking altered calcium handling and mechanical stress to hypertrophic gene transcription. Experimental studies in transgenic animals, human myocardial tissue, and induced pluripotent stem cell-derived cardiomyocytes demonstrate that sustained calcineurin activation promotes NFAT nuclear translocation and reactivation of fetal gene programs characteristic of HCM. Pharmacologic inhibition of calcineurin attenuates pathological hypertrophy in multiple preclinical models, although systemic toxicity and inconsistent efficacy limit clinical translation. Consequently, novel therapeutic strategies, including cardiac-targeted gene therapy, NFAT decoy oligonucleotides, peptide-based inhibitors, and modulation of regulatory signaling nodes, have been developed to achieve pathway-specific suppression with improved safety. Despite challenges related to signaling redundancy, disease heterogeneity, and optimal timing of intervention, selective targeting of calcineurin-NFAT signaling represents a promising disease-modifying approach for HCM, with the potential to shift management beyond symptomatic treatment toward precision-based molecular therapy.

Atherosclerotic cardiovascular disease originates in childhood, and cumulative exposure to low-density lipoprotein cholesterol (LDL-C) is a major determinant of lifetime cardiovascular risk. Multiple professional societies have published guidelines for lipid screening, diagnosis, and management in pediatric populations; yet important differences exist among these recommendations. Our objective is to review and compare major pediatric dyslipidemia guidelines and identify areas of consensus, disagreement, and remaining evidence gaps. A narrative review was conducted to compare recommendations from major professional society guidelines on lipid screening, diagnostic criteria, lifestyle management, pharmacologic therapy, and management of hypertriglyceridemia. Across guidelines, there is broad agreement that lifestyle modification is first-line therapy and that statins are safe and effective for children with familial hypercholesterolemia. Key differences exist around universal screening, the age and LDL-C thresholds for statin initiation, LDL-C treatment targets, and the role of genetic testing. More recent guideline updates support earlier identification and treatment of pediatric dyslipidemia, particularly in children with familial hypercholesterolemia. Pediatric dyslipidemia guidelines are evolving toward earlier detection and more intensive management of lipid disorders in children. However, important evidence gaps remain, including limited long-term cardiovascular outcome data following childhood lipid-lowering therapy, insufficient pediatric evidence for newer lipid-lowering agents, and persistent disparities in access to screening.

Gastrointestinal (GI) disease complicates anticoagulation by simultaneously increasing bleeding risk and maintaining high thromboembolic vulnerability. Mucosal injury, portal hypertension, malignancy, inflammatory bowel disease, and vascular lesions predispose to hemorrhage, whereas interruption of therapy increases the risk of stroke, venous thromboembolism, and stent thrombosis. Contemporary management follows an indication-first, risk-balanced approach that integrates thrombotic urgency, GI disease phenotype, and patient-specific bleeding-risk factors. Direct oral anticoagulants demonstrate heterogeneous GI bleeding profiles, with higher risk observed with dabigatran and rivaroxaban, while apixaban is comparatively safer in high-risk populations. Periprocedural management is guided by procedural bleeding risk, renal function, and drug pharmacokinetics, with strategies emphasizing appropriate interruption and minimal use of bridging. In acute GI bleeding, management prioritizes hemodynamic stabilization, restrictive transfusion strategies, and early endoscopic or interventional radiology-guided source control, with selective use of reversal agents in severe cases. Adjunctive measures, including proton pump inhibitor therapy and Helicobacter pylori eradication, reduce recurrent bleeding risk. Resumption of anticoagulation is generally associated with improved survival and reduced thromboembolic events when timed appropriately. Key knowledge gaps remain regarding optimal reversal strategies, lesion-specific restart timing, and management in cirrhotic populations.

Childhood obesity is a growing global public health concern influenced by genetic, environmental, behavioral, psychological, and socioeconomic factors. Increasing consumption of ultra-processed foods and increasingly sedentary lifestyles have contributed significantly to rising obesity rates among children and adolescents. Childhood obesity is associated with serious long-term health complications, including type 2 diabetes, cardiovascular disease, and psychological disorders. Current childhood obesity management emphasizes early identification and intensive lifestyle intervention through nutrition counseling, physical activity promotion, behavioral therapy, and family-based treatment. Recent advances in pharmacologic therapy, particularly glucagon-like peptide-1 receptor agonists, as well as bariatric surgery, have demonstrated meaningful improvements in body mass index and metabolic outcomes in adolescents with severe obesity. This review summarizes the epidemiology, risk factors, clinical consequences, prevention strategies, and emerging treatment approaches for childhood obesity.

