Cardiovascular Disease In Patients Research Articles

Multiplicative Impact of Adverse Social Determinants of Health on Outcomes in Lupus Nephritis: A Meta-analysis and Systematic Review.

Social determinants of health (SDoH) likely contribute to outcome disparities in lupus nephritis (LN). Understanding the overall burden and contribution of each domain could guide future health equity-focused interventions to improve outcomes and reduce disparities in LN. Objectives of this meta-analysis were to 1) determine the association of overall SDoH and specific SDoH domains on LN outcomes and 2) develop a framework for the multidimensional impact of SDoH on LN outcomes. We performed a comprehensive search of studies measuring associations between SDoH and LN outcomes. We examined pooled odds of poor LN outcomes including death, end-stage kidney disease, or cardiovascular disease in patients with and without adverse SDoH. Additionally, we calculated the pooled odds ratios of outcomes by four SDoH domains: individual (eg, insurance), health care (eg, fragmented care), community (eg, neighborhood socioeconomic status), and health behaviors (eg, smoking). Among 531 screened studies, 31 meeting inclusion criteria and 13 with raw data were included in meta-analysis. Pooled odds of poor outcomes were 1.47-fold higher in patients with any adverse SDoH. Patients with adverse SDoH in individual and health care domains had 1.64-fold and 1.77-fold higher odds of poor outcomes. We found a multiplicative impact of having two or more adverse SDoH on LN outcomes. Black patients with public insurance and fragmented care had 12-fold higher odds of poor LN outcomes. Adverse SDoH is associated with poor LN outcomes. Having two or more adverse SDoH, specifically in different SDoH domains, had a multiplicative impact leading to worse LN outcomes, widening disparities.

Dietary habits and compliance with dietary guidelines in patients with established cardiovascular disease.

Unhealthy dietary habits are an important risk factor for cardiovascular disease (CVD) and adopting a healthy diet is a central recommendation in CVD prevention. This study assessed the dietary habits of patients with established CVD, their compliance to dietary guidelines, and the relationship between guideline-compliance and recurrent cardiovascular event risk. 2656 patients with established CVD from the Utrecht Cardiovascular Cohort-Secondary Manifestations of ARTerial disease (UCC-SMART) prospective cohort study, were included between 1996 and 2022. Data on dietary intake was retrospectively collected for all participants in December 2022 using a 160-item food frequency questionnaire. Compliance with dietary guidelines was quantified using an amended version of the Dutch Healthy Diet 2015 (DHD-15) index (range: 0-135). Cox proportional hazard models were used to quantify the relationship with cardiovascular events (stroke and myocardial infarction). Among 2656 CVD patients (77% male, mean age 59 ± 9 years), median energy intake was 1922 [IQR: 1536-2351] kcal/day. The median DHD-15 index was 81.7 [IQR 71.2-92.0], with high compliance scores for recommendations on legumes and fish, and low scores for recommendations on whole grains, red meat, processed meat, and dairy. A higher DHD-15 score was associated with lower stroke risk (HR 0.78, 95% CI 0.66-0.92 per 10-point increase) but not with myocardial infarction. Compliance with dietary guidelines was suboptimal in patients with established CVD. High compliance was associated with a clinically significant reduction in stroke risk in patients with established CVD, emphasizing the importance of dietary counseling.

HEART + score: integrating carotid ultrasound to chest pain assessment in the emergency department.

The HEART score is a clinical decision tool that stratifies patients into categories of low, moderate, and high-risk of major adverse cardiac events in the emergency department (ED) but cannot identify underlying cardiovascular disease in patients without prior history. The presence of atherosclerosis can easily be detected at the bedside using carotid ultrasound. Plaque quantification is well established, and plaque composition can be assessed using ultrasound grayscale pixel distribution analysis. This study aimed to determine whether carotid plaque burden and/or composition correlated with risk of events and could improve the sensitivity of the HEART score in risk stratifying ED patients with chest pain. The HEART score was calculated based on history, electrocardiogram, age, risk factors, and initial troponin in patients presenting to the ED with chest pain (n = 321). Focused carotid ultrasound was performed, and maximum plaque height and total plaque area were used to determine plaque burden (quantity). Plaque composition (% blood, fat, muscle, fibrous, calcium-like tissue) was assessed by pixel distribution analysis. Carotid plaque height and area increased with HEART score (p < 0.0001). Carotid plaque % fibrous and % calcium also increased with HEART score. The HEART score had a higher area under the curve (AUC = 0.84) in predicting 30-day events compared to the plaque variables alone (AUCs < 0.70). Integrating plaque quantity into the HEART score slightly increased test sensitivity (62-69%) for 30-day events and reclassified 11 moderate-risk participants to high-risk (score 7-10). Plaque burden with advanced composition features (fibrous and calcium) was associated with increased HEART score. Integrating plaque assessment into the HEART score identified subclinical atherosclerosis in moderate-risk patients.

