- Association of Non-HDL Cholesterol, Homocysteine and Vitamin D in Acute Coronary Syndrome. [Journal Article]
- JAJ Assoc Physicians India 2018; 66(8):22-25
- CONCLUSIONS: Non-HDL cholesterol was a better predictor of cardiovascular diseases than LDL-C, HDL-C or total cholesterol.
- Prevalence of coronary artery calcification in young patients with SLE of predominantly Hispanic and African-American descent. [Journal Article]
- LSLupus Sci Med 2019; 6(1):e000330
- CONCLUSIONS: Patients with SLE aged ≤45 years have an increased prevalence of detectable CAC compared with the general population. Our data suggest that subclinical atherosclerosis in SLE develops early and warrants timely screening and cardioprotective interventions.
- Stent malapposition occurred 17 days following percutaneous coronary intervention for a severe calcified lesion in acute myocardial infarction. [Case Reports]
- JCJ Cardiol Cases 2019; 20(1):4-7
- The occurrence of stent malapposition and coronary artery aneurysm (CAA) during the early phase of drug-eluting stent (DES) implantation is rare. This report presents the case of a 55-year-old man wh…
The occurrence of stent malapposition and coronary artery aneurysm (CAA) during the early phase of drug-eluting stent (DES) implantation is rare. This report presents the case of a 55-year-old man who underwent DES implantation to the left circumflex artery with full-arc severe calcified lesion owing to inferior acute myocardial infarction. Coronary angiography and optical coherence tomography (OCT) at 17 days following percutaneous coronary intervention (PCI) revealed stent malapposition and CAA of diameter 6.5 mm in the distal part of the stented vessel. OCT findings at 5 months following PCI revealed a dilated CAA of diameter 7.5 mm and a luminal structure outside the stent. Based on these findings, it was suggested that the cause of CAA in the early phase following DES implantation to the severe calcified lesion was related to coronary sequelae of Kawasaki disease. <Learning Objective: This was a case of coronary artery aneurysm (CAA) in the stented lesion at early phase post percutaneous coronary intervention (PCI). Despite the patient's young age and low coronary risk, there was full-arc severe calcification lesion. Optical coherence tomography after PCI showed luminal structure outside of the stent. It was similar to recanalized CAA of Kawasaki disease (KD). These findings suggested that CAA in early phase following PCI might be related to the sequelae of coronary arteritis, especially KD.>.
- [Coronary artery calcium: pathogenesis and cardiovascular risk]. [Journal Article]
- GIG Ital Cardiol (Rome) 2019 Jul-Aug; 20(7):401-408
- Atherosclerosis is an almost universal disease of human kind and involves infiltration of lipids, inflammation and calcification in the subintimal space. Coronary artery calcium (CAC) accumulates wit…
Atherosclerosis is an almost universal disease of human kind and involves infiltration of lipids, inflammation and calcification in the subintimal space. Coronary artery calcium (CAC) accumulates within the context of subintimal atherosclerosis and is a highly specific marker of pre-clinical disease. The prognostic significance of CAC has been elucidated during the past 20 years of research and it is now considered the best non-invasive marker to enhance prediction of adverse events in the general population as well as several disease states, such as diabetes mellitus, chronic kidney disease and HIV. However, the prognostic significance of CAC is not the same for all carriers of this marker, although it is well established that its absence is associated with an extremely low and long-lasting probability of cardiovascular events even in subjects at high risk. In this review, we discuss the current knowledge of the epidemiology and clinical significance of CAC in patients of different race, sex and age and summarize the current recommendations on its use in clinical practice.
