Perioperative hyperglycemia in cardiac surgery is associated with wound infection, acute kidney injury, and death, yet the intravenous insulin used to treat it is itself coupled to hypoglycemia. Glucagon-like peptide-1 receptor agonists lower glucose only when glucose is elevated and might therefore separate glycemic control from hypoglycemic risk. We searched PubMed/MEDLINE, Scopus, Web of Science, and CENTRAL through September 2025 for randomized controlled trials of perioperative subcutaneous liraglutide versus placebo or insulin-based usual care in adults undergoing cardiac surgery. Two reviewers screened, extracted data, and applied the Cochrane Risk of Bias 2 tool independently; certainty was graded using GRADE. Effects were pooled by inverse variance, fixed-effect when I2 was below 50%. Seven reports of 4 trials, enrolling 446 randomized patients, were eligible. Liraglutide did not alter 30-day mortality (1/161 vs 3/160; risk ratio [RR] 0.42, 95% confidence interval [CI], 0.06-2.81), the composite of any postoperative complication (68/129 vs 76/132; RR 0.92; 95% CI, 0.74-1.14), cardiac adverse events (RR 1.08; 95% CI, 0.83-1.40), hypoglycemia (8/165 vs 9/166; RR 0.85; 95% CI, 0.34-2.13), or postoperative nausea and vomiting (RR 3.01; 95% CI, 0.26-35.27).
Microvascular disease of the eye encompasses both structural and functional changes to the retinal vessels. Cardiometabolic disorders, such as hypertension and diabetes, are associated with early, measurable abnormalities in the retinal microvascular network that often emerge before cardiovascular disease becomes detectable. These features can be directly, noninvasively assessed with a multitude of evolving imaging techniques. Furthermore, these vascular changes can be used to predict future cardiac events, making them promising biomarkers for systemic disease. Early detection is essential, as retinal microvascular pathology not only reflects systemic health but, in certain conditions, can be detrimental to vision. Therefore, clinical evaluation requires a combination of ocular-specific strategies and a focus on underlying metabolic risk factors. As screening techniques advance, integrating assessment of the ocular microcirculation into broader cardiovascular care may become increasingly valuable.
In 2025, the US Food and Drug Administration (FDA) removed its prior class-wide boxed warnings for menopausal hormone therapy (MHT), paving the way for increased clinical use. Menopause accelerates cardiovascular risk independently of chronological aging, manifesting as a 7.5% increase in carotid-femoral pulse wave velocity within 1 year and a hypertension prevalence of 66.6% in women aged 55-64 years. Risk stratification for MHT hinges on the timing of initiation and the administered formulation. The 2025 Women's Health Initiative secondary analysis suggests that in symptomatic women aged 50-59 years, combination (estrogen-progestogen) MHT maintains atherosclerotic neutrality while reducing vasomotor symptoms by 59%. Conversely, atherosclerotic risk increases in women aged 70-79 years (hazard ratio 3.22 for combined therapy). Route of administration dictates the metabolic effect: oral estrogens undergo hepatic first-pass metabolism, elevating venous thromboembolism risk and increasing triglycerides by 5-15%, whereas transdermal formulations bypass hepatic first-pass metabolism, decrease triglycerides by 5-30%, and carry a neutral thromboembolic risk profile. When concurrent progestogen therapy is required, natural micronized progesterone is favored over synthetic medroxyprogesterone acetate to preserve estrogen-mediated vascular benefits. Oral or transdermal systemic MHT can be considered for vasomotor symptom management in women <60 years or within 10 years of menopause with a 10-year atherosclerotic cardiovascular disease risk of <5% and a coronary artery calcium score of zero.
Coronary artery disease coexists in approximately 50% of transcatheter aortic valve implantation candidates, yet the role of percutaneous coronary intervention (PCI) remains uncertain. We conducted a systematic review and meta-analysis of randomized controlled trials comparing PCI with conservative management or deferral in transcatheter aortic valve implantation candidates with coronary artery disease. We searched 4 databases from inception to June 19, 2026. Odds ratios (ORs) were pooled using random-effects models with restricted maximum likelihood estimation and Hartung-Knapp-Sidik-Jonkman adjustment. Individual patient data were reconstructed from published Kaplan-Meier curves. Risk of bias and certainty of evidence were assessed. Three randomized controlled trials (n = 1156 patients) were included. PCI showed no significant reductions in all-cause death (OR 0.88; 95% confidence interval [CI], 0.62-1.25; I2 = 0%), cardiovascular death (OR 0.72; 95% CI, 0.40-1.29; I2 = 0%), or myocardial infarction (OR 0.85; 95% CI, 0.17-4.18; I2 = 51.8%). Stroke was significantly reduced with PCI (OR 0.68; 95% CI, 0.48-0.95; I2 = 0%). PCI was associated with a trend toward increased any bleeding (OR 2.26; 95% CI, 0.81-6.29; I2 = 69.8%) and major bleeding (OR 1.70; 95% CI, 0.63-4.60; I2 = 35.9%).
