Risk Of Atherosclerotic Heart Disease Research Articles

Explainable artificial intelligence for LDL cholesterol prediction and classification

IntroductionMonitoring LDL-C levels is essential in clinical practice because there is a direct relation between low-density lipoprotein cholesterol (LDL-C) levels and atherosclerotic heart disease risk. Therefore, measurement or estimate of LDL-C is critical. The present study aims to evaluate Artificial Intelligence (AI) and Explainable AI (XAI) methodologies in predicting LDL-C levels while emphasizing the interpretability of these predictions. Materials and methodsWe retrospectively reviewed data from the Laboratory Information System (LIS) of Ankara Etlik City Hospital (AECH). We included 60.217 patients with standard lipid profiles (total cholesterol [TC], high-density lipoprotein cholesterol, and triglycerides) paired with same-day direct LDL-C results. AI methodologies, such as Gradient Boosting (GB), Random Forests (RF), Support Vector Machines (SVM), and Decision Trees (DT), were used to predict LDL-C and compared directly measured and calculated LDL-C with formulas. XAI techniques such as Shapley additive annotation (SHAP) and locally interpretable model-agnostic explanation (LIME) were used to interpret AI models and improve their explainability. ResultsPredicted LDL-C values using AI, especially RF or GB, showed a stronger correlation with direct measurement LDL-C values than calculated LDL-C values with formulas. TC was shown to be the most influential factor in LDL-C prediction using SHAP and LIME. The agreement between the treatment groups based on NCEP ATPIII guidelines according to measured LDL-C and the LDL-C groups obtained with AI was higher than that obtained with formulas. ConclusionsIt can be concluded that AI is not only a reliable method but also an explainable method for LDL-C estimation and classification.

Sitosterolaemia presenting with consistent skin xanthomas in a pair of monozygotic twins who responded to ezetimibe treatment.

We described for the first time, to the best of our knowledge, sitosterolaemia in monozygotic twins. They presented with almost identical skin xanthomas that responded well to treatment. Raising awareness of sitosterolaemia is crucial, as early diagnosis and treatment are imperative to prevent the associated risk of atherosclerotic heart disease.

Is calcium a link between inflammatory bone resorption and heart disease?

Several epidemiologic studies associate bone-resorbing chronic inflammatory conditions with increased risk of atherosclerotic heart disease. These include post-menopausal osteoporosis, spinal cord injury, rheumatoid arthritis, and osteoarthritis. Additional studies have noted that the use of anti-resorptive agents following hip fracture, during rheumatoid arthritis, and prior to intensive care management have resulted in reduced overall mortality and mortality from cardiovascular disorders. The careful study of burn patients has allowed us to detect that children and adolescents have a mechanism that protects them from the entry of calcium into the circulation following inflammatory bone resorption. That is, they respond to pro-inflammatory cytokines by up-regulating the parathyroid calcium-sensing receptor (CaSR) with consequent development of hypocalcemic hypoparathyroidism and hypercalciuria. As extracellular calcium appears to exacerbate and/or prolong the inflammatory response, this responsiveness of the CaSR to inflammatory cytokines may be the factor that reduces cardiovascular morbidity and mortality. In adults with chronic inflammatory conditions, the ability of the CaSR to respond to pro-inflammatory cytokines is lost, suggesting that the calcium that enters the circulation following inflammatory bone resorption may persist in the circulation, entering the small coronary blood vessels and favoring the formation of coronary artery calcification, inflammation, and consequent cardiovascular disease.

PSAT033 Increased Risks of Atherosclerotic Heart Disease, Malignancy and Sleep Apnea with Primary Aldosteronism: A Case Report

