Hasil untuk "Diseases of the circulatory (Cardiovascular) system"

M. Bellemare, M. Chetrit, I. Voron Kostychuk et al.

L. J. Spielman, D. Gibson, A. Klegeris

&NA; The number of bacterial cells living within the human body is approximately equal to, or greater than, the total number of human cells. This dynamic population of microorganisms, termed the human microbiota, resides mainly within the gastrointestinal tract. It is widely accepted that highly diverse and stable microbiota promote overall human health. Colonization of the gut with maladaptive and pathogenic microbiota, a state also known as dysbiosis, is associated with a variety of peripheral diseases ranging from type 2 diabetes mellitus to cardiovascular and inflammatory bowel disease. More recently, microbial dysbiosis has been associated with a number of brain pathologies, including autism spectrum disorder, Alzheimer's disease (AD), Parkinson's disease (PD), and amyotrophic lateral sclerosis (ALS), suggesting a direct or indirect communication between intestinal bacteria and the central nervous system (CNS). In this review, we illustrate two pathways implicated in the crosstalk between gut microbiota and CNS involving 1) the vagus nerve and 2) transmission of signaling molecules through the circulatory system and across the blood‐brain barrier (BBB). We summarize the available evidence of the specific changes in the intestinal microbiota, as well as microorganism‐induced modifications to intestinal and BBB permeability, which have been linked to several neurodegenerative disorders including ALS, AD, and PD. Even though each of these diseases arises from unique pathogenetic mechanisms, all are characterized, at least in part, by chronic neuroinflammation. We provide an interpretation for the substantial evidence that healthy intestinal microbiota have the ability to positively regulate the neuroimmune responses in the CNS. Even though the evidence is mainly associative, it has been suggested that bacterial dysbiosis could contribute to an adverse neuroinflammatory state leading to increased risk of neurodegenerative diseases. Thus, developing strategies for regulating and maintaining healthy intestinal microbiota could be a valid approach for lowering individual risk and prevalence of neurodegenerative diseases. HighlightsDiverse and stable human intestinal microbiota are associated with brain health.Intestinal microbiota regulate neuroimmune responses in the central nervous system.Gut bacteria communicate with the brain via the vagus nerve and circulatory system.Microbial dysbiosis increase the risk of developing neurodegenerative diseases.Microbial dysbiosis may cause adverse neuroinflammation in neurodegenerative diseases.

Zhi-Yuan Zhang, Feng Li, Chi Geng et al.

Background: Left atrial appendage closure (LAAC) has been reported to be a viable alternative to prevent thromboembolic events for atrial fibrillation (AF) patients. Interatrial communication closure, such as atrial septal defect (ASD) and patent foramen ovale (PFO) closure could significantly decrease the occurrence of stroke. For AF patients with interatrial communication, the success rate as well as the long-term outcomes of ‘One stop’ closure remain elusive. Methods: Studies were systematically screened using online databases (including PubMed, Cochrane Library, Web of Science, Embase, China National Knowledge Infrastructure (CNKI) database, and WanFang database) from their establishment to 1st August 2024. We utilized a fixed-effect model to synthesize the success rate and the long-term outcomes. Subgroup analysis was performed to identify the potential confounders. Results: A total of 7 studies comprising 156 patients were included. ASD/PFO closure combined with LAAC showed a high degree of feasibility, with a success rate of 1.00 (95% CI: 0.99, 1.00; p < 0.001). Meanwhile, ‘One stop’ ASD/PFO closure combined with LAAC exhibited a high long-term safety and a low occurrence of complications. Moreover, subgroup analysis revealed that the bleeding event occurrence was relatively higher in the male proportion ≥50% subgroup and HAS-BLED score ≥3 subgroup, respectively. Conclusions: ASD/PFO closure combined with LAAC has a satisfying performance on AF patients with interatrial communication. The PROSPERO Registration: CRD42023462221, https://www.crd.york.ac.uk/prospero/display_record.php?ID=CRD42023462221.

Daniela Renedo, Tanyeri Barak, Jonathan DeLong et al.

