Greater Incidence Of Cardiovascular Disease Research Articles

A 20-year population study of peripartum cardiomyopathy.

The epidemiology of peripartum cardiomyopathy (PPCM) in Europe is poorly understood and data on long-term outcomes are lacking. A retrospective, observational, population-level study of validated cases of PPCM in Scotland from 1998 to 2017 was conducted. Women hospitalized with presumed de novo left ventricular systolic dysfunction around the time of pregnancy and no clear alternative cause were included. Each case was matched to 10 controls. Incidence and risk factors were identified. Morbidity and mortality were examined in mothers and children. The incidence of PPCM was 1 in 4950 deliveries. Among 225 women with PPCM, obesity, gestational hypertensive disorders, and multi-gestation were found to be associated with having the condition. Over a median of 8.3 years (9.7 years for echocardiographic outcomes), 8% of women with PPCM died and 75% were rehospitalized for any cause at least once. Mortality and rehospitalization rates in women with PPCM were ∼12- and ∼3-times that of controls, respectively. The composite of all-cause death, mechanical circulatory support, or cardiac transplantation occurred in 14%. LV recovery occurred in 76% and, of those who recovered, 13% went on to have a decline in LV systolic function despite initial recovery. The mortality rate for children born to women with PPCM was ∼5-times that of children born to controls and they had an ∼3-times greater incidence of cardiovascular disease over a median of 8.8 years. PPCM affected 1 in 4950 women around the time of pregnancy. The condition is associated with considerable morbidity and mortality for the mother and child. There should be a low threshold for investigating at-risk women. Long term follow-up, despite apparent recovery, should be considered.

Liver disease is a significant risk factor for cardiovascular outcomes – A UK Biobank study

Chronic liver disease (CLD) is associated with increased cardiovascular disease (CVD) risk. We investigated whether early signs of liver disease (measured by iron-corrected T1-mapping [cT1]) were associated with an increased risk of major CVD events. Liver disease activity (cT1) and fat (proton density fat fraction [PDFF]) were measured using LiverMultiScan® between January 2016 and February 2020 in the UK Biobank imaging sub-study. Using multivariable Cox regression, we explored associations between liver cT1 (MRI) and primary CVD (coronary artery disease, atrial fibrillation [AF], embolism/vascular events, heart failure [HF] and stroke), and CVD hospitalisation and all-cause mortality. Liver blood biomarkers, general metabolism biomarkers, and demographics were also included. Subgroup analysis was conducted in those without metabolic syndrome (defined as at least three of: a large waist, high triglycerides, low high-density lipoprotein cholesterol, increased systolic blood pressure, or elevated haemoglobin A1c). A total of 33,616 participants (mean age 65 years, mean BMI 26kg/m2, mean haemoglobin A1c 35mmol/mol) had complete MRI liver data with linked clinical outcomes (median time to major CVD event onset: 1.4 years [range: 0.002-5.1]; follow-up: 2.5 years [range: 1.1-5.2]). Liver disease activity (cT1), but not liver fat (PDFF), was associated with higher risk of any major CVD event (hazard ratio 1.14; 95% CI 1.03-1.26; p= 0.008), AF (1.30; 1.12-1.51; p <0.001); HF (1.30; 1.09-1.56; p= 0.004); CVD hospitalisation (1.27; 1.18-1.37; p <0.001) and all-cause mortality (1.19; 1.02-1.38; p= 0.026). FIB-4 index was associated with HF (1.06; 1.01-1.10; p= 0.007). Risk of CVD hospitalisation was independently associated with cT1 in individuals without metabolic syndrome (1.26; 1.13-1.4; p <0.001). Liver disease activity, by cT1, was independently associated with a higher risk of incident CVD and all-cause mortality, independent of pre-existing metabolic syndrome, liver fibrosis or fat. Chronic liver disease (CLD) is associated with a twofold greater incidence of cardiovascular disease. Our work shows that early liver disease on iron-corrected T1 mapping was associated with a higher risk of major cardiovascular disease (14%), cardiovascular disease hospitalisation (27%) and all-cause mortality (19%). These findings highlight the prognostic relevance of a comprehensive evaluation of liver health in populations at risk of CVD and/or CLD, even in the absence of clinical manifestations or metabolic syndrome, when there is an opportunity to modify/address risk factors and prevent disease progression. As such, they are relevant to patients, carers, clinicians, and policymakers.