Abstract Introduction Primary aldosteronism (PA) demonstrates an increased risk of atherosclerotic heart disease. A less commonly known fact is that PA is often associated with increased risks of malignancy, especially renal cell carcinoma (RCC) and sleep apnea. We are reporting a 51-year-old male with a long history of untreated PA caused by an adenoma (APA) who developed coronary artery disease (CAD), RCC, and sleep apnea during the course of his illness. Case presentation A 51-year-old male was evaluated in the endocrine clinic for secondary hypertension. Patient developed hypertension and hypokalemia at the age of 39 years and laboratory tests showed plasma renin activity PRA 0.06 ng/mL/hr, aldosterone 6 ng/dL, plasma metanephrines 79 pg/mL (ref 0–145), normetanephrine 22 pg/mL (ref 0-62), a serum cortisol value of 0.8 mcg/dL after 1 mg dexamethasone suppression. Despite using several anti-hypertensive medications, including quinapril, amlodipine, and potassium chloride, both his hypertension and hypokalemia remained poorly controlled. He also was diagnosed with sleep apnea at the age of 44 years, treated with CPAP. Abdominal CT showed normal adrenals and angiomyolipoma involving the right interior pole of the kidney. At the age of 47 years, a diagnosis of Liddle syndrome was considered, and the patient was placed on amiloride. At the age of 48 years, the patient developed chest pain and further diagnostic tests confirmed coronary artery disease, and a stent was placed in the left anterior descending artery. Due to the poor control of hypertension, carvedilol and eplerenone were also added to the regimen. Another abdominal CT done at the age of 50 years showed a left adrenal adenoma 1.2 cm, left kidney lower pole cyst 2.9 cm, and atherosclerotic calcification of aorta. Family history was negative for endocrine diseases. Physical examination: HR 62/min, BP 160/90 mmHg, normal examination of the heart, lungs, and abdomen. No clinical features of Cushing syndrome was observed. Repeat laboratory evaluations showed plasma renin activity < 0.167 ng/ml/hr, plasma aldosterone 111.4 ng/dL, concerning for PA. A follow-up CT of the abdomen confirmed left adrenal adenoma and a 1.8 cm left renal lesion suggestive of RCC. The patient underwent an adrenal venous sampling, which localized the left adrenal adenoma as the cause of PA. The patient underwent left adrenalectomy and left partial nephrectomy and pathology confirmed left adrenal adenoma and RCC. One week after surgery plasma aldosterone was 1.9 ng/dL and his hypertension was controlled with fewer medications and he did not require potassium supplements. Conclusion Our case illustrates that delayed diagnosis of PA (poorly treated PA) may be associated with an increased risk of CAD, malignancy and sleep apnea. Early diagnosis and surgical intervention are recommended for PA, especially caused by an adenoma. Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.

Studies Detail Heart Risks for Firefighters

Studies Detail Heart Risks for Firefighters

Inflammatory associated microRNAs expression in cardiomyocytes and blood serum in CAD patients

Abstract Objective To evaluate inflammatory associated microRNAs: miRNA-27a, miRNA-133a and miRNA-203 expression in CAD patients and to explore whether tissue expression is correlated with serum miRNA expression. Methods This cross-sectional observational study comprised 100 subjects (mean age 60.9±1.0 years old; 67% men). The left atrial and blood serum expression of the miRNA-27a, miRNA-133a and miR-203 was analyzed using real-time PCR in. 80 patients referred for CABG surgery (40 of them with multi-vessel CAD) and 20 control patients undergoing heart valve surgery. Patients with CAD did not have a history of myocardial infarction, they were patients with stable chronic CAD with planned coronary arteries bypass graft surgery (CABG). Results The levels of miRNA-27a, miRNA-133a and miRNA-203 myocardial and serum expression in patients with clinically relevant three-vessel coronary stenosis were significantly higher than in patients with 1–2 vessel disease, and significantly higher in both CAD cohorts compared to subjects without coronary atherosclerosis. The myocardial expression of miRNA-27a and miRNA-133a was significantly higher than serum expression, while miRNA-203 myocardial expression was lower serum expression. Serum miRNA-203 expression displayed the greatest differences between compared groups. Decision tree method established that the risk of atherosclerotic heart disease increases five-fold if miRNA-203 serum expression was more than 101.00 REU (OR 5.9 & CI 94.21–107.93). Conclusions Myocardial miRNA-27a, miRNA-133a and miRNA-203 expression in the left atrium and blood serum is higher in CAD patients than in non-CAD subjects, and the expression level is strongly associated with the number of affected coronary vessels. Although larger studies are required to confirm our findings, our results suggest that serum miRNA-203 expression level is correlated with myocardial tissue expression, severity of coronary atherosclerosis and might be proposed as a marker of the CAD extent. Funding Acknowledgement Type of funding source: None