Background Ischemic stroke results in significant morbidity and mortality. By examining gene expression of cells comprising stroke clots, we aim to gain valuable insights into the underlying mechanisms of this disease and identify potential biomarkers of stroke cause. Methods We employed single‐cell RNA sequencing to analyze 10 clot samples from patients diagnosed with large vessel occlusion stroke. We aimed to identify and compare the immune cell compositions and gene expression profiles between stroke clots (atrial fibrillation vs carotid atherosclerosis). We also used Multi‐marker Analysis of Genomic Annotation and genome‐wide association studies summary statistics from the GIGASTROKE consortium to assess associations between genetic variants and cell type‐specific gene expression within the stroke subtypes. Results Our analysis revealed distinct immune cell populations, including monocytes, macrophages, dendritic cells, neutrophils, and T cells in both clot types. Notably, we observed significant differences in gene expression within the mononuclear phagocytic system cells between clots from patients with atrial fibrillation and carotid atherosclerosis. We identified specific genes associated with atherosclerosis and stroke‐related processes, such as CD74, HLA‐DRB1*01, HTRA1, C1Q, CD81, and CR1 from patients with carotid atherosclerosis. In atrial fibrillation clots, CD8 T cells and natural killer cells show upregulated expression of genes such as GZMH, GZMB, S100A4, FCGBP2, HLA‐A, TIMP1, CLIC1, and IFITM2, indicating their involvement in cytotoxic activities and potential tissue damage. The Multi‐marker Analysis of Genomic Annotation approach highlighted significant genetic associations within leukocytes underscoring the potential roles of B cells, T cells, and macrophages in clot pathogenesis. Conclusions This study illuminates the immune and transcriptomic landscape within clots, offering potential biomarkers and lays the foundation for future research.

Ana I. Vargas, Samar A. Tarraf, Turner Jennings et al.

Maternal mortality due to cardiovascular disease is a rising concern in the U.S. Pregnancy triggers changes in the circulatory system, potentially influencing the structure of the central vasculature. Evidence suggests a link between a woman’s pregnancy history and future cardiovascular health, but our understanding remains limited. To fill this gap, we examined the passive mechanics of the murine ascending thoracic aorta during late gestation. By performing biaxial mechanical testing on the ascending aorta, we were able to characterize the mechanical properties of both control and late-gestation tissues. By examining mechanical, structural, and geometric properties, we confirmed that remodeling of the aortic wall occurred. Morphological and mechanical properties of the tissue indicated an outward expansion of the tissue, as reflected in changes in wall thickness (~ 12% increase) and luminal diameter (~ 6% increase) at its physiologically loaded state in the pregnant group. With these geometric adaptations and despite increased hemodynamic loads, pregnancy did not induce significant changes in the tensile wall stress at the similar physiological pressure levels of the pregnant and control tissues. The alterations also included reduced intrinsic stiffness in the circumferential direction (~ 18%) and reduced structural stiffness (~ 26%) in the pregnant group. The observed vascular remodeling maintained the elastic stored energy of the aortic wall under systolic loads, indicating preservation of vascular function. Data from our study of pregnancy-related vascular remodeling will provide valuable insights for future investigations of maternal cardiovascular health.

Richard M Monaghan, Richard W. Naylor, Daisy Flatman et al.

Abstract Aims Rare, deleterious genetic variants in FLT4 are associated with Tetralogy of Fallot (TOF), the most common cyanotic congenital heart disease. The distinct genetic variants in FLT4 are also an established cause of Milroy disease, the most prevalent form of primary hereditary lymphoedema. The phenotypic features of these two conditions are non-overlapping, implying pleiotropic cellular mechanisms during development. Methods and results In this study, we show that FLT4 variants identified in patients with TOF, when expressed in primary human endothelial cells, cause aggregation of FLT4 protein in the perinuclear endoplasmic reticulum, activating proteostatic and metabolic signalling, whereas lymphoedema-associated FLT4 variants and wild-type (WT) FLT4 do not. FLT4 TOF variants display characteristic gene expression profiles in key developmental signalling pathways, revealing a role for FLT4 in cardiogenesis distinct from its role in lymphatic development. Inhibition of proteostatic signalling abrogates these effects, identifying potential avenues for therapeutic intervention. Depletion of flt4 in zebrafish caused cardiac phenotypes of reduced heart size and altered heart looping. These phenotypes were rescued with coinjection of WT human FLT4 mRNA, but incompletely or not at all by mRNA harbouring FLT4 TOF variants. Conclusion Taken together, we identify a pathogenic mechanism for FLT4 variants predisposing to TOF that is distinct from the known dominant negative mechanism of Milroy-causative variants. FLT4 variants give rise to conditions of the two circulatory subdivisions of the vascular system via distinct developmental pleiotropic molecular mechanisms.

