High Risk For Coronary Disease Research Articles

Association of Lipoprotein (a) With Coronary-Computed Tomography Angiography-Assessed High-Risk Coronary Disease Attributes and Cardiovascular Outcomes.

Lipoprotein(a) [Lp(a)] is a risk factor for cardiovascular events. This study evaluated the relationship between Lp(a) and high-risk attributes by coronary computed tomography angiography as well as their prognostic value. Lp(a) and coronary computed tomography angiography from 377 consecutive patients at Zhongshan Hospital (Shanghai, China) were evaluated. High-risk attributes were defined as high-risk morphological attributes (low attenuation plaque, positive remodeling, napkin-ring sign, spotty calcification, minimum lumen area <4 mm2, or plaque burden [ratio between cross-sectional plaque area at the site of maximum stenosis and cross-sectional vessel area] ≥70%); inflammatory attribute represented by fat attenuation index; high-risk physiological attributes [lesion-specific ischemia defined by fractional flow reserve by coronary computed tomography angiography ≤0.8, physiologic diffuseness defined by fractional flow reserve by coronary computed tomography angiography pullback pressure gradient]. Total plaque volume in mm3 was also quantified. Quintiles or binary classification of Lp(a) levels were used to evaluate its relationships with plaque features and clinical outcomes with ANOVA, Cox models, and log-rank tests, as appropriate. The major adverse cardiovascular event included cardiovascular death, nonfatal myocardial infarction, and target vessel revascularization. Lp(a) was significantly associated with total plaque volume (P=0.004), fat attenuation index (P=0.031), and fractional flow reserve by coronary computed tomography angiography pullback pressure gradient (P=0.038). Patients with a high Lp(a) level had a higher total plaque volume (393.3 mm3 versus 293.9 mm3, P<0.001), lower pullback pressure gradient (0.62 versus 0.69, P=0.023), higher fat attenuation index (-70.5HU versus -73.9HU, P=0.004), and higher incidence of major adverse cardiovascular event (14.5% versus 6.3%, adjusted hazard ratio: 2.52, 95% CI: 1.12-5.63, P=0.025). In a 4-group classification according to Lp(a) and high-risk attributes, patients with high Lp(a) and ≥3 high-risk attributes had the highest risk of major adverse cardiovascular event (25.9%; overall P<0.001). Causal mediation analysis revealed that around 40% of the prognostic effect of Lp(a) was mediated by high-risk attributes. Lp(a) level is associated with coronary computed tomography angiography high-risk characteristics, including morphologic, physiologic, and inflammatory attributes as well as major adverse cardiovascular event. This effect is partly mediated by inflammation and vulnerable plaque. URL: https://www. gov; Unique identifier: NCT05323227.

Design and Characterization of Sustained Release Tablet Formulation Containing Metformin Hydrochloride and Simvastatin

The aim of the present work was to develop pharmaceutical combinational dosage form for simultaneous treatment of patients with type 2 diabetes with at high-risk of coronary disease associated co-morbidities. Metformin, an antidiabetic drug is used to treat the diabetic patient and combined with Simvastatin which is HMG-CoA reductase inihibitor drug to treat the high-risk coronary disease simultaneously. In this formulation, three batches were prepared by the direct compression method. Preformulation parameters such as identification, solubility, melting point, compatibility studies, Pre-compression parameters such as bulk density, tapped density, angle of repose, Hausner ratio, compressibility index, and Post-compression parameters like weight uniformity, hardness, drug content, thickness, in-vitrodrug release. In-vitrodrug release of all formulations, B1, B2, and B3 was carried out in 0.1N HCl for 2hrs and 10 hrs in phosphate buffer (pH 6.8) dissolution media. Among all the formulations, B3 was an optimized batch. B3 formulations showed drug release of 85% for Metformin Hydrochloride and 93% for Simvastatin over a period of 12hrs.©2022iGlobal Research and PublishingFoundation. All rights reserved.