- Imaging residual inflammatory cardiovascular risk. [Journal Article]
- EHEur Heart J 2019 Jul 16
- Targeting residual cardiovascular risk in primary and secondary prevention, would allow deployment of novel therapeutic agents, facilitating precision medicine. For example, lowering vascular inflamm…
Targeting residual cardiovascular risk in primary and secondary prevention, would allow deployment of novel therapeutic agents, facilitating precision medicine. For example, lowering vascular inflammation is a promising strategy to reduce the residual inflammatory cardiovascular risk in patients already receiving optimal medical therapy, but prescribing novel anti-inflammatory treatments will be problematic due to the lack of specific companion diagnostic tests, to guide their targeted use in clinical practice. Currently available tests for the detection of coronary inflammation are either non-specific for the cardiovascular system (e.g. plasma biomarkers) or expensive and not readily available (e.g. hybrid positron emission tomography imaging). Recent technological advancements in coronary computed tomography angiography (CCTA) allow non-invasive detection of high-risk plaque features (positive remodelling, spotty calcification, low attenuation plaque, and napkin-ring sign) and help identify the vulnerable patient, but they provide only indirectly information about coronary inflammation. Perivascular fat attenuation index (FAI), a novel method for assessing coronary inflammation by analysing routine CCTA, captures changes in the perivascular adipose tissue composition driven by inflammatory signals coming from the inflamed coronary artery, by analysing the three-dimensional gradients of perivascular attenuation, followed by adjustments for technical, anatomical, and biological factors. By detecting vascular inflammation, perivascular FAI enhances cardiovascular risk discrimination which could aid more cost-effective deployment of novel therapeutic agents. In this article, we present the existing non-invasive modalities for the detection of coronary inflammation and provide a practical guide for their use in clinical practice.
- Arterial tissue transcriptional profiles associate with tissue remodeling and cardiovascular phenotype in children with end-stage kidney disease. [Journal Article]
- SRSci Rep 2019 Jul 16; 9(1):10316
- Chronic kidney disease (CKD) greatly increases the risk for cardiovascular disease (CVD). However, molecular mechanisms underlying CKD-induced arterial remodeling are largely unknown. We performed a …
Chronic kidney disease (CKD) greatly increases the risk for cardiovascular disease (CVD). However, molecular mechanisms underlying CKD-induced arterial remodeling are largely unknown. We performed a systematic analysis of arterial biopsies from children with stage 5 predialysis CKD participating in the Cardiovascular Comorbidity in Children with Chronic Kidney Disease (4 C) study. For comparison, we studied biopsies from children without CKD, coronary bypass vessels from adults with atherosclerotic coronary heart disease without CKD and aortic sections of subtotally nephrectomized rats. In pediatric CKD patients, gene expression was correlated to the cardiovascular phenotype assessed by surrogate end-points. The arterial calcium content correlated with the intima-media thickness (IMT) of biopsied vessels from pediatric CKD patients, was markedly increased compared to biopsies from children without CKD and comparable to adult coronary bypass patients. Significant transcriptional changes included ECM components, pro-calcifying factors, and physiological calcification inhibitors; most were highly accordant with changes observed in adults with atherosclerosis and in uremic rats. Individual gene expression levels were significantly associated with the left ventricular mass index and carotid intima media thickness. Thus, inflammatory processes (TNF, IL-10), calcification inhibitors (CA2), the Wnt-pathway (FGF-2) and foremost, ECM components (HMGA1, VNN1, VCAN), impact pathobiological responses in arteries from children with CKD.
- Orbital atherectomy for treatment of complex severely calcified coronary artery lesions: Insights from a Veterans Affairs cohort. [Journal Article]
- CRCardiovasc Revasc Med 2019 Jun 28
- CONCLUSIONS: This single-center VA cohort demonstrates that patients with severely calcified and anatomically complex coronary artery lesions treated with OA had a low rate of angiographic complications and a high rate of one-year freedom from MACE. Moreover, this study included demographics underrepresented in clinical trials, including those with acute myocardial infarction, left main coronary artery disease, and bifurcation lesions.