Study of thyroid dysfunction in metabolic syndrome in patients of Amalapuram, Andhra Pradesh, India

Background: Both metabolic syndrome and thyroid dysfunction are associated with increased risk of atherosclerotic heart disease. The present study was conducted to study the Association of thyroid dysfunction and Metabolic syndrome and to find out the type of thyroid dysfunction in metabolic syndrome patients.Methods: Sixty cases were defined according to the IDF Criteria. Detailed history and necessary investigations like fasting blood sample was analyzed for total triiodothyronine (T3), total thyroxine (T4), thyroid-stimulating hormone (TSH), lipid profile, and blood glucose were undertaken.Results: In this study population of metabolic syndrome cases, the thyroid dysfunction is present in 16.7% patients. Among the thyroid dysfunction, sub clinical hypothyroidism is highly prevalent - 11.7%, The hypothyroidism is 3.3% prevalent in metabolic syndrome patients (one patient had TSH levels of more than 150 mU/L) and sub clinical hyperthyroidism is 1.7% prevalent. There were no overt hyperthyroidism patients in the study.Conclusions: This study clearly shows that, one sixth of metabolic syndrome patients or every sixth metabolic syndrome had hypothyroidism either overt or subclinical. This finding indicates a need for investigating the presence of Thyroid dysfunction during managing metabolic syndrome patients

Evaluation of epicardial adipose tissue and carotid intima-media thickness as a marker of atherosclerosis in patients with inflammatory bowel disease.

this study aimed to compare carotid intima media (CIMT) and epicardial adipose tissue (EAT) measurements, which are considered as markers for the detection of early atherosclerosis in healthy controls and inflammatory bowel disease (IBD) cases. a total of 60 IBD patients (25 Crohn's disease and 35 ulcerative colitis) and 60 healthy patients (as a control group) were included in the study. The measurements of CIMT and EAT were performed using echocardiography and ultrasonography, respectively. Statistical analysis was used to determine the relationship between the parameters. the thickness of bilateral (right and left) CIMT and EAT were significantly higher in IBD than in the control group (p < 0.05). There was a positive correlation between EAT and bilateral (right and left) CIMT in IBD patients (p < 0.05). IBD is associated with an increased thickness of EAT and CIMT. Chronic inflammation in IBD may increase the risk of atherosclerotic heart disease. Thus, only measuring the thickness of EAT and CIMT can be used as an objective, easy, simple, affordable, non-invasive and accessible assessment method in order to screen for this risk.

Clonal hematopoiesis of indeterminate potential-associated mutations and risk of comorbidities in patients with myelodysplastic syndrome.

Clonal hematopoiesis of indeterminate potential (CHIP)-associated mutations increase the risk of atherosclerotic heart disease. Comorbidities significantly impact the prognosis of patients with myelodysplastic syndromes (MDS). The objective of this study was to determine the association and impact of CHIP mutations with comorbidities in patients with MDS. This retrospective analysis of 566 consecutive patients with MDS was conducted at The University of Texas MD Anderson Cancer Center from August 2013 to December 2016. The 27-item Adult Comorbidity Evaluation (ACE-27) scale was used to assess the severity of comorbid conditions. Next-generation sequencing was used to detect the presence of CHIP mutations in bone marrow aspirates. Spearman correlations and logistic regression analyses were used to determine the association between mutations and comorbidities. Mutations in the genes tet methylcytosine dioxygenase 2 (TET2), ASXL transcriptional regulator 1 (ASXL1), DNA methyltransferase 3α (DNMT3A), Janus kinase 2 (JAK2), and tumor protein 53 (TP53) were noted in 20%, 18%, 9%, 2%, and 21% of patients, respectively. Patients with DNMT3A and JAK2 mutations had higher likelihoods of a prior history of myocardial infarction (odds ratio, 2.62; P=.03) and veno-occlusive disease (odds ratio, 6.48; P=.02), respectively. TP53 mutation was associated with a prior history of malignancy. Patients with TET2 mutation had no association with any comorbidity. A prognostic model including the revised International Prognostic Scoring System classification, the ACE-27 score, and TP53 mutation status (the I-RAT model) predicted median overall survival. In patients with MDS, the presence of CHIP-associated mutations is associated with comorbidities. DNMT3A and JAK2 mutations were associated with higher likelihoods of prior myocardial infarction and thrombotic events. There was no association between comorbidity and TET2 mutation. Incorporating the revised International Prognostic Scoring System classification with the ACE-27 and TP53 mutation status improved outcome prediction in patients with MDS.