Cardiovascular Disease Continuum

Peripheral artery disease (PAD) is an occlusive disease of extremities, which used to be diagnosed and treated as an isolated disease of the limbs or other parts of the body. Nowadays, the role of PAD transcends the affected limb; instead, the cardiovascular system must be observed as a whole, with PAD having a prognostic role. About 200 million people are affected by PAD worldwide. The prevalence of PAD is likely to increase steadily in the future due to the global aging of the population and the predominantly sedentary lifestyle, along with the expected universal increase in the major PAD risk factors such as smoking habit, diabetes mellitus, dyslipidemia and hypertension. Patients with PAD are at a higher risk of coronary disease and cardiovascular events in comparison to healthy control subjects. The severity of PAD correlates with the development and complications of cardiovascular disease. In PAD patients, percutaneous coronary intervention is more demanding, associated with more comorbidities, more complex lesions, and poorer procedural success as compared with PAD-free patients. For a year now, the use of antiplatelet therapy with acetylsalicylic acid in combination with low (vascular) dose of a direct oral anticoagulant has been recommended for cardiovascular and lower limb protection in PAD patients. In the future, we expect a better understanding of atherosclerotic disease, stronger modulation of systemic inflammation, and the discovery of new therapies. In the meantime, it is necessary to identify the risk population and aggressively treat the classic factors – control of blood pressure, glycemia and lipids with antiplatelet and new anticoagulant therapy. The goal is to protect the limb and preserve the cardiovascular continuum. The negative consequences of COVID- 19 on treatment CVD will be estimated in the following years.

Procedure and Effectiveness of Extracorporeal Membrane Oxygenation in Percutaneous Coronary Intervention for High-risk Complex Coronary Disease

Objective: It has been demonstrated that performing percutaneous coronary intervention (PCI) in the absence of mechanical circulation support (MCS) for patients with complex high-risk coronary artery disease bears a high risk. Alternatively, to figure out the procedure effectiveness and the mid-term prognosis of PCI for complex high-risk coronary artery disease, we accomplished the whole process by the assistance of extracorporeal membrane oxygenation (ECMO). Methods: Between July 2016 and October 2017, 6 consecutive complex and high-risk coronary disease patients underwent routine ECMO-supported PCI. Results: The average age of the patients was 70.5±11.98, and half of them (50%) were male. The mean creatinine (Cr) was 188.67±151.68 µmol/L. The average scores for SYNTAX, SYNTAX II, and LVEF pre the procedure was 41.33±12.14, 47.87±9.45 / 31.55±8.82, and 44.40±12.58%, respectively. The mean supporting duration of ECMO was 10.50±7.79 h. Regarding the postoperative complication, one case observed lower limp venous thrombosis and another reported infection at the access site. Two patients (33.3%) died for refractory heart failure during the follow-up course of 17.00±9.51 months, and the average net improvement index (NII) was 28.30±25.11% for this period. Conclusion: With the support of ECMO, the prognosis of complex high-risk coronary disease has shown to be improved by intervention in our study.

Invasive therapy improved angina health status in patients with high-risk stable coronary disease and more frequent angina.

Spertus JA, Jones PG, Maron DJ, et al. Health-status outcomes with invasive or conservative care in coronary disease. N Engl J Med. 2020;382:1408-19. 32227753.

The relationship between sleep problems and cortisol in people with type 2 diabetes

BackgroundSleep problems are linked with negative health outcomes, including coronary heart disease. Neuroendocrine dysfunction has been associated with sleep problems and may be a pathway linking sleep and ill health. Dysregulated cortisol output has observed in people with type 2 diabetes (T2D), though little is known about the links between sleep and cortisol in this population at high risk of coronary disease. MethodThis study investigated the association between sleep problems and cortisol over the course of an ordinary day and in response to acute laboratory stress in a sample of 129 individuals with T2D. Sleep problems were assessed using the Jenkins sleep problems questionnaire. Mental stress was induced using two five-minute laboratory stress tasks: a mirror-tracing task and the Stroop color-word interference task. ResultsSleep problems were positively associated with daily cortisol area under the curve (B = 17.051, C.I. = 6.547 to 27.554, p = 0.002) adjusting for age, sex, marital status, education, household income, body mass index and smoking; suggesting that those with greater sleep problems had greater cortisol concentrations over the course of an ordinary day. Participants reporting greater sleep problems also had raised evening cortisol levels (B = 0.96, C.I. = 0.176 to 1.746, p = 0.017) in adjusted models. In the laboratory sleep problems were negatively associated with cortisol immediately post-task (B = -0.030, C.I. = -0.059 to 0.000, p = 0.048) and 45 minutes post-task (B = -0.037, C.I. = -0.072 to -0.002, p = 0.039) in fully adjusted models; indicating that those who experienced greater sleep problems had lower cortisol concentrations after stress. ConclusionsSleep problems were associated with disturbances in cortisol responses to stress, as well as changes diurnal cortisol output in people with T2D. Further research is needed to assess if neuroendocrine disturbance increases the risk of cardiovascular disease in this population.

