Search Results (106)

Thyroid hormones play a crucial role in regulating metabolism and cardiovascular function, with even mild dysfunction—such as subclinical hypothyroidism—negatively impacting heart health. While previous studies have confirmed the effects of iodine, selenium, and vitamin D on thyroid regulation and inflammation, the combined role of these nutrients in reducing cardiovascular disease (CVD) risk in autoimmune thyroid disorders remains insufficiently understood. This review explores the influence of specific micronutrients—including selenium, iodine, and zinc—and dietary patterns, particularly the Mediterranean diet, on the pathophysiology of hypothyroidism and Hashimoto’s thyroiditis. We introduce a novel framework that integrates emerging data on sex-specific micronutrient interactions and nutritional immunomodulation. Unlike the existing literature, this review introduces original hypotheses related to sex-specific nutritional immunomodulation and proposes a novel framework for micronutrient-driven dietary intervention in Hashimoto’s thyroiditis. Full article

Primary aldosteronism (PA), the most common cause of secondary hypertension, is increasingly recognized as an independent driver of adverse cardiac remodeling, mediated through mechanisms beyond elevated blood pressure alone. Chronic aldosterone excess leads to myocardial fibrosis, left ventricular hypertrophy, and diastolic dysfunction via mineralocorticoid receptor activation, oxidative stress, inflammation, and extracellular matrix dysregulation. These changes culminate in a distinct cardiomyopathy phenotype, often underrecognized in early stages. Multimodality cardiac imaging, led primarily by conventional and speckle-tracking echocardiography, and complemented by exploratory cardiac magnetic resonance (CMR) techniques such as T1 mapping and late gadolinium enhancement, enables non-invasive assessment of structural, functional, and tissue-level changes in aldosterone-mediated myocardial damage. While numerous studies have established the diagnostic and prognostic relevance of imaging in PA, several gaps remain. Specifically, the relative sensitivity of different modalities in detecting subclinical myocardial changes, the long-term prognostic significance of imaging biomarkers, and the differential impact of adrenalectomy versus medical therapy on cardiac reverse remodeling require further clarification. Moreover, the lack of standardized imaging-based criteria for defining and monitoring PA-related cardiomyopathy hinders widespread clinical implementation. This narrative review aims to synthesize current knowledge on the pathophysiological mechanisms of aldosterone-induced cardiac remodeling, delineate the strengths and limitations of existing imaging modalities, and critically evaluate the comparative effects of surgical and pharmacologic interventions. Emphasis is placed on early detection strategies, identification of imaging biomarkers with prognostic utility, and integration of multimodal imaging into clinical decision-making pathways. By outlining current evidence and highlighting key unmet needs, this review provides a framework for future research aimed at advancing personalized care and improving cardiovascular outcomes in patients with PA. Full article

Background and Objectives: Type 2 diabetes mellitus (T2DM) is associated with subclinical cardiovascular changes, such as increased arterial stiffness and myocardial dysfunction. Vitamin D deficiency has been recognized as a potential contributing factor to vascular disease; however, its impact on early cardiac changes associated with T2DM remains poorly understood. Our aim was to evaluate the association between serum levels of 25-hydroxyvitamin D3 [25(OH)D3], arterial stiffness, and left ventricular global longitudinal strain (LV GLS) in patients with T2DM who do not have a clinically evident cardiovascular disease. Material and methods: This cross-sectional study evaluated the carotid intima–media thickness (IMT), aortic pulse wave velocity (PWVao), LV GLS, and serum 25(OH)D3 levels in patients diagnosed with T2DM (n = 65) compared to healthy control subjects (n = 55). Independent predictors of arterial stiffness were identified by a multivariate logistic regression analysis. Results: Patients with T2DM showed a significant increase in IMT and PWVao, a reduction in LV GLS, and low levels of 25(OH)D3 compared to subjects in the control group (all p < 0.05). Both vitamin D deficiency and T2DM were found to be independently associated with an increased arterial stiffness, with odds ratios of 2.4 and 4.8, respectively. A significant inverse relationship was identified between 25(OH)D3 levels and markers of arterial stiffness, as well as LV GLS, suggesting a possible association between the vitamin D status and the early onset of cardiovascular dysfunction. Conclusions: Patients with T2DM show early signs of heart and blood vessel problems, even with an ejection fraction that remains within normal limits. There is a significant correlation between vitamin D deficiency and increased arterial stiffness, along with impaired LV GLS, indicating its possible involvement in cardiovascular complications associated with diabetes. These findings support the utility of integrating vascular, myocardial, and vitamin D assessments in early cardiovascular risk stratification for T2DM patients. Full article

