Search Results (1,719)

Hemostasis and thrombosis reflect a delicate balance, regulated by the interplay between procoagulant and anticoagulant mechanisms. Hemophilia is traditionally viewed as a bleeding disorder, but emerging evidence highlights the paradoxical risks of thrombosis in hemophilia patients. We explore the landscape of hemophilia management, emphasizing challenges of balancing hemostasis in the context of aging, novel non-factor replacement therapies (NRTs), and comorbidity-driven thrombotic complications. Therapeutic approaches, including innovative NRTs, such as emicizumab, or rebalancing agents (e.g., concizumab, marstacimab, fitusiran), offer promising advancements in bleeding prophylaxis but may increase thrombotic risks. Conversely, novel anticoagulants, such as FXI inhibitors, offer potential thrombosis protection with minimal bleeding risk. Our review examines the impact of aging-related comorbidities, including cardiovascular disease, atrial fibrillation, HIV-associated complications, and acute coronary syndromes, on thrombotic risk in hemophilia patients. Evidence-based strategies for balancing hemostasis and thrombosis are outlined alongside experimental models, thrombin generation assays, and advancements in rebalancing coagulation through natural anticoagulant modulation. FXI inhibition emerges as a paradigm shift in thrombosis management, offering reduced bleeding risks while preserving vascular health. Finally, this review highlights the need for global laboratory assays to personalize treatments, emphasizing strategies to optimize safety and efficacy, particularly as hemophilia patients live longer with complex comorbidity profiles. Full article

High platelet reactivity (HPR) in patients with coronary artery disease receiving P2Y12 inhibitors increases ischemic risk. Chronic kidney disease (CKD) is an established contributor to HPR during clopidogrel therapy. The objective of the study was to assess whether CKD influences platelet reactivity (PR) in patients treated with clopidogrel or ticagrelor. This double-blind, double-dummy study enrolled 106 stable patients more than one year after an acute coronary syndrome, with or without CKD. Participants were matched by age and sex and randomized to clopidogrel or ticagrelor. PR was measured using the VerifyNow™ P2Y12 assay, and HPR was defined as P2Y12 reaction units (PRU) ≥ 208. Median glomerular filtration rates were 80 mL/min/1.73 m² in non-CKD patients and 41 mL/min/1.73 m² in CKD patients (p < 0.01). Ticagrelor produced similarly low PR in both groups (36 vs. 35 PRU; p = 0.61). Clopidogrel resulted in a numerically higher PR in CKD patients (209 vs. 180 PRU; p = 0.07). The magnitude of PR reduction with ticagrelor relative to clopidogrel was greater in CKD patients (p-interaction = 0.09). HPR was markedly more common with clopidogrel, particularly in CKD (difference 37%; adjusted OR 4.42; p = 0.01). In conclusion, CKD significantly impairs clopidogrel responsiveness but does not affect ticagrelor, resulting in a greater relative advantage of ticagrelor in patients with CKD. Full article

Factor XII is a molecule of unclear physiological function that has attracted increasing research interest across multiple medical disciplines. In recent years, a substantial body of evidence has emerged regarding the contribution of factor XII to the pathogenesis of inflammatory and prothrombotic conditions. FXII has been shown to play a protective role in FXII-driven coagulation during host defence against infections and to protect against multi-organ failure in animal models of sepsis. In acute respiratory distress syndrome (ARDS), FXII activity contributes to the release of pro-inflammatory mediators and is associated with severe clinical outcomes; it also induces fibroblast migration in idiopathic pulmonary fibrosis. FXII deficiency has been associated with reduced neutrophil adhesion and migration in sterile skin wounds and immune complex-induced vasculitis. In neurological conditions, FXII deficiency significantly reduced the number and severity of multiple sclerosis relapses and decreased the volume of post-traumatic brain oedema. In heart failure pathogenesis, FXII deficiency and pharmacological inhibition of FXII activity blocked activation of the renin–angiotensin–aldosterone system (RAAS) in dilated cardiomyopathy, increased median survival, and delayed heart failure onset in murine models. Importantly, FXII inhibition prevented arterial thrombosis without affecting haemostasis. This review summarises the latest findings on the contribution of FXII to inflammatory and prothrombotic states across multiple medical fields, including cardiology. Pharmacological inhibition of FXII has generated considerable interest as a potential future therapeutic strategy; however, to date, human studies remain limited. Full article