Non-occlusive lower limbs arteriopathy in hypertensive type 2 diabetes: Should we get interested?

Occlusive peripheral artery disease (OPAD) is a strong marker of cardiovascular events. Screening for PAD is recommended by all guidelines; however, there is no consensus on the benefit for detecting the non-occlusive stage of PAD (NOPAD). Therefore, when screening for OPAD, all patients with NOPAD are usually merged with those having normal arteries. WE aimed to assess the bio-clinical profile and morbidity related to diabetes complications in patients with NOPAD and to compare them to those with OPAD and with normal arteries at ultrasonography (UNA). In a cross-sectional, observational, prospective study with a sub-group analysis, we recruited 327 consecutive newly diagnosed type 2 diabetics, aged from 40 to 70 year from January 2009 to December 2014. We collected clinical, biological data and screened exhaustively for macro and microvascular complications. All patients had an Ankle-Brachial Index measurement and a duplex ultrasonography (DUS). The diagnosis of PAD was done on DUS. We considered as NOPAD the presence of atherosclerosis plaque and/or medial artery calcifications without stenosis. We selected the sub-group of hypertensive diabetics for analysis. Coronary risk was calculated by using the Framingham score. Among 327 newly diagnosed type 2 diabetics, 202 had hypertension, 129 women and 73 men; 12 patients had OPAD (5.9%), 111 had NOPAD (54.9%) and 79 had UNA (39.2%), aged respectively 54.8 ± 8.3, 57.1 ± 7.8 and 50.4 ± 7.9 years ( P < 10 −6 ). Arterial DUS showed both atherosclerosis and medial arterial calcifications in 90% in the PAD groups. We didn’t find significant difference between the three groups on smoking ( P = 0.824), body mass index ( P = 0.962), arterial blood pressure ( P = 0.058), glycemic status ( P = 0.975) and prevalence of metabolic syndrome ( P = 0.431). OPAD and NOPAD patients had higher LDL ( P = 0.005), higher coronary disease risk ( P = 10 −4 ), lower glomerular filtration rate ( P = 0.011) and significantly more chronic kidney disease ( P = 0.0009), coronary artery disease ( P = 0.008), atherothrombotic events ( P = 10 −4 ), peripheral diabetic neuropathy ( P = 0.024) and cognitive impairment ( P = 0.006) than those with UNA. No significant difference has been found while comparing the OPAD and NOPAD groups on all studied parameters except for cardiovascular events that are more prevalent in the OPAD group ( P = 0.009). Non-occlusive as well as occlusive PAD, is associated with a high cardiovascular morbidity when associated with type 2 diabetes and hypertension. A screening of NOPAD could help to risk stratification in hypertensive diabetics allowing them to benefit of an earlier preventive action on cardiovascular events. Clinicaltrials.gov ID: NCT02002091

Low, borderline and normal ankle-brachial index as a predictor of incidents outcomes in the Mediterranean based-population ARTPER cohort after 9 years follow-up.