Background: Psoriasis is a chronic inflammatory skin disease linked to systemic comorbidities, including metabolic, cardiovascular, and autoimmune disorders. Thyroid dysfunction, particularly hypothyroidism, has been observed in patients with moderate-to-severe psoriasis, suggesting possible shared inflammatory pathways. Objectives: This study aims to explore the relationship between psoriasis and thyroid dysfunction in adults with moderate-to-severe psoriasis undergoing biologic therapy to determine whether psoriasis predisposes individuals to thyroid disorders and to identify demographic or clinical factors influencing this association. Materials and Methods: A cross-sectional study included adult patients with moderate-to-severe psoriasis receiving biologic therapy, recruited from the Psoriasis Unit at the Dermatology Department of Hospital Universitario San Cecilio in Granada, Spain, from 2017 to 2023. Patients with mild psoriasis or those treated with conventional systemic therapies were excluded. The data collected included demographics and clinical characteristics, such as age, sex, BMI (body mass index), and psoriasis severity (psoriasis severity was evaluated using the Psoriasis Area Severity Index (PASI), body surface area (BSA) involvement, Investigator’s Global Assessment (IGA), pruritus severity using the Numerical Rating Scale (NRS), and impact on quality of life through the Dermatology Life Quality Index (DLQI)). Thyroid dysfunction, including hypothyroidism and subclinical hypothyroidism, was assessed based on records from the Endocrinology Department. Results: Thyroid dysfunction was found in 4.2% of patients, all classified as hypothyroidism, primarily subclinical. The affected patients were generally older, with a mean age of 57.4 years. No significant differences in psoriasis severity (PASI, BSA) or treatment response were observed between patients with and without thyroid dysfunction. Conclusion: Our findings suggest hypothyroidism is the main thyroid dysfunction in psoriatic patients, independent of psoriasis severity. The lack of impact on psoriasis severity suggests hypothyroidism may be an independent comorbidity, warranting further research into shared inflammatory mechanisms. Full article

Cardiovascular disease remains the leading global cause of mortality, with inflammation now recognized as a central driver of atherosclerosis and other cardiometabolic conditions. Recent advances have repositioned perivascular adipose tissue from a passive structural element to an active endocrine and immunomodulatory organ, now a key focus in cardiovascular and metabolic research. Among the most promising tools for assessing perivascular adipose tissue inflammation is the fat attenuation index, a non-invasive imaging biomarker derived from coronary computed tomography angiography. This review explores the translational potential of the fat attenuation index for cardiovascular risk stratification and treatment monitoring in both coronary artery disease and systemic inflammatory or metabolic conditions (psoriasis, systemic lupus erythematosus, inflammatory bowel disease, obesity, type 2 diabetes, and non-obstructive coronary syndromes). We summarize evidence linking perivascular adipose tissue dysfunction to vascular inflammation and adverse cardiovascular outcomes. Clinical studies reviewing the fat attenuation index highlight its ability to detect subclinical inflammation and monitor treatment response. As research advances, standardization of measurement protocols and imaging thresholds will be essential for routine clinical implementation. Full article

