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  Site Guide ··   
Coronary Artery Disease: HELP
Articles by Dan Atar
Based on 10 articles published since 2008
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Between 2008 and 2019, Dan Atar wrote the following 10 articles about Coronary Artery Disease.
 
+ Citations + Abstracts
1 Guideline [European practice guidelines on prevention of cardiovascular diseases: executive summary]. 2008

Graham, Ian / Atar, Dan / Borch-Johnsen, Knut / Boysen, Gudrun / Burell, Gunilla / Cifkova, Renata / Dallongeville, Jean / De Backer, Guy / Ebrahim, Shah / Gjelsvik, Bjørn / Herrmann-Lingen, Christoph / Hoes, Arno / Humphries, Steve / Knapton, Mike / Perk, Joep / Priori, Silvia G / Pyorala, Kalevi / Reiner, Zeljko / Ruilope, Luis / Sans-Menendez, Susana / Reimer, Wilma Scholteop / Weissberg, Peter / Wood, David / Yarnell, John / Zamorano, Jose Luis / Anonymous970596 / Anonymous980596. ·European Society of Cardiology ·G Ital Cardiol (Rome) · Pubmed #18383763.

ABSTRACT: -- No abstract --

2 Editorial Sudden cardiac death--the challenge to cardiology. 2010

Kjeldsen, Keld / Atar, Dan / Hallén, Jonas / Vardas, Panos / Zannad, Faiez / Haunsø, Stig. · ·Fundam Clin Pharmacol · Pubmed #20854303.

ABSTRACT: -- No abstract --

3 Review Choosing a particular oral anticoagulant and dose for stroke prevention in individual patients with non-valvular atrial fibrillation: part 1. 2017

Diener, Hans-Christoph / Aisenberg, James / Ansell, Jack / Atar, Dan / Breithardt, Günter / Eikelboom, John / Ezekowitz, Michael D / Granger, Christopher B / Halperin, Jonathan L / Hohnloser, Stefan H / Hylek, Elaine M / Kirchhof, Paulus / Lane, Deirdre A / Verheugt, Freek W A / Veltkamp, Roland / Lip, Gregory Y H. ·Department of Neurology, University Hospital Essen, Essen, Germany. · Icahn School of Medicine at Mount Sinai, New York, USA. · Hofstra North Shore/LIJ School of Medicine, Hempstead, USA. · Division of Medicine, Oslo University Hospital, Ullevål and University of Oslo, Oslo, Norway. · Division of Rhythmology, Department of Cardiovascular Medicine, Hospital of the University Münster, Münster, Germany. · Population Health Research Institute, McMaster University, Hamilton, ON, Canada. · Cardiovascular Research Foundation, New York, NY, USA. · Thomas Jefferson University Sidney Kimmel Medical College, Philadelphia, PA, USA. · Lankenau Medical Center, Wynnewood, PA, USA. · Department of Medicine, Duke University, Durham, NC, USA. · Icahn School of Medicine at Mount Sinai, Mount Sinai Medical Center, New York, NY, USA. · Division of Clinical Electrophysiology, Department of Cardiology, J. W. Goethe University, Frankfurt, Germany. · Boston Medical Center, Boston University School of Medicine, Boston, MA, USA. · Institute of Cardiovascular Sciences, University of Birmingham, SWBH and UHB NHS Trusts, Birmingham, UK. · Department of Cardiovascular Medicine, Hospital of the University of Münster, Münster, Germany. · University of Birmingham, Institute of Cardiovascular Sciences, City Hospital, Birmingham, UK. · Afdeling Cardiologie, Hartcentrum OLVG, Amsterdam, The Netherlands. · Stroke Medicine, Imperial College London, London, UK. · University of Birmingham, Birmingham, UK. · Aalborg Thrombosis Research Unit, Department of Clinical Medicine, Aalborg University, Aalborg, Denmark. ·Eur Heart J · Pubmed #26848149.

ABSTRACT: Patients with atrial fibrillation (AF) have a high risk of stroke and mortality, which can be considerably reduced by oral anticoagulants (OAC). Recently, four non-vitamin-K oral anticoagulants (NOACs) were compared with warfarin in large randomized trials for the prevention of stroke and systemic embolism. Today's clinician is faced with the difficult task of selecting a suitable OAC for a patient with a particular clinical profile or a particular pattern of risk factors and concomitant diseases. We reviewed analyses of subgroups of patients from trials of vitamin K antagonists vs. NOACs for stroke prevention in AF with the aim to identify patient groups who might benefit from a particular OAC more than from another. In the first of a two-part review, we discuss the choice of NOAC for stroke prevention in the following subgroups of patients with AF: (i) stable coronary artery disease or peripheral artery disease, including percutaneous coronary intervention with stenting and triple therapy; (ii) cardioversion, ablation and anti-arrhythmic drug therapy; (iii) mechanical valves and rheumatic valve disease, (iv) patients with time in therapeutic range of >70% on warfarin; (v) patients with a single stroke risk factor (CHA2DS2VASc score of 1 in males, 2 in females); and (vi) patients with a single first episode of paroxysmal AF. Although there are no major differences in terms of efficacy and safety between the NOACs for some clinical scenarios, in others we are able to suggest that particular drugs and/or doses be prioritized for anticoagulation.

4 Article Effects of FX06 in vitro on platelet, coagulation, and fibrinolytic biomarkers in volunteers and patients with documented