BackgroundGuidelines recommended adopting the same cardiovascular risk modification strategies used for coronary disease in case of low Ankle-brachial index (ABI), but here exist few studies on long-term cardiovascular outcomes in patients with borderline ABI and even fewer on the general population.AimThe aim of the present study was to analyze the relationship between long-term cardiovascular events and low, borderline and normal ABI after a 9-year follow up of a Mediterranean population with low cardiovascular risk.Design and settingA population-based prospective cohort study was performed in the province of Barcelona, Spain.MethodA total of 3,786 subjects >49 years were recruited from 2006–2008. Baseline ABI was 1.08 ± 0.16. Subjects were followed from the time of enrollment to the end of follow-up in 2016 via phone calls every 6 months, systematic reviews of primary-care and hospital medical records and analysis of the SIDIAP (Information System for Primary Care Research) database to confirm the possible appearance of cardiovascular events.Results3146 individuals participated in the study. 2,420 (77%) subjects had normal ABI, 524 (17%) had borderline ABI, and 202 (6.4%) had low ABI.In comparison with normal and borderline subjects, patients with lower ABI had more comorbidities, such as hypertension, hypercholesterolemia and diabetes.Cumulative MACE incidence at 9 years was 20% in patients with low ABI, 6% in borderline ABI and 5% in normal ABI.The annual MACE incidence after 9 years follow-up was significantly higher in people with low ABI (26.9/1000py) (p<0.001) than in borderline (6.6/1000py) and in normal ABI (5.6/1000py).Subjects with borderline ABI are at significantly higher risk for coronary disease (HR: 1.58; 95% CI: 1.02–2, 43; p = 0,040) compared to subjects with normal ABI, after adjustment.ConclusionThe results of the present study support that low ABI was independently associated with higher incidence of MACE, ICE, cardiovascular and no cardiovascular mortality; while borderline ABI had significantly moderate risk for coronary disease than normal ABI.

High sensitive TROponin levels In Patients with Chest pain and kidney disease: A multicenter registry - The TROPIC study.

Accuracy of high sensitive troponin (hs-cTn) to detect coronary artery disease (CAD) in patients with renal insufficiency is not established. The aim of this study was to evaluate the prognostic role of hs-cTn T and I in patients with chronic kidney disease (CKD). All consecutive patients with chest pain, renal insufficiency (eGFR < 60 mL/min/1.73 m2) and high sensitive troponin level were included. The predictive value of baseline and interval troponin (hs-cTnT and hs-cTnI) for the presence of CAD was assessed. One hundred and thirteen patients with troponin I and 534 with troponin T were included, with 95 (84%) and 463 (87%) diagnosis of CAD respectively. There were no differences in clinical, procedural and outcomes between the two assays. For both, baseline hs-cTn values did not differ be-tween patients with/without CAD showing low area under the curve (AUC). For interval levels, hs-cTnI was significantly higher for patients with CAD (0.2 ± 0.8 vs. 8.9 ± 4.6 ng/mL; p = 0.04) and AUC was more accurate for troponin I than hs-cTnT (AUC 0.85 vs. 0.69). Peak level was greater for hs-cTnI in patients with CAD or thrombus (0.4 ± 0.6 vs. 15 ± 20 ng/mL; p = 0.02; AUC 0.87: 0.79-0.93); no differences were found for troponin T assays (0.8 ± 1.5 vs. 2.2 ± 3.6 ng/mL; p = 1.7), with lower AUC (0.73: 0.69-0.77). Peak troponin levels (both T and I) independently predicted all cause death at 30 days. Patients with CKD presenting with altered troponin are at high risk of coronary disease. Peak level of both troponin assays predicts events at 30 days, with troponin I being more accurate than troponin T. (Cardiol J 2017; 24, 2: 139-150).

A Comparison of the Abdominal Fat Distribution and Coronary Risk Markers in Body Mass Index-matched Subjects with and without Fatty Liver.