Fibrinogen, Coagulation, and Ageing.

The World Health Organization estimates that the world's population over 60years of age will nearly double in the next 30years. This change imposes increasing demands on health and social services with increased disease burden in older people, hereafter defined as people aged 60years or more. An older population will have a greater incidence of cardiovascular disease partly due to higher levels of blood fibrinogen, increased levels of some coagulation factors, and increased platelet activity. These factors lead to a hypercoagulable state which can alter haemostasis, causing an imbalance in appropriate coagulation, which plays a crucial role in the development of cardiovascular diseases. These changes in haemostasis are not only affected by age but also by gender and the effects of hormones, or lack thereof in menopause for older females, ethnicity, other comorbidities, medication interactions, and overall health as we age. Another confounding factor is how we measure fibrinogen and coagulation through laboratory and point-of-care testing and how our decision-making on disease and treatment (including anticoagulation) is managed. It is known throughout life that in normal healthy individuals the levels of fibrinogen and coagulation factors change, however, reference intervals to guide diagnosis and management are based on only two life stages, paediatric, and adult ranges. There are no specific diagnostic guidelines based on reference intervals for an older population. How ageing relates to alterations in haemostasis and the impact of the disease will be discussed in this chapter. Along with the effect of anticoagulation, laboratory testing of fibrinogen and coagulation, future directions, and implications will be presented.

Individuals with Acute Spinal Cord Injury Display Impaired Biomarkers of Cardiometabolic Health

Individuals with spinal cord injuries (SCI) have a greater incidence of cardiovascular disease (CVD) than the non‐injured. Contributing to the increased CVD is decreased cardiometabolic health including increased insulin resistance, central adiposity, and dyslipidemia. In fact, cross‐sectional analyses of individuals with chronic SCI (up to 50 years post injury) indicates that up to 70% are classified as overweight/obese and 25‐60% have either insulin resistance or dyslipidemia. However, current understanding of cardiometabolic health in SCI derives from those with chronic injury, hence it is unknown if biomarkers are adversely affected in those with more acute injuries. Therefore, we assessed cardiometabolic health in individuals with SCI &lt;3 yrs. Cardiometabolic health was assessed through fasting blood glucose, insulin, triglycerides, low density lipoprotein (LDL), high density lipoprotein (HDL), total cholesterol, C‐reactive protein (CRP), and hemoglobin A1C (HbA1C). In addition, oral glucose tolerance testing (OGTT) was performed, and body composition was estimated via dual energy x‐ray absorptiometry (DXA). Five individuals (1F, 4M) aged 20 to 34 yo with SCI at neurologic level of injury ranging from spinal cord segments C6 to T4 (ASIA A and B) at 9 to 27 months post‐injury participated. All subjects displayed at ≥1 marker of impaired cardiometabolic health, while one displayed five markers. Body fat ranged from 27 to 42%, and one subject was classified as obese, two as overweight, and two as normal weigh based on BMI. Dyslipidemia was prominent in four of five subjects: one had elevated total cholesterol (&gt;200 mg/dL), one had elevated triglycerides (&gt;150 mg/dL), three had low HDL (&lt;40 mg/dL), and two had elevated LDL (&gt;100 mg/dL). Glucose tolerance test data and fasting insulin measurements showed normal fasting glucose (&lt;100 mg/dl), HOMA‐IR (&lt;2.0), and HbA1C (&lt;5.7%) in all individuals, but one subject displayed impaired glucose tolerance during the OGTT (1 hr post &gt;200 mg/dL, 2hr post &gt;180 mg/dL). Three of five subjects had CRP levels &gt;3.0, suggesting an increased inflammatory state. These preliminary results strongly suggest that cardiometabolic health may be impaired within 3 years after SCI. These biomarkers of altered cardiometabolic health, specifically related to lipid dysregulation, may reflect adipose tissue dysfunction, possibly in response to the accumulation of adipose tissue and/or the decreased physical activity, increased sedentary activity, and skeletal muscle atrophy that typically occurs following a spinal injury. More research is needed to determine the mediators of impaired cardiometabolic health in subjects with SCI and determine effective strategies to mitigate the detrimental effects of SCI on cardiometabolic health.

