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Rationale: Microparticles are cell-derived membrane vesicles, relevant to a range of biological responses and known to be elevated in cardiovascular disease. Objective: To investigate microparticle release during cardiac stress and how this response differs in those with vascular disease. Methods and Results: We measured a comprehensive panel of circulating cell-derived microparticles by a standardized flow cytometric protocol in 119 patients referred for stress echocardiography. Procoagulant, platelet, erythrocyte, and endothelial but not leukocyte, granulocyte, or monocyte-derived microparticles were elevated immediately after a standardized dobutamine stress echocardiogram and decreased after 1 hour. Twenty-five patients developed stress-induced wall motion abnormalities suggestive of myocardial ischemia. They had similar baseline microparticle levels to those who did not develop ischemia, but, interestingly, their microparticle levels did not change during stress. Furthermore, no stress-induced increase was observed in those without inducible ischemia but with a history of vascular disease. Fourteen patients subsequently underwent coronary angiography. A microparticle rise during stress echocardiography had occurred only in those with normal coronary arteries. Conclusions: Procoagulant, platelet, erythrocyte, and endothelial microparticles are released during cardiac stress and then clear from the circulation during the next hour. This stress-induced rise seems to be a normal physiological response that is diminished in those with vascular disease.

Background: Chronic renal disease (CRD) is a well-known risk factor for bleeding complications in acute coronary syndrome patients. Aim: To determine the impact of CRD with ST segment elevation myocardial infarction (STEMI) treated with primary percutaneous coronary intervention (pPCI) on periprocedural complications. Methods: 103 patients with STEMI treated with pPCI were prospectively observed for in-hospital complications and analysed according to kidney function status. Endpoints included clinical and periprocedural outcomes. Major and minor bleedings were reported according to TIMI, REPLACE2 and EASY classifications. Results: Patients with CRD were at greater risk of major bleeding defined by RAPLACE-2 (20.0% vs. 2.7%; p = 0.007) and TIMI(13.3% vs. 1.3%, p = 0.018) classifications and had more grade 2 EASY scale haematomas (20.0% vs. 2.7%; p = 0.007). Vascular access crossover during PCI occurred eight-fold more often among CRD patients (33.3% vs. 4.0%, p < 0.001). Grade 3 TIMI flow was achieved less frequently in CRD patients (60% vs. 89.3%, p = 0.004). CRD predisposed to contrast-induced nephropathy (35.7% vs. 5.7%; p < 0.001) and ischaemic stroke (14.3% vs. 0.0%; p = 0.004). Conclusions: CRD in STEMI patients undergoing pPCI is a risk factor for major and minor bleeding complications including major bleeding, moderate haematomas, contrast-induced nephropathy and ischaemic stroke. Treatment and diagnostic measures should be taken in CRD patients to reduce the severity of periprocedural complications.

Preterm birth is associated with higher blood pressure, which could be because preterm birth alters early aortic elastin and collagen development to cause increased arterial stiffness. We measured central and conduit artery size and multiple indices of arterial stiffness to define the extent and severity of macrovascular changes in individuals born preterm. A total of 102 young adults born preterm and 102 controls who were born after an uncomplicated pregnancy underwent cardiovascular magnetic resonance on a Siemens 1.5 T scanner to measure the aortic cross-sectional area in multiple locations. Ultrasound imaging with a Philips CX50 and linear array probe was used to measure carotid and brachial artery diameters. Carotid-femoral pulse wave velocity and the augmentation index were measured by SphygmoCor, brachial-femoral pulse wave velocity by Vicorder and aortic pulse wave velocity by cardiovascular magnetic resonance. The cardio-ankle vascular index (CAVI) was used as a measurement of global stiffness, and ultrasound was used to assess peripheral vessel distensibility. Adults born preterm had 20% smaller thoracic and abdominal aortic lumens (2.19 ± 0.44 vs. 2.69 ± 0.60 cm(2), P