- Homoarginine Supplementation Prevents Left Ventricular Dilatation and Preserves Systolic Function in a Model of Coronary Artery Disease. [Journal Article]
- JAJ Am Heart Assoc 2019 Jul 16; 8(14):e012486
- Background Homoarginine (hA rg) has been shown to be cardioprotective in a model of ischemic heart failure; however, the mechanism remains unknown. hA rg can inhibit tissue-nonspecific alkaline phosp…
Background Homoarginine (hA rg) has been shown to be cardioprotective in a model of ischemic heart failure; however, the mechanism remains unknown. hA rg can inhibit tissue-nonspecific alkaline phosphatase (TNAP), an enzyme that promotes vascular calcification. We hypothesized that hA rg will exert beneficial effects by reducing calcification in a mouse model of coronary artery disease associated with TNAP overexpression and hypercholesterolemia. Methods and Results TNAP was overexpressed in the endothelium in mice homozygous for a low-density lipoprotein receptor mutation (wicked high cholesterol [ WHC ] allele). WHC and WHC -endothelial TNAP mice received placebo or hA rg supplementation (14 mg/L in drinking water) starting at 6 weeks of age simultaneously with an atherogenic diet. Outcomes were compared between the groups after 4 to 5 weeks on treatment. Experiments were performed in males, which presented a study limitation. As expected, WHC -endothelial TNAP mice on the placebo had increased mortality (median survival 27 days, P<0.0001), increased coronary calcium and lipids (P<0.01), increased left ventricular end-diastolic diameter (P<0.0001), reduced ejection fraction (P<0.05), and increased myocardial fibrosis (P<0.0001) compared with WHC mice. Contrary to our hypothesis, hA rg neither inhibited TNAP activity in vivo nor reduced coronary artery calcification and atherosclerosis in WHC -endothelial TNAP mice; however, compared with the placebo, hA rg prevented left ventricular dilatation (P<0.01), preserved ejection fraction (P<0.05), and reduced myocardial fibrosis (P<0.001). Conclusions The beneficial effect of hA rg supplementation in the setting of calcified coronary artery disease is likely due to its direct protective actions on the myocardial response to the ischemic injury and not to the inhibition of TNAP activity and calcification.
- Association between acute aortic dissection and the distribution of aortic calcification. [Journal Article]
- PlosPLoS One 2019; 14(7):e0219461
- CONCLUSIONS: We identified the associations between AC-related variables and the location of IT in patients with AAD. However, AC was not an independent risk factor for AAD. The distribution of AC was different between patients with type A and type B AAD.
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- Increased apolipoprotein C3 drives cardiovascular risk in type 1 diabetes. [Journal Article]
- JCIJ Clin Invest 2019 Jul 11; 130
- Type 1 diabetes mellitus (T1DM) increases the risk of atherosclerotic cardiovascular disease (CVD) in humans by poorly understood mechanisms. Using mouse models of T1DM-accelerated atherosclerosis, w…
Type 1 diabetes mellitus (T1DM) increases the risk of atherosclerotic cardiovascular disease (CVD) in humans by poorly understood mechanisms. Using mouse models of T1DM-accelerated atherosclerosis, we found that relative insulin deficiency rather than hyperglycemia elevated levels of apolipoprotein C3 (APOC3), an apolipoprotein that prevents clearance of triglyceride-rich lipoproteins (TRLs) and their remnants. We then showed that serum APOC3 levels predict incident CVD events in subjects with T1DM in the Coronary Artery Calcification in Type 1 Diabetes (CACTI) study. To explore underlying mechanisms, we investigated the impact of Apoc3 antisense oligonucleotides (ASOs) on lipoprotein metabolism and atherosclerosis in a mouse model of T1DM. Apoc3 ASO treatment abolished the increased hepatic Apoc3 expression in diabetic mice - resulting in lower levels of TRLs - without improving glycemic control. APOC3 suppression also prevented arterial accumulation of APOC3-containing lipoprotein particles, macrophage foam cell formation, and the accelerated atherosclerosis in diabetic mice. Our observations demonstrate that relative insulin deficiency increases APOC3 and that this results in elevated levels of TRLs and accelerated atherosclerosis in a mouse model of T1DM. Because serum levels of APOC3 predicted incident CVD events in the CACTI study, inhibiting APOC3 might reduce CVD risk in T1DM patients.