Study of serum lipid profile before and after hepatitis C virus treatment

Objective To study the lipid profile in hepatitis C virus (HCV) patients before and after treatment with daclatasvir (DAV)+sofosbuvir (SOF)±ribavirin (RBV) to determine the effect of virus clearance on the lipid profile. Background Chronic HCV infection is associated with lipid and lipid protein metabolism disorders. There is a marked increase in serum low-density lipoprotein-cholesterol (LDL-C) in HCV-infected patients treated with SOF and RBV. Participants and methods A total of 100 chronic hepatitis C patients were included in a case–control study from February 2017 to August 2017. Twenty healthy individuals volunteered as a control group. Lipid profile changes were analyzed at baseline, after the end of treatment, and 12 weeks after treatment. Results Before treatment, the levels of serum LDL-C, cholesterol and triglycerides (TGs) were significantly lower in patients than the controls. At the end of treatment and 12 weeks after treatment with DCV + SOF + RBV, there was a significant increase in serum LDL-C, high-density lipoprotein-cholesterol, cholesterol, and TGs (P = 0.0001, 0.0001, 0.0001, and 0.007), respectively, and there was also a significant increase in patients treated with DCV + SOF (P = 0.035, 0.036, 0.01, and 0.0001), respectively. 100% of the treated patients achieved a sustained viral response (week 24). Conclusion Eradication of HCV was associated with an increase in the serum level of total cholesterol, TGs, LDL-C, and high-density lipoprotein-cholesterol; so follow up of the patient's lipid profile after Hepatitis C virus treatment is very important to avoid hyperlipidemia which is a risk for atherosclerotic heart disease.

Associations of genetic markers of the sympathoadrenal system and endothelial dysfunction with coronary heart disease on the example of a small Shoriya population

Aim . To establish associations of polymorphisms of candidate genes coding for the components of the endothelial (NOS3, MTHFR) and sympathoadrenal systems (ADRB1, ADRA2B) with coronary heart disease (CHD) in the cohort of the small population of Mountain Shoriya. Material and methods . A clinical and epidemiological study was conducted in the areas of Mountain Shoriya (Orton, Ust-Kabyrza, Sheregesh, Tashtagol). Analysis of risk factors included recording the age, sex, body mass index, waist circumference, presence/absence of arterial hypertension (AH), smoking, and the presence of disorders of lipid and carbohydrate metabolism. CHD diagnosis was made by three epidemiological criteria: coding of the electrocardiogram according to the Minnesota code, Rose questionnaire, and a history of myocardial infarction. The patient underwent molecular genetic testing. DNA isolation from blood was carried out by the method of phenol-chloroform extraction. Statistical processing was carried out using the programs STATISTICA 6.1 (StatSoft Inc., USA) and SNPStats. Results . The prevalence of CHD in the Shoriya cohort was 9,7%. The results of our study established the relationship of genetic markers of the sympathoadrenal and endothelial systems with coronary atherosclerosis in the indigenous population of Shoriya. The high risk of atherosclerotic heart disease was associated with the 4b/4a genotype of the NOS3 gene (OR 2,57 95% CI (1,12-5,86), p=0,026) according to the dominant mode of inheritance. The relationship of the T/T genotype of the MTHFR gene with CHD by recessive inheritance was established (OR 13,28; 95% CI (1,79-98,40), p=0,024). Conclusion . Due to genetic research, there is a real opportunity not only to carry out accurate molecular diagnostics, but also to determine an underlying risk for a disease. Detection of genetic disposition to CHD can be carried out long before the onset of clinical symptoms, which can effectively prevent its development.