Background— Preterm birth leads to an early switch from fetal to postnatal circulation before completion of left ventricular in utero development. In animal studies, this results in an adversely remodeled left ventricle. We determined whether preterm birth is associated with a distinct left ventricular structure and function in humans. Methods and Results— A total of 234 individuals 20 to 39 years of age underwent cardiovascular magnetic resonance. One hundred two had been followed prospectively since preterm birth (gestational age=30.3±2.5 week; birth weight=1.3±0.3 kg), and 132 were born at term to uncomplicated pregnancies. Longitudinal and short-axis cine images were used to quantify left ventricular mass, 3-dimensional geometric variation by creation of a unique computational cardiac atlas, and myocardial function. We then determined whether perinatal factors modify these left ventricular parameters. Individuals born preterm had increased left ventricular mass (66.5±10.9 versus 55.4±11.4 g/m 2 ; P r = −0.22, P =0.03). Preterm-born individuals had short left ventricles with small internal diameters and a displaced apex. Ejection fraction was preserved ( P >0.99), but both longitudinal systolic (peak strain, strain rate, and velocity, P P P =0.05 and P =0.006; net twist angle, P =0.02) movement were significantly reduced. A diagnosis of preeclampsia during the pregnancy was associated with further reductions in longitudinal peak systolic strain in the offspring ( P =0.02, n=29). Conclusions— Individuals born preterm have increased left ventricular mass in adult life. Furthermore, they exhibit a unique 3-dimensional left ventricular geometry and significant reductions in systolic and diastolic functional parameters. Clinical Trial Registration— URL: http://www.clinicaltrials.gov . Unique identifier: NCT01487824.

Risk of hypertension in mother and offspring after preeclampsia is greater if preeclampsia develops early in pregnancy. We investigated whether those who develop early onset disease have unique adverse blood pressure characteristics. One hundred forty women were studied 6 to 13 years either after a pregnancy complicated by preeclampsia (45 women with early onset preeclampsia before 34 weeks gestation and 45 women with late-onset preeclampsia) or after a normotensive pregnancy (50 women). Forty-seven offspring from these pregnancies also participated. Data on maternal antenatal and postnatal blood pressures were extracted from maternity records and related to peripheral, central, and ambulatory blood pressure measurements in later life. Compared with late-onset preeclampsia, early onset preeclampsia was associated with higher diastolic blood pressure 6 weeks postnatally (86.25±13.46 versus 75.00±5.00 mm Hg, P P =0.04, and 67.00±7.25 versus 58.60±5.79 mm Hg, P =0.002). Furthermore, at age 6 to 13 years their offspring had higher systolic blood pressure compared with those born to late-onset preeclampsia (96.27±7.30 versus 88.39±7.57 mm Hg, P =0.005). Mothers who developed early onset preeclampsia, and the offspring of that pregnancy display specific adverse blood pressure characteristics later in life. These are not evident in mothers and offspring after late-onset preeclampsia or normotensive pregnancy.

AIMS: As obesity-related cardiovascular mortality, although elevated when compared with normal weight, is lower in females than in males at every body mass index (BMI) level, we aimed to investigate gender-specific differences in left ventricular (LV) hypertrophy in obesity, which themselves have been shown to have varying prognostic value. METHOD AND RESULTS: In total, 741 subjects (female, n = 399) without identifiable cardiovascular risk factors (BMI 15.7-59.2 kg/m(2)) underwent cardiovascular magnetic resonance (1.5 T) to determine LV mass, end-diastolic volume (EDV, mL), and LV mass/volume ratio (LVM/VR). Across both sexes, there was a strong positive correlation between BMI and LV mass (male r = 0.44, female r = 0.57, both P < 0.001), with males showing a greater LV hypertrophic response (male +2.3 vs. female +1.6 g per BMI point increase, P = 0.001). Concentric hypertrophy was present in both sexes and LVM/VR positively correlated to BMI (male r = 0.45, female r = 0.29, both P < 0.001) on linear regression analysis. However, the degree of concentric hypertrophy was greater in males (male +0.13 vs. female +0.06 LVM/VR increase per BMI point increase, P = 0.001). On the other hand, females showed a greater LV cavity dilatory response (female +1.1 vs. male +0.3 mL per BMI point increase, P < 0.001). Indeed, in contrast to females, where BMI and LV-EDV were positively correlated (r = 0.38, P < 0.001), BMI did not correlate with EDV in men (r = 0.03, P = 0.62). CONCLUSION: In the absence of traditional cardiovascular risk factors, obese men show predominantly concentric hypertrophy, whereas obese women exhibit both eccentric and concentric hypertrophy. As concentric hypertrophy is more strongly related to cardiovascular mortality than eccentric hypertrophy, our observations may explain the observed gender difference in obesity-related mortality.