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.
Atrial fibrillation (AF) recurrence remains a major challenge after catheter ablation, and whether dronedarone or amiodarone should be preferred during the post-ablation blanking period is unresolved. We performed a systematic review and meta-analysis comparing these 2 agents after AF catheter ablation. Five single-center Chinese studies (1 open-label randomized trial and 4 retrospective cohorts) enrolling 996 patients (507 dronedarone and 489 amiodarone) were included. In reconstructed individual patient data from 4 studies, AF recurrence did not differ between dronedarone and amiodarone (hazard ratio [HR] 1.06; 95% confidence interval [CI], 0.75-1.50; P = 0.746), confirmed by a 30-day landmark analysis (HR 1.08; 95% CI, 0.75-1.56; P = 0.690), by study-level pooling of HRs (HR 1.06; 95% CI, 0.74-1.52; I2 = 0%), and by restricted mean survival time analysis. Recurrence also did not differ during the blanking period (risk ratio [RR] 1.09; 95% CI, 0.85-1.40) or over long-term follow-up (RR 1.17; 95% CI, 0.89-1.55). Dronedarone was associated with lower risks of QTc-interval prolongation (RR 0.39; 95% CI, 0.19-0.80) and thyroid dysfunction (RR 0.37; 95% CI, 0.24-0.57) but higher risks of gastrointestinal (RR 7.72; 95% CI, 2.10-28.37) and dermatologic (RR 4.20; 95% CI, 1.06-16.53) adverse events. Dronedarone and amiodarone appear equally effective at preventing AF recurrence after catheter ablation but differ in safety, so selection should be individualized according to patient-specific tolerability and toxicity risk.
The Myval and Myval Octacor transcatheter heart valves (THVs) are newer-generation balloon-expandable devices for transcatheter aortic valve implantation (TAVI) in severe aortic stenosis (AS), but comprehensive synthesis of 1-year outcomes incorporating recent randomized data remains limited. We searched PubMed/MEDLINE, Embase, and CENTRAL through June 2026 for randomized controlled trials and propensity-matched or adjusted observational studies comparing Myval/Myval Octacor with contemporary THVs in adults undergoing transfemoral TAVI for severe symptomatic AS. The primary outcome was 1-year all-cause mortality; secondary outcomes included cardiovascular death, stroke, new permanent pacemaker implantation (PPI), mean transvalvular gradient, effective orifice area, and moderate-to-severe aortic regurgitation. Random-effects meta-analyses generated pooled risk ratios (RRs) and mean differences with 95% confidence intervals. Five studies (2 randomized trials, 3 propensity-matched/adjusted cohorts; 2327 patients: 1107 Myval, 1220 contemporary THV recipients) were included. At 1 year, Myval showed comparable outcomes to contemporary THVs for all-cause mortality (RR 0.89, 0.66-1.21), cardiovascular death (RR 0.92, 0.55-1.55), and stroke (RR 1.41, 0.91-2.18), with similar new PPI rates (RR 0.82, 0.47-1.42). Among randomized trials, Myval had lower mean transvalvular gradients (MD -1.28 mm Hg, -1.73 to -0.82) and larger effective orifice area (mean difference +0.15 cm2, 0.09-0.20) than SAPIEN, with no significant difference in moderate-to-severe aortic regurgitation (RR 1.28, 0.19-8.71). Myval demonstrated comparable all-cause mortality, cardiovascular death, stroke, and PPI rates to contemporary THVs at 1 year, along with favorable hemodynamics versus SAPIEN, supporting Myval as an effective contemporary TAVI platform; longer-term studies are needed to confirm durability and clinical outcomes.
Chronic wounds are a major source of patient morbidity and healthcare expenditure, with impaired tissue oxygenation recognized as a notable obstacle to successful repair. Supersaturated oxygen (SSO2) therapies have gained increasing traction as adjunctive treatments to improve the local wound environment and support the healing process. This review examines the current research and applications of SSO2 therapy in wound healing, including its proposed biological effects, methods of administration, clinical outcomes, and safety considerations. Current research suggests that oxygen-enriched therapies may support tissue regeneration through multiple mechanisms, including the promotion of vascularization, support of extracellular matrix formation, optimization of cellular energy production, and modulation of host inflammatory and antimicrobial processes. Clinical studies have also reported improved outcomes in chronic wounds, particularly diabetic foot ulcers, with additional positive findings in venous leg ulcers, pressure ulcers, and select postoperative wounds. Although limitations remain regarding ideal patient selection and long-term financial impacts, current data support SSO2 therapy as a promising adjunctive therapy within comprehensive wound management.