Objective The close relationship between fatty liver and metabolic syndrome suggests that individuals with fatty liver may have multiple coronary risk factors. In the present study, we investigated the relationships among fatty liver, abdominal fat distribution, and coronary risk markers. Methods and Results Eighty-seven pairs of men and 42 pairs of women who were matched for age and body mass index were enrolled in the present study. The obesity-related markers, abdominal fat distribution (examined by CT), and coronary risk markers were compared in subjects with and without fatty liver. The visceral fat area was significantly larger in the men with fatty liver than in the men without fatty liver. The plasma levels of triglyceride and low-density lipoprotein cholesterol (LDL-C), as well as the homeostasis model assessment-insulin resistance level, were higher in both males and females with fatty liver than in those without fatty liver, while the plasma levels of high-density lipoprotein cholesterol (HDL-C) and adiponectin were lower in the males and females with fatty liver. The plasma levels of apolipoprotein B, remnant-like particle cholesterol (RLP-C), and oxidized LDL were higher in men with fatty liver, but not in women with fatty liver. Conclusion Both males and females with fatty liver had lower insulin sensitivity, lower plasma levels of HDL-C and adiponectin, and higher triglyceride and LDL-C levels. However, the plasma levels of apolipoprotein B, RLP-C, and oxidized LDL were only higher and closely associated with fatty liver in men. Men with fatty liver had a higher risk of coronary disease than women with fatty liver.

Italian Diffuse/Multivessel Disease ABSORB Prospective Registry (IT-DISAPPEARS). Study design and rationale.

The Absorb Bioresorbable Vascular Scaffold System (Absorb BVS) is an everolimus-eluting bioresorbable vascular scaffold able to provide temporary scaffolding and antiproliferative drug delivery for the treatment of coronary artery disease. This temporary scaffolding could be the true feature to overcome the limitations of the conventional metallic stents. A growing body of evidence worldwide is supporting its implementation into daily practice as being associated with comparable results as the second-generation everolimus-eluting stent. However, these pieces of evidence come from 'studies in which the majority of the patients had low-risk stenoses', whereas patients with more complex coronary artery disease could benefit the most from the Absorb BVS technology. The aim of the IT-DISAPPEARS is to investigate the procedural and clinical performance of the Absorb BVS in patients with long (>24 mm), single-vessel coronary disease or with multivessel disease. At least 50 centers across the Italian territory will enroll 1000 patients with either stable or acute coronary syndromes. Follow-up will end up at 5 years. Primary endpoint will be the cumulative hierarchical incidence of major adverse cardiac events at 1 year, defined as: cardiac death, nonfatal target vessel myocardial infarction, or clinically driven target lesion revascularization. The efficacy as well as safety parameters will be evaluated along with a detailed evaluation of the dual antiplatelet therapy duration/interruption. The IT-DISAPPEARS could provide the first evidence worldwide concerning the performance of Absorb BVS in patients with high-risk diffuse coronary disease.

TCT-293 Quantifying Total Atherosclerotic Burden Non-Invasively Through Coronary Computed Tomography Angiography: A Comparison With Multivessel Intravascular Ultrasound Data

Introduction: The extension of atherosclerotic disease is one the most powerful predictors of cardiovascular outcomes. Accurate methods that quantify coronary disease extension may be useful in assessing prognosis, guiding treatment and evaluating disease progression. While intravascular ultrasound (IVUS) is the gold-standard method to quantify atherosclerosis, coronary computed tomography angiography (CCTA) is a promising non-invasive alternative. Hypothesis: We compared previously proposed and novel CCTA scores to multivessel IVUS parameters in order to explore the best way to non-invasively assess the global extent of coronary atherosclerotic disease. Methods: Patients with high risk coronary disease referred for percutaneous coronary intervention were prospectively enrolled. For all cases, CCTA and multivessel IVUS imaging were obtained. Calcium score and 4 previously reported CCTA scores were calculated and compared to average IVUS derived percent atheroma volume (PAV). A novel score was created through comparison with IVUS. Spearman’s correlation coefficients were used to correlate score data with IVUS PAV. Receiver-operating characteristics (ROC) curves were created to establish the ability of each score to predict a PAV above the median. Results: 62 patients with a mean age of 59.7 ± 9.2 years were enrolled. 67.7% were males, 41.9% diabetics and 75.8% had multivessel coronary disease. In average, 3.8 ± 0.7 vessels, comprising 123.8 ± 31.3 mm in length, were imaged with IVUS per patient. All evaluated scoring systems, with the exception of the CONFIRM score, correlated significantly with IVUS derived percent atheroma volume. A novel “soft plaque” CCTA score, that excludes segments with purely calcified plaques, showed the strongest correlation with IVUS PAV (ρ=0.73, p Conclusion: A soft plaque score that takes into account the number of segments with significant non-calcified or mixed plaques correlates strongly - and better than previously described scores - with multivessel IVUS percent atheroma volume. This is possibly the most sensible way to quantify total coronary atherosclerotic burden non-invasively through CCTA.