Jong S. Kim

In patients with stroke caused by cardiac embolism, the responsible heart diseases include atrial fibrillation, acute myocardial infarction, sick sinus syndrome, valvular disease, and significant heart failure. When there is no clear source of the embolism, the condition is referred to as “embolic stroke with unknown source (ESUS).” Recent studies have shown that the most common cause of ESUS is a right-to-left cardiac shunt through a patent foramen ovale (PFO). However, considering that PFOs are found in up to 25% of the general population, their presence does not necessarily indicate causality. In patients with ESUS associated with a PFO, either anticoagulants or antiplatelets are used for the prevention of future strokes or transient ischemic attacks. However, it currently remains unclear which treatment is superior. Nevertheless, recent randomized clinical trials have shown that percutaneous closure of the PFO more effectively reduces the incidence of recurrent strokes compared to medical therapy alone in patients with PFO-related strokes. This benefit is especially significant when the PFO carries high-risk features, such as a large shunt or the presence of an atrial septal aneurysm. Furthermore, the effectiveness of PFO closure has been well documented in young patients (<60 years) with a high-risk PFO development. In other cases, the therapeutic decision should be made through discussion among neurologists, cardiologists, and patients. Notably, in ESUS patients without a PFO, the underlying heart condition itself may be the source of embolism, with left atrial enlargement being the most important factor. Theoretically, anticoagulants such as non-vitamin K antagonist oral anticoagulants (NOACs) would be an effective therapy in these cases. However, recent trials have failed to show that NOACs are superior to antiplatelets in preventing further strokes in these patients. This may be due to the still uncertain definition of emboligenic cardiopathy and the presence of other potential embolic sources, such as mild but emboligenic arterial diseases. Overall, further research is needed to elucidate the source of embolism and to determine an effective management strategy for patients with ESUS.

Joseph J. Cuthbert, Oliver I. Brown, Pierpaolo Pellicori et al.

Abstract Aims Approximately half of patients with heart failure and a reduced ejection fraction (HeFREF) are discharged from hospital on triple therapy [angiotensin‐converting enzyme inhibitors (ACE‐Is) or angiotensin receptor blockers (ARBs), beta‐blockers (BBs), and mineralocorticoid receptor antagonists (MRAs)]. We investigated what proportion of patients are on optimal doses prior to discharge and how many might be eligible for initiation of sacubitril–valsartan or sodium‐glucose co‐transporter‐2 inhibitors (SGLT2Is). Methods and results Between 2012 and 2017, 1277 patients admitted with suspected heart failure were enrolled at a single hospital serving a local community around Kingston upon Hull, UK. Eligibility for sacubitril–valsartan or SGLT2I was based on entry criteria for the PIONEER‐HF, DAPA‐HF, and EMPEROR‐Reduced trials. Four hundred fifty‐five patients had HeFREF with complete data on renal function, heart rate, and systolic blood pressure (SBP) prior to discharge. Eighty‐three per cent of patients were taking an ACE‐I or ARB, 85% a BB, and 63% an MRA at discharge. More than 60% of patients were eligible for sacubitril–valsartan and >70% for SGLT2I. Among those not already receiving a prescription, 37%, 28%, and 49% were eligible to start ACE‐I or ARB, BB, and MRA, respectively. Low SBP (≤105 mmHg) was the most frequent explanation for failure to initiate or up‐titrate therapy. Conclusions Most patients admitted for heart failure are eligible for initiation of life‐prolonging medications prior to discharge. A hospital admission may be a common missed opportunity to improve treatment for patients with HeFREF.

Shuangshuang Zhang, Yong Wang, Jinsong Cheng et al.

Purine metabolism in the circulatory system yields uric acid as its final oxidation product, which is believed to be linked to the development of gout and kidney stones. Hyperuricemia is closely correlated with cardiovascular disease, metabolic syndrome, and chronic kidney disease, as attested by the epidemiological and empirical research. In this review, we summarize the recent knowledge about hyperuricemia, with a special focus on its physiology, epidemiology, and correlation with cardiovascular disease. This review also discusses the possible positive effects of treatment to reduce urate levels in patients with cardiovascular disease and hyperuricemia, which may lead to an improved clinical treatment plan.

