179 research outputs found
Cardiovascular Disease in Diabetics: Pharmacology and Revascularization
Diabetes has become a public health crisis. With the incidence of obesity rising in the United States, the number of diabetics will grow considerably. Of greatest concern is the impact this trend will have on cardiovascular disease. Diabetics demonstrate accelerated coronary atherosclerosis, and the prognosis is worse following cardiac events. Moreover, our interventions have achieved uneven success in treating this subset of patients. This paper will review the metabolic abnormalities that promote atherosclerosis in diabetics and the current methods for treating and preventing the development of coronary artery disease in diabetics, principally through a combination of medications and revascularization
Reply Underutilization of High-Intensity Statin Therapy After Hospitalization for Coronary Heart Disease: A Cause for Concern, But a Few Words of Caution
A doença de Chagas como um modelo mecanicista para testar uma nova hipótese
The association between depression and cardiovascular disease is well documented. Nevertheless, the process through which they are linked remains unknown, as does the direction of this relationship. Studies have suggested both that depression is a risk factor for heart disease and that heart disease is a risk factor for depression. A number of studies have established that a relationship exists between depression and inflammation, with alterations in the levels of inflammatory markers (IL-1, IL-6, TNF-alpha and others). Depressive symptoms have also been identified in many diseases characterized by inflammatory processes e.g. rheumatoid arthritis, bronchial asthma, diabetes, tuberculosis and cardiovascular diseases. In this brief viewpoint, we explain and propose how to use Chagas disease, a disorder characterized by inflammatory processes and leading to cardiovascular and autonomic problems, as a model for studying the directionality of the relationship between heart disease and depression.A associação entre depressão e doença cardiovascular está bem documentada. Não obstante, o processo pelo qual está associada permanece desconhecido, assim como o sentido desta associação. Estudos têm sugerido que tanto a depressão é um fator de risco para a doença cardiovascular quanto esta o é para a depressão. Uma série de trabalhos tem estabelecido que uma relação existe entre depressão e inflamação, com alterações evidenciadas por marcadores de inflamação (IL-1, IL-6, TNF alfa e outros). Sintomas de depressão também têm sido identificados em diversas doenças caracterizadas por processos inflamatórios, tais como artrite reumatoide, asma brônquica, diabete, tuberculose e doenças cardiovasculares. Nesta breve opinião é explicitado e proposto como empregar a doença de Chagas, um agravo caracterizado por processos inflamatórios e indutor de problemas cardiovasculares e autonômicos, como um modelo de estudo da direcionalidade da relação entre doença cardíaca e depressão
The complementary roles of dynamic contrast-enhanced MRI and 18F-fluorodeoxyglucose PET/CT for imaging of carotid atherosclerosis
Inflammation and neovascularization in vulnerable atherosclerotic plaques are key features for severe clinical events. Dynamic contrast-enhanced (DCE) MRI and FDG PET are two noninvasive imaging techniques capable of quantifying plaque neovascularization and inflammatory infiltrate, respectively. However, their mutual role in defining plaque vulnerability and their possible overlap has not been thoroughly investigated. We studied the relationship between DCE-MRI and [supersript 18]F-FDG PET data from the carotid arteries of 40 subjects with coronary heart disease (CHD) or CHD risk equivalent, as a substudy of the dal-PLAQUE trial (NCT00655473)
Relationship of Serum Inflammatory Biomarkers With Plaque Inflammation Assessed by FDG PET/CT The dal-PLAQUE Study