Background and Objectives: SGLT2 inhibitors are foundational in heart failure therapy, yet their impact on left ventricular (LV) remodeling immediately following acute coronary syndrome (ACS) remains less defined. This study evaluated the association between early SGLT2 inhibitor initiation and structural recovery in a real-world post-ACS cohort. Materials and Methods: We conducted a retrospective observational study including 238 revascularized ACS patients, stratified into an SGLT2 inhibitor group (n = 71) and a control group (n = 167). Changes in LV ejection fraction (LVEF) and indexed LV mass (LVMi) were assessed by echocardiography at baseline and follow-up (mean 286 days). Multivariable regression models were adjusted for baseline imbalances and tested for interactions with diabetes status. Results: A significant “confounding by indication” was observed; the SGLT2 group presented a high-risk phenotype with higher diabetes prevalence (56.3% vs. 25.7%, p < 0.001), lower baseline LVEF (38.3% vs. 43.3%), and greater hypertrophy. After adjustment, statistical independence was attenuated by baseline severity, yet the SGLT2 group achieved follow-up structural outcomes comparable to lower-risk controls. Interaction analysis indicated these trends were consistent regardless of diabetes status (p > 0.05). Conclusions: In this high-risk ACS population, early SGLT2 inhibitor therapy was associated with stabilization of cardiac structure. Despite a profound baseline disadvantage, the recovery trajectory effectively aligned with that of a lower-risk population, highlighting a clinically relevant pattern of structural stabilization consistent across metabolic subgroups. Full article

Understanding thrombosis in acute coronary syndromes (ACSs) has evolved through advances in biomarkers, intracoronary imaging, and emerging analytical tools, improving diagnostic accuracy and risk stratification in high-risk patients. This narrative review provides an integrative overview of contemporary evidence from clinical trials, meta-analyses, and international guidelines addressing circulating biomarkers, intracoronary imaging modalities—including optical coherence tomography (OCT), intravascular ultrasound (IVUS), and near-infrared spectroscopy (NIRS)—artificial intelligence–based analytical approaches, and emerging antithrombotic therapies. High-sensitivity cardiac troponins and natriuretic peptides remain the most robust and guideline-supported biomarkers for diagnosis and prognostic assessment in ACS, whereas inflammatory markers and multimarker strategies offer incremental prognostic information but lack definitive validation for routine therapeutic guidance. Intracoronary imaging with IVUS or OCT is supported by current guidelines to guide percutaneous coronary intervention in selected patients with ACS and complex coronary lesions, leading to improved procedural optimization and clinical outcomes compared with angiography-guided strategies. Beyond procedural guidance, OCT enables detailed plaque characterization and mechanistic insights into ACS, while NIRS provides complementary information on lipid-rich plaque burden, primarily for risk stratification based on observational evidence. Artificial intelligence represents a rapidly evolving tool for integrating clinical, laboratory, and imaging data, with promising results in retrospective and observational studies; however, its clinical application in thrombosis management remains investigational due to the lack of outcome-driven randomized trials. In the therapeutic domain, factor XI inhibitors have demonstrated favorable safety profiles with reduced bleeding and preserved antithrombotic efficacy in phase II and early phase III studies, but their definitive role in ACS management awaits confirmation in large, outcome-driven randomized trials. Overall, the integration of biomarkers, intracoronary imaging, and emerging analytical and pharmacological strategies highlights the potential for more individualized cardiovascular care. Nevertheless, careful interpretation of existing evidence, rigorous validation, and alignment with guideline-directed practice remain essential before widespread clinical adoption. Full article