J. Nawrot, J. Gornowicz‑Porowska, J. Budzianowski et al.

COVID-19 infection causes complications, even in people who have had a mild course of the disease. The most dangerous seem to be neurological ailments: anxiety, depression, mixed anxiety–depressive (MAD) syndromes, and irreversible dementia. These conditions can negatively affect the respiratory system, circulatory system, and heart functioning. We believe that phytotherapy can be helpful in all of these conditions. Clinical trials confirm this possibility. The work presents plant materials (Valeriana officinalis, Melissa officinalis, Passiflora incarnata, Piper methysticum, Humulus lupulus, Ballota nigra, Hypericum perforatum, Rhodiola rosea, Lavandula officinalis, Paullinia cupana, Ginkgo biloba, Murraya koenigii, Crataegus monogyna and oxyacantha, Hedera helix, Polygala senega, Pelargonium sidoides, Lichen islandicus, Plantago lanceolata) and their dominant compounds (valeranon, valtrate, apigenin, citronellal, isovitexin, isoorientin, methysticin, humulone, farnesene, acteoside, hypericin, hyperforin, biapigenin, rosavidin, salidroside, linalool acetate, linalool, caffeine, ginkgolide, bilobalide, mihanimbine, epicatechin, hederacoside C,α-hederine, presegenin, umckalin, 6,7,8-trixydroxybenzopyranone disulfate, fumaroprotocetric acid, protolichesteric acid, aucubin, acteoside) responsible for their activity. It also shows the possibility of reducing post-COVID-19 neurological, respiratory, and cardiovascular complications, which can affect the functioning of the nervous system.

D. S. Bogdanov, D. Cherkashin, S. V. Efimov et al.

A problem of the novel coronavirus infection pandemic is the absence of specific biomarkers, the determination of which would make it possible to assess the likelihood of a severe disease course, development of complications, immediate and long-term consequences, and effective etiotropic (antiviral) therapy. The severity of the novel coronavirus infection depends on various factors such as the initial state of health, immune status, age, smoking status, concomitant cardiovascular diseases, and diabetes mellitus. However, a severe disease course is also observed in patients without the aforementioned risk factors. The development of the disease and its complications depends on sex and geographical identity. Angiotensin-converting enzyme 2 (ACE2), associated by gene-gene interaction with ACE, plays a main role in the pathogenesis of the penetration of severe acute respiratory syndrome-2 coronavirus into the cell. The main body of information on this problem is represented by systematic meta-analyses and results of single-center cohort studies, which offer insufficient information to unequivocally assert the associations of ACE and ACE2 gene polymorphisms with pathological changes in the circulatory system during and after a new coronavirus infection. Differences in the incidence of ACE and ACE2 alleles may explain the differences between susceptible populations and/or response to the severe coronavirus infection. The above studies were carried out on the effect of the coronavirus in the initial period of the pandemic. For a more complete molecular genetic picture of the influence of polymorphism, persons with different strains of the coronavirus must be considered. In addition, no data are available regarding the expressions of ACE and ACE2 genes in response to a coronavirus infection. Moreover, the identification of the polymorphic variants of the genes of the reninangiotensinaldosterone system and ACE2 associated with a high risk of developing and worsening cardiovascular diseases may be one of the promising areas for the early diagnosis and prevention of post-COVID-19 changes. Therefore, all scientific interest research is aimed at studying genetic factors, such as single nucleotide polymorphisms that affect susceptibility to infection, severity of the disease course, and development of circulatory system consequences. In general, polymorphic variants of ACE and ACE2 and their interaction will help us understand this problem and systematize knowledge for further research in this area.

C. Mátyás, G. Haskó, L. Liaudet et al.

Ashok Kumar Karamsi

Lin Li, Congping Su, Xiangyang Chen et al.

Chlorogenic acids (CGAs) have gained considerable attention as pervasive human dietary constituents with potential cardiovascular-preserving effects. The main sources include coffee, yerba mate, Eucommia ulmodies leaves, and Lonicerae Japonicae Flos. CGAs consumption can reduce the risks of hypertension, atherosclerosis, heart failure, myocardial infarction, and other factors associated with cardiovascular risk, such as obesity and type 2 diabetes. This review recapitulates recent advances of CGAs in the cardiovascular-preserving effects, pharmacokinetics, sources and safety. Emerging evidence indicates that CGAs exhibit circulatory guarding properties through the suppression of oxidative stress, leukocyte infiltration, platelet aggregation, platelet-leukocyte interactions, vascular remodeling, and apoptosis as well as the regulation of glucose and lipid metabolism, and vasodilatory action in the cardiovascular system. CGAs exert these effects by acting on complex signaling networks, but the global mechanisms are still not clear. The oral bioavailability of CGA is poor and there is a potential sensitization concern about CGA. The bioactive metabolites, systematic toxicity, and optimized structure are needed to further identify.