BACKGROUND AND OBJECTIVE: Preeclampsia is an independent cardiovascular risk factor for the mother, and recent studies reveal that offspring of affected pregnancies also may have an increased cardiovascular risk. Our objective was to examine evidence for increased cardiovascular risk factors in children exposed to preeclampsia in utero. METHODS: We performed a systematic review and meta-analysis on studies reporting traditional cardiovascular risk factors in those exposed to preeclampsia compared to controls. Information was extracted on the classic cardiovascular risk factors, including blood pressure, lipid profile, glucose metabolism, and BMI from articles published between 1948 and August 2011 in Medline and Embase. RESULTS: Eighteen studies provided cumulated data on 45 249 individuals. In utero exposure to preeclampsia was associated with a 2.39 mm Hg (95% confidence interval: 1.74–3.05; P < .0001) higher systolic and a 1.35 mm Hg (95% confidence interval: 0.90–1.80; P < .00001) higher diastolic blood pressure during childhood and young adulthood. BMI was increased by 0.62 kg/m2 (P < .00001). Associations were similar in children and adolescents, for different genders, and with variation in birth weight. There was insufficient evidence to identify consistent variation in lipid profile or glucose metabolism. CONCLUSIONS: Young offspring of pregnancies complicated by preeclampsia already have increased blood pressure and BMI, a finding that may need to be considered in future primary prevention strategies for cardiovascular disease.

Summary Across both genders, obesity, in the absence of traditional cardiovascular risk factors, is characterized by concentric LV remodeling. Whereas males show predominantly concentric remodeling, females exhibit eccentric and concentric hypertrophy. This may explain the observed gender difference in obesity related cardiovascular mortality. Background Obesity related cardiovascular mortality, although elevated when compared to normal weight, is lower in females (♀ )t han males ( ♂ )a t every body mass index (BMI) level. Given the fact that males have less fat tissue than females at each BMI level, the reasons behind this trend are unlikely to be attributable to the effects of excess adiposity alone. As different patterns of left ventricular (LV) remodeling have been shown to have varying prognostic value, with concentric hypertrophy being more strongly predictive of cardiovascular mortality than eccentric hypertrophy, our aim was to investigate whether sex-specific differences in LV remodeling could provide an additional explanation for the observed gender difference in obesity related mortality. Methods 703 subjects (♀ n= 390, ♂ n=313) without identifiable cardiovascular risk factors, (BMI range 15.7-59.2 Kg/ M2) underwent cardiovascular magnetic resonance at 1.5 Tesla for the assessment of LV mass (g), enddiastolic volume (EDV; ml) and LV mass/volume ratio (LVM/VR).

Summary Robust pre-contrast reference T1 values using ShMOLLI in 231 normal human controls aged 11 to 81 years demonstrate little dependence on gender, age or heart rates. Background Quantitative T1-mapping is rapidly becoming a clinical Cardiovascular Magnetic Resonance (CMR) imaging tool that can distinguish normal from diseased myocardium. The usefulness of any quantitative measurement to identify disease lies in its ability to detect significant differences from an established normal range of values. In this study we aim to establish a large database for the normal range of T1 values in healthy human myocardium and to examine any differences based on age and gender.