Post-traumatic cardiac dysfunction is a clinically under-recognized complication of polytrauma, often occurring in the absence of overt structural injury. Traditional diagnostic tools frequently fail to detect early or subclinical myocardial impairment, underscoring the need for more sensitive assessment methods. This review explores the utility of global longitudinal strain (GLS), derived from speckle-tracking echocardiography (STE), as a sensitive biomarker for identifying and managing cardiac dysfunction following traumatic injury. It outlines the complex pathophysiology of trauma-induced myocardial impairment, including mechanical injury, systemic inflammation, oxidative stress, and neuro-hormonal activation. The limitations of conventional diagnostic approaches, such as electrocardiography, left ventricular ejection fraction (LVEF), and cardiac biomarkers, are critically assessed and contrasted with the enhanced diagnostic performance of GLS. GLS has demonstrated superior sensitivity in detecting subclinical myocardial dysfunction even when LVEF remains preserved and is associated with increased risk of long-term cardiovascular complications, including arrhythmias and heart failure. The manuscript highlights the clinical utility of GLS in early diagnosis, risk stratification, treatment monitoring, and long-term follow-up. Integration of GLS with inflammatory and oxidative biomarkers (e.g., IL-6, TNF-α, and MPO) and artificial intelligence-based diagnostic models offers potential for improved precision in trauma cardiology. Full article

Cardiovascular disease remains the leading cause of morbidity and mortality worldwide, especially in regions like Eastern Europe, South Asia, and Latin America. A significant portion of these cases (80%) is linked to atherosclerosis, which can lead to severe conditions like ischemic heart disease and stroke, with atherosclerosis (ATS) responsible for the majority of cases. This review explores the multifaceted relationship between insulin resistance (IR) and ATS, highlighting their roles as both independent and interrelated contributors to cardiovascular risk. ATS is characterized by lipid accumulation and chronic inflammation within arterial walls, driven by factors such as hypertension, dyslipidemia, and genetic predisposition, with endothelial dysfunction as a key early event. The early detection of subclinical ATS is critical and can be achieved through a combination of non-invasive imaging techniques—such as coronary artery calcium scoring and carotid ultrasound—and comprehensive risk profiling. IR, marked by impaired glucose uptake in liver, muscle, and adipose tissue, often precedes early diabetes and is associated with metabolic disturbances, including dyslipidemia and chronic inflammation. The diagnosis of IR relies on surrogate indices such as HOMA-IR, the QUICKI, and the TyG index, which facilitate screening in clinical practice. Compelling evidence indicates that IR independently predicts the progression of atherosclerotic plaques, even in non-diabetic individuals, and operates through both traditional risk factors and direct vascular effects. Understanding and targeting the IR–ATS axis is essential for the effective prevention and management of cardiovascular disease. Full article

Background: Over the last 15 years, few echocardiographic studies have examined the biventricular mechanics by speckle tracking echocardiography (STE) in patients affected by chronic obstructive pulmonary disease (COPD) without advanced lung disease. We aimed to summarize the main findings of these studies and quantify the overall effect of COPD on biventricular mechanics in patients without severe airflow obstruction. Methods: Eligible studies assessing cardiac function by conventional transthoracic echocardiography (TTE), implemented with a STE analysis of left ventricular (LV)-global longitudinal strain (GLS) and/or right ventricular (RV)-GLS in COPD patients without severe airflow obstruction vs. healthy controls, were selected from the PubMed, Embase and Scopus databases. The primary endpoint was to quantify the effect of COPD on LV-GLS and RV-GLS in individuals without advanced lung disease. Continuous data [LV-GLS, RV-GLS, left ventricular ejection fraction (LVEF) and tricuspid annular plane systolic excursion (TAPSE)] were pooled as the standardized mean difference (SMD) comparing COPD cohorts with healthy controls. Results: Ten studies were included, totaling 682 COPD patients and 316 healthy controls. Overall, COPD showed a large effect on LV-GLS (SMD −1.296; 95%CI −2.010, −0.582, p < 0.001) and RV-GLS (SMD −1.474; 95% CI −2.142, −0.805, p < 0.001), a medium-to-large effect on TAPSE (SMD −0.783, 95% CI −0.949, −0.618, p < 0.001) and a small effect on LVEF (SMD −0.366, 95% CI −0.659, −0.074, p = 0.014). The I² statistic value for the LV-GLS (91.1%), RV-GLS (88.2%) and LVEF (76.7%) studies suggested a high between-study heterogeneity, while that for the TAPSE (38.1%) studies was compatible with a low-to-moderate between-study heterogeneity. Egger’s test yielded a p-value of 0.16, 0.48, 0.58 and 0.50 for LV-GLS, RV-GLS, LVEF and TAPSE studies, respectively, indicating an absence of publication bias. Meta-regression analyses excluded that the effect of COPD on biventricular mechanics might be influenced by potential confounders (all p > 0.05). Sensitivity analysis confirmed the robustness of the LV-GLS, RV-GLS and TAPSE studies’ results. Conclusions: COPD appears to be independently associated with a mild attenuation of biventricular mechanics in patients with moderate airflow limitations, despite a preserved LVEF and TAPSE on conventional TTE. STE analysis may allow clinicians to identify COPD patients with subclinical myocardial dysfunction and an increased risk of heart failure and cardiovascular complications early. Full article