#2141 Lipoprotein a levels and atherosclerotic cardiovascular disease in hemodialysis patients

Abstract Background and Aims Lipoprotein a (Lp(a)) is an LDL cholesterol-like particle to which two apolipoprotein(a) molecules are attached. Epidemiological and genetic studies strongly support a causal and continuous association between Lp(a) concentration and atherosclerotic cardiovascular (CV) disease, including aortic valve stenosis, even with low levels of low-density lipoprotein cholesterol. On the other hand, it is well known that patients on hemodialysis (HD) have high comorbidity due to cardiovascular pathology. Method We conducted a cross-sectional, observational, retrospective study in a cohort of patients on HD, with the aim of evaluating whether there was any correlation between Lp(a) concentration and atherosclerotic cardiovascular disease (ASCVD). For this purpose, in December 2023 we measured Lp(a) levels (in nmol/L) in all prevalent HD patients in the province of Cáceres (Spain) and collected their major adverse coronary events (MACE): acute myocardial infarction (AMI) and angina, as well as major adverse non-coronary cardiovascular events (MANCE): cerebrovascular disease and peripheral artery disease. Aortic valve stenosis/calcification was also assessed by echocardiography. SPSS version 21 software was used for statistical analysis. Results A total of 214 patients were included, 68.7% male, with a mean age of 70.5 years. The mean Lp(a) value was 76.9 nmol/L, without differences in both sexes. A total of 66.4% had Lp(a) &amp;lt; 75 nmol/L and 23.8% had levels ≥ 125 nmol/L. The main cardiovascular event was peripheral artery disease (14.9%), followed by AMI (14.1%), aortic valve stenosis (10.7%), stroke (8.4%), angina (2.8%) and transient ischemic attack (1.4%). Some 23.4% (50 patients) had a CV event and, among them, almost half (42%) had Lp(a) levels &amp;gt;75 nmol/L. A statistically significant linear correlation was found between Lp(a) concentration and AMI (p 0.03) and aortic valve stenosis (p 0.001). No correlation was observed between Lp(a) and the other CV events analyzed (peripheral artery disease, stroke, angina, transient ischemic attack), nor between Lp(a) and sex. Conclusion There is a linear and positive correlation between Lp(a) levels and coronary pathology, and with aortic valve stenosis in HD patients in the cohort studied. Studies are needed to assess whether reducing their levels reduces cardiovascular disease in these patients.

#302 Proteomic study reveals indoxyl sulfate induced changes in endothelial cells: role of extracellular vesicles in cardiovascular disease

Abstract Background and Aims Chronic kidney disease (CKD) lead to the accumulation of uremic toxins in the bloodstream, among which indoxyl sulfate (IS) is the most prominent. IS causes damage to endothelial cells lining blood vessels, ultimately leading to cardiovascular diseases in patients with CKD. Under physiological conditions, extracellular vesicles (EVs) are released by cells as intercellular communicators; however, after damage, the cargo of the EVs can be modified. This makes EV potential markers of damage, possibly carrying proteins of interest. This study aimed to investigate the impact of IS on endothelial cells and the release of EVs to identify potential therapeutic targets for preventing endothelial injury. Method Human umbilical vein endothelial cells (HUVEC) were cultured under control conditions and with IS exposure (250 μM IS, 24 h, n = 5). The released EVs were isolated from the supernatants by differential centrifugation and characterized by TEM and flow cytometry to confirm their identity as EVs (following the MISEV2018 guidelines). Proteome profiles of both cells and EVs were analyzed using a mass spectrometer (Orbitrap Exploris™ 240), followed by a Gene Set Enrichment Analysis (GSEA) which revealed altered functions. Results A total of 5871 proteins were identified in the proteomic analysis of cells, and 3614 proteins in EVs (with a False Discovery Rate (FDR) &amp;lt; 1%). In cells, 30 proteins were upregulated and 46 were found downregulated in response to IS, while in EVs, 51 proteins were found upregulated and 47 downregulated (IS vs C). GSEA revealed that IS potentiated adipogenesis (p-value &amp;lt; 0.001), TNF-α signaling via NFкB (p-value = 0.006), and xenobiotic metabolism in cells (p-value = 0.012). In contrast, EVs from cells treated with IS exhibited downregulation of extracellular matrix components (p-value = 0.003), myogenesis (p-value 0.009), genes downregulated in response to ultraviolet radiation (p-value = 0.014) and TNF-α signaling via NFкB (p-value = 0.041). Conclusion IS induces a change in protein expression in cells and their EVs, potentiating inflammation and atherosclerotic plaque formation with extracellular matrix loss. All these modifications contribute to endothelial dysfunction, which is the first step in the development of cardiovascular disease in patients with CKD. This study shed light on novel targets for intervention strategies to mitigate cardiovascular complications in patients with CKD. Funding Grants from the Instituto de Salud Carlos III (ISCIII) and cofounded by Fondos Europeo de Desarrollo Regional (FEDER): “PI19/00240” and “PI20/01321” and “FI20/00018” contract by the Instituto de Salud Carlos III and Ayuda de la Línea de Actuación “Excelencia para el Profesorado Universitario de la UAH” (EPU-INV-UAH/2022/001) from Alcala University.

