Microplastics and Cardiovascular Disease: Should Clinicians Be Paying Attention?

Recognizing Pregnancy-Associated Cardiovascular Risk Factors

Asymmetric dimethylarginine in end-stage renal disease patients: A biomarker modifiable by calcium blockade and angiotensin II antagonism?

Usefulness of Brachial Artery Flow-Mediated Dilation to Predict Long-Term Cardiovascular Events in Subjects Without Heart Disease

Crucial advances in our understanding of basic pathogenic mechanisms involved in atherogenesis have been achieved during the past 2 decades. The historical hypothesis of pathogenesis (“lipid accumulation”) has evolved to integrate several causal events contributing to the initiation and evolution of atherosclerosis. Vascular inflammation and apoptosis may play a joint pivotal role in its progression and onset. Hypercholesterolemia and hypertension have synergistic deleterious effects on coronary endothelial function.1 Impaired fasting glucose, triglycerides and triglyceride-rich lipoprotein remnants, lipoprotein(a), homocysteine, and high-sensitivity C-reactive protein (hsCRP) might contribute to an increased risk of atherosclerosis.2 The disease also has been related to infiltration of immune cells, which are involved in both systemic and local, innate as well as adaptive, immune responses.3 Distinct pathways of atherothrombosis seem to develop at different sites of the vascular system (brain, heart, and peripheral circulation). Endothelial dysfunction induced by cardiovascular risk factors is considered to be 1 of the earliest stages in vascular damage and is associated independently with cardiovascular events.4 There is a synergic action between genetic, ambient, local, and systemic factors, and ultimately the progression of atherosclerosis is responsible for coronary heart disease (CHD) and its complications (such as unstable “in crescendo” angina, myocardial infarction, and sudden death), peripheral arterial disease, and ischemic stroke. The evolution of atherosclerosis, however, is characterized by a long lag time between onset and clinical manifestation, thereby providing an opportunity for implementation of early detection, prevention, and intervention strategies. Because the development of atherosclerosis commences early in humans, we need to rethink the timing of what is currently considered to be “primary” prevention of atherosclerosis-related diseases. It is likely that we need to start administering effective treatments much earlier than previously assumed. Indeed, much attention would be important when subjects are in a state of wellness before the …

As reports show cardiovascular (CV) risks in first-degree relatives (FDR) of type2 diabetics, and autonomic imbalance predisposing to CV risks, in the present study we have assessed the contribution of sympathovagal imbalance (SVI) to CV risks in these subjects. Body mass index (BMI), waist-to-hip ratio (WHR), basal heart rate (BHR), blood pressure (BP), rate pressure product (RPP), and spectral indices of heart rate variability (HRV) were reordered and analyzed in FDR of type2 diabetics (study group, n=293) and in subjects with no family history of diabetes (control group, n=405). The ratio of low-frequency (LF) to high-frequency (HF) power of HRV (LF-HF), a sensitive marker of SVI, was significantly increased (P<0.001) in the study group compared with the control group. The SVI in the study group was due to concomitant sympathetic activation (increased LF) and vagal inhibition (decreased HF). In the study group, the LF-HF ratio was significantly correlated with BMI, WHR, BHR, BP and RPP. Multiple regression analysis showed an independent contribution of LF-HF to hypertension status (P=0.000), and bivariate logistic regression showed significant prediction (odds ratio 2.16, confidence interval 1.130-5.115) of LF-HF to increased RPP, the marker of CV risk, in the study group. Sympathovagal imbalance in the form of increased sympathetic and decreased parasympathetic activity is present in FDR of type2 diabetics. Increased resting heart rate, elevated hypertension status, decreased HRV and increased RPP in these subjects make them vulnerable to CV risks. SVI in these subjects contributes to CV risks independent of the degree of adiposity.

<i>Circulation</i> Editors’ Picks

Impact of psychological status on cardiovascular diseases: Is it time for upgrading risk score charts?

Are We There Yet? Pediatric Screening for Inflammatory Biomarkers and Low Cardiorespiratory Fitness to Identify Youth at Increased Risk of Cardiovascular Disease

Editorial: Modifying Cardiovascular Risk Factors: Newer Advances in Cardiovascular Metabolism and Diagnostic Technologies.