Association of Bulimia Nervosa With Long-term Risk of Cardiovascular Disease and Mortality Among Women

Bulimia nervosa is associated with short-term cardiovascular complications in women, but its long-term consequences on cardiovascular health are unknown. To study the association of bulimia nervosa with the long-term risk of cardiovascular disease and mortality in women. In this longitudinal cohort study, 416 709 women hospitalized in Quebec, Canada, including women hospitalized for bulimia nervosa and those for pregnancy-related events as a comparison group, were followed up for 12 years from 2006 to 2018 to identify incidences of cardiovascular disease and death. At least 1 hospitalization for bulimia nervosa. The study participants were followed up to identify future incidences of cardiovascular disease and deaths. Cox proportional hazards regression was used to estimate hazard ratios (HRs) and 95% CIs to assess the association of bulimia nervosa with future outcomes after adjustment for patient characteristics. The study population comprised 818 women who were hospitalized for bulimia nervosa (mean [SD] age, 28.3 [13.4] years) and 415 891 hospitalized for pregnancy-related events (mean [SD] age, 28.3 [5.4] years). Patients were followed up for a total of 2 957 677 person-years. The women hospitalized for bulimia nervosa had a greater incidence of cardiovascular disease compared with those hospitalized for pregnancy-related events (10.34 [95% CI, 7.77-13.76] vs 1.02 [95% CI, 0.99-1.06] per 1000 person-years). Incidence of future cardiovascular disease was even higher for women with 3 or more bulimia admissions (25.13 [95% CI, 13.52-46.70] per 1000 person-years). Women hospitalized for bulimia nervosa had 4.25 (95% CI, 2.98-6.07) times the risk of any cardiovascular disease and 4.72 (95% CI, 2.05-10.84) times the risk of death compared with women hospitalized for pregnancy-related events. Bulimia nervosa was found to be associated with ischemic heart disease (HR, 6.63; 95% CI, 3.34-13.13), atherosclerosis (HR, 6.94; 95% CI, 3.08-15.66), and cardiac conduction defects (HR, 2.99; 95% CI, 1.57-5.71). Bulimia was also associated with 21.93 (95% CI, 9.29-51.74) times the risk of myocardial infarction at 2 years of follow-up and 14.13 (95% CI, 6.02-33.18) times the risk at 5 years of follow-up. This study's findings suggest that bulimia nervosa may be associated with the long-term risk of any cardiovascular disease, such as ischemic cardiac events and conduction disorders, as well as with death among women. The findings also suggest that women with a history of bulimia nervosa should be screened regularly for ischemic cardiovascular disease and may benefit from prevention of and treatment for cardiovascular risk factors.

Prospective Study of Dietary Zinc Intake and Risk of Cardiovascular Disease in Women.

Several animal and human studies have shown that zinc is associated with cellular damage and cardiac dysfunction. This study aims to investigate dietary zinc and the zinc-iron ratio, as predictors of incident cardiovascular disease (CVD) in a large longitudinal study of mid-age Australian women (aged 50–61 years). Data was self-reported and validated food frequency questionnaires were used to assess dietary intake. Energy-adjusted zinc was ranked using quintiles and predictors of incident CVD were examined using stepwise logistic regression. After six years of follow-up, 320 incident CVD cases were established. A positive association between dietary zinc intake, zinc-iron ratio and risk of CVD was observed even after adjusting for potential dietary and non-dietary confounders. Compared to those with the lowest quintile of zinc, those in the highest quintile (Odds Ratio (OR) = 1.67, 95% Confidence Interval (CI) = 1.08–2.62) and zinc-iron ratio (OR = 1.72, 95% CI = 1.05–2.81) had almost twice the odds of developing CVD (p trend = 0.007). This study shows that high dietary zinc intake and zinc-iron ratio is associated with a greater incidence of CVD in women. Further studies are required detailing the source of zinc and iron in diet and their precise roles when compared to other essential nutrients.