#3011 Pathophysiological link between renal and cardiovascular disease in patients with type 2 diabetes mellitus: preliminary results from a proteomic study

Abstract Background and Aims Diabetic kidney disease (DKD) affects nearly 40% of people with diabetes and is the leading cause of chronic kidney disease (CKD). A high prevalence of cardiovascular disease (CVD) is known in this population. Indeed, DKD and CVD are often related and lead to worse outcomes in type 2 diabetes mellitus (T2D), i.e. cardiac fibrosis and CV events are frequently described in patients with DKD. However, specific associations and accurate prediction biomarkers for DKD and CVD progression in T2D are still lacking as various proteins may play a multi-mechanistic role. Lipocalin-2 (LCN2) is involved in several pathophysiological processes (inflammation, renal disease and cardiometabolic complications in CKD). Its leukocyte-chemoattractant effect has shown to reduce CVD in experimental models of cardiomyopathy when suppressed. Excess LCN2 in CKD is a determinant of disease progression, but also a potent mediator of cardiac injury in CKD. Insulin-like growth factor binding proteins (IGFBPs) also play an important role in cell homeostasis by regulating cell transcription, migration, and apoptosis. IGFBP-3 down-regulation has demonstrated to be a predictor of rapid renal progression in T2DM. On the other hand, IGFBP-6 increases when GFR drops, being involved in the pathophysiological process of CKD as an apoptosis-inducing protein In this context, a proteomic-based approach would optimise the clinical utility of multiple plasma biomarkers. The aim was to identify proteins associated with DKD, cardiac fibrosis (estimated by the PICP biomarker) and the presence of a new CV event. Method A prospective cohort of 91 T2D patients, with a minimum follow-up of 3 years (mean: 4 years) was analysed. We evaluated the association between rates of change in GFR and PICP during follow-up (fold-change: end/initial) and their interaction with the development of a composite of cardiovascular (CV) events: CV death, stroke, ischaemic heart disease, atrial fibrillation, valvular heart disease and CV-related hospitalisation. In addition, ninety-two proteins were quantified in serum samples using a multiplex proximity extension assay with high-throughput protein detection technology (Olink proteomics, Cardiometabolic panel). Associations between variations in these proteins and changes in PICP and eGFR (all expressed as fold change from baseline) were assessed using linear regression analyses adjusted for their respective baseline values. All analyses were adjusted by multiple testing (Benjamini-Hochberg, FDR = 0.05%) using R software. Results Sixty-eight (74.7%) men and 23 (25.3%) women were included in the analysis. The mean age at baseline was 65.8 years, and the mean follow-up was 4 years (minimum 3 years). Sixteen cardiovascular events were recorded. An inverse association was observed between GFR and PICP (p = 0.003). Interaction analysis showed that this correlation occurred only in patients with incident CV events (p for interaction &amp;lt;0.001) (Fig. 1). By proteomic analysis (Fig. 2) several proteins were found to be significantly related to one of the three parameters studied (change in GFR, change in PICP and change with cardiovascular event), of which 3 proteins presented an overlap for all the parameters analysed: Lipocalin 2 (LCN2) and Insulin-like growth factor binding proteins 3 and 6 (IGFBP3 and IGFBP6). Interestingly, LCN2 and IGFBP6 were more highly expressed in patients with CV events whereas IGFBP3 was downregulated in these patients. Conclusion In patients with DKD, worsening enal function is associated with elevated circulating levels of the collagen synthesis biomarker PICP, particularly in those who developed at least one CV event. The link shown with LCN2, IGFBP-6 and IGFBP-3 shed light on possible multi-mechanistic pathways involved in DKD and narrow the scope towards a common pathway involving an interaction between pro-apoptotic and local inflammatory factors.

#1841 Trimethylamine N-oxide (TMAO) induces the formation of endothelial extracellular vesicles

Abstract Background and Aims Endothelial dysfunction caused by the accumulation of uremic toxins is an important contributor to the development of cardiovascular disease in patients with chronic kidney disease (CKD). The uremic toxin trimethylamine n-oxide (TMAO) is associated with oxidative stress, vascular calcification, and inflammation, triggering the release of several proinflammatory molecules and Extracellular Vesicles (EVs). Clinical studies have shown that patients with CKD have high levels of circulating EVs, however, their role is still poorly understood. In this dysfunctional scenario, EVs can be used as damage biomarkers for CKD, as they carry information from their cells of origin. Here, we aim to elucidate the formation of EVs in endothelial cells exposed to TMAO. Method Human endothelial cells (EA.hy926, ATCC CRL-2922) were exposed for 24 h with TMAO at uremic concentrations (7.49 mg/L). EVs were isolated by differential ultracentrifugation. Protein concentration was analyzed by Pierce™ BCA Protein Assay Kit, and particle size and particle concentration were analyzed by NanoParticle Tracking Analysis (NTA), Transmission Electron Microscopy (TEM), and Scanning Electron Microscopy (SEM). EVs were stained with calcein and their internalization in endothelial cells was analyzed with Fluorescence Confocal Microscopy. Results TMAO treatment at uremic concentration induced the formation of EVs with a size of 202.8 ± 3.1 nm (image 1B) and 1.09 × 109 ± 2.68 × 107 particles/mL and a total protein concentration of 88.57 µg/mL. The morphological features of EVs are shown in images 1C-1F. TMAO-induced EVs were incorporated by endothelial cells, being dispersed in the cytoplasm or perinuclear regions (images 1G and end 1H). Conclusion TMAO was able to induce the formation of EVs in endothelial cells, with characteristics morphological features. When compared to control EVs (image 1A), TMAO-EVs have a more heterogeneous size, which indicate a change in the size pattern, and thus the nature of the EVs induced by TMAO. TMAO-EVs were able to be internalized by human endothelial cells. This uptake can be closely related to the effects of EVs in endothelial cells, but more experiments need to be performed. Taken together, these data could contribute to understanding how the formation and uptake of TMAO-EVs by the endothelium occurs, relating their effects to the cardiovascular complications of CKD.