Polycystic ovary syndrome (PCOS) affects an estimated 11-13% of reproductive-age women worldwide and is increasingly recognized as a condition with significant cardiometabolic abnormalities, beyond its reproductive manifestations. This focused narrative review synthesizes contemporary evidence on the mechanistic, subclinical, and clinical links between PCOS and cardiovascular disease. We examine how hyperandrogenism may contribute to insulin resistance and related abnormalities, including dyslipidemia, hypertension, metabolic dysfunction-associated steatotic liver disease, and endothelial dysfunction, which collectively may increase atherosclerotic risk. Chronic low-grade inflammation and sympathetic overactivation are identified as additional, body mass index-independent amplifiers of this risk. Subclinical markers of vascular dysfunction, including increased carotid intima-media thickness, elevated coronary artery calcium, and elevated biomarkers such as asymmetric dimethylarginine and plasminogen activator inhibitor-1, are consistently elevated in women with PCOS relative to controls. A 2024 meta-analysis of over 300,000 women with PCOS demonstrates pooled odds ratios of 2.50 for myocardial infarction and 1.71 for stroke. Importantly, cardiovascular risk is not limited to women with elevated body mass index; lean women with PCOS carry a substantial and underappreciated metabolic burden. Current risk stratification tools inadequately account for PCOS, and cardiology guidelines have not yet formally designated PCOS as an atherosclerotic cardiovascular disease risk-enhancing condition. We review guideline-based cardiovascular risk assessment and interventions that improve cardiometabolic risk factors, including lifestyle modification, metformin, statins, and glucagon-like peptide-1 receptor agonists. Lastly, we identify priority areas for future research in this underserved population.
Cardiorenal syndrome (CRS) represents a complex bidirectional interaction between the heart and kidneys whereby acute or chronic failure of one organ precipitates dysfunction in the other. CRS occurring in the setting of cardiogenic shock (CS), or CRS-CS, remains one of the most severe manifestations, contributing substantially to morbidity and mortality. Historically, CRS-CS was attributed to renal hypoperfusion from reduced cardiac output. Contemporary evidence suggests that venous congestion and right ventricular dysfunction play equally important roles in the development of acute kidney injury and resultant CRS-CS. Advanced hemodynamic monitoring has further refined our understanding of this dynamic interplay. This review discusses the epidemiology, pathophysiology, hemodynamic determinants, diagnosis, and contemporary management of CRS-CS, emphasizing the importance of forward flow, venous congestion, and right ventricular performance when evaluating renal dysfunction.
Loop diuretics are widely used in the treatment of hypertension and edema caused by cardiovascular, renal, and hepatic dysfunction. Furosemide and bumetanide are 2 of the more commonly prescribed loop diuretics. Sharing a common mechanism of action of blocking the Na+-K+-2Cl- cotransporter in the thick ascending loop of Henle, these drugs can be used to promote diuresis and electrolyte excretion. This article reviews the uses of these loop diuretics and compares and contrasts the pharmacology, efficacy in treating congestive heart failure, adverse effects, and clinical trials comparing the 2 drugs to evaluate whether one drug has higher efficacy and under which circumstances it is preferable to use one drug over another. Numerous studies have shown that furosemide and bumetanide are both equally effective in treating congestive heart failure and the peripheral edema associated with it. As they both possess side effects that can be caused by low electrolyte levels, it is important to monitor these values during administration. Furosemide possesses a lower relative dose ratio to bumetanide, allowing the dosage to be more easily titrated for individual requirements, while bumetanide has a lower risk of ototoxicity and has a higher bioavailability.
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.
Pacemaker insertion in children presents unique challenges because of their small size and developing anatomy. Since pacemaker insertion is relatively uncommon in pediatric patients, and as a result, specialized technologies for this population remain limited and under-researched. The most common indication for pacemaker insertion in children is congenital or acquired heart block. Congenital heart block is often associated with maternal autoimmune disease, in which autoantibodies damage the developing cardiac conduction system. It may also occur in association with congenital heart disease. Acquired heart block can result from several causes, including postoperative conductive abnormalities and complications of myocarditis. Several types of pacemakers have been studied in pediatric patients, including leadless, transvenous, and epicardial pacemakers. Smaller devices designed specifically for neonates are also being investigated. In addition, temporary pacemakers may be used in acute settings or as a bridge to permanent therapy because they can be implanted more rapidly.