Carotid magnetic resonance imaging in persons living with HIV and 10-year atherosclerotic cardiovascular disease risk score

Both traditional and HIV-specific risk factors contribute to greater incidence of cardiovascular disease in persons living with HIV (PLWH). Using state-of-the-art, high-resolution magnetic resonance (MR) imaging of the common carotid arteries, this study aimed to evaluate the relationship between carotid vessel wall thickness (c-VWT) and atherosclerotic cardiovascular disease (ASCVD) risk score in PLWH. Cross-sectional determinations of c-VWT using MR imaging in virally suppressed PLWH without known cardiovascular disease (n=32) and matched controls (n=13) were completed. Clinical data, including ASCVD risk and c-VWT, were compared between groups and regression analyses performed to identify predictors of c-VWT. PLWH had significantly higher c-VWT (1.15 ±0.11 mm versus 1.08 ±0.08 mm; P=0.02) as well as higher diastolic blood pressure compared to controls, but exhibited no differences in 10-year ASCVD risk score, systolic blood pressure or smoking. Ten-year ASCVD risk score (r=0.53, P-value =0.0002), age (r=0.30, P-value <0.05), triglycerides (r=0.33, P-value =0.03) and waist circumference (r=0.36, P-value =0.02) were significantly associated with increased c-VWT. Among PLWH, c-VWT did not differ by protease inhibitor use. In a multivariate regression analysis, ASCVD risk score was the only variable significantly associated with c-VWT (P-value =0.02), whereas, HIV status was not. In this cross-sectional study MR imaging demonstrated that c-VWT, a known marker for CVD risk, was increased in PLWH relative to controls, and that 10-year ASCVD risk was closely related to c-VWT, independent of HIV infection. Our data suggest that traditional cardiovascular disease risk factors in PLWH are adequately captured in the ASCVD risk score which was closely associated with subclinical carotid disease.

Epigenetics and Preeclampsia: Programming of Future Outcomes.

Pregnancy is known to induce rapid, progressive, and substantial changes to the cardiovascular system, ultimately facilitating successful pregnancy outcomes. Women who develop hypertensive disorders during pregnancy are considered to have "failed" the cardiovascular stress test of pregnancy and likely represent a subpopulation with inadequate cardiovascular accommodation. Preeclampsia is a serious complication with a myriad of manifestations in both mother and offspring. This pregnancy syndrome is a polygenic disease and has now been linked to a greater incidence of cardiovascular disease. Moreover, offsprings born to preeclamptic mothers exhibit an elevated risk of cardiovascular disease, stroke, and mental disorders during adulthood. This suggests that preeclampsia not only exposes the mother and the fetus to complications during pregnancy but also programs chronic diseases during adulthood in the offspring. The etiology of preeclampsia remains unknown, with various theories being suggested to explain its origin. It is primarily thought to be associated with poor placentation and entails excessive maternal inflammation and endothelial dysfunction. It is well established now that the maternal immune system and the placenta are involved in a highly choreographed cross talk that underlies adequate spiral artery remodeling required for uteroplacental perfusion and free flow of nutrients to the fetus. Although it is not clear whether immunological alterations occur early during pregnancy, studies have proposed that dysregulated systemic and placental immunity contribute to impaired angiogenesis and the onset of preeclampsia. Recently emerged strong evidence suggests a potential link among epigenetics, microRNAs (miRNAs), and pregnancy complications. This chapter will focus on important aspects of epigenetics, immunological aspects, and cardiovascular and vascular remodeling of preeclampsia.