Background: Subclinical atherosclerosis is a “silent” cardiovascular disease that can be devastating when combined with other illnesses. Its presence may affect therapy responses but can potentially worsen hematological malignancies due to most chemotherapy regimens’ cardiovascular adverse effects. Thus, cardiovascular risk factor (CVRF) assessment is required before chemotherapy. Unfortunately, this rarely happens. Aim: we aim to examine the impact of CVRFs on hemodynamic parameters of acute leukemia (AL) patients before chemotherapy. Methods: Overall, 45 AL patients and 26 controls were included. Intima-media thickness (IMT), ankle brachial index (ABI), pulse wave velocity (PWV), and functional cardiac parameters were used. CVRFs were found in 26 AL patients (36.6%), while 19 AL (26.8%) patients lacked CVRFs. CVRFs were also found in 26 controls (36.6%). Results: Left ventricular ejection fraction (LVEF) significantly decreased for patients with CVRFs (59.26 ± 5.62) compared to those without CVRFs (64.05 ± 7.43, p < 0.05). Hypertensive and diabetic patients had a significantly higher left IMT (mm) of 0.92 ± 0.01 compared to those without them (0.76 ± 0.03, p < 0.05). Patients with acute myeloid leukemia (AML) with CVRFs had a significantly higher PWV (m/s) of 8.4 ± 0.12 compared to those without CVRFs (6.87 ± 0.66) (p < 0.05). Conclusions: AL and cardiovascular risk factors interacted before chemotherapy. To decrease cardiotoxicity, AL patients need cardiovascular risk assessment. Subclinical atherosclerosis and echocardiography help chemotherapy patients to choose a treatment regimen, predict long-term outcomes, and predict cardiovascular issues. Full article

Background: Over the last two decades, a fair number of echocardiographic studies have investigated the influence of metabolic dysfunction-associated steatotic liver disease (MASLD) on myocardial strain and strain rate parameters assessed by speckle tracking echocardiography (STE) in individuals without overt heart disease, reporting not univocal results. We aimed at analyzing the main findings of these studies. Methods: All studies examining conventional echoDoppler parameters by transthoracic echocardiography (TTE) and left ventricular (LV) mechanics [LV-global longitudinal strain (GLS), LV-global strain rate in systole (GSRs), in early diastole (GSRe) and late diastole (GSRl)] by STE in MASLD patients without known heart disease vs. healthy individuals, were searched on PubMed, Embase and Scopus databases. The primary endpoint was to quantify the effect of MASLD on LV-GLS in individuals without overt cardiac disease. Continuous data [LV-GLS, LV-GLSRs, LV-GLSRe, LV-GLSRl and left ventricular ejection fraction (LVEF)] were pooled as the standardized mean difference (SMD) comparing MASLD cohorts with healthy controls. Results: A total of 11 studies were included, totaling 1348 MASLD patients and 6098 healthy controls. Overall, MASLD showed a medium effect on LV-GLS (SMD −0.6894; 95%CI −0.895, −0.472, p < 0.001) and LV-GLSRs (SMD −0.753; 95%CI −1.501, −0.006, p = 0.048), a large effect on LV-GLSRe (SMD −0.837; 95%CI −1.662, −0.012, p = 0.047) and a small and not statistically significant effect on LV-GLSRl (SMD −0.375; 95%CI −1.113, 0.363, p = 0.319) and LVEF (SMD −0.134; 95%CI −0.285, 0.017, p = 0.083). The overall I² statistic was 86.4%, 89.4%, 90.9%, 89.6% and 72.5% for LV-GLS, LV-GLSRs, LV-GLSRe, LV-GLSRl and LVEF studies, respectively, indicating high between-study heterogeneity. Egger’s test for LV-GLS studies gave a p value of 0.11, 0.26, 0.40, 0.32 and 0.42 for LV-GLS, LV-GLSRs, LV-GLSRe, LV-GLSRl and LVEF studies, respectively, thus excluding publication bias. Meta-regression analysis excluded any correlation between potential confounders and LV-GLS in MASLD individuals (all p > 0.05). Sensitivity analysis confirmed the robustness of study results. Conclusions: MASLD has a medium effect on LV-GLS, independently of demographics, anthropometrics and the cardiovascular disease burden. STE analysis may allow early detection of subclinical LV systolic dysfunction in MASLD patients, potentially identifying those who may develop heart failure later in life. Full article