Paranthaman M, Yaathash B, S. S et al.

One of the most important structures in the human body is the heart. It is at the focal point of the circulatory framework. Heart disease is a potentially fatal condition that can result in death or severe long-term impairment. Therefore, efficient techniques for uncovering hidden linkages and there are no clear patterns in e-health data. Medical diagnosis is a difficult task that is crucial to preserving lives, so it must be done correctly and quickly. To lower the cost of performing clinical tests, a suitable and precise computer-based automated decision support system is necessary. The use of machine learning in health analytics has been presented as a way to anticipate reliable patient data analysis. The information generated by the healthcare industry is not mined. In the medical industry, data mining techniques can be utilized to create an intelligent model employing data sets that include patient risk factors. The emergence of ideas and techniques for making use of data has surprised knowledge discovery in databases (KDD). This study delves into the usage of deep learning and machine learning approaches in disease diagnosis. In recent years, many data mining classifiers have been created to aid in the accurate and timely identification of illnesses. This study offers a heart attack forecasting model based on deep learning methodologies, notably Multi-Layer Perceptron (MLP), to anticipate a patient's likelihood of acquiring heart disease. MLP is an advanced type approach that employs the Artificial Neural Network's Deep Learning approach. Deep learning and data mining are used in the suggested approach to get reliable and error-free outcomes.

Tao Jiang, Dewei Peng, Wei Shi et al.

AimsCytokine storm is closely related to the initiation and progression of sepsis, and the level of IL-6 is positively correlated with mortality and organ dysfunction. Sepsis-induced myocardial dysfunction (SIMD) is one of the major complications. However, the role of the IL-6/STAT3 signaling in the SIMD remains unclear.Methods and ResultsSeptic mice were induced by intraperitoneal injection of LPS (10 mg/kg). Echocardiography, cytokines detection, and histologic examination showed that sepsis mice developed cardiac systolic and diastolic dysfunction, increase of inflammatory cytokines in serum, activated STAT3 and TLR4/NFκB pathway in heart, and raised myocardial apoptosis, which were attenuated by IL-6/STAT3 inhibitor, Bazedoxifene. In vitro, we found that LPS decreased cell viability in a concentration-dependent manner and activated STAT3. Western blot and immunofluorescence results indicated that STAT3 phosphorylation induced by LPS was inhibited by Bazedoxifene. Bazedoxifene also suppressed LPS-induced IL-6 transcription. sIL-6R caused LPS-induced p-STAT3 firstly decreased and then significantly increased. More importantly, we found STAT3-knockdown suppressed LPS-induced expression of FUNDC1, a protein located in mitochondria-associated endoplasmic reticulum membranes (MAMs). Overexpression of STAT3 led to an increase in FUNDC1 expression. Dual-luciferase reporter assay was used to confirm that STAT3 was a potential transcription factor for FUNDC1. Moreover, we showed that LPS increased MAMs formation and intracellular Ca2+ levels, enhanced the expression of Cav1.2 and RyR2, decreased mitochondrial membrane potential and intracellular ATP levels, and promoted mitochondrial fragmentation, the expression of mitophagy proteins and ROS production in H9c2 cells, which were reversed by knockdown of FUNDC1 and IL-6/STAT3 inhibitor including Bazedoxifene and Stattic.ConclusionsIL-6/STAT3 pathway plays a key role in LPS-induced myocardial dysfunction, through regulating the FUNDC1-associated MAMs formation and interfering the function of ER and mitochondria. IL-6/STAT3/FUNDC1 signaling could be a new therapeutic target for SIMD.