BACKGROUND: A phenomenon of endothelial impairment, independent of classical cardiovascular risk factors, has been observed in young people. We identified subjects with persistently reduced, or declining, endothelial function during adolescence and early adulthood, without apparent cardiovascular risk, and investigated the clinical relevance of this finding. METHODS: Endothelial vasomotor responses were assessed by brachial artery flow-mediated dilatation (FMD) at age 15 years in 47 subjects (22 males) who returned for a repeated measurement at age 25. Subjects underwent quantification of left ventricular mass (LVM) and function by cardiovascular magnetic resonance, central arterial stiffness by applanation tonometry, and common carotid artery intima-media thickness using ultrasound on their visit at age 25. RESULTS: Individuals with low average FMD over 10-year period, although normotensive, had 5 mm Hg higher systolic blood pressure and, significantly greater LVM (73.48 ± 7.73 vs. 56.25 ± 9.54 g/m(2), P = 0.0001), carotid intima-media thickness (cIMT) (0.53 ± 0.06 vs. 0.47 ± 0.04 mm, P = 0.03), and pulse wave velocity (5.97 ± 0.63 vs. 5.29 ± 0.59 m/s, P = 0.02) than those with higher endothelial responses. Subjects with the greatest decline in FMD over 10 years had a significant increase in mean arterial pressure but similar cardiovascular phenotype. CONCLUSION: Persistently reduced, or declining, endothelial function during adolescence, in the absence of overt cardiovascular disease, is a sensitive early marker associated with subclinical changes in blood pressure (BP) and an adverse cardiovascular phenotype. The findings highlight the potential importance of endothelial responses during adolescence in primary prevention strategies for hypertension.

Vascular endothelial dysfunction is a key biological process underlying the development of cardiovascular disease and therefore of potential importance as a target for gene-based therapy. Modification of nitric oxide bioavailability through gene therapy is possible in animal studies and of clinical relevance because of the central role for nitric oxide in vascular homeostasis. However, most clinical trials have so far focused on endothelial-related pathways, in particular, vascular endothelial growth factor, to induce angiogenesis, with variable results. The slow progress of the development of gene-therapy targeted at the endothelium relates to a range of complexities of design of therapy including mode of gene delivery. This is usually achieved through the use of viral or non-viral vectors but the best physical and vector methods for delivery of complimentary DNA to the vascular endothelium remains under investigation. More recently there has been emerging interest into other genome-based methods to alter vascular phenotype, in particular, gene-based modification of endothelial progenitor cell function and whether gene function might be modifiable through induced epigenetic changes.

Activation of peroxisome proliferator-activated receptor-gamma (PPARgamma) signaling after stroke may reduce brain injury, but this effect will depend on the levels of receptor and cofactors. Here, we showed that the direct effect of PPARgamma signaling to protect neurons from ischemic injury requires a novel cofactor LMO4, because this effect was lost in LMO4-null cortical neurons. PPARgamma agonist also failed to reduce cerebral infarction after transient focal ischemia in CaMKIIalphaCre/LMO4loxP mice with LMO4 ablated in neurons of the forebrain. Expressing LMO4 in LMO4-null cortical neurons rescued the PPARgamma-protective effect. PPARgamma signaling activates the promoter of the antioxidant gene SOD2 and this process requires LMO4. Addition of a superoxide dismutase mimetic MnTBAP [manganese(III)tetrakis(4-benzoic acid)porphyrin] bypassed the deficiency in PPARgamma signaling and was able to directly rescue LMO4-null cortical neurons from ischemic injury. Like LMO4, PPARgamma and PGC1alpha (PPARgamma coactivator 1alpha) levels in neurons are elevated by hypoxic stress, and absence of LMO4 impairs their upregulation. Coimmunoprecipitation and mammalian two-hybrid assays revealed that LMO4 interacts in a ligand-dependent manner with PPARgamma. LMO4 augments PPARgamma-dependent gene activation, in part, by promoting RXRalpha (retinoid X receptor-alpha) binding to PPARgamma and by increasing PPARgamma binding to its target DNA sequence. Together, our results identify LMO4 as an essential hypoxia-inducible cofactor required for PPARgamma signaling in neurons. Thus, upregulation of LMO4 expression after stroke is likely to be an important determinant of neuron survival.