Background/Objectives: This is the first systematic review and meta-analysis investigating early myocardial dysfunction in children/adolescents with celiac disease and the effect of a gluten-free diet by comparing early echocardiographic markers between patients and healthy individuals and between compliant and non-compliant celiac disease patients (based on serum antibody titers). Methods: A systematic literature search was conducted across major electronic databases, with data collection extending up to 3 March 2024. Results: In total, 15 studies with 916 children/adolescent patients with celiac disease and 569 healthy individuals were included. Our results showed a trend toward reduced myocardial function in all echocardiographic parameters (conventional and advanced), with statistical significance in fractional shortening and the myocardial performance index. However, these parameters did not differ significantly after adherence to a gluten-free diet. Conclusions: Therefore, we recommend that an examination of the cardiovascular system should be incorporated into the routine investigations of children with celiac disease in order to detect early subclinical myocardial dysfunction based on echocardiography. Although the results of our meta-analysis indicate that the myocardial performance index may serve as a useful, non-invasive marker for assessing myocardial function in children and adolescents with celiac disease, further research is needed in order to confirm its reliability and clinical applicability in this population. The improvement of echocardiographic parameters after long-term compliance to a gluten-free diet is yet to be evaluated. Full article

Background: The Metabolic Score for Insulin Resistance (METS-IR) is a newly developed index that has been described to predict cardiovascular (CV) events. In this study, we calculated the METS-IR index in patients with rheumatoid arthritis (RA), a condition linked to an elevated CV risk. We then examined its relationship with disease characteristics and CV comorbidities, including disease activity, lipid profile, subclinical carotid atherosclerosis, and insulin resistance indices. Methods: A total of 515 RA patients were recruited. Disease-related characteristics and disease activity indices, including the Disease Activity Score (DAS28), the Clinical Disease Activity Index (CDAI), and the Simple Disease Activity Index (SDAI) were calculated. Additionally, the complete lipid profile, insulin resistance indices, metabolic syndrome criteria, and carotid ultrasound for intima–media thickness and carotid plaque detection were assessed. METS-IR was calculated. A multivariable linear regression analysis was performed to examine the associations between the disease characteristics and METS-IR. Results: METS-IR was positively correlated with age, body mass index, and traditional cardiovascular risk factors such as metabolic syndrome and insulin resistance indices. Carotid intima–media thickness—but not the presence of carotid plaque—was associated with significantly higher METS-IR values. Regarding disease-related characteristics, C-reactive protein and disease activity indices demonstrated a significant positive association with METS-IR after multivariable adjustment. Specifically, C-reactive protein was associated with higher METS-IR values (beta coefficient 0.2, 95% CI: 0.1–0.3, p < 0.001). All disease activity indices, except CDAI, showed a significant positive relationship with METS-IR. Conclusions: METS-IR is linked not only to CV risk factors but also, independently, to inflammatory disease activity in patients with RA. Its association with CV events in the general population and disease activity in RA highlights the significant role of inflammation in driving excessive cardiovascular risk in RA. This underscores the intricate relationship between metabolic dysfunction, systemic inflammation, and CV outcomes in RA. Full article