#1372 Association of plasma beta-2-microglobulin with risk of cardiovascular disease in patients with chronic kidney disease

Abstract Background and Aims In patients with chronic kidney disease(CKD), beta 2 microglobulin (B2MG) can be used to assess renal function, and predialysis serum B2MG levels can predict mortality risk. In addition to the kidney, B2MG regulates the expression of interleukin 1 and tumor necrosis factor, participates in the pathogenesis of vascular damage, and is a marker that can detect the formation of amyloid, therefore it is important in the diagnosis of cardiovascular disease (CVD). To assess the correlation of serum B2MG levels with some metabolic and cardiovascular function factors in patients with chronic kidney disease. Method 119 people with chronic kidney disease and 52 healthy control groups were selected as a case-control study and blood samples were analyzed for creatinine, urea, cholesterol, triglycerides, LDL, calcium, phosphorus, albumin, total protein, and B2MG with Cobas 6000 fully automatic analyzer and echocardiography was performed. Renal function was evaluated by CKD EPI crea-cys combined calculation. In the group with CKD, a person with eGFR &amp;lt;90 ml/min/1.73 m² was not included in the study due to the study exclusion criteria. Results The average age of the group with CKD was 54.92, and the average age of the healthy group was 50.66. B2MG has a significantly higher (P &amp;lt; 0.000) statistically significant correlation in the group with CKD compared to the control group. B2MG was significantly associated with creatinine (g = 0.516, P &amp;lt; 0.000), phosphorus (g = 0.342, P &amp;lt; 0.000), cystatin C (g = 0.700, P &amp;lt; 0.000), urea (g = 0.326, P &amp;lt; 0.000), and echocardiography with directly indicators LVMI(g = 0.113, P &amp;lt; 0.000), LVESD (r = 0.265, P &amp;lt; 0.000), thus BMI (g = −0.274, P &amp;lt; 0.000), tTSH (r = −0.516, P &amp;lt; 0.000), calcium ( g = −0.137, P &amp;lt; 0.000), albumin (g = −0.180, P &amp;lt; 0.000), total protein (r = −0.080, P &amp;lt; 0.000), cholesterol (g = −0.215, P &amp;lt; 0.000), BNLP (r = −0.163, P &amp;lt; 0.000), triglycerides (g = −0.142, P &amp;lt; 0.000), and EV of echocardiography (g = −0.292, P &amp;lt; 0.000) have inverse statistical significance. Conclusion B2MG levels have been shown to predict CVD risk and CVD-related mortality in all stages of chronic kidney disease. According to our study, B2MG is directly related to kidney function biomarkers, phosphorus, LVMI, and LVESD indicators of cardiac echocardiography, and inversely correlated with parameters of eGFR, protein, triglycerides, calcium, and cardiac echocardiogram EV indicators, which is similar to studies conducted in other countries. Therefore, B2MG can be used to detect the risk of CVD in people with severe CKD. Figure: Will be uploaded on our poster if accepted.

#1258 Moderate-severe intrarenal arteriosclerosis and circulating GDF-15 levels may influence the cardiac-renal prognosis of IgAN patients