Di-peptidyl peptidase-4 inhibitor sitagliptin protects vascular function in metabolic syndrome: possible role of epigenetic regulation.

Metabolic syndrome (MetS) is a complex medical disorder characterized by insulin resistance, hypertension, and high risk of coronary disease and stroke. Microvascular rarefaction and endothelial dysfunction have also been linked with MetS, and recent evidence from clinical studies supports the efficacy of incretin-based antidiabetic therapies for vascular protection in diabetes. Previous studies pointed out the importance of dipeptidyl peptidase-4 (DPP-4) inhibition in endothelial cells due to getting protection against metabolic pathologies. We therefore aimed to investigate the acute effects of a DPP-4 inhibitor, sitagliptin, on vascular function in rats with high-sucrose diet-induced MetS. In order to elucidate the mechanisms implicated in the effects of DPP-4 inhibition, we tested the involvement of NO pathway and epigenetic regulation in the MetS. Acute use of sitagliptin protects the vascular function in the rats with MetS in part due to NO pathway via restoring the depressed aortic relaxation responses mediated by receptors. Application of sitagliptin enhanced the depressed phosphorylation levels of both the endothelial NO synthase and the apoptotic status of protein kinase B, known as Akt, in endothelium-intact thoracic aorta from rats with MetS. One-hour application of sitagliptin on aortic rings from rats with MetS also induced remarkable histon posttranslational modifications such as increased expression of H3K27Me3, but not of H3K27Me2, resulting in an accumulation of the H3K27Me3. Our findings suggest that, in addition to its well-known hypoglycemic action, sitagliptin may also have beneficial effects on hyperglycemia-induced vascular changes in an endotheium-dependent manner. These present results with sitagliptin aside from the glycaemic control, may demonstrate its important role in the treatment of patients with MetS.

Metabolic syndrome ifluences the severity of sleep apnea syndrome: from the cordioprev study

Introduction Sleep Apnea Syndrome (SAHS) represents a significant risk factor for the development of cardiovascular disease and evidence suggests a relation with Metabolic Syndrome (MetS). However, it is not clear whether SAHS exacerbates the metabolic abnormalities in patients with MetS. Objectives : To determine the relationship between the MetS and the number of components of MetS and the severity of SAHS. Materials and methods The CordioPrev study (NCT00924937) is an ongoing prospective, controlled trial with a mean follow up of five years duration, including patients with high-risk coronary disease. Among 245 patients from the CordioPrev cohort, SAHS was diagnosed from the nocturnal polysomnography (Apnea–Hipopnea Index (AHS) >5) and MetS was evaluated according to the diagnostic criteria of Adult Panel Treatment III. MetS patients (120 men and 30 women; aged between 45 and 68 years) were divided into three groups based on the number of MetS components: subjects with 3, 4 and 5 MetS components ( N = 86, 41 and 23 respectively). Insulin resistance and other cardiometabolic parameters were analyzed. Results 150 patients were fulfilling MetS criteria. As expected, the SAHS severity defined for AHI was significantly higher in patients with MetS ( p = 0.04). However, no differences were observed between the AHI and the number of components of MetS ( p = 0.27). Interestingly body mass index (BMI) was correlated independently with AHI ( p = 0.003) and men with MetS presented major nocturnal desaturation compared with the rest of the population ( p = 0.014). We did not find any association between SAHS severity and HOMA-IR ( p = 0.39). Conclusion Patients with MetS showed a high prevalence and severity of SAHS independently of the number of components. Moreover, obesity is an independent risk factor for the SAHS development, influencing its severity. These findings may need to be taken into consideration when treating these related diseases. Acknowledgement To Dra. Feu Collado for her critical Reading of this paper.