ObjectivesThis study sought to longitudinally investigate the relationship between a broad spectrum of serum inflammatory biomarkers and plaque inflammation assessed by 18F-fluorodeoxyglucose positron emission tomography/computed tomography (FDG-PET/CT).BackgroundBoth plaque inflammation and serum biomarkers of inflammation are associated with atherothrombotic events; however, the relationship between them is unclear.MethodsWe conducted a post hoc analysis of the dal-PLAQUE (A Randomized Placebo-Controlled Study of the Effect of RO4607381 on Progression or Regression of Atherosclerotic Plaque in Patients With Coronary Heart Disease [CHD] Including Patients With Other CHD Risk Factors), a randomized, placebo-controlled study of dalcetrapib, a cholesteryl ester transfer protein inhibitor, in 130 patients with coronary heart disease, or coronary heart disease risk equivalents on stable lipid-lowering therapy. Baseline and change after 3-month follow-up in inflammatory biomarker levels and baseline and change after 3-month follow-up in aorta and carotid 18F-FDG PET/CT (mean maximum target-to-background ratio of the most diseased segment [TBRmds]) were analyzed.ResultsBaseline myeloperoxidase positively correlated with baseline carotid TBRmds (rho = 0.25, p = 0.02). This correlation remained at the 3-month follow-up and was independent of traditional cardiovascular disease risk factors. Baseline lipoprotein-associated phospholipase A2 mass correlated with aorta TBRmds (rho = 0.21, p = 0.03). However, this correlation disappeared at the 3-month follow-up and was not independent of cardiovascular disease risk factors. There was no association between change from baseline in myeloperoxidase or lipoprotein-associated phospholipase A2 mass and change from baseline in aorta and carotid TBRmds. Baseline and change from baseline in high sensitivity C-reactive protein, interleukin 6, soluble P-selectin, soluble E-selectin, soluble intracellular adhesion molecule 1, soluble vascular cell adhesion molecule 1, and matrix-metalloproteinase 3 and 9 did not correlate with baseline or change from baseline in carotid or aorta TBRmds.ConclusionsOur data show that, in patients with coronary heart disease or at high risk of coronary heart disease on stable lipid-lowering therapy, circulating myeloperoxidase levels are associated with carotid plaque inflammation. (A Randomized, Placebo-controlled Study of the Effect of RO4607381 on Progression or Regression of Atherosclerotic Plaque in Patients With Coronary Heart Disease [CHD] Including Patients With Other CHD Risk Factors [dal-PLAQUE]; NCT00655473
Cardiovascular and cerebrovascular events among patients receiving omalizumab: Results from EXCELS, a prospective cohort study in moderate to severe asthma
BackgroundEXCELS, a postmarketing observational cohort study, was a commitment to the US Food and Drug Administration to assess the long-term safety of omalizumab in an observational setting, focusing predominantly on malignancies.ObjectiveThe aim of this study was to examine a potential association between omalizumab and cardiovascular (CV)/cerebrovascular (CBV) events in EXCELS.MethodsPatients (≥12 years of age) with moderate to severe allergic asthma and who were being treated with omalizumab (n = 5007) or not (n = 2829) at baseline were followed up for ≤5 years. Analyses included overall CV/CBV events, but focused on the subset of arterial thromboembolic events (ATEs), comprising CV death, myocardial infarction, ischemic stroke, transient ischemic attack, and unstable angina. A prespecified analysis of the end point of ATE was conducted to control for available potential confounders. A blinded independent expert panel adjudicated all events.ResultsAt baseline, the 2 cohorts had similar demographic characteristics, but severe asthma was more common in the omalizumab versus the non-omalizumab group (50% vs 23%). Omalizumab-treated patients had a higher rate of CV/CBV serious adverse events (13.4 per 1,000 person years [PYs]) than did non–omalizumab-treated patients (8.1 per 1,000 PYs). The ATE rates per 1,000 PYs were 6.66 (101 patients/15,160 PYs) in the omalizumab cohort and 4.64 (46 patients/9,904 PYs) in the non-omalizumab cohort. After control for available confounding factors, the hazard ratio was 1.32 (95% CI, 0.91-1.91).ConclusionThis observational study demonstrated a higher incidence rate of CV/CBV events in the omalizumab versus the non-omalizumab cohort. Differences in asthma severity between cohorts likely contributed to this imbalance, but some increase in risk cannot be excluded
Una combinación nueva en Erica (Ericaceae).