Abstract Background and Aims The cardiovascular risk among patients with IgA nephropathy (IgAN) is gradually garnering increased attention. The KDIGO guidelines explicitly emphasize the importance of evaluating cardiovascular risk in the management of IgAN patients and implementing appropriate interventions when necessary. The aim of this study was to investigate the risk factors affecting cardiac-renal prognosis in patients with IgAN. Method This is a retrospective study. A total of 353 IgAN patients with regular follow-up for at least 1 year at Beijing Anzhen Hospital were recruited. Patients were divided into group A (n = 85, yes) and group B (n = 268, no) according to the occurrence of cardio-renal composite endpoint events. Clinical and pathological characteristics of the two groups were compared and analyzed. The risk factors affecting the cardiac and renal prognosis in IgAN patients were analyzed by univariate and multivariate Cox models. In addition, serum GDF-15 of IgAN patients were detected. Results Approximately 14.7% (52/353) of IgAN patients presented with cardiovascular diseases at the time of renal biopsy. 55.8% (197/353) patients presented with hypertension. Prognostic analysis showed that hypertension (HR, 1.810; 95% confidence interval, 1.073 to 3.053; P = 0.026), 24-hour urinary protein (24 hUTP) (HR, 1.081; 95% confidence interval, 1.006 to 1.162; P = 0.033), eGFR (HR, 0.980; 95% confidence interval, 0.973 to 0.987; P&amp;lt;0.001), the presence of endocapillary proliferation (E1) (HR, 1.697; 95% confidence interval, 1.079 to 2.669; P = 0.022), tubular atrophy/interstitial fibrosis (T2) (HR, 3.757; 95% confidence interval, 1.959 to 7.203; P &amp;lt; 0.001), and moderate-severe intrarenal arteriosclerosis (HR, 3.320; 95% confidence interval, 1.289 to 8.548; P = 0.013) are independent risk factors affecting the cardiac-renal prognosis of IgAN. In IgAN patients with moderate-severe intrarenal arteriosclerosis, 24-hour urinary protein (24 hUTP) (HR, 1.131; 95% confidence interval, 1.014 to 1.261; P = 0.028), eGFR (HR, 0.982; 95% confidence interval, 0.971 to 0.993; P = 0.001) and E1 (HR, 2.583; 95% confidence interval, 1.379 to 4.841; P = 0.003) are independent risk factors affecting the cardiac-renal prognosis of IgAN patients. The serum GDF-15 level is positively correlated with 24 hUTP (r = 0.405, P &amp;lt; 0.001) and negatively correlated with eGFR (r = −0.606, P &amp;lt; 0.001). Compared with those with benign cardio-renal composite outcome, the serum level of GDF-15 in IgAN with poor cardio-renal composite outcome were significantly higher (1591.69 (1001.65, 2546.36) pg/ml vs 775.85 (546.82, 1310.29) pg/ml, P &amp;lt; 0.001). Conclusion The occurrence of cardiovascular diseases in patients with IgAN is frequently observed. In addition to the conventional risk factors associated with IgAN, including hypertension, initial proteinuria, eGFR, E1 and T2 lesion, moderate-severe intrarenal arteriosclerosis also contributes to the cardiac-renal prognosis of individuals with IgAN. In IgAN patients with moderate-severe intrarenal arteriosclerosis, Oxford-E lesion is an independent risk factor affecting the cardiac-renal prognosis of IgAN patients. This study suggested that the impairment of endothelial cells could potentially serve as a link between heart and kidney disease. The circulating levels of GDF-15 might contribute to the cardiac-renal prognosis of IgAN.

#2610 Low skeletal muscle mass and low skeletal muscle quality are associated with thoracic aorta calcification in dialysis patients

Abstract Background and Aims Cardiovascular disease (CVD) is the leading cause of mortality in dialysis patients. Thoracic aorta calcification (TAC) is a common cardiovascular complication in dialysis patients and is independently associated with CVD. Sarcopenia, particularly low skeletal muscle mass, has been found to be associated with increased cardiovascular risk in dialysis patients. This study aims to explore the relationship between skeletal muscle quality and skeletal muscle mass at the first lumbar vertebra (L1) level determined by opportunistic CT scans (chest CT) and TAC, with the goal of providing valuable opportunities for identifying and intervening in high-risk CVD patients. Method We included 2514 patients for cross-sectional analysis, who underwent dialysis in four centers in China from 2020 to 2023 and all had chest CT scans including the L1 level. Additionally, we conducted a follow-up study on TAC in patients who initiated dialysis between 2014 and 2019 as part of the earlier research, including 215 patients who had undergone at least two chest CT scans for cohort analysis. At the L1 level, we assessed skeletal muscle quality [by skeletal muscle density (SMD), HU] and skeletal muscle mass [by skeletal muscle index (SMI), cm2/m2] in dialysis patients. Measurements of thoracic aorta calcification scores (TACS) and calcification scores for three segments of the thoracic aorta, including ascending aorta calcification score (ATACS), aortic arch calcification score (AoACS), and descending thoracic aorta calcification score (DTACS), were obtained in dialysis patients. Patients were divided based on their annual calcification score growth rate: those with a rate greater than or equal to the average annual increase were classified into the rapid progression group, while those with a rate less than the average were classified into the slow progression group (including those with no progression). Multivariable linear regression models were employed to assess the relationships between SMI and SMD with TACS. Multivariable logistic regression models were used to evaluate the associations of SMl and SMD with the risk of rapid progression of TACS. Results The mean (SD) age of participants was 56 (15) years, with 58.2% being male. The prevalence of TAC was 82.2%, while the prevalence of ascending thoracic aorta calcification (ATAC), aortic arch calcification (AoAC), and descending thoracic aorta calcification (DTAC) was 21.4%, 75.3%, and 68.8%, respectively. Over an average follow-up period of 3.22 years, the progression rate of TAC was 85.6%. Comparing the highest quartile of SMD to the lowest quartile, a significant inverse association was observed with TAC (beta −1.19, 95% CI −1.55— −0.83; P &amp;lt; 0.001). Similarly, comparing the highest quartile of SMI to the lowest quartile, a significant inverse association was found with TAC (beta −0.59, 95% CI −0.92— −0.26; P = 0.001). SMI and SMD, as continuous variables, were both significantly negatively correlated with TAC. Higher SMD was associated with a reduced risk of rapid progression of TAC; after full adjustment, for every 1 SD increase in SMD, the risk of TAC rapid progression decreased by 46% (aOR 0.54, 95% CI 0.32—0.91; P = 0.021). SMI showed no significant association with the rapid progression of TAC. The associations of SMI and SMD with AoAC and DTAC were consistent with their associations with TAC, except for ATAC. The ROC curve analysis indicated that incorporating SMD into the model enhanced the discriminative ability for stratifying the risk of rapid progression of thoracic aorta calcification. Conclusion After adjusting for cardiovascular risk factors and inflammatory markers, higher skeletal muscle quality and higher skeletal muscle mass were significantly associated with lower TAC. Improving skeletal muscle quality in initial dialysis patients may reduce the risk of rapid TAC progression.