1B.10

Objective:Evidence suggests an interarm difference (IAD) of >=10mmHg in blood pressure (BP) is associated with a greater incidence of cardiovascular disease. Effect of ethnicity on the prevalence of this difference has not been reported.Design and method:The Blood Pressure in Ethnic Groups Study (BP

Vascular Dysfunction and Chronic Obstructive Pulmonary Disease

Chronic obstructive pulmonary disease (COPD) is characterized by low pulmonary function, inflammation, free radical production, vascular dysfunction, and subsequently a greater incidence of cardiovascular disease. By administering an acute oral antioxidant cocktail to patients with COPD (n=30) and controls (n=30), we sought to determine the role of redox balance in the vascular dysfunction of these patients. Using a double-blind, randomized, placebo-controlled, crossover design, patients with COPD and controls were ingested placebo or the antioxidant cocktail (vitamin C, vitamin E, α-lipoic acid) after which brachial artery flow-mediated dilation and carotid-radial pulse wave velocity were assessed using ultrasound Doppler. The patients exhibited lower baseline antioxidant levels (vitamin C and superoxide dismutase activity) and higher levels of oxidative stress (thiobarbituic acid reactive species) in comparison with controls. The patients also displayed lower basal flow-mediated dilation ( P &lt;0.05), which was significantly improved with antioxidant cocktail (3.1±0.5 versus 4.7±0.6%; P &lt;0.05; placebo versus antioxidant cocktail), but not controls (6.7±0.6 versus 6.9±0.7%; P &gt;0.05; placebo versus antioxidant cocktail). The antioxidant cocktail also improved pulse wave velocity in patients with COPD (14±1 versus 11±1 m·s −1 ; P &lt;0.05; placebo versus antioxidant cocktail) while not affecting controls (11±2 versus 10±1 m·s −1 ; P &gt;0.05; placebo versus antioxidant). Patients with COPD exhibit vascular dysfunction, likely mediated by an altered redox balance, which can be acutely mitigated by an oral antioxidant. Therefore, free radically mediated vascular dysfunction may be an important mechanism contributing to this population’s greater risk and incidence of cardiovascular disease.

Diffuse myocardial fibrosis is subclinical and is associated with impaired myocardial deformation characteristics in systemic lupus erythematosus: a cardiovascular magnetic resonance study

Background Systemic lupus erythematosus (SLE) is a systemic autoimmune disorder that commonly affects the heart, resulting in a 7 to 9 times greater incidence of cardiovascular disease (CVD) in SLE patients compared to healthy controls. Female patients with SLE between 35 and 44 years old have an incidence of myocardial infarction over 50 times greater than that observed in the Framingham cohort. Diffuse myocardial fibrosis can be detected non-invasively by extracellular volume (ECV) mapping based on pre- and postcontrast T1 measurements using cardiovascular magnetic resonance (CMR). We aimed to detect subclinical diffuse myocardial fibrosis in SLE using CMR T1 mapping. Methods 23 SLE patients (22 female, mean age 41 ± 9 years) and 23 matched controls (22 female, mean age 42 ± 9 years) without previously known cardiovascular disease underwent CMR at 1.5T. CMR evaluation included late gadolinium enhancement (LGE) [IV gadoterate meglumine at 0.15 mmol/kg], T1 mapping pre- and postcontrast, cine, tagging, and T2-weighted imaging. Results Regional fibrosis on LGE imaging was found in 5 SLE patients (22%) compared to none of controls. Presence of diffuse myocardial fibrosis in SLE was confirmed by significantly higher precontrast T1 values (981 ± 31 vs. 960 ± 21 ms, p = 0.010), decreased postcontrast T1 values (445 ± 31 vs. 470 ± 24 ms, p = 0.005) and expansion of ECV (31.8 ± 4.1 vs. 28.9 ± 2.0 %, p = 0.004). Diffuse myocardial fibrosis was evident in SLE regardless of the presence of any regional fibrosis. Left ventricular volumes, mass and ejection fraction were similar between SLE patients and controls. However, peak systolic circumferential strain (-17.0 ± 1.6 vs. -19.3 ± 1.1, p < 0.001) and peak diastolic strain rate (79 ± 26 vs. 119 ± 15 s-1, p < 0.001) were impaired in SLE. Presence of diastolic dysfunction is SLE was further supported by larger left atrial diameters (31 ± 5 vs. 26 ± 4 mm, p < 0.001). Abnormal myocardial systolic strain and diastolic strain rate correlated with diffuse myocardial fibrosis indices. There was no evidence of myocardial edema in SLE. Conclusions Cardiac involvement is common in SLE patients with no cardiovascular symptoms, and includes both focal and diffuse myocardial fibrosis, which is associated with impaired systolic and diastolic strain parameters. CMR is a robust non-invasive tool for the assessment of diffuse myocardial fibrosis and subclinical cardiac involvement in inflammatory heart disease.