The role of small noncoding RNAS in the pathogenesis of coronary arteries atherosclerosis

Background.Cardiovascular disease, including coronary artery disease (CAD), remains a leading cause of mortality. The results of recent studies demonstrate that microRNA engages in pathogenesis of different pathological states, including coronary atherosclerosis and its clinical manifestation — CAD.Objective.To evaluate microRNA-27а, microRNA-133а and microRNA-203 expression in cardiomyocytes and blood serum of CAD patients with different degrees of coronary artery lesion.Design and methods. 100 patients were included in the study, they formed 3 groups: 40 patients with CAD and significant atherosclerosis of 1-2 coronary arteries; 40 patients with multi arterial coronary disease and 20 persons without CAD and significant comorbidity. The microRNA-27a, microRNA-133а and microRNA-203 expression was determined in cardiomyocytes and blood serum of these patients by real-time polymerase chain reaction.Results.Level of microRNA-27a, microRNA-133а and microRNA-203 expression in left atrium cardiomyocytes of CAD patients with significant stenosis of 3 or more coronary arteries was higher, then their expression in the patients with 1-2-vessel and in group without coronary atherosclerosis. Examination of the microRNA expression level in blood serum and in left atrium cardiomyocytes revealed a significant difference. The expression of microRNA-27a and microRNA-133а in cardiomyocytes is above than in blood serum, while the expression of microRNA-203 in the myocardium is lower, than in the blood serum. Level of microRNA-27a, microRNA-133а and microRNA-203 expression in blood serum in CAD patients with significant stenosis of 3 or more coronary arteries was significantly higher, than in patients with 1-2 stenosis of coronary arteries. Furthermore, classification tree method established that risk of atherosclerotic heart disease increases five-fold if microRNA-203 expression in blood serum is more than 100 REU.Conclusion.MicroRNA-27а and microRNA-133а expression in cardiomyocytes of left atrium is higher than in blood serum in CAD patients. MicroRNA-203 expression level in blood serum may be a new predictive marker of coronary artery degree atherosclerotic stenosis in CAD patients.

Molecular Pathways Underlying Cholesterol Homeostasis.

Cholesterol is an essential molecule that exerts pleiotropic actions. Although its presence is vital to the cell, its excess can be harmful and, therefore, sustaining cholesterol homeostasis is crucial to maintaining proper cellular functioning. It is well documented that high plasma cholesterol concentration increases the risk of atherosclerotic heart disease. In the last decades, several studies have investigated the association of plasma cholesterol concentrations and the risk of cardiovascular diseases as well as the signaling pathways involved in cholesterol homeostasis. Here, we present an overview of several mechanisms involved in intestinal cholesterol absorption, the regulation of cholesterol synthesis and uptake. We also discuss the importance of reverse cholesterol transport and transintestinal cholesterol transport to maintain cholesterol homeostasis and prevent atherosclerosis development. Additionally, we discuss the influence of dietary cholesterol on plasma cholesterol concentration and the new recommendations for cholesterol intake in a context of a healthy dietary pattern.

PCSK9 INHIBITION: REAL WORLD APPLICATION AND CHALLENGES TO ACHIEVE UNMET CHOLESTEROL TARGETS IN CANADIAN ATHEROSCLEROTIC HEART DISEASE, THE PRACTICAL STUDY

LDL cholesterol reduction is a cornerstone of atherosclerotic heart disease risk reduction. The landmark Fourier study showed continued benefits with further cholesterol reductions below 1 mmol/L. Yet achieving even traditional targets of LDL below 2 mmol/L has been a challenge in clinical practice

Role of Estrogens in the Regulation of Liver Lipid Metabolism.