Exploring mitochondrial DNA copy number in circulating cell-free DNA and extracellular vesicles across cardiovascular health status: A prospective case-control pilot study.

Cardiovascular disease (CVD) is a leading global cause of mortality, difficult to predict in advance. Evidence indicates that the copy number of mitochondrial DNA (mtDNAcn) in blood is altered in individuals with CVD. MtDNA released into circulation may act as a mediator of inflammation, a recognized factor in the development of CVD, in the long distance. This pilot study aims to test if levels of mtDNAcn in buffy coat DNA (BC-mtDNA), in circulating cellfree DNA (cf-mtDNA), or in DNA extracted from plasma extracellular vesicles (EV-mtDNA) are altered in CVD patients and if they can predict heart attack in advance. A group of 144 people with different CVD statuses (50 that had CVD, 94 healthy) was selected from the LifeLines Biobank according to the incidence of new cardiovascular event monitored in 6 years (50 among controls had heart attack after the basal assessment). MtDNAcn was quantified in total cf-DNA and EV-DNA from plasma as well as in buffy coat. EVs have been characterized by their size, polydispersity index, count rate, and zeta potential, by Dynamic Light Scattering. BC-mtDNAcn and cf-mtDNAcn were not different between CVD patients and healthy subjects. EVs carried higher mtDNAcn in subject with a previous history of CVD than controls, also adjusting the analysis for the EVs derived count rate. Despite mtDNAcn was not able to predict CVD in advance, the detection of increased EV-mtDNAcn in CVD patients in this pilot study suggests the need for further investigations to determine its pathophysiological role in inflammation.

Prevalence estimation of sarcopenia using bioelectrical impedance analysis in elderly people in Lahore

Sarcopenia is the loss of muscle mass and strength, or both, and physiological functions through aging. Early detection of muscle weakness results in better care and interventions regarding dietary habits and protein intake in older adults. The objective of this study was to investigate the prevalence of sarcopenia in a Pakistani population and to correlate dietary habits and lifestyle with the prevalence of sarcopenia. A sample size of 150 individuals, both male and female, of age sixty and above was used. Cardiovascular disease and renal failure patients were excluded. The research field was the community of Lahore. Muscle power was calculated using a handgrip strength dynamometer, and gait speed was calculated using a pedometer. After screening, muscle mass was calculated using bioelectrical impedance analysis, from which sarcopenia was diagnosed. In the age group of 60–65 years, 123 individuals (82%) had low muscle strength and 93 (83%) had low muscle mass. In the age group of 66–70 years, 15 individuals (83.3%) had low muscle strength. In the age group of 71–75 years, 9 individuals (90%) had low muscle strength. The percentage of low muscle strength in the age group of 76+ years was 100%. The percentage of severe sarcopenia was 6%, and moderate sarcopenia was approximately 10% for individuals 60 years of age and older. The prevalence rates of sarcopenia were 21.53% in males and 11.76% in females. Sarcopenia is an emerging health issue in older adults, and early detection and lifestyle modification will lead to a better health outcome and correlate dietary habits and lifestyle with the prevalence of sarcopenia.

Dutch cardio-oncology cohort: Incident cardiovascular disease predisposes to a higher cancer mortality rate.

Cardiovascular disease (CVD) and cancer are the two leading causes of death worldwide. Given their high prevalence, it is important to understand the disease burden of cancer mortality in CVD patients. We aimed to evaluate whether patients with incident CVD have a higher risk of malignancy-related mortality, compared to the general population without CVD. We performed a national population-based cohort study selecting patients with incident CVD in the Netherlands between 01 April 2000 and 31 December 2005. A reference cohort was selected from the Dutch population using age, sex and ethnicity. Mortality follow-up data were evaluated after data linkage of national registries from Statistics Netherlands until 31 December 2020. A total of 2,240,879 individuals were selected with a mean follow-up of 12 years (range 0.4-21.0), of which 738,666 patients with incident CVD with a mean age of 71 ± 15 years. Malignancy mortality per 1000 person years was 84 for the reference group and 118 for patients with CVD, with the highest rate of 258 in patients with heart failure. Patients with CVD had a higher malignancy mortality risk, compared to the reference group: HR 1.35 (95%CI 1.33-1.36). Highest risks were observed in patients with venous diseases (HR 2.27, 95%CI 2.17-2.36) and peripheral artery disease (HR 1.87, 95%CI 1.84-2.01). Results show that CVD predisposes to a higher cancer mortality rate. Of all CVD subtypes, HF patients have the highest cancer mortality rate and the hazards were highest in patients with venous diseases and peripheral artery disease.