Abstract 350: Influence of HIV-1 Infection and Antiretroviral Therapy on the Coagulation System

HIV-1-infected individuals have a two- to four-fold greater incidence of cardiovascular disease and atherothrombotic events compared with the general population. The mechanisms responsible for this heightened cardiovascular risk are not fully understood. We have previously reported that the capacity of the endothelium to release tissue-type plasminogen activator (t-PA), the primary activator of fibrinolysis and a key endogenous defense mechanism against intravascular fibrin deposition and thrombosis, is impaired in HIV-1-seropositive adults. Whether diminished fibrinolytic activity is coupled with a hypercoagulative state in this population is unknown. Elevations in specific coagulation markers such as tissue factor and Factor VII are associated with increased thrombotic risk. The experimental aim of this study was to determine the influence of HIV-1 infection and antiretroviral therapy (ART) on markers of coagulation. To address this aim we studied 33 men: 16 HIV-1-seronegative (age: 41±3 yr); 7 HIV-1-seropositive treatment-naïve (34±2 yr); and 10 HIV-1-seropositive receiving ART (42±3 yr; efavirenz-based regimen). All subjects were non-obese, normotensive and free of overt cardiometabolic disease. Circulating concentrations of tissue factor, Factor VII, Factor VIII and Factor X were determined by immunoassay. There were no significant differences in plasma concentrations of tissue factor (32+3 vs 40+3 pg/mL), Factor VII (103+9 vs 100+5 %), Factor VIII (111+13 vs 117+8 %) and Factor X (89+5 vs 91+2 %) between HIV-1-seropositive treatment-naïve and healthy men. Moreover, there was no influence of ART on these circulating markers. Plasma tissue factor (41+5 pg/mL), Factor VII (107+6 %), Factor VIII (103+7 %) and Factor X (90+3%) were similar in the HIV-1-seropositive receiving ART compared with HIV-1-seropositive treatment-naïve and seronegative groups. These data suggest that neither HIV-1 infection per se nor ART are associated with unfavorable changes in specific coagulation markers. Thus, changes in the coagulation system that have been linked to increased thrombotic burden are not apparent in HIV-1-seropositive adults.

100 SYSTEMIC LUPUS ERYTHEMATOSUS IS ASSOCIATED WITH IMPAIRED MYOCARDIAL STRAIN AND VASCULAR FUNCTION, INCREMENTAL TO THAT CAUSED BY TRADITIONAL RISK FACTORS: A CARDIOVASCULAR MAGNETIC RESONANCE STUDY