Ischemic heart disease (IHD) remains a leading cause of global morbidity and mortality despite advances in prevention, diagnosis, and therapy. Traditional clinical risk scores and biomarkers often fail to fully capture the complex molecular processes underlying atherosclerosis, myocardial infarction, and ischemic cardiomyopathy, leaving substantial residual risk. MicroRNAs have emerged as promising regulators and biomarkers of cardiovascular disease, among which microRNA-21 (miR-21) has attracted particular attention. MiR-21 is deeply involved in key pathophysiological mechanisms of IHD, including endothelial dysfunction, vascular inflammation, vascular smooth muscle cell proliferation, plaque development and vulnerability, cardiomyocyte survival, and myocardial fibrosis. Accumulating clinical evidence suggests that circulating miR-21 holds diagnostic value across the ischemic continuum, from stable coronary artery disease to acute coronary syndromes, myocardial infarction, and ischemic heart failure. Moreover, miR-21 demonstrates prognostic relevance, correlating with plaque instability, adverse remodeling, heart failure progression, and long-term cardiovascular outcomes. Preclinical studies further indicate that miR-21 represents a double-edged therapeutic target, offering cardio protection in acute ischemic injury while contributing to fibrosis and maladaptive remodeling if dysregulated. This narrative review summarizes current evidence on the diagnostic, prognostic, and therapeutic utility of miR-21 in IHD, highlighting its clinical promise as well as key limitations and future translational challenges. Full article

Atherosclerosis (AS) is a disease characterized by chronic vascular wall inflammation and lipid deposition. Although lipid-lowering drugs such as statins have significantly reduced cardiovascular event rates, “residual inflammatory risk” remains a key factor driving disease progression and plaque rupture. As a central regulator of the inflammatory response, the nuclear factor-κappaB (NF-κB) signaling network comprises both canonical pro-inflammatory pathways and functionally more complex non-canonical pathways. Increasing evidence in recent years indicates that abnormal and sustained activation of the non-canonical NF-κB signaling pathway plays a pivotal role in driving plaque rupture. This review first elaborates on the shift in AS strategies from “lipid-lowering” to “anti-inflammatory” approaches, followed by an in-depth analysis of the molecular activation mechanisms of the NF-κB signaling pathway and its distinctiveness in the AS pathological process, along with its epigenetic regulation. It emphasizes how this pathway drives pathological angiogenesis and regulates vascular smooth muscle cell (VSMC) phenotypic switching and macrophage function, thereby forming a vicious cycle that amplifies inflammation and structural damage, ultimately leading to acute cardiovascular events. Finally, we systematically summarize current progress and challenges in drug development targeting the NF-κB pathway (e.g., targeting key kinases like NIK and IKKα), aiming to provide theoretical foundations and future directions for novel therapeutic strategies to stabilize coronary plaques and prevent acute coronary syndromes. Full article

Air pollution from lignite combustion represents a major environmental and public health concern, particularly for cardiovascular disease. This study investigated the relationship between ambient air pollution and hospital admissions for Acute Coronary Syndromes (ACS) and Atrial Fibrillation (AF) in Western Macedonia, Greece—a region historically dominated by lignite mining and power generation. Air quality data for PM₁₀, SO₂, and NO_x from 2011–2014 and 2021 were analyzed alongside hospital admission records from four regional hospitals (Kozani, Ptolemaida, Florina, Grevena). Spatial analyses revealed significantly higher pollutant concentrations and cardiovascular admissions in high-exposure areas near power plants compared with the control area. Temporal analyses demonstrated a pronounced decline in pollutant levels between 2014 and 2021, coinciding with lignite phase-out and accompanied by a marked reduction in ACS and AF hospitalizations, particularly in the high-exposure areas of Ptolemaida and Florina. Correlation analyses indicated modest but significant positive associations between monthly pollutant concentrations and cardiovascular admissions. These findings provide real-world evidence that reductions in air pollution following lignite decommissioning were associated with improved cardiovascular outcomes. The study underscores the medical importance of air quality improvement and highlights emission reduction as a critical strategy for cardiovascular disease prevention in transitioning energy regions. Full article

We report the case of an 80 yo female patient with cardiovascular risk factors and previous diagnosis of Tako-Tsubo syndrome, who was referred to our institution one year after a previous diagnosis, due to symptoms suggestive of acute coronary syndrome (SCA) after severe emotional stress. After ruling out suspected CAD by cardiac computed tomography (CCT) and subsequent invasive coronary angiography (ICA) confirming no significant stenosis but presence of vulnerable plaque, the patient underwent further investigation by cardiac magnetic resonance (CMR) that confirmed a clinical picture compatible with recurrence of Tako-Tsubo syndrome. Our case underlines the importance of multimodality imaging to guide diagnosis and treatment in this specific clinical scenario. Full article