Contemporary data on national mortality trends, projections, and evolving disparities remains limited. National rheumatic heart disease mortality data from 1999 to 2024 was assessed using Centers for Disease Control and Prevention's Wide-ranging Online Data for Epidemiologic Research database. Age adjusted mortality rates (AAMR) per 100,000 were calculated. Trends were assessed using joinpoint regression to compute the average annual percent change (AAPC), and predictive models were adopted to estimate rates through 2050. A total of 177,342 deaths were recorded from chronic rheumatic heart disease in the US between 1999 and 2024 with an AAPC of -0.46 [95% confidence interval, -1.20 to 0.26]. Mortality declined significantly between 1999 and 2010 [annual percent change (APC): 3.79: P < 0.001]; however, increased between 2017 and 2021 (APC: 6.04; P < 0.001). Females had a higher mortality burden than males (AAMR: 3.36 vs 2.65). AAMR declined across all racial groups, most prominently in Asian (AAPC: -0.82, P = 0.04) and Hispanics (AAPC: -0.87, P = 0.01). Mortality was higher in non-metropolitan areas (AAMR: 3.25) than metropolitan areas (AAMR: 2.91), though both showed significant decline (metropolitan: AAPC: -1.49, P < 0.001; non-metropolitan: AAPC: -0.54, P = 0.04). Geographically, the West had the highest AAMR (3.80), while Northeast experienced the steepest decline (AAPC: -1.06, P < 0.01). Mortality increased sharply with age, with those ≥65 years experiencing the highest mortality (AAMR: 12.57).

Ischemic heart disease remains the leading cause of cardiovascular mortality globally, yet the burden in Southeast Asia, East Asia, and Oceania has followed a distinct trajectory that contrasts with global trends. Despite declining age-standardized rates reported in higher-income regions, these areas continue to experience rising absolute prevalence, mortality, and disability-adjusted life years, reflecting the combined effects of population aging, rapid urbanization, and persistent metabolic and environmental risk factors. Smaller nations and lower-resource settings, including Timor-Leste, the Maldives, Papua New Guinea, Indonesia, and parts of China, have experienced the steepest increases, highlighting widening regional disparities. Air pollution has emerged as a particularly important contributor to ischemic heart disease mortality, emphasizing the growing influence of environmental exposures alongside traditional cardiometabolic determinants such as hypertension, diabetes, hypercholesterolemia, and tobacco use. The increasing burden in these regions underscores the need for tailored, region-specific strategies that integrate public health, environmental, and cardiovascular prevention priorities. Early identification and management of modifiable risk factors, improvements in air quality, and expanded access to acute and preventive cardiac care are essential to curb future disease burden. Understanding the interplay between demographic shifts, environmental challenges, and persistent metabolic risks is critical for guiding policy and clinical interventions, particularly in lower-resource countries, and may offer a roadmap for mitigating emerging disparities and preventing avoidable cardiovascular deaths across diverse populations.

Coronary artery disease assessment has long focused on stenosis severity, yet luminal narrowing alone fails to capture ischemic burden, plaque vulnerability, or myocardial health. This mismatch drives unnecessary invasive coronary angiography and delays preventive therapy. Cardiac computed tomography (CT) has evolved from a simple anatomical gatekeeper into a comprehensive, noninvasive platform that addresses this gap. This review synthesizes current evidence and provides practical guidance for clinicians, with an emphasis on artificial intelligence integration. High-quality coronary CT angiography now serves as a foundational anatomical roadmap, with trials demonstrating its feasibility for planning complex revascularization (SYNTAX III REVOLUTION) and safely reducing invasive procedures (DISCHARGE). CT-derived fractional flow reserve improves diagnostic specificity, reduces nonobstructive catheterization, and guides revascularization decisions, though prognostic evidence remains mixed and image-quality constraints apply. Quantitative plaque characterization, particularly low-attenuation and total plaque volumes, strongly predicts myocardial infarction and mortality, outperforming stenosis severity and supporting proactive preventive therapy even in nonobstructive disease. Emerging applications include CT-derived extracellular volume for detecting diffuse fibrosis and cardiac amyloidosis, with prognostic value across aortic stenosis and heart failure.