Objectives Offspring of hypertensive pregnancies have increased cardiovascular risk factors during childhood. We hypothesised that offspring of hypertensive pregnancies would demonstrate increased clinical levels of hypertension by young adult life, which would be proportional to the severity of the pregnancy complication. Design Prospective birth cohort study Setting Tertiary obstetric hospital. Participants 2868 young adult offspring of women enrolled during pregnancy into the Western Australia Pregnancy Cohort (Raine) Study. Main outcome measures Cardiovascular risk, including incidence of hypertension and metabolic disease, in those born to hypertensive compared to normotensive pregnancies. Results Young adult offspring of hypertensive pregnancies were 2.5 times (95% CI 1.32 to 4.56, p=0.004) more likely to have global lifetime risk (QRISK) scores above the 75th centile. Thirty per cent of 20 year olds with hypertensive blood pressures were born following a hypertensive pregnancy. Pre-eclampsia or hypertension resulting in preterm birth associated with a threefold (95% CI 1.3 to 7.0, p=0.01) greater risk of being hypertensive by age 20 years, with no differences in body mass index. Whereas pregnancy-induced hypertension associated with a smaller 3±1 mm Hg blood pressure rise (p=0.001) and a twofold (95% CI 1.5 to 2.8, p=0.001) greater risk of being obese or overweight. Risk factor associations were consistent throughout early life and independent of other birth-factors. Conclusions Incidence of offspring hypertension was significantly increased in those whose mothers had a more complicated pregnancy history, including preterm birth and pre-eclampsia.

Objective Children born to hypertensive pregnancies are known to have higher levels of cardiovascular risk factors. We studied whether by age 20 years they have developed hypertension or metabolic disorders that may warrant intervention. Methods We quantified cardiovascular risk in young adults born to hypertensive pregnancies using data fromthe 2868 offspring of women enrolled during pregnancy into Western Australia Pregnancy Cohort (Raine) Study, taking into account whether risk varies with severity of the hypertensive pregnancy syndrome and degree of prematurity. Results Young adults born to hypertensive pregnancies accounted for 30% of those with hypertensive blood pressures at age 20 years. Detailed pregnancy medical records demonstrated that a more complicated history, characterised as preeclampsia or preterm birth due to maternal hypertension, associated with a 3-fold (95% CI 1.3 to 7.0, p = 0×01) greater risk of hypertension, whereas, pregnancy-induced hypertension at term associated with a smaller blood pressure rise. Although incidence of overweight and obesity was 2-fold (95% CI 1.5 to 2.8, p = 0×001) higher in the pregnancy-induced hypertension group, body size did not account for blood pressure variation in either group and metabolic risk markers did not vary. Associations were consistent throughout life and independent of other birth-related factors. Conclusions Adults born following a complicated hypertensive pregnancy are significantly more likely to be hypertensive by age 20 years and exhibit a specific hypertensive phenotype without metabolic changes. Consideration of maternal pregnancy history may be of value to provide insight into why some young adults present with hypertension.

Background Preterm birth leads to a switch from fetal to postnatal circulation before completion of in utero cardiac development. We hypothesised that those born preterm would have a unique adult cardiac phenotype and that this would develop during postnatal life. Methods 234 young adults underwent cardiovascular magnetic resonance, of which 102 had been followed prospectively since preterm birth. We then studied 200 infants, longitudinally from birth to three months of age using echocardiography, of which 111 were born preterm. To define cardiac shape and function in adult and neonatal life we developed in-house 3D computational approaches and applied novel deformation imaging tools. Results born preterm had increased LV and RV mass index ( P .001 and P .001), proportional to severity of prematurity ( P = 0 .03 and P .001), and reduced chamber volumes and length (P P = 0 .006), as were LV systolic and diastolic myocardial deformation. At birth, preterm-born infants had similar LV mass index, appropriate for gestational body size, as term-born infants ( P = 0 .13). However, by three months a greater percentage increase ( P = 0 .01) resulted in significantly greater LV mass index in those born preterm (P = 0 .04). Interestingly, their LV end-diastolic volume index was already smaller at birth ( P = 0 .003) and this difference persisted at three months ( P = 0 .05). Conclusions Birth is associated with a unique adult cardiac phenotype. Disproportionate increases in mass occur during postnatal life alongside persistent shape changes. Postnatal life may be a critical window for modification of cardiac development, relevant to the adult cardiovasculature.