Introduction

a disturbance of endothelial function is considered as a key event in the development of atherosclerosis ([63][1]). Thus reliable assessment of endothelial function in humans appears highly desirable. With respect to the major endothelial functions, this aim can be achieved by different approaches:

Background/Aims COVID-19 has led to substantial changes in the provision of emergency healthcare services. International data suggest that COVID-19 is associated with increased morbidity and mortality in patients with pre-existing cardiovascular disease and cardiovascular risk factors. This study aimed to explore the association between pre-existing cardiovascular disease and/or cardiovascular risk factors and COVID-19 disease severity and outcomes in an Irish hospital. Methods This retrospective study obtained data from a bioresource database of patients with confirmed COVID-19 infection (n=649) in a large hospital in Dublin. Data were collected on patients' demographic characteristics, cardiovascular diseases, cardiovascular disease risk factors and medications taken for cardiovascular conditions. The World Health Organization progression scale was used to assess the severity of COVID-19 infection in each patient. Cross-tabulation analysis was used to analyse associations between variables, with a P value of ≤0.05 indicating significance. Results Mortality rates were six times greater in patients with cardiovascular disease compared to those without cardiovascular disease (18.6% vs 3.1%). A higher percentage of patients with one or more cardiovascular risk factors had moderate (53.4%) or severe (19.1%) COVID-19 and higher mortality rates (10.7%) than those without cardiovascular risk factors. Of the patients who died from COVID-19 (n=40), 60.0% (n=24) had one or more cardiovascular diseases, while 80.0% (n=32) had one or more cardiovascular risk factors. Conclusions Existing cardiovascular disease and cardiovascular risk factors increase the risk of more severe disease and worse clinical outcomes in patients with COVID-19. Many cardiovascular risk factors are modifiable, so it is important to consider preventative education strategies designed to reduce modifiable risk factors to improve outcomes for patients with COVID-19.

Importance of Low-Grade Albuminuria

For children and adolescents, comprehensive guidelines for the diagnosis and management of elevated cholesterol have been published once, by the National Cholesterol Education Program in 1992.1 Since then, substantial research on early atherosclerosis and in related clinical areas has been conducted; simultaneously, the obesity epidemic has added the metabolic syndrome and its related high-triglyceride/low–high-density lipoprotein (HDL) phenotype to the agenda of those interested in establishing a consensus approach to early cardiovascular disease prevention.2 Article p 1056 Before assuming that new knowledge and secular trends in risk factors demand substantial revision of cardiovascular health guidelines for children, we must first consider several valuable, often prescient aspects of the 1992 report. First is an emphasis on the importance of nutritional management over pharmacological management of elevated low-density lipoprotein (LDL) cholesterol, unless levels clearly associated with premature cardiovascular disease exist and children are sufficiently old that advanced atherosclerotic lesions may be presumed to be present. Two randomized trials of dietary intervention, the DISC (Dietary Intervention Study in Children) and STRIP (Special Turku coronary Risk factor Intervention Project for babies) studies, have shown that the diet recommended by the 1992 report is safe and mildly effective in lowering LDL cholesterol and thus can be implemented in population-based strategies of cardiovascular disease risk lowering.3,4 Furthermore, the PDAY (Pathobiological Determinants of Atherosclerosis in Youth) study has shown that advanced, irreversible atherosclerotic lesions (American Heart Association grades IV and V) are rarely present before 19 years of age and that the relationship of risk to atherosclerosis in late adolescence is with regard to reversible early lesion grades (American Heart Association grades I through III).5 A second and woefully underrecognized virtue of the 1992 report is the definition of risk strata for LDL cholesterol, with borderline values being 110 to 129 mg/dL and high …

Previous studies suggested that the lectin-complement pathway plays a complex role in cardiovascular disease (CVD). To date, no prospective human studies have investigated the relationship between the initiating factor of the lectin pathway, that is, mannose-binding lectin (MBL), and low-grade inflammation, endothelial dysfunction, or carotid intima-media thickness (cIMT). Moreover, MBL-associated proteases (MASPs) and MBL-associated proteins (MAps), which mediate downstream complement activation, have not been studied in the development of CVD. In a prospective cohort (n=574; age 60±7 years; 7-year follow-up), we investigated longitudinal associations of plasma MBL, MASP-1, MASP-2, MASP-3, and MAp44 with biomarker scores that reflect low-grade inflammation and endothelial dysfunction, respectively, and with cIMT. We also investigated their associations with incident CVD (n=73). In adjusted analyses, low-grade inflammation was lowest in the middle tertile (TMiddle) of MBL, that is, TMiddle was 0.19 SD (0.03 to 0.34) lower than TLow, and 0.15 SD (-0.02 to 0.31) lower than THigh. cIMT was 28 μm (-50 to -5) lower in the highest MBL tertile (THigh) than in TMiddle and did not differ between TLow and TMiddle. MBL was not associated with endothelial dysfunction or CVD. MASP-1 and MASP-2 were not associated with any cardiovascular outcomes. MASP-3 and MAp44 were, independently of MBL levels, associated with endothelial dysfunction (per 1 SD higher MASP-3: β=0.10 SD [0.02 to 0.18]; per 1 SD higher MAp44 β=0.12 SD [0.04 to 0.20]) but not with low-grade inflammation, cIMT, or CVD. High MBL may contribute to low cIMT, whereas the association of MBL with low-grade inflammation was nonlinear. MASP-1 and MASP-2 were not associated with adverse cardiovascular outcomes. MASP-3 and MAp44 may play a role in endothelial dysfunction, potentially independent of lectin-pathway activation.