Osimertinib, a third-generation EGFR-TKI, is now the standard first-line treatment for EGFR-mutant non-small cell lung cancer and is increasingly given in the adjuvant setting for up to 3 years and in combination with chemotherapy. As exposure has lengthened and shifted toward curative-intent settings, its cardiac effects have acquired greater clinical weight, because patients may remain on therapy for years and survive long enough for cardiovascular outcomes to matter. This review argues that the dominant cardiac phenotype, a decline in left ventricular ejection fraction, with or without clinical heart failure, is best understood as an often reversible functional cardiomyopathy rather than structural myocardial injury. The neuregulin-1/ErbB signaling axis, which maintains adult cardiomyocyte function and whose disruption by trastuzumab causes a comparable reversible dysfunction, provides the lens for this interpretation, and off-target inhibition of ErbB2/ErbB4 has been proposed as a mechanism for osimertinib cardiotoxicity. That account is incomplete: the EGFR-TKIs that inhibit HER2 most potently do not carry the largest clinical signal, and a recently described GATA4-MYLK3-MYL2 contractile pathway offers an alternative, not clearly ErbB-dependent, mechanism. The proximal cause, therefore, remains unresolved, but across the available evidence, the dominant phenotype appears functional, contractile, and often reversible.

Resistant hypertension affects approximately 10-15% of hypertensive patients despite optimized pharmacologic therapy, necessitating novel interventions. Atrioventricular Interval Modulation (AVIM) therapy is an emerging device-based approach that utilizes dual-chamber pacemakers to simultaneously address standard pacing indications and uncontrolled blood pressure. Unlike conventional pacing, AVIM leverages continuous cycles of short atrioventricular delays to effectively reduce ventricular preload and arterial afterload. These short delays are strategically interspersed with native-like, longer atrioventricular intervals that generate intermittent, higher-pressure pulses. This cyclical asymmetry tricks the body's baroreflex, successfully suppressing compensatory sympathetic vasoconstriction and lowering total peripheral resistance. Pilot trials (MODERATO I and II) demonstrate significant, durable reductions in ambulatory systolic blood pressure while maintaining cardiac contractility and energy efficiency. Furthermore, integrating AVIM with modern conduction system pacing, specifically left bundle branch area pacing, has refined the therapy. Left bundle branch area pacing-AVIM preserves native-like electrical synchrony and substantially outperforms traditional right ventricular pacing, achieving systolic blood pressure reductions of up to 24.1 mm Hg. The therapy also demonstrates rapid, restorative benefits for patients with concurrent diastolic dysfunction, promoting favorable reverse left ventricular remodeling. Ultimately, AVIM presents a continuous, nonpharmacological alternative for managing hypertension, circumventing the pervasive challenges of polypharmacy and medication nonadherence.

Heart failure (HF), particularly heart failure with preserved ejection fraction (HFpEF), disproportionately affects women, yet female-specific and iatrogenic contributors to HF risk remain deeply underrecognized. Bilateral oophorectomy (BO) results in abrupt estrogen deprivation and has increasingly been associated with adverse cardiovascular outcomes, particularly when performed before natural menopause. This review examines the mechanistic and epidemiologic evidence linking BO to cardiovascular disease and HF, with particular attention to age at oophorectomy, estrogen deprivation, and the potential modifying role of estrogen replacement therapy (ERT). Growing evidence associates BO with increased cardiovascular morbidity, mortality, and HF risk, with the greatest risk observed among women undergoing premenopausal BO. Abrupt estrogen loss may contribute through endothelial dysfunction, increased vascular stiffness, adverse metabolic and inflammatory changes, neurohormonal activation, and myocardial remodeling-mechanisms that substantially overlap with HFpEF pathophysiology. ERT may mitigate some cardiovascular consequences of premature surgical menopause, although its effects appear dependent on age, timing of initiation, and route of administration. Recognition of BO as a female-specific cardiovascular risk factor may serve as a critical opportunity for earlier risk identification, targeted prevention, and individualized multidisciplinary care to reduce long-term cardiovascular and HF risk in women worldwide.

Systemic sclerosis (SSc) is a heterogeneous autoimmune connective tissue disease characterized by immune dysregulation, microvascular dysfunction, and progressive fibrosis. It frequently involves the cardiopulmonary system, resulting in many different and serious complications. Cardiovascular manifestations include heart failure, myocarditis, pericardial disease, arrhythmias, coronary artery disease, and treatment-related toxicities such as hydroxychloroquine-induced cardiomyopathy. Pulmonary complications, particularly interstitial lung disease and pulmonary arterial hypertension, remain the leading causes of morbidity and mortality in SSc. Diagnosis relies on multidisciplinary and multimodal evaluation, including serologic testing, advanced imaging, and hemodynamic assessment. Management strategies are disease-specific and include guideline-directed medical therapy, immunosuppression, antifibrotic agents, and targeted pulmonary vasodilator therapy. This review provides a clinically focused overview of the major cardiopulmonary manifestations of SSc, with emphasis on diagnosis, management, and emerging therapeutic considerations.