Comments on the guidelines (2023) of the ESC on the management of cardiovascular diseases in patients with diabetes

Comments on the guidelines (2023) of the ESC on the management of cardiovascular diseases in patients with diabetes

Evaluation of novel indices of walking performance taking oxygen desaturation into account during six-minute walk test in cardiovascular disease patients.

In pulmonary disease patients since oxygen desaturation during 6-min walk test (6MWT) affects walk distance (6MWD), some novel indices such as desaturation/distance ratio [DDR, oxygen desaturation area (DAO2)/6MWD] and distance-saturation product [DSP, 6MWD × minimum peripheral oxygen saturation (SpO2)] are evaluated. However, there has been no study examining these indices that consider exercise-induced desaturation (EID) in patients with cardiovascular disease. In 94 cardiovascular disease patients without pulmonary complications, 6MWT and echocardiography were performed at the entry of cardiac rehabilitation. SpO2 was measured during 6MWT using a continuously monitorable pulse oximeter, and DSP and DDR were calculated using minimum SpO2 and DAO2 [sum of (100-SpO2) per second during 6MWT], respectively. EID was defined as SpO2 decrease of ≥ 4% or minimum SpO2 of < 90% during 6MWT. DSP was slightly lower and DDR was markedly higher in patients with EID than in those without. When examining correlations of DSP and DDR with their components, DSP was correlated with 6MWD much closely than minimum SpO2, while DDR was correlated as closely with DAO2 as 6MWD. Furthermore, DAO2, but not minimum SpO2, had a direct correlation with 6MWD. As for associations with cardiac function, DSP was correlated with several cardiac parameters, but DDR was not correlated with any of these parameters. Our findings suggest that oxygen desaturation during 6MWT affects walking distance in cardiovascular disease patients even without pulmonary complications and that DDR is more appropriate than DSP as an index of walking performance that takes EID into consideration, independently of cardiac function.

A multiple technology-based and individually-tailored Sit Less program for people with cardiovascular disease: A randomized controlled trial study protocol.

Sedentary behavior, a key modifiable risk factor for cardiovascular disease, is prevalent among cardiovascular disease patients. However, few interventions target sedentary behavior in this group. This paper describes the protocol of a parallel two-group randomized controlled trial for a novel multi-technology sedentary behavior reduction intervention for cardiovascular disease patients (registered at Clinicaltrial.gov, NCT05534256). The pilot trial (n = 70) will test a 12-week "Sit Less" program, based on Habit Formation theory. The 35 participants in the intervention group will receive an instructional goal-setting session, a Fitbit for movement prompts, a smart water bottle (HidrateSpark) to promote hydration and encourage restroom breaks, and weekly personalized text messages. A control group of 35 will receive the American Heart Association's "Answers by Heart" fact sheets. This trial will assess the feasibility and acceptability of implementing the "Sit Less" program with cardiovascular disease patients and the program's primary efficacy in changing sedentary behavior, measured by the activPAL activity tracker. Secondary outcomes include physical activity levels, cardiometabolic biomarkers, and patient-centered outcomes (i.e. sedentary behavior self-efficacy, habit strength, and fear of movement). This study leverages commonly used mobile and wearable technologies to address sedentary behavior in cardiovascular disease patients, a high-risk group. Its findings on the feasibility, acceptability and primary efficacy of the intervention hold promise for broad dissemination.

Independent predictors of MACE in patients with cancer

Abstract Funding Acknowledgements None. Background/Introduction Cardiovascular disease and cancer are the leading causes of death worldwide. Both disease entities share common risk factors. More importantly, the main cause of death after disease progression is cardiovascular disease in patients with cancer. Despite the recent advancements in the field of cardio-oncology, the main prognostic factors of major adverse cardiovascular events (MACE) remain elusive. Purpose To investigate prognostic factors of MACE in a single center cardio-oncology registry. Methods Consecutive patients referred to the cardio-oncology outpatient clinic of a tertiary center for cardiologic consultation were included. All patients were followed up clinically or by telephone. Data from national records were also used. Results In total, 115 patients were included in the analysis. Of them, 60 (52.2%) were female and the majority of study population suffered from breast cancer (27%). Thirteen patients (11.3%) had hematologic malignancies and the rest solid tumors. Chemotherapy was received by a total of 94 patients (81,7%). The mean follow -up duration was 446 days. During follow up, 32 MACEs (27.8%) occurred. Death from any cause occurred in 21 patients (including 2 cardiac deaths), hospitalization due to heart failure in 6, myocardial infarction in 2, pulmonary embolism in 3 and stroke in 1 patient. In multivariate logistic regression analysis, diabetes mellitus was an independent predictor of MACE, after adjustment for cardiovascular risk factors and body mass index (OR=3.37, 95% CI 1.14-9.99). In Kaplan Meier plots patients with diabetes mellitus showed higher incidence of MACE (log rank p=0.03). Conclusions In the present single center study, diabetes mellitus emerged as an independent predictor of MACE. This finding confirms the important and primary role of cardio-oncology units in the strict management of cardiovascular risk factors, leading to improved prognosis of this patient-population.Kaplan Meier Curve