Background: Intentional occlusion of the internal iliac artery (IIA) during endovascular repair of aorto-iliac aneurysms may predispose patients to pelvic ischemic complications such as gluteal claudication, erectile dysfunction, and bowel ischemia. Iliac branch devices (IBDs) have been developed to preserve hypogastric perfusion. E-Liac (Artivion/Jotec) is one of the latest modular IBDs yet reports on mid-term performance are limited to small single-center cohorts with short follow-up. The CAMpania PugliA bRanch IliaC (CAMPARI) study is a multicenter investigation of E-Liac outcomes. Methods: A retrospective observational cohort study was conducted across five Italian vascular centers. All consecutive patients undergoing E-Liac implantation for aorto-iliac or isolated iliac aneurysms between January 2015 and December 2024 were identified from prospectively maintained registries. Inclusion criteria comprised elective or urgent endovascular repair of aorto-iliac aneurysms in which an adequate distal sealing zone was not available without covering the IIA and suitability for the E-Liac device according to its instructions for use (IFU). Patients with a life expectancy < 1 year or hostile anatomy incompatible with the IFU were excluded. The primary end point was freedom from branch instability (occlusion/stenosis, kinking, or detachment of the bridging stent). Secondary end points included freedom from any endoleak, freedom from device-related reintervention, freedom from gluteal claudication, aneurysm-related and all-cause mortality, acute renal failure, and sac regression > 5 mm. Results: A total of 69 consecutive patients (68 male, 1 female, median age 72.0 years) received 74 E-Liac devices, including 5 bilateral implantations. The mean infrarenal aortic diameter was 45 mm and the mean CIA diameter 34 mm; 14 patients (20.0%) had a concomitant IIA aneurysm (>20 mm). Concomitant fenestrated or branched aortic repair was performed in 23% of procedures. Two patients received a standalone IBD without implantation of a proximal aortic endograft. Technical success was achieved in 71/74 cases (96.0%); three failures occurred due to inability to catheterize the IIA. Distal landing was in the main IIA trunk in 58 cases and in the posterior branch in 13 cases. Over a median follow-up of 18 (6; 36) months, there were four branch instability events (5.4%): three occlusions and one bridging stent detachment. Seven patients (9.5%) developed endoleaks (one type Ib, two type II, two type IIIa, and two type IIIc). Five patients (6.8%) required reintervention, and five (6.8%) reported gluteal claudication. There were seven all-cause deaths (10%), none within 30 days or related to aneurysm rupture; causes included COVID-19 pneumonia, acute coronary syndrome, melanoma, gastric cancer, and stroke. No acute renal or respiratory failure occurred. Kaplan–Meier analysis showed 92% (95% CI 77–100) freedom from branch instability in the main-trunk group and 89% (60–100) in the posterior-branch group (log-rank p = 0.69). Freedom from any endoleak at 48 months was 87% (95% CI 75–95), and freedom from reintervention was 93% (95% CI 83–98). Conclusions: In this multicenter cohort, the E-Liac branched endograft demonstrated high technical success and favorable early–mid-term outcomes. Preservation of hypogastric perfusion using E-Liac was associated with low rates of branch instability, endoleak, and reintervention, with no 30-day mortality or aneurysm-related deaths. These findings support the safety and efficacy of E-Liac for aorto-iliac aneurysm management, although larger prospective studies with longer follow-up are needed. Full article

Background/Objectives: Diagnostic performance of angiography-derived physiological measures has been benchmarked against two-dimensional (2D) and three-dimensional (3D) quantitative coronary angiography (QCA), which are known for their poor correlation with hemodynamic lesion severity. Relying on the statistical concept of the wisdom of the crowd, we devised a human-performance reference for FFR surrogates, called vox populi FFR (vpFFR), and examined the comparative diagnostic performance of vpFFR, as well as 2D- and 3D-QCA, using invasively measured FFR as the gold standard. Methods: Analyses were performed in a single-center, prospective registry of consecutive FFR procedures. We calculated vpFFR as a mean of five independent, blinded predictions of the invasively measured FFR. Pearson’s correlation coefficient and receiver operating characteristic (ROC) curve analyses were used for diagnostic performance comparisons. Results: In 116 patients (156 vessels), Pearson’s correlation coefficients for vpFFR, 2D-, and 3D-QCA with invasively measured FFR are 0.56, −0.26, and −0.01, respectively (p < 0.001, p = 0.001 and p = 0.918). vpFFR has a sensitivity of 56%, specificity of 84%, positive predictive value of 67%, and negative predictive value of 76%. It correctly classified hemodynamic severity of lesions in 73% of vessels compared to 65% and 51% for 2D- and 3D-QCA, respectively. vpFFR has a larger area under the ROC curve than 2D- and 3D-QCA for predicting positive FFR (0.78, 0.63, and 0.45, respectively, p < 0.001). Conclusions: vpFFR, a mean value of five predictions of invasively measured FFR, has moderate diagnostic performance, superior to 2D- and 3D-QCA using FFR as the gold standard, and can be used as a human-performance reference for existing and emerging angiography-derived physiological measures. Full article