Eduardo Z. Romo, Angela M. Zivkovic

High-density lipoprotein (HDL) particles, long known for their critical role in the prevention of cardiovascular disease (CVD), were recently identified to carry a wide array of glycosylated proteins, and the importance of this glycosylation in the structure, function and metabolism of HDL are starting to emerge. Early studies have demonstrated differential glycosylation of HDL-associated proteins in various pathological states, which may be key to understanding their etiological role in these diseases and may be important for diagnostic development. Given the vast array and specificity of glycosylation pathways, the study of HDL-associated glycosylation has the potential to uncover novel mechanisms and biomarkers of CVD. To date, no large studies examining the relationships between HDL glycosylation profiles and cardiovascular outcomes have been performed. However, small pilot studies provide promising preliminary evidence that such a relationship may exist. In this review article we discuss the current state of the evidence on the glycosylation of HDL-associated proteins, the potential for HDL glycosylation profiling in CVD diagnostics, how glycosylation affects HDL function, and the potential for modifying the glycosylation of HDL-associated proteins to confer therapeutic value.

Qiang Feng, Ying Zhao, Haiyan Wang et al.

PurposeAs a second-generation drug-eluting stent, the restenosis risk factors of the everolimus-eluting stent (EES) lack sufficient evidence. Therefore, the study investigated the in-stent restenosis occurrence and its predictive factors among patients with coronary heart disease (CHD) who underwent percutaneous coronary intervention (PCI) with EES.Materials and methodsTotally, 235 patients with CHD who underwent PCI with EES were included. At 1 year post PCI with EES (or earlier if clinically indicated), coronary angiography was performed to evaluate the in-stent restenosis status.ResultsWithin 1 year post-operation, 20 patients developed in-stent restenosis while 215 patients did not develop in-stent restenosis, resulting in a 1-year in-stent restenosis rate of 8.5%. Diabetes mellitus, hypercholesteremia, hyperuricemia, fasting blood glucose, serum uric acid (SUA), high-sensitivity C-reactive protein (HsCRP), target lesions in the left circumflex artery, patients with two target lesions, length of target lesions and length of stent positively correlated with in-stent restenosis risk, while high-density lipoprotein cholesterol negatively associated with in-stent restenosis risk. Notably, diabetes mellitus, hypercholesteremia, SUA, HsCRP levels, and patients with two target lesions were independent predictive factors for in-stent restenosis risk by multivariate logistic regression analysis. Then, the in-stent restenosis risk prediction model was established based on these independent predictive factors, which exhibited an excellent value in predicting in-stent restenosis risk (area under the curve: 0.863; 95% CI: 0.779–0.848) by receiver operating characteristic analysis.ConclusionIn-stent restenosis risk prediction model, consisting of diabetes mellitus, hypercholesteremia, SUA, HsCRP, and patients with two target lesions, may predict in-stent restenosis risk in patients with CHD who underwent post-PCI with EES.

Mitra Mastali, Anum Asif, Qin Fu et al.

Background: Associations between elevated circulating cardiac troponin I (cTnI) levels and adverse cardiac outcomes were established prior to the ability to measure extremely low levels of cTnI. Immunoassays that achieve precise ultra-highly sensitive quantification of cTnI (u-hs-cTnI) will allow accurate measurement in healthy subjects. We aimed to evaluate the distribution of u-hs-cTnI values measured by (Simoa HD-1 Analyzer, Quanterix Corporation, Lexington, MA) in healthy subjects and characterize relations to sex and age. Methods: Two independent, healthy cohorts (total of 200 women, 200 men) aged 18–86 years were analyzed in duplicate using the u-hs-cTnI Immunoassay. The u-hs-cTnI 99th percentiles were calculated as the upper limits considering a robust estimation against outliers with 90% confidence intervals. The Quanterix immunoassay analytical performance was established and compared to an existing clinical assay (ARCHITECT STAT High Sensitivity Troponin I, Abbott Laboratories, Wiesbaden, Germany). Results: The lower limit of detection of the u-hs-cTnI assay was calculated to be 0.005 ng/L; we accurately quantified u-hs-cTnI in 95% of healthy individuals. The Quanterix immunoassay within overlapping concentrations correlated with the Abbott assay (R2 = 0.932). The calculated combined 99th percentile was 7.94 ng/L (90% Confidence Interval [CI], 5.47–10.52). Women had lower mean u-hs-cTnI concentrations than men under the age of 40 years. The sex-specific 99th percentile for female vs. male individuals was 4.89 ng/L (90%CI, 3.71–6.25) and 10.49 ng/L (90%CI, 5.19–15.06), respectively. Conclusion: The Quanterix immunoassay provides precise quantification in 95% of healthy individuals. Women under the age of 40 years have significantly lower levels of u-hs-cTnI than men.

Juliette Vahdat, Nathalie Lalevée, Julien Fromonot et al.