Prediction of mortality in young adults with cardiovascular disease using artificial intelligence

&lt;b&gt;Background:&lt;/b&gt; Young mortality is prevalent among patients with cardiovascular disease (CVD). To develop prediction models for CVD mortality in young adults, it is crucial to assess CVD risks. Early detection of cardiac disorders using machine learning algorithms, a branch of artificial intelligence (AI) is crucial for preventing more damage to coronary arteries and saving lives.&lt;br /&gt; &lt;b&gt;Aims:&lt;/b&gt; To predict mortality versus a life outcome among young adults (18-45 years) with CVD using AI technique known as Chi-squared automatic interaction detector (CHAID) algorithms.&lt;br /&gt; &lt;b&gt;Methods:&lt;/b&gt; A large-scale dataset was extracted from the electronic health records of 809 young adult patients diagnosed with CVD using a retrospective design. Information was retrieved regarding young adults from Jordan who were admitted to public health institutions between 2015 and the end of 2021.&lt;br /&gt; &lt;b&gt;Results:&lt;/b&gt; CHAID algorithms were chosen among seven prediction models based on accuracy and area under curve to predict mortality vs life in young individuals (18-45 years old) with CVD. The mortality prediction algorithms started with pulse pressure, then diastolic blood pressure, then ischemic heart disease, and last geographical location.&lt;br /&gt; &lt;b&gt;Conclusions:&lt;/b&gt; CHAID model used in our study indicated how the death rate was classified and distributed among a variety of parameters. As a result, we may argue that AI model could provide additional information on how many aspects are articulated in connection to CVD patient fatality situations.

Atopic dermatitis is associated with an increased risk of cardiovascular diseases: A large-scale, propensity-matched US-based retrospective study.

Atopic dermatitis is a chronic relapsing inflammatory skin disease characterized by intense itch impacting heavily on patients' and caregivers' quality of life. Its clinical presentation is accompanied by a variety of type 2 comorbidities, e.g. asthma, hay fever, food allergies. However, current data on cardiovascular comorbidities are inconsistent. To identify risk of cardiovascular diseases in patients with atopic dermatitis. Data from Electronic Health Records (EHRs) of 1,070,965 atopic dermatitis patients and equally propensity score matched controls were retrieved from the US Collaborative Network part of the federated TriNetX network. Hazard ratios for risk of onset of cardiovascular diseases with a prevalence of ≥1% in both cohorts within 20 years after diagnosis were determined. A total of 55 cardiovascular diseases belonging to 8 major cardiovascular groups were identified. Of those, 53 diagnoses displayed a significantly increased risk in atopic dermatitis patients. Different diagnoses of heart failure and heart disease were found most often, followed by valve insufficiencies, arrhythmia, tachycardia, atrial fibrillation, flutter, but also MACE and venous thromboembolism. The individual diagnoses venous insufficiency, atherosclerosis of native arteries of the extremities, and unspecified diastolic (congestive) heart failure displayed highest hazard ratios. Atopic dermatitis is associated with an increased risk for multiple cardiovascular diseases.

Circulating perturbation of phosphatidylcholine (PC) and phosphatidylethanolamine (PE) is associated to cardiac remodeling and NLRP3 inflammasome in cardiovascular patients with insulin resistance risk

Lipidome perturbation occurring during meta-inflammation is associated to left ventricle (LV) remodeling though the activation of the NLRP3 inflammasome, a key regulator of chronic inflammation in obesity-related disorders. Little is known about phosphatidylcholine (PC) and phosphatidylethanolamine (PE) as DAMP-induced NLRP3 inflammasome. Our study is aimed to evaluate if a systemic reduction of PC/PE molar ratio can affect NLRP3 plasma levels in cardiovascular disease (CVD) patients with insulin resistance (IR) risk.Forty patients from IRCCS Policlinico San Donato were enrolled, and their blood samples were drawn before heart surgery. LV geometry measurements were evaluated by echocardiography and clinical data associated to IR risk were collected. PC and PE were quantified by ESI-MS/MS. Circulating NLRP3 was quantified by an ELISA assay.Our results have shown that CVD patients with IR risk presented systemic lipid impairment of PC and PE species and their ratio in plasma was inversely associated to NLRP3 levels. Interestingly, CVD patients with IR risk presented LV changes directly associated to increased levels of NLRP3 and a decrease in PC/PE ratio in plasma, highlighting the systemic effect of meta-inflammation in cardiac response. In summary, PC and PE can be considered bioactive mediators associated to both the NLRP3 and LV changes in CVD patients with IR risk.