<h3>Introduction</h3> Systemic lupus erythematosus (SLE) is a systemic autoimmune disorder that commonly affects the heart. The impact of SLE on the heart is a 7–9 times greater incidence of cardiovascular disease(CVD) in SLE patients compared to healthy controls. Moreover, female patients with SLE between 35 and 44 years old have an incidence of myocardial infarction over 50 times greater than that observed in the Framingham cohort. The exact cause of this excess CVD burden in SLE is poorly understood, but is thought to be multi-factorial. Cardiovascular magnetic resonance (CMR) has the capacity of simultaneously assessing non-invasively cardiac function, altered vascular distensibility, myocardial strain and fibrosis. <h3>Objective</h3> The purpose of this study was to assess cardiac and vascular function and myocardial strain in patients with SLE and to determine their relation to the presence of cardiovascular risk factors (CVRFs) and SLE disease duration. <h3>Methods</h3> 11 SLE patients with no CVRFs (11 female, mean age 37±7), 19 SLE patients with CVRFs (18 female, mean age 47±11), 39 normal controls (39 female, mean age 45±12), and 11 controls with CVRFs (11 female, mean age 52±9), underwent CMR at 1.5 T. All patients with previously known CVD were excluded. CVRFs, disease activity index and duration of disease were recorded for each subject. Biventricular volumes and function, LGE, myocardial strain and vascular function were assessed by CMR. Aortic distensibility and pulse wave velocity (PWV) were measured in the ascending aorta, proximal descending aorta and distal descending aorta. <h3>Results</h3> There were no differences in left ventricular (LV) volumes and LV ejection fraction between the four groups (table&nbsp;1). SLE patients with CVRFs showed the greatest reduction in mid short axis circumferential systolic strain, peak diastolic strain rate, and vascular indices. SLE patients without CVRFs showed a similar degree of vascular dysfunction and deformational abnormality as controls with CVRFs. Aortic distensibility (Rs=−0.59, p&lt;0.001) and total pulse wave velocity (Rs=0.29, p=0.01) correlated with SLE disease duration (table&nbsp;2). <h3>Conclusions</h3> Evidence of impaired circumferential systolic strain and vascular function in SLE is demonstrated on CMR assessment, which is independent and incremental to that due to traditional CVRFs.

Increased Framingham 10-year CVD risk in Chinese patients with schizophrenia

Background & hypothesisSchizophrenia is associated with increased mortality rates, which has been attributed to the greater incidence of cardiovascular disease (CVD) events. The Framingham risk score (FRS) is a widely-used age- and gender-specific algorithm to estimate 10-year CVD risk and vascular age. The main aim of this study was to determine the cardiovascular risk profile in schizophrenia and examine the effect of metabolic syndrome (MetS) as a predictor of CVD risk. We hypothesized that patients with schizophrenia have an increased 10-year CVD risk. Methods83 Chinese patients with schizophrenia and 243 Chinese community controls were recruited. Their medical and smoking histories were obtained, and anthropometric parameters measured. All subjects provided fasted venous blood samples for lipid and glucose measurements. 10-year CVD risk and the difference between vascular and actual age (VAdiff) for each participant were computed using the FRS and compared between patients and controls. ResultsSchizophrenia patients had a higher mean 10-year CVD risk of 4.6%, as compared with 3.1% in controls, and a greater VAdiff of 4.6years vs. 0.6years. Both smoking and MetS contributed significantly to the 10-year CVD risk in patients with schizophrenia, with smoking having a greater effect than MetS on this risk. ConclusionThis study found a significantly elevated mean 10-year CVD risk and VAdiff in patients with schizophrenia compared with controls. Findings point towards the importance of smoking cessation and screening for MetS to decrease the excess CVD risk in patients with schizophrenia.

Patients with systemic lupus erythematosus have impaired strain and vascular function which is incremental to that caused by traditional risk factors: insights from Cardiovascular Magnetic Resonance

Background Systemic lupus erythematosus (SLE) is a systemic autoimmune disorder that commonly affects the heart. The impact of SLE on the heart is a 7 to 9 times greater incidence of cardiovascular disease (CVD) in SLE patients compared to healthy controls. Moreover, female patients with SLE between 35 and 44 years old have an incidence of myocardial infarction over 50 times greater than that observed in the Framingham cohort. The exact cause of this excess CVD burden in SLE is poorly understood, but is thought to be multi-factorial. Cardiovascular magnetic resonance (CMR) has the capacity of simultaneously assessing non-invasively cardiac function, altered vascular distensibility, myocardial strain and fibrosis. The purpose of this study was to assess cardiac and vascular function and myocardial strain in patients with SLE and to determine their relation to the presence of cardiovascular risk factors (CVRFs) and SLE disease duration.