Before menopause, women are protected from atherosclerotic heart disease associated with obesity relative to men. Sex hormones have been proposed as a mechanism that differentiates this risk. In this review, we discuss the literature around how the endogenous sex hormones and hormone treatment approaches after menopause regulate fatty acid, triglyceride, and cholesterol metabolism to influence cardiovascular risk.The important regulatory functions of estrogen signaling pathways with regard to lipid metabolism have been in part obscured by clinical trials with hormone treatment of women after menopause, due to different formulations, routes of delivery, and pairings with progestins. Oral hormone treatment with several estrogen preparations increases VLDL triglyceride production. Progestins oppose this effect by stimulating VLDL clearance in both humans and animals. Transdermal estradiol preparations do not increase VLDL production or serum triglycerides.Many aspects of sex differences in atherosclerotic heart disease risk are influenced by the distributed actions of estrogens in the muscle, adipose, and liver. In humans, 17β-estradiol (E2) is the predominant circulating estrogen and signals through estrogen receptor alpha (ERα), estrogen receptor beta (ERβ), and G-protein-coupled estrogen receptor (GPER). Over 1000 human liver genes display a sex bias in their expression, and the top biological pathways are in lipid metabolism and genes related to cardiovascular disease. Many of these genes display variation depending on estrus cycling in the mouse. Future directions will likely rely on targeting estrogens to specific tissues or specific aspects of the signaling pathways in order to recapitulate the protective physiology of premenopause therapeutically after menopause.

The LDL/HDL ratio and atherosclerosis in ankylosing spondylitis.

In ankylosing spondylitis (AS) patients, cardiac and vascular involvement may manifest as atherosclerosis and coronary artery disease. Systemic inflammation, oxidative stress, increased low-density lipoprotein (LDL) cholesterol and decreased high-density lipoprotein (HDL) cholesterol constitute asignificant risk for atherosclerosis. This study investigated the relationship between carotid intima-media thickness (CIMT), LDL/HDL ratio, total oxidant status (TOS; an indicator of oxidative stress) and ischemic modified albumin (IMA; an ischemic marker in AS patients). Sixty AS patients were diagnosed using the Modified New York Criteria; 54age- and gender-matched participants were included as controls. CIMT, LDL/HDL ratio, TOS and IMA were measured using the most appropriate methods. IMA was higher in AS patients compared to controls (p <0.0001). TOS was also increased in AS patients (p= 0.005); as was CIMT (p <0.0001). The LDL/HDL ratio was also greater in AS patients compared to controls (p= 0.047). Apositive correlation was found between CIMT and LDL/HDL ratio among AS patients. Elevated CIMT, IMA and TOS levels suggest an increased risk of atherosclerotic heart disease in AS patients. The LDL/HDL ratio was higher in AS patients compared to controls, and there was acorrelation between LDL/HDL ratio and CIMT, albeit statistically weak. Therefore, the LDL/HDL ratio is not areliable marker to predict atherosclerotic heart disease in AS patients.

The Lipid Parameters and Lipoprotein(a) Excess in Hashimoto Thyroiditis.

Objective. The risk of atherosclerotic heart disease is increased in autoimmune thyroiditis, although the reason is not clear. Lipoprotein(a) (Lp(a)) excess has been identified as a powerful predictor of premature atherosclerotic vascular diseases. The aim of this study is to investigate the relationship between Lp(a) levels and thyroid hormones in Hashimoto patients. Method. 154 premenopausal female Hashimoto patients (48 patients with overthypothyroid (OH), 50 patients with subclinical hypothyroid (SH), and 56 patients with euthyroid Hashimoto to (EH)) were enrolled in this study. The control group consists of 50 age matched volunteers. In every group, thyroid function tests and lipid parameters with Lp(a) were measured. Lp(a) excess was defined as Lp(a) > 30 mg/dL. Results. Total-C, LDL-C, TG, and Lp(a) levels were increased in Hashimoto group. Total-C, LDL-C, and TG levels were higher in SH group than in the control group. Total-C and LDL-C levels were also higher in EH group compared to controls. Lp(a) levels were similar in SH and EH groups with controls. However, excess Lp(a) was more common in subclinical hypothyroid and euthyroid Hashimoto group than in the control group. Conclusion. The Total-C and LDL-C levels and excess Lp(a) were higher even in euthyroid Hashimoto patients. Thyroid autoimmunity may have some effect on Lp(a) and lipid metabolism.