Introduction Young adults with cardiovascular risk factors, such as hypertension, may gain long-term risk benefits from effective targeted lifestyle interventions. We compared the effectiveness of lifestyle interventions with defined physical activity components targeting change in blood pressure, in young adults (aged 20 to 40) with established cardiovascular risk factors. Methods We searched databases including CENTRAL, MEDLINE, EMBASE, CINAHL (from earliest dates available to May 2014) and assessed reference lists of relevant articles for potential titles. Study selection criteria including: randomised control trials with at least 12 weeks follow-up; reporting blood pressure as the primary outcome; targeting participants aged between 20 to 40 years or within one standard deviation of this age range. Four authors (WW, PK, AL, HR), independently screened the eligibility of trials. Titles selected for full review were discussed and disagreement settled with an independent pair of authors (CF and PL). Meta-analysis was completed using Review Manager (RevMan) Version 5.2 using a random effects model imputing post intervention blood pressures. Study protocol available on PROSPERO 2014:CRD42014009604. Results 13 studies satisfied all inclusion criteria, baseline mean age of participants was 42.7 years (SD 6.4) (n = 3338). 11 trials targeted increased moderate to vigorous physical activity (MVPA) either via supervised exercise (n = 8) or via behavioural counselling (n = 3). One trial investigated effects of resistance exercise and 1 study implemented a yoga trial. Meta-analysis was restricted to the trials targeting increased MVPA with analysis performed according to duration of follow-up. In total 10 studies (n = 2716) reported 3 to 6 months outcomes, mean reduction in systolic BP was –4.4 mmHg (95% CI -5.8 to -3) and mean reduction in diastolic BP was –4.3 mmHg (95% CI -5.6 to -3.0). The effects of intervention on blood pressure at 3 to 5 year follow-up (3 studies, n = 2553) was positive but with significant heterogeneity. Mean reduction in systolic BP was -1.3 mmHg (95% CI -2.9 to 0.3, I 2 80%) and mean reduction in diastolic BP was –1.2 mmHg (95% CI -2.3 to -0.2, I 2 74%). Conclusions Our review found that interventions targeting an increased dose of MVPA through supervised and self-directed programmes achieved significant short-term improvements in blood pressure. However, studies targeting blood pressure reduction in participants below the age of 40 years with cardiovascular risk factors are limited in number. The clinical and statistical heterogeneity of the studies limits conclusions on the effectiveness of individual components of the interventions. It remains unclear how to translate short-term intervention effects into sustained reduction in blood pressure and cardiovascular risk. As understanding increases of young adult populations predisposed to early cardiovascular disease more research is needed on primary and secondary prevention in these groups.

A pregnancy complicated by preeclampsia identifies both a mother and child with an unusual predisposition to develop cardiovascular diseases.1,2 Therefore, characterization of biological pathways common to both preeclampsia and cardiovascular disease may provide novel insights into both conditions.3 One particular area of interest is whether known triggers for preeclampsia, such as hypoxia, inflammation, and angiogenic imbalance, may also trigger the cardiac dysfunction that has been observed in women with preeclampsia.4 Article see p 734 Early in pregnancy, women who subsequently develop preeclampsia display an increased cardiac output compared with women who have a normotensive pregnancy5,6 (Table). As the clinical syndrome of preeclampsia develops the cardiac output significantly drops,5,10,12 a change that coincides with increases in total vascular resistance. Some studies report a reduction in left ventricular ejection fraction, although within normal limits,11 and tissue Doppler imaging has been used to demonstrate reduced cardiac longitudinal systolic function. Diastolic function, assessed by mitral valve inflow and tissue Doppler imaging of the mitral annulus, …