Evaluation of the dual peroxisome proliferator–activated receptor α/γ agonist aleglitazar to reduce cardiovascular events in patients with acute coronary syndrome and type 2 diabetes mellitus: Rationale and design of the AleCardio trial

Peroxisome proliferator-activated receptors (PPARs) regulate transcription of genes involved in glucose uptake, lipid metabolism, and inflammation. Aleglitazar is a potent dual PPAR agonist with insulin-sensitizing and glucose-lowering actions and favorable effects on lipid profiles and biomarkers of cardiovascular risk. The AleCardio trial examines whether the addition of aleglitazar to standard medical therapy reduces the risk of cardiovascular morbidity and mortality in patients with type 2 diabetes mellitus and recent acute coronary syndrome. AleCardio is a phase 3, multicenter, randomized, double-blind, placebo-controlled trial. A total of 7,228 patients were randomized to aleglitazar 150 μg or placebo daily in addition to standard medical therapy. The primary efficacy end point is time to the first event of cardiovascular death, myocardial infarction, or stroke. Principal safety end points are hospitalization due to heart failure and changes in renal function. Treatment will continue until 7,000 patients are followed up for at least 2.5 years and 950 primary end point events are adjudicated. AleCardio will establish whether the PPAR-α/γ agonist aleglitazar improves cardiovascular outcomes in patients with diabetes and high-risk coronary disease.

Impact of Percutaneous Coronary Intervention Performance Reporting on Cardiac Resuscitation Centers

Patients who experience out-of-hospital cardiac arrest (OHCA) have high mortality rates. Acute coronary occlusions and high-risk coronary obstructive disease are common in this population, especially in patients with ventricular tachycardia or ventricular fibrillation (VF) as the presenting cardiac arrest (CA) rhythm. In one recent series, 32% of patients with OHCA and sustained return of spontaneous circulation (ROSC) had ST-segment elevation on their first documented ECG.1 The vast majority of patients are unable to give a history of prearrest symptoms on hospital arrival because they are comatose. The “2010 American Heart Association (AHA) Guidelines for Cardiopulmonary Resuscitation (CPR) and Emergency Cardiovascular Care (ECC)” state that “appropriate treatment of ACS or STEMI, including PCI, should be initiated regardless of coma (Class I, LOE B)” and “coma and the use of induced hypothermia are not contraindications or reasons to delay PCI.”2 The 2010 AHA Guidelines for CPR and ECC also state that “PCI after ROSC in subjects with arrest of presumed cardiac etiology may be reasonable, even in the absence of a clearly defined STEMI (Class IIb, LOE B).” Quality postarrest care was thought to make such a significant contribution to overall survival after CA that the AHA added a fifth link to the Chain of Survival to emphasize the importance of care after resuscitation treatments. The AHA recently issued a policy statement calling for the establishment of regional systems of care to manage OHCA patients.3 The proposed model is patterned after similar successful major trauma, ST-segment elevation myocardial infarction (STEMI), and stroke programs. The policy statement recommends a comprehensive, regionalized approach to postresuscitation care that includes therapeutic hypothermia, multidisciplinary goal-directed management of critical physiological functions (ie, organ perfusion, ventilation, metabolic management), and early coronary angiography/percutaneous coronary intervention (PCI) when indicated. The AHA policy statement defines 2 levels of cardiac …

FRI0365 Metabolic syndrome and tumor necrosis factor in childhood-onset systemic lupus erythematosus

BackgroundPatients with systemic lupus erythematosus (SLE) have a higher incidence of metabolic syndrome (MetS). Among the possible causes we may mention the inflammation associated with increased levels of triglycerides and...

AB0722 Prevalence of metabolic syndrome in patients with systemic lupus erythematosus

BackgroundSystemic lupus erythematosus (SLE) is a multisystem inflammatory disease characterized by varied clinical manifestations. It mainly affects women of childbearing age and varies in intensity from a mild disease with...