Post-cardiac arrest syndrome (PCAS) remains a major cause of mortality and neurological impairment following successful resuscitation, yet the mechanisms linking global ischemia–reperfusion injury to microvascular and systemic dysfunction are not yet completely understood. While prior work has focused on inflammation, endothelial injury, and circulatory collapse, the central role of platelets in coordinating these pathological processes has not been comprehensively examined. This review provides the first integrated framework positioning platelets as core modulators, rather than secondary participants, in PCAS pathophysiology. We synthesize emerging evidence demonstrating that ischemia and reperfusion transform platelets into potent thromboinflammatory effectors through oxidative stress, DAMP-mediated pattern recognition signaling, and mitochondrial dysfunction. Hyperactivated platelets drive cerebral microthrombus formation, coronary no-reflow, and peripheral organ hypoperfusion, while platelet–leukocyte aggregates, neutrophil extracellular traps, and platelet-derived microparticles amplify systemic inflammation and endothelial injury. We further highlight the clinical significance of dynamic platelet dysfunction in coagulopathy, prognostication, and responses to post-arrest therapies including targeted temperature management and ECMO. Finally, we outline a novel, platelet-centered therapeutic paradigm, emphasizing selective interventions, such as GPVI inhibition, P-selectin blockade, FXI/XIa inhibition, and NETosis modulation, that target pathological platelet activity while preserving essential hemostatic function. In this review, by reframing platelets as the central determinants of PCAS, we report new mechanistic insights and therapeutic opportunities that are complementary to the existing post-arrest strategies and have the potential to improve survival and neurological outcomes after cardiac arrest. Full article

Background/Objectives: The Lancet Commission proposes a new obesity definition that combines body mass index (BMI) with anthropometric measurements to distinguish adipose tissue excess more effectively. This study aims to determine the prevalence of obesity based on the new definition and to examine cardiometabolic risk factors and lifestyle habits across different obesity phenotypes in the urban population of Lithuania. Methods: This study was conducted among residents of Kaunas city from 2020 to 2024. A total of 3426 adults aged 25–69 years (57.1% of the random sample) were participated. Three individuals were excluded due to missing anthropometric data. Participants were categorized into three phenotypes: (1) no obesity (BMI < 30 kg/m² and no or one elevated anthropometric measure, (2) anthropometric-only obesity (BMI < 30 kg/m² and at least 2 elevated anthropometric measures), and (3) BMI-plus-anthropometric obesity (BMI ≥ 30 kg/m² plus at least one elevated anthropometric measure or BMI ≥ 40 kg/m²). Standardized anthropometric, biochemical, and clinical measurements were collected, along with self-reported dietary habits and leisure-time physical activity. Results: Anthropometric-only obesity was highly prevalent, affecting 36.1% of males and 22.7% of females (p < 0.05). The prevalence of BMI-plus-anthropometric obesity was 24.1% among males and 21.4% among females. Individuals with anthropometric-only obesity had significantly higher odds of metabolic syndrome (OR 8.64; 95% CI 6.97–10.71), diabetes (OR 3.01; 95% CI 1.72–5.25), coronary heart disease (OR 1.48; 95% CI 1.12–1.97), and several lipid abnormalities compared with those without obesity. The highest cardiometabolic risk was observed in the BMI-plus-anthropometric obesity group. Greater adiposity was associated with higher intake of red meat, junk foods, and sugary drinks, while physical activity levels declined across obesity categories. Conclusions: Anthropometric-only obesity is a common and metabolically adverse phenotype that cannot be detected using BMI alone. A new obesity definition enhances identification of high-risk individuals and supports targeted prevention strategies. Full article