[EN] A new nomenclatural status and combination is proposed for Erica cinerea var. numidica. New data about the morphology,
chorology and ecology of this taxon are given.[ES] Una combinación nueva en Erica (Ericaceae).- Se propone un nuevo estatus y combinación nomenclatural para Erica
cinerea var. numidica. Se aportan nuevos datos sobre la morfología, corología y ecología de este taxón.This work
has been supported by “Ajuts a grups de recerca
consolidats: 2005SGR00344 and 2009SGR0439,
Generalitat de Catalunya” and "Proyectos Intramurales
de Incorporación del CSIC: 2009930I161".Peer reviewe
Cardiovascular magnetic resonance parameters of atherosclerotic plaque burden improve discrimination of prior major adverse cardiovascular events
<p>Abstract</p> <p>Aims</p> <p>Patients with prior major cardiovascular or cerebrovascular events (MACE) are more likely to have future recurrent events independent of traditional cardiovascular disease risk factors. The purpose of this study was to determine if patients with traditional risk factors and prior MACE had increased cardiovascular magnetic resonance (CMR) plaque burden measures compared to patients with risk factors but no prior events.</p> <p>Methods and Results</p> <p>Black blood carotid and thoracic aorta images were obtained from 195 patients using a rapid extended coverage turbo spin echo sequence. CMR measures of plaque burden were obtained by tracing lumen and outer vessel wall contours. Patients with prior MACE had significantly higher MR plaque burden (wall thickness, wall area and normalized wall index) in carotids and thoracic aorta compared to those without prior MACE (Wall thickness carotids: 1.03 ± 0.03 vs. 0.93± 0.03, p = 0.001; SD wall thickness carotids: 0.137 ± 0.0008 vs. 0.102 ± 0.0004, p < 0.001; wall thickness aorta: 1.63 ± 0.10 vs. 1.50 ± 0.04, p = 0.009; SD wall thickness aorta: 0.186 ± 0.035 vs. 0.139 ± 0.012, p = 0.009 respectively). Plaque burden (wall thickness) and plaque eccentricity (standard deviation of wall thickness) of carotid arteries were associated with prior MACE after adjustment for age, sex, and traditional risk factors. Area under ROC curve (AUC) for discriminating prior MACE improved by adding plaque eccentricity to models incorporating age, sex, and traditional CVD risk factors as model inputs (AUC = 0.79, p = 0.05).</p> <p>Conclusion</p> <p>A greater plaque burden and plaque eccentricity is prevalent among patients with prior MACE.</p
Anticoagulation in Patients With COVID-19: JACC Review Topic of the Week.
Clinical, laboratory, and autopsy findings support an association between coronavirus disease-2019 (COVID-19) and thromboembolic disease. Acute COVID-19 infection is characterized by mononuclear cell reactivity and pan-endothelialitis, contributing to a high incidence of thrombosis in large and small blood vessels, both arterial and venous. Observational studies and randomized trials have investigated whether full-dose anticoagulation may improve outcomes compared with prophylactic dose heparin. Although no benefit for therapeutic heparin has been found in patients who are critically ill hospitalized with COVID-19, some studies support a possible role for therapeutic anticoagulation in patients not yet requiring intensive care unit support. We summarize the pathology, rationale, and current evidence for use of anticoagulation in patients with COVID-19 and describe the main design elements of the ongoing FREEDOM COVID-19 Anticoagulation trial, in which 3,600 hospitalized patients with COVID-19 not requiring intensive care unit level of care are being randomized to prophylactic-dose enoxaparin vs therapeutic-dose enoxaparin vs therapeutic-dose apixaban. (FREEDOM COVID-19 Anticoagulation Strategy [FREEDOM COVID]; NCT04512079).Dr Farkouh has received research grants from Amgen, Novo Nordisk,
and Novartis. Dr Stone has received speaker honoraria from Infraredx; has served as a consultant to Valfix, TherOx, Robocath, HeartFlow, Ablative Solutions, Miracor, Neovasc, Abiomed, Ancora,
Vectorious, Elucid Bio, Occlutech, CorFlow, Apollo Therapeutics,
Impulse Dynamics, Cardiomech, Gore, and Amgen; and has equity/
options from Ancora, Cagent, Applied Therapeutics, Biostar family of
funds, SpectraWave, Orchestra Biomed, Aria, Cardiac Success, Valfix,
and Xenter. Dr Godoy is supported by the Frederick Banting and
Charles Best Canada Graduate Scholarship (Doctoral Research Award)
from the Canadian Institutes of Health Research. All other authors
have reported that they have no relationships relevant to the contents of this paper to disclose.S
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