Abstract 18582: Correlation Between Reductions in LDL-cholesterol, Apolipoprotein B, and Lipoprotein(a) with Mipomersen in FH and Other Hypercholesterolemic Patients at High Risk for Coronary Disease

Introduction: Familial hypercholesterolemia (FH) is characterized by markedly elevated LDL-cholesterol (LDL-c) and, if untreated, premature atherosclerosis. Current treatment modalities are directed toward lowering LDL-c, although other atherogenic lipoproteins such as lipoprotein(a) [Lp(a)] are also considered independent causal risk factors for CHD. Lp(a) levels are about 2-fold higher in FH patients. However the LDL receptor is probably not the major route of Lp(a) clearance as statin therapy does not lower Lp(a). As Apo B is an integral component of Lp(a), inhibiting Apo B would be expected to reduce Lp(a) levels. Methods : We evaluated the relationship between the reduction in LDL-c, Apo B, and Lp(a) levels in patients with FH or hypercholesterolemia at high risk for CHD (N=256)and already receiving maximum tolerated lipid-lowering therapy, following treatment with mipomersen, an antisense Apo B synthesis inhibitor. Results: Table shows the absolute and percent changes in lipoprotein parameters pre/post mipomersen 200mg SC weekly for 26 weeks.Percent reductions in LDL-c and Apo B pre/post treatment were tightly correlated (r =0.95, p&lt;0.0001). There was also a positive, but moderate, linear correlation between the percent reductions in Apo B and Lp(a) pre/post treatment (r =0.43, p&lt;0.0001 ). Conclusion: Inhibiting Apo B synthesis with mipomersen reduced not only LDL-c and Apo B, but also Lp(a), and therefore represents a novel potential approach to reducing all three of these atherogenic lipid fractions. *LDL-c and Apo B results are in mean (SD) and Lp(a) in median (CI)

Maladie de Kawasaki : ce qu’il faut savoir

Kawasaki disease (KD) is an acute systemic vasculitis syndrome occurring mostly in children younger than 5 years of age. Especially young infants (<1 year) have an increased risk of coronary artery lesions (CAL). Whereas the etiology of KD is still unknown, progress in treatment during its acute phase has decreased the incidence of CAL from 25-30% to 3-5%. In "atypical KD", the clinical picture is dominated by an unusual symptom as seizure, bloody diarrhea, compressive cervical adenopathy, nephrotic syndrome or hyponatremia. To make a diagnosis in case of "incomplete KD", the supplementary criteria (clinical and biological) suggested by the American Heart Association can be helpful. Once the diagnosis established, the treatment of choice is the intravenous administration of immunoglobulin associated to aspirin at anti-inflammatory dose. However, some patients remain feverish within 36 hours following the end of immunoglobulin administration. This treatment resistance seems increasing in some regions of the globe and can touch up 20% of patients. The unsatisfactory answer to the initial treatment is associated to a higher risk of CAL. Predictive criteria of resistance have been identified and allow to strengthen the medical treatment with a second administration of immunoglobulins. Moreover, methylprednisolone pulse therapy and tumor necrosis factor-alpha blockade (infliximab) appear to be interesting therapeutic options in the future. At last, other treatments have not been the object of controlled studies yet but are alternatives in refractory forms e.g. cytotoxic agents (cyclosporine A, cyclophosphamide, methotrexate), plasmapheresis, plasma exchange or abciximab, especially in patients with aneurysms. Sclerotic vascular changes are often observed in post-Kawasaki disease patients, including those without coronary lesions during the acute phase. Indeed, endothelial dysfunction and risk factors for the development of atherosclerosis, such as dyslipidemia, decreased vascular elasticity, increased C-reactive protein, oxidative stress, and inflammatory cytokines, are known to be present in the late phase of KD. However, it is not clearly established that the survivors of KD carry a higher risk of coronary disease. The epidemiological studies of the next decade should give clearer answers as far as these patients henceforth achieved the age of the atherosclerosis. In conclusion, the diagnosis of KD imposes a strict supervision by a pediatric cardiologist initially. The follow-up is organized according to the existence or non-existence of coronary artery lesions. Late complications as stenosis or coronary thrombosis can occur but remain rare. Thus, it is necessary to be reassuring with the parents, especially for those whose children had no or regressive CAL, while recommending a prevention of the cardiovascular risk factors in the adulthood.