Cardiovascular diseases (CVDs) are devastating disorders and the leading cause of mortality worldwide. The pathophysiology of cardiovascular diseases is complex and multifactorial and, in the past years, mitochondrial dysfunction and excessive production of reactive oxygen species (ROS) have gained growing attention. Indeed, CVDs can be considered as a systemic alteration, and understanding the eventual implication of circulating blood cells peripheral blood mononuclear cells (PBMCs) and or platelets, and particularly their mitochondrial function, ROS production, and mitochondrial DNA (mtDNA) releases in patients with cardiac impairments, appears worthwhile. Interestingly, reports consistently demonstrate a reduced mitochondrial respiratory chain oxidative capacity related to the degree of CVD severity and to an increased ROS production by PBMCs. Further, circulating mtDNA level was generally modified in such patients. These data are critical steps in term of cardiac disease comprehension and further studies are warranted to challenge the possible adjunct of PBMCs’ and platelets’ mitochondrial dysfunction, oxidative stress, and circulating mtDNA as biomarkers of CVD diagnosis and prognosis. This new approach might also allow further interesting therapeutic developments.

Lung diseases such as chronic obstructive pulmonary disease, asthma, pulmonary arterial hypertension, or idiopathic pulmonary fibrosis are major causes of morbidity and mortality. Complex, their physiopathology is multifactorial and includes lung mitochondrial dysfunction and enhanced reactive oxygen species (ROS) release, which deserves increased attention. Further, and importantly, circulating blood cells (peripheral blood mononuclear cells-(PBMCs) and platelets) likely participate in these systemic diseases. This review presents the data published so far and shows that circulating blood cells mitochondrial oxidative capacity are likely to be reduced in chronic obstructive pulmonary disease (COPD), but enhanced in asthma and pulmonary arterial hypertension in a context of increased oxidative stress. Besides such PBMCs or platelets bioenergetics modifications, mitochondrial DNA (mtDNA) changes have also been observed in patients. These new insights open exciting challenges to determine their role as biomarkers or potential guide to a new therapeutic approach in lung diseases.

Background: Coronary and carotid artery diseases are manifestations of a systemic atherosclerotic process, often coexisting in patients affected by both conditions. This association emphasizes the importance of evaluating both coronary and carotid atherosclerosis in high-risk individuals. Ultrasound 2D shear-wave elastography (2D-SWE) has shown promise as a noninvasive technique for assessing carotid plaque stiffness. This prospective pilot study aimed to assess carotid plaque stiffness in patients undergoing coronary artery bypass grafting (CABG) and those not scheduled for the procedure as a control group. Methods: 32 patients (17 CABG and 15 controls) were recruited, collectively presenting 43 carotid plaques. Bilateral carotid ultrasound was performed using a high-resolution linear transducer. Plaque stiffness was quantified via 2D-SWE, expressed in shear-wave velocity (SWV, m/s) and Young’s modulus (YM, kPa). Plaque characteristics, including GSM, were quantified. Intra-observer reproducibility was evaluated with intraclass correlation coefficients (ICCs) and Bland–Altman plots. Statistical differences and correlations were assessed using Mann–Whitney U and Spearman’s correlation tests. Results: Carotid plaques in the CABG group exhibited significantly lower stiffness compared to controls (median stiffness SWV: 3.64 m/s vs. 4.91 m/s, p < 0.0001; YM: 20.96 kPa vs. 72.54 kPa, p < 0.0001). ICCs demonstrated excellent reproducibility for stiffness measurements (SWV: ICC = 0.992; YM: ICC = 0.992), with minimal bias in measurements. A positive correlation was observed between 2D-SWE and GSM values (SWV: r = 0.343, p = 0.024; YM: r = 0.340, p = 0.026). Conclusions: Ultrasound 2D-SWE has shown promise as a reliable tool for quantifying carotid plaque stiffness, demonstrating high reproducibility and a significant correlation with GSM. The observed reduction in plaque stiffness among CABG patients highlights its potential as a valuable parameter for identifying high-risk plaques and assessing cerebrovascular risk in patients undergoing CABG.

Introduction: The mitochondrial function of circulating peripheral blood mononuclear cells (PBMCs) is an interesting new approach to cardiac diseases. Thus, PBMC’s mitochondrial respiration decreases in relation to heart failure severity. However, no data are available on heart-transplanted patients (Htx). Population and Methods: We determined PBMCs mitochondrial respiration by high-resolution respirometry (Oroboros Instruments) and superoxide anion production using electron paramagnetic resonance (Bruker-Biospin) in 20 healthy subjects and 20 matched Htx and investigated clinical, biological, echocardiographic, coronarography and biopsy characteristics. Results: PBMCs mitochondrial respiratory chain complex II respiration was decreased in Htx (4.69 ± 0.84 vs. 7.69 ± 1.00 pmol/s/million cell in controls and Htx patients, respectively; p = 0.007) and complex IV respiration was increased (24.58 ± 2.57 vs. 15.68 ± 1.67 pmol/s/million cell; p = 0.0035). Superoxide anion production was also increased in Htx (1.47 ± 0.10 vs. 1.15 ± 0.10 µmol/min; p = 0.041). The leucocyte-to-lymphocyte ratio was increased in Htx, whom complex II correlated with leucocyte number (r = 0.51, p = 0.02) and with the left ventricular posterior wall peak early diastolic myocardial velocity (r = −0.62, p = 0.005). Complex IV was increased in the two patients with acute rejection and correlated negatively with Htx’s isovolumetric relation time (r = −0.45, p = 0.045). Discussion: Although presenting with normal systolic function, Htx demonstrated abnormal PBMC’s mitochondrial respiration. Unlike immunosuppressive therapies, subclinical diastolic dysfunction might be involved in these changes. Additionally, lymphopenia might reduce complex II, and acute rejection enhances complex IV respirations. Conclusion: PBMC’s mitochondrial respiration appears modified in Htx, potentially linked to cellular shift, mild diastolic dysfunction and/or acute rejection.