Sex differences in vascular function: implication of endothelium-derived hyperpolarizing factor

The vascular endothelium plays a crucial role in the regulation of vascular homeostasis by controlling vascular tone, coagulation, and inflammatory responses. These actions are exerted by endothelial factors including nitric oxide, prostacyclin, and endothelium-derived hyperpolarizing factor (EDHF). The greater incidence of cardiovascular disease (CVD) in men and postmenopausal women compared with premenopausal women implies a vasoprotective phenotype of females, which may be influenced by sex hormones. These hormones, particularly estrogen, have modulatory effects on the endothelium and circulating cells that have been implicated in vascular inflammation and in the development of CVD. EDHF seems to be the predominant endothelial factor in the resistance vasculature of females and this mediator could afford the beneficial cardiovascular risk profile observed in premenopausal woman. In this review, we discuss sex differences in EDHF biology and how sex hormones can modulate EDHF responses. We also review the implication of sex hormone-dependent regulation of EDHF in inflammatory processes, platelet function, and repair after vascular damage, each of which have a critical role in several aspects of the pathogenesis of CVD.

Salacia oblonga improves cardiac fibrosis and inhibits postprandial hyperglycemia in obese zucker rats

Diabetes has a markedly greater incidence of cardiovascular disease than the non-diabetic population. The heart shows a slowly developing increase in fibrosis in diabetes. Extended cardiac fibrosis results in increased myocardial stiffness, causing ventricular dysfunction and, ultimately, heart failure. Reversal of fibrosis may improve organ function survival. Postprandial hyperglycemia plays an important role in the development of type 2 diabetes and cardiovascular complications, and has been proposed as an independent risk factor for cardiovascular diseases. Salacia oblonga (S.O.) is traditionally used in the prevention and treatment of diabetes. We investigated the effects of its water extract on cardiac fibrosis and hyperglycemia in a genetic model of type 2 diabetes, the obese Zucker rat (OZR). Chronic administration of the extract markedly improved interstitial and perivascular fibrosis in the hearts of the OZR. It also reduced plasma glucose levels in non-fasted OZR, whereas it had little effect in the fasted animals, suggesting inhibition of postprandial hyperglycemia in type 2 diabetic animals, which might play a role in improvement of the cardiac complications of OZR. Furthermore, S.O. markedly suppressed the overexpression of mRNAs encoding transforming growth factor βs 1 and 3 in the OZR heart, which may be an important part of the overall molecular mechanisms. S.O. dose-dependently inhibited the increase of plasma glucose in sucrose-, but not in glucose-loaded mice. S.O. demonstrated a strong inhibition of α-glucosidase activity in vitro, which is suggested to contribute to the improvement of postprandial hyperglycemia.

Diabetic cardiomyopathy: The significance of creatine

Diabetics exhibit a greater incidence of cardiovascular disease than non-diabetics. The vascular changes that occur are well documented and are thought to promote other clinical manifestations such as cardiomyopathy. Research has shown that the pathogenic events in the myocyte may occur independently of atherosclerotic processes. The atherosclerotic changes in diabetes involve non-enzymatic glycation of extracellular basement membrane proteins. We hypothesize that intracellular glycation events occur in cardiac tissue that alter intermediary metabolism, particularly Cat+ homeostasis, which leads to cell dysfunction. Additionally, we hypothesize that the high steady state intracellular concentrations of unphosphorylated creatine may offer protection against the formation of advanced glycation endproducts by reacting directly with glucose metabolites that may have reached toxic levels in the myocyte of diabetics.

MENOPAUSE AND RISK OF CARDIOVASCULAR DISEASE. THE FRAMINGHAM STUDY

The relation of menopause to cardiovascular disease incidence was examined in women less than 55 years old from the cohort of 2873 women in the initial Framingham examination. Although the number of person-years of experience during the 20 years of observation was nearly the same for premenopausal and postmenopausal status, there were only 20 cardiovascular events among the premenopausal women in this age group whereas 70 events occurred among the postmenopausal women of the same age. In each specific age group studied incidence rates were lower in premenopausal than postmenopausal women. This was also true for coronary heart disease. Contrast for hard diagnoses of cardiovascular disease (excluding diagnoses of angina pectoris and intermittent claudication) was in the same direction. Although cholesterol and hemoglobin did rise somewhat more steeply in women undergoing the menopause, this greater incidence of cardiovascular disease in postmenopausal women could not be explained by the influence of the menopause on the usual cardiovascular risk factors.