Background: Acute coronary syndrome (ACS) continues to be a major contributor to morbidity and mortality worldwide. While percutaneous coronary interventions (PCIs) have significantly evolved, coronary artery bypass grafting (CABG) has retained a role in emergency revascularization. Nevertheless, ongoing debate persists about how to select candidates for surgery, when to operate, and which surgical techniques offer the greatest safety and efficacy. Methods: A comprehensive literature search was conducted, yielding 2302 records, of which 25 studies met predefined screening criteria and were included for detailed analysis. Given that timing remains one of the most controversial issues in the management of ACS, our primary aim was to determine the optimal timing for CABG in this patient population. Additionally, we examined how preoperative antiplatelet therapy and the presence of cardiogenic shock influence clinical outcomes, and what revascularization strategy may be most appropriate for these patients. Results: Of the 2302 initially identified studies, 25 were selected for a detailed analysis, supplemented by 28 additional key references. Among the included studies, 17 focused primarily on the effects of surgical timing and 8 on comparisons between the outcomes of CABG and PCI. The analysis comprised 15 database or multicentre retrospective cohort studies, 8 single-centre retrospective studies, and 2 prospective investigations. Conclusion and limitations: Although the topic of non-elective coronary surgery has been with us for several decades, a number of inherent biases hinder thorough statistical investigation in this complex population. Although a number of contradictory findings hinder drawing simple conclusions, being reluctant to perform early surgery solely based on poorer unfiltered outcomes might miss a point. Full article

Background/Objectives: Hypothyroidism is highly prevalent among HD patients, due to cumulative disturbances in thyroid hormone synthesis, metabolism, and clearance. Subclinical hypothyroidism—defined by elevated TSH with normal fT₄—is common in HD, along with a distinct entity, the low-T₃ syndrome. This study aims to examine the predictors of hypothyroidism in HD and its impact on cardiovascular morbidity and mortality. Methods: We conducted a retrospective cohort study including 282 hemodialysis (HD) patients, with evaluated thyroid function and monitored from January 2022 to June 2025. A total of 66 (23.4%) patients with hypothyroidism were identified, 15 (5.31%) of whom had autoimmune thyroiditis. Subclinical hypothyroidism was documented in 31.81% of the hypothyroid patients. Results: Hypothyroidism occurred predominantly in females (63.63% vs. 41.2%, p ≤ 0.001) and was associated with higher BMI (27.856 ± 6.216 vs. 25.759 ± 6.080, p = 0.017), hypoalbuminemia (3.534 ± 0.547 vs. 3.725 ± 0.471, p = 0.006), elevated LDL-cholesterol and triglyceride levels, as well as with amiodarone use. Hypothyroidism was further associated with atrial fibrillation (33.33 vs. 19.9%, p = 0.022), coronary artery revascularization procedures (18.18% vs. 9.72%, p = 0.047), neoplastic disease (25.75% vs. 12.03%, p = 0.008), and cancer-related mortality (10.6% vs. 1.85%, p = 0.001). Multivariable regression analysis revealed the following predictors of hypothyroidism: female sex (OR 3.848, 95%CI 1.704–8.693, p = 0.001), BMI (OR 1.072, 95%CI 1.007–1.146, p = 0.031), hypoalbuminemia (OR 0.412, 95%CI 0.177–0.962, p = 0.040), hypertriglyceridemia (OR 1.088, 95% CI 1.001–1.016, p = 0.022) and amiodarone use (OR 6.698, 95%CI 1.744–25.722, p = 0.006). Patients with autoimmune thyroiditis did not exhibit clinical or biochemical differences compared with other hypothyroid patients. Subclinical hypothyroidism was associated with longer HD duration (10.476 ± 7.910 vs. 6.567 ± 5.541, p = 0.003), dyslipidemia, hypertension, atrial fibrillation and amiodarone use. Cardiovascular conditions—particularly atrial fibrillation and ischemic coronary disease requiring revascularization—are more common in HD patients with clinical or subclinical hypothyroidism. However, in our cohort, the Kaplan–Meier survival curves at 12, 24, and 36 months for patients with both subclinical and clinical hypothyroidism do not show significant differences in cardiac or overall mortality. Conclusions: The increased incidence of hypothyroidism in HD patients, together with its impact on cardiovascular pathology, underscores the need for multidisciplinary management and supports annual routine assessment of thyroid hormones—particularly in overweight or dyslipidemic patients and in those receiving amiodarone. Full article