Background/Objectives: Ultrasound shear-wave elastography (SWE) enables quantitative assessment of tissue stiffness and may provide a non-invasive biomarker of carotid plaque vulnerability. This study aimed to evaluate the ability of SWE to differentiate symptomatic from asymptomatic carotid plaques and to assess its reproducibility. Methods: A systematic search of PubMed, Web of Science, EMBASE, and the Cochrane Library was conducted in the last ten years until January 2026 for publications evaluating carotid plaques using ultrasound SWE. Inclusion criteria required original publications that used quantitative ultrasound SWE parameters for the evaluation of carotid plaque in symptomatic and asymptomatic patients and/or investigated the reproducibility of SWE parameters for carotid plaques; non-carotid studies, non-original articles, and studies not comparing symptomatic versus asymptomatic plaques or not reporting reproducibility were excluded. Fourteen studies comprising 1781 carotid plaques were included. Quantitative SWE measurements were meta-analyzed using random effects. Differences between symptomatic and asymptomatic plaques were assessed using standardized mean differences (SMDs). The reproducibility of SWE measurements was evaluated using pooled correlation coefficients. Publication bias was evaluated using funnel plots and Egger’s regression test. Results: Ten studies including 1246 plaques compared SWE stiffness between symptomatic (n = 472) and asymptomatic plaques (n = 774). The meta-analysis demonstrated significantly lower stiffness values in symptomatic plaques compared with asymptomatic plaques (SMD −1.10, p < 0.001). Reproducibility analysis of correlation coefficients extracted from seven studies demonstrated excellent agreement for SWE measurements (r = 0.92, n = 602). Heterogeneity was observed across the included studies. No statistically significant evidence of publication bias was detected. Conclusions: Ultrasound SWE is a promising approach for assessing carotid plaque vulnerability, with lower SWE stiffness observed in symptomatic plaques compared to asymptomatic plaques. This finding should be interpreted with consideration of methodological heterogeneity and the cross-sectional nature of the available assessed evidence. Further prospective studies with standardized imaging protocols and longitudinal follow-up are needed to determine clinically applicable stiffness thresholds and evaluate the prognostic value of ultrasound SWE in cerebrovascular risk stratification.

Background: Ultrasound is the primary imaging modality for evaluating thyroid nodules, with echogenicity and nodule size serving as parameters for malignancy risk stratification. Though the TI-RADS classification system is standardized, interpretation varies among observers due to subjectivity, and can affect diagnostic consistency. This study aimed to evaluate the diagnostic and interobserver agreement of quantitative ultrasound gray-scale analysis and nodule area in differentiating benign from malignant solid thyroid nodules. Methods: This retrospective study reviewed 600 patients who underwent thyroid ultrasound at King Abdulaziz University Hospital, Jeddah, Saudi Arabia, in 2023 and 2024. Of these 600, 107 adult patients with 116 solid thyroid nodules (96 benign and 20 malignant) who subsequently underwent ultrasound-guided fine-needle aspiration were included in the final analysis. From B-mode ultrasound images, the grayscale median (GSM) values of each nodule and adjacent normal thyroid tissue were measured using Adobe Photoshop. The GSM ratio (GSMr) was calculated by dividing nodule GSM by normal tissue GSM. Nodule size, taken as cross-sectional area, was assessed using ImageJ software version 1.53. The Mann–Whitney U test was used to compare GSMr and the area between benign and malignant nodules. Inter-observer agreement was evaluated using the intraclass correlation coefficient (ICC). Results: Malignant nodules had significantly lower GSMr compared to benign nodules (malignant: median 0.76, IQR 0.27; benign: median 0.88, IQR 0.55, p = 0.02). Malignant nodules were also significantly larger than benign nodules (malignant: median 2.77 cm², IQR: 5.08; benign: median 1.78 cm², IQR 1.65, p = 0.02). Inter-observer reproducibility was excellent for both GSMr (ICC = 0.998) and area (ICC = 0.997). Conclusions: Quantitative ultrasound assessment of grayscale echogenicity and nodule area provides valuable diagnostic information for differentiating benign from malignant solid thyroid nodules. These objective measures may enhance diagnostic confidence and support more precise clinical decision-making in thyroid nodule evaluation.