Recent studies have highlighted the association between polycystic ovary syndrome (PCOS) and cardiometabolic diseases, leading to an improved understanding of the underlying mechanistic factors. PCOS significantly increases cardiovascular risk by predisposing individuals to various subclinical and clinical conditions, including atherosclerosis and type 2 diabetes mellitus. Additionally, it interacts synergistically with other traditional cardiovascular risk factors, such as obesity, hyperlipidemia, and insulin resistance. Several molecular mechanisms involving genetics, epigenetics, adipokine secretion, hyperandrogenemia, and hyperinsulinemia play a role in the relationship between PCOS and these comorbidities. For instance, androgen excess has been implicated in the development of hypertension, type 2 diabetes mellitus, endothelial dysfunction, and ultimately, broader cardiovascular disease. A deeper understanding of these underlying mechanisms facilitates the development of diagnostic, preventative, and therapeutic strategies directed at reducing cardiometabolic morbidity. This narrative review summarizes the current evidence, explores the potential clinical implications of these findings, and discusses emerging therapies to reduce cardiometabolic morbidity in women with PCOS. Full article

There is growing evidence linking growth differentiation factor 15 (GDF15) to both metabolic dysfunction-associated steatotic liver disease (MASLD) and cardiovascular (CV) risk. Nevertheless, the potential relationship between circulating levels of GDF15 and key features of MASLD being predisposed to atherosclerotic CV disease is not fully unveiled. The aim of this study was to deepen into the role of circulating GDF15 levels on metabolic-associated liver injury and atherosclerotic CV disease. We determined the serum GDF15 levels in 156 participants of a metabolic patient-based cohort, and cross-sectionally explored its associations with liver injury and an advanced atherosclerotic lipoprotein profile assessed by nuclear magnetic resonance (¹H-NMR). Additionally, we prospectively evaluated the association between GDF15 levels at baseline and incident atherosclerotic CV disease after a 10-year follow-up. GDF15 was related to liver injury and inflammatory hallmarks, and it increased the likelihood for liver steatosis independently of confounding factors. Likewise, GDF15 was positively associated with an atherogenic profile, particularly with the number of very-low-density lipoproteins (VLDL) particles and its cholesterol and triglyceride content, and with an indicator of subclinical atherosclerosis (i.e., carotid intima–media thickness (cIMT)). The baseline serum GDF15 levels were higher in the patients with atherosclerotic CV disease (10.6%) after a 10-year follow-up than in the individuals without CV disease. Altogether, this study provides new insights into the role of GDF15 in both MASLD and CV disease. Full article

Background/Objectives: Familial Mediterranean fever (FMF) is a chronic autoinflammatory disease. Throughout the disease, subclinical inflammation persists into the remission period. It is known that chronic inflammation causes endothelial dysfunction and, as a consequence, arterial stiffness occurs. In this study, carotid and aortic intima–media thicknesses (IMT) and arterial stiffness were measured in FMF patients to evaluate the risk of possible vascular damage due to chronic inflammation. Methods: The study included pediatric patients with FMF who had been in remission for a minimum of 3 months. Carotid and aortic IMT and arterial stiffness measurements were conducted using sonoelastography. The acute-phase reactants were also evaluated in all participants. Results: Carotid artery stiffness measurements by strain elastography were significantly higher in the patient group than in the control group. However, the aortic and carotid IMT were similar between the two groups. The acute-phase reactants were significantly higher in the patient group than in the control group. Conclusions: This study demonstrated that arterial stiffness increased in pediatric FMF patients. According to the results of the present study, the effects of chronic inflammation on arterial tissues may lead to atherosclerotic changes in the later stages of the disease and may pose a risk for coronary diseases. Arterial ultrasonographic and elastographic measurements to be performed periodically in children with FMF are noninvasive methods that can be used to evaluate the course of endothelial damage. We aimed to show that arterial stiffness may be a marker of early cardiovascular disease. Full article