We used the National Inpatient Sample from 2016 to 2022 to compare complete revascularization with culprit-only percutaneous coronary intervention in adults hospitalized with non-ST-elevation myocardial infarction and multivessel disease. Hospitalizations complicated by cardiogenic shock, cardiac arrest, coronary artery bypass grafting, or mechanical circulatory support were excluded. Complete revascularization was defined as intervention on at least 2 native coronary territories during the index admission. We performed 1:1 propensity score matching on 52 covariates. The primary outcome was in-hospital major bleeding. Among 713,844 weighted hospitalizations (142,769 unweighted), 27.5% underwent complete revascularization. Matching yielded 37,048 well-balanced pairs (all standardized mean differences <0.01). Complete revascularization was associated with more major bleeding (12.22% vs 10.52%; odds ratio 1.18; 95% confidence interval, 1.13-1.24; P < 0.001), whereas in-hospital mortality was similar (1.01% vs 0.98%; P = 0.684). Major adverse cardiovascular events trended lower (14.61% vs 15.10%; P = 0.062), driven by less recurrent myocardial infarction (P = 0.034). Complete revascularization was also associated with a longer stay (3 vs 2 days) and higher cost ($127,536 vs $91,771; both P < 0.001). The excess bleeding was consistent across 17 subgroups and greatest in patients younger than 65 years (P for interaction < 0.001).
Pompe disease (glycogen storage disease type 2, acid maltase deficiency) is an uncommon, progressive, autosomal recessive lysosomal storage disorder caused by a lack of the enzyme acid α-glucosidase. The enzyme deficiency results in the abnormal buildup of glycogen in lysosomes, especially in skeletal, cardiac, and smooth muscle. The disease can affect multiple organ systems, notably the cardiovascular system. The introduction and approval of enzyme replacement therapy (alglucosidase alfa; Myozyme/Lumizyme) in 2006 dramatically changed the outlook for infantile-onset Pompe disease, transforming what was once a uniformly fatal cardiomyopathy into a treatable condition. Nonetheless, long-term follow-up of patients receiving enzyme replacement therapy has uncovered ongoing cardiac issues; persistent conduction defects, arrhythmias, and residual myocardial fibrosis highlight the need for continued cardiovascular monitoring in these individuals.
Pompe disease (glycogen storage disease type 2, acid maltase deficiency) is an uncommon, progressive, autosomal recessive lysosomal storage disorder caused by a lack of the enzyme acid α-glucosidase. The enzyme deficiency results in the abnormal buildup of glycogen in lysosomes, especially in skeletal, cardiac, and smooth muscle. The disease can affect multiple organ systems, notably the cardiovascular system. The introduction and approval of enzyme replacement therapy (alglucosidase alfa; Myozyme/Lumizyme) in 2006 dramatically changed the outlook for infantile-onset Pompe disease, transforming what was once a uniformly fatal cardiomyopathy into a treatable condition. Nonetheless, long-term follow-up of patients receiving enzyme replacement therapy has uncovered ongoing cardiac issues; persistent conduction defects, arrhythmias, and residual myocardial fibrosis highlight the need for continued cardiovascular monitoring in these individuals.
Ebstein's anomaly is an uncommon congenital defect of the tricuspid valve, marked by the apical displacement of the septal and posterior leaflets, leading to the "atrialization" of the right ventricle and subsequent dysfunction on the right side. Clinical manifestations vary from asymptomatic adults to neonates exhibiting severe cyanosis and heart failure. Advancements in diagnostic imaging, therapeutic interventions, and surgical techniques have significantly enhanced the prognosis for individuals afflicted by this historically serious condition. This review provides an in-depth examination of Ebstein's anomaly, discussing its embryological origins, underlying pathophysiology, clinical manifestations, diagnostic assessment, medical treatment protocols, and surgical interventions. Particular emphasis is placed on contemporary surgical options, including cone reconstruction, the Starnes procedure, one-and-a-half ventricle repair, and valve replacement.
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.
Valvular heart disease (VHD) and psychiatric disorders are each highly prevalent, yet their co-occurrence is underappreciated in clinical practice. Patients carrying both diagnoses present particular management challenges because the pathologic relationship between the two conditions is bidirectional and mechanistically diverse. This narrative review examines the mechanistic, clinical, and therapeutic interplay between VHD and psychiatric illness, with the aim of providing cardiologists and psychiatrists with an integrated framework for recognition and management. We conducted a systematic search of PubMed, MEDLINE, and EMBASE for publications through April 2025, supplemented by a review of the reference lists of retrieved articles. Three mechanistic directions are identified. First, VHD precipitates psychiatric symptoms through hemodynamic burden, neurohormonal activation, cerebral microembolism, and the psychological impact of serious illness. Second, psychiatric disorders and their treatments contribute to VHD through catecholamine-mediated valve stress, chronic inflammation, serotonergic drug-induced valvulopathy, and behavioral risk factors. Third, both conditions share common upstream pathways, including systemic inflammation, oxidative stress, genetic pleiotropy, and adverse social determinants of health. The interplay between VHD and psychiatric disorders calls for structured multidisciplinary care, with psychiatric screening warranted in selected valve populations and echocardiographic vigilance warranted in selected psychiatric cohorts. Adequately powered clinical trials are needed to validate these approaches.