Aortic stiffness: pathophysiology, clinical implications, and approach to treatment.

Aortic stiffness is a hallmark of aging, and classic cardiovascular risk factors play a role in accelerating this process. Current changes in medicine, which focus on preventive care, have led to a growing interest in noninvasive evaluation of aortic stiffness. Aortic stiffness has emerged as a good tool for further risk stratification because it has been linked to increased risk of atherosclerotic heart disease, myocardial infarction, heart failure, and stroke. This has led to the invention and validation of multiple methods to measure aortic stiffness. Pulse wave velocity is emerging as the gold standard for evaluation of aortic stiffness. This review focuses on the pathophysiology involved in aortic stiffness, methods available for evaluation of aortic stiffness, the importance of central pressure as a predictor of future cardiovascular events, and therapies that affect aortic stiffness.

Evaluation of the Future Atherosclerotic Heart Disease with Oxidative Stress and Carotid Artery Intima Media Thickness in Gestational Diabetes Mellitus

Background and objective. In this study our aim was to evaluate paraoxonase (PON1) activity and free sulfhydryl groups (–SH) as antioxidative parameters and lipid hydroperoxide (LOOH) as oxidative parameter in the serum of women with gestational diabetes mellitus (GDM) and determine their relation with the degree of subclinical atherosclerosis. Material and methods. Serum samples from 39 pregnant women complicated with GDM and 40 healthy pregnant women were collected for the analysis of oxidative markers. Common carotid artery intima media thickness (CIMT) was measured for both groups to assess future atherosclerotic heart disease risk. PON1 activity and –SH were measured spectrophotometrically. LOOH levels were measured by ferrous oxidation with a xylenol orange assay. Results. CIMT and LOOH levels were significantly higher (p = 0.01, p < 0.001, respectively) in GDM group compared to controls, whereas PON1 and –SH levels were significantly lower (p < 0.001 for both). CIMT values were significantly correlated with body mass index (BMI), 50 g oral glucose tolerance test (OGTT), and mean arterial blood pressure (MABP) (p = 0.003, p = 0.02, and p = 0.03, respectively). However, there was no correlation between CIMT and oxidative markers. Conclusions. Increased levels of LOOH and decreased levels of PON1 and –SH showed disturbance of antioxidative mechanisms in GDM. These changes were associated with increased BMI and MABP which may be relevant to GDM pathophysiology. Furthermore, increased CIMT values in GDM compared to healthy controls designate increased risk of future atherosclerotic heart disease.

Secondhand Smoke Exposure and Quality of Life in Patients With Heart Failure

Secondhand smoke (SHS) exposure is associated with an increased risk of atherosclerotic heart disease and cardiac events. We sought to assess the effect of SHS on health-related quality of life (HRQOL) in patients with heart failure. Current nonsmokers with heart failure (N = 205) were enrolled in a cohort study. Exposure to SHS was assessed with a validated exposure questionnaire and a high-sensitivity assay for urinary cotinine level. Multidimensional HRQOL was evaluated with the RAND 36-Item Short Form Health Survey, which assesses 8 domains on a scale of 0 (worst) to 100 (best): physical functioning, bodily pain, role limitations due to physical health problems (role physical), role limitations due to emotional/personal problems (role emotional), emotional well-being, social functioning, energy/fatigue, and general health perceptions. A subset of patients (n = 75) agreed to assessment of functional status with a 6-minute walk test. Self-reported exposure to SHS was associated with generally lower HRQOL scores in univariate analysis, with statistically and clinically significant reductions in 3 subscale scores: role physical (22.2 points), emotional well-being (11.0 points), and role emotional (16.2 points). Even after adjustment for clinical factors, such as age, sex, New York Heart Association class of heart failure, comorbidities, and medications, exposure to SHS remained an independent predictor of HRQOL scores in these domains. When increasing quartiles of urinary cotinine level were used as the exposure measure, qualitatively similar results were obtained. Even low levels of SHS are associated with lower scores in several aspects of HRQOL. Physicians should advise patients with heart failure and their families to avoid SHS exposure.