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.
M. Moore, R. Hirani, Samy Khessib et al.· Cardiology in Review· 0 citations
Three-dimensional (3D) bioprinting is an evolving biofabrication approach in regenerative medicine with the potential to overcome many limitations of conventional reconstructive techniques, including donor-site morbidity, limited tissue availability, and suboptimal restoration of form and function. Recent advances in biofabrication have accelerated the development of patient-specific living constructs for reconstructive applications. This narrative review synthesizes contemporary evidence on the use of 3D bioprinting in reconstructive surgery, emphasizing developments most relevant to plastic surgery. The current literature on bioprinting technologies, bioinks, tissue-specific applications, translational studies, and regulatory considerations was critically reviewed. Significant progress has been achieved in the bioprinting of skin, cartilage, bone, osteochondral tissues, vascularized constructs, and composite craniofacial tissues. Advances in extrusion-, inkjet-, laser-, and stereolithography-based printing, together with increasingly sophisticated natural and synthetic bioinks, have improved construct fidelity, cellular viability, and tissue-specific functionality. In situ bioprinting, patient-specific computer-aided design, and hybrid biomaterial strategies have further expanded the clinical potential of bioprinted tissues. Despite these advances, major barriers remain, including inadequate vascularization of large constructs, limited mechanical maturation of load-bearing tissues, manufacturing standardization, regulatory uncertainty, and the absence of robust long-term clinical outcomes. Three-dimensional bioprinting is enabling increasingly personalized tissue fabrication, although most applications remain preclinical. Clinical translation will require further advances in biomaterials, vascular engineering, manufacturing standardization, and regulatory science.
R. Hirani, Sarina Iraj, Mathew Trandafirescu et al.· Cells· 0 citations
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