Introduction Offspring born to hypercholesterolaemic mothers have increased fatty streak formation in the fetal aorta, which persists into adolescence. To understand whether exposure to elevated cholesterol in early life, independent of a maternal history of hypercholesterolaemia, also has a long-term impact on the cardiovascular system we studied the vascular phenotype of adults in whom cholesterol levels were artificially elevated for a short period postnatally. Methods We prospectively followed-up 102 subjects born premature now aged 23 to 28 years. Individuals exposed to maternal hypercholesterolaemia were excluded. 18 received intravenous (IV) lipids during the first nine weeks of life and were matched 2:1 for pregnancy and early life complications, age, sex, birthweight and gestational age with controls that did not receive IV lipids. Aortic pulse wave velocity (aPWV), regional aortic distensibility, left ventricular mass and ejection fraction were determined by cardiovascular magnetic resonance. Detailed lifestyle information and anthropometric measurements were collected during childhood and adolescence. Metabolic parameters were measured multiple times per week for the first 9 weeks of life and again at follow-up visits. Results Individuals that received IV lipids achieved significantly higher maximum cholesterol levels during the first 9 weeks of life than those that did not (mean±SD=4.38±1.65 vs 3.12±0.78 mmol/l, p=0.006). Dose given and number of days on IV lipids also associated with maximum cholesterol level during this period (r=0.557, p 3 , p=0.012). There were no differences between the groups in other vascular or left ventricular measures. In a stepwise regression model, maximum cholesterol level achieved in the first few weeks of life was an independent predictor of aPWV in young adulthood (β=0.596, p Conclusions Brief artificial elevation of cholesterol level in immediate postnatal life is associated with long term changes in aortic function independent of later cholesterol levels. The association is graded depending on the degree of elevation of circulating cholesterol. High cholesterol exposure during sensitive periods of early postnatal life may have long term impacts on the cardiovascular system.

Background Although it is widely accepted that obesity is related to increased aortic size, to date, there is no large study assessing the effect of obesity, in the absence of co-morbidities, on regional aortic diameter. In addition, despite the fact that magnetic resonance imaging (MRI) is generally regarded as the gold standard technique for imaging the aorta, the vast majority of data comes from 2D echo, which has marked limitations in the setting of obesity. As a result, we aimed to use MRI to 1) establish a large

Background In the elderly, reduced left ventricular function is related to elevated carotid intima media thickness (IMT), a well-established subclinical marker of atherosclerosis. Cardiovascular magnetic resonance (CMR) allows for precise quantification of changes in myocardial structure and function. We therefore sought to determine if in young adults, without overt cardiovascular risk factors, there was already evidence of early changes in systolic function related to subclinical atherosclerosis. Methods We studied 81 individuals (44 females, 37 males) without cardiovascular risk factors and with a mean age of 28.42±5.36 years (mean±SD). Peak mid-ventricular myocardial circumferential systolic strain and left ventricular mass adjusted for body surface area (LVM) were assessed by CMR. Carotid IMT was measured as a marker of subclinical atherosclerosis using ultrasound. Demographic and anthropometric characteristics were measured as well as metabolic parameters and peripheral and central blood pressure. Results Individuals with reduced peak myocardial circumferential systolic strain had higher carotid IMT (r=0.392, p Conclusions We have shown for the first time that subclinical changes in cardiac function and subclinical atherosclerosis are closely interrelated in young adults, with associations that extend to those in the normal range of cardiovascular risk. This study further establishes the ability of CMR to detect early changes in cardiovascular disease development.

Introduction and objectives Primary percutaneous coronary intervention infarction became the preferred method of treatment for myocardial ST segment elevation. Improved safety was reported in transradial access (radial) compared to transfemoral access (femoral). The aim of this study was to compare the cost between the two access points in ST segment elevation myocardial infarction. Methods This is a subanalysis of the OCEAN RACE trial in which 103 myocardial infarction patients were randomized to either the radial (n=52) or femoral (n=51) groups. The clinical safety and efficacy were recorded during the hospital stay. The procedural metrics were meticulously logged, and costs were evaluated using the micro-cost method. The indirect costs were estimated using the human capital approach. Results Clinical success was numerically higher in the radial group (90.4 vs. 80.4%, p=0.123). There were no differences in major adverse cardiac events (9.6% vs. 11.8%, p=0.48) and death (2.0% vs. 6.0%, p=0.31). The average in-hospital cost per patient was 2,740 ± 1,092 EUR. The cost of therapeutic success was lower in the radial group at 3,060 EUR vs. 3,374 EUR. The indirect costs related to absence at work were 138 EUR per patient, which were lower in the radial group compared to the femoral group. Conclusions The total in-hospital costs were similar between the study groups. The indirect costs were lower in the radial group. Introduction of radial access as the default approach in all centers may significantly reduce the overall financial burden from a social perspective.

Previous studies have shown that myocardial steatosis occurs with age, diabetes, and the metabolic syndrome and that myocardial triglyceride content (MTGC) is related to concentric left ventricular hypertrophy (LVH) [(1)][1] and diastolic dysfunction [(2)][2], suggesting a direct negative effect on

Background Excess body fat is a known risk factor for cardiovascular mortality and morbidity. However, obesity, hypertension, hyperlipidaemia and insulin resistance are closely interlinked, both in their causes (eg sedentary lifestyle, social class, diet & age) and effects (endothelial function, increased left ventricular mass, increased myocardial fatty acid uptake). Thus it has been difficult to determine the exact effects of excess weight alone on myocardial function and metabolism. Myocardial triglyceride deposition and impaired strain have been clearly shown in adult diabetic cardiomyopathy. Recently, similar findings have been demonstrated in obese non-diabetic women. We set out to see if obesity alone, in the absence of other components of the Metabolic Syndrome, was also associated with cardiac steatosis and/or impaired peak circumferential strain in adults of both sexes and in adolescent boys. Methods We recruited 100 adults (44 lean, 28 overweight & 28 obese) and 22 boys aged 10-15 years (11 lean & 11 obese) by open poster advertisement. Exclusion criteria were heart failure, valvular disease, the use of any cardiovascular medications and any classical risk factors (hypertension, hyperlipidaemia, diabetes mellitus, smoking and obstructive sleep apnoea). Body mass index (BMI) and waist circumference were measured in all subjects. Left ventricular (LV) mass, volumes, function and peak circumferential strain were measured with 3T cardiac MR imaging and tagging. Myocardial triglyceride content (MTGC) was determined by ECG-gated localised proton spectroscopy to calculate the lipid : water ratio in the interventricular septum. Image and spectroscopy data were anonymised prior to analysis. Results There was a clear increase in myocardial lipid content in overweight and obese adults compared to the lean control group (Figure 1). Body mass index and waist circumference were associated with a linear increase in MTGC (a 10kg/m 2 increase in BMI was associated with a 48% increase in MTGC, p < 0.05), but gender had no impact. There was also an 11% reduction in the peak circumferential strain of obese adults compared to their lean peers (median -18.0 v -21.4, p = 0.01), despite similar LV ejection fractions. LV mass was 16% higher in overweight and 20% higher in obese adults (p

Background Cardiac MRI has become the reference imaging modality used to assess left ventricular (LV) remodelling. Ventricles are generally characterised by bulk metrics such as cavity volume, mass or wall thickness. We introduce a workflow that aims to improve the stratification power of conventional analysis by providing 3D shape metrics through the construction of computational cardiac atlases.

Background Cardiovascular magnetic resonance (CMR) allows quantification of early changes in systolic myocardial function. In the elderly, reduced left ventricular systolic function is related to elevated carotid intima media thickness (IMT), a well-established marker of atherosclerosis. We therefore sought to determine if peak myocardial systolic strain was also related to subclinical variation in carotid IMT and cardiovascular risk factors in young adults. Methods We recruited 68 individuals (39 females, 29 males) with a mean age of 28.29±5.45 (mean±SD). Peak midventricular myocardial circumferential systolic strain and left ventricular mass adjusted for body surface area (LVM) were assessed by CMR. Carotid IMT was measured as a marker of subclinical atherosclerosis using ultrasound. Demographic and anthropometric characteristics were measured as well as metabolic parameters and peripheral blood pressure. Results Individuals with reduced peak myocardial circumferential systolic strain had higher carotid IMT (r=0.406, P=0.001). Elevated total cholesterol and waist to hip ratio were both significantly associated with reduced myocardial strain. Increased LVM, peripheral systolic blood pressure, pulse pressure, glucose, triglycerides, age, BMI and WHR, as well as reduced HDL, were all significantly associated with increased carotid IMT (P

Background and aim Obesity confers an enormous burden of cardiovascular morbidity and mortality worldwide. Lipotoxicity has been implicated as a potential common pathway in myocyte dysfunction and ultimately apoptosis. Fat deposition in the peritoneum, the liver and around vascular structures has been linked to metabolic syndrome and subsequent cardiomyopathy. Therefore this study sought to determine the relationship between excess body fat and intracardiac lipids as assessed by 3T proton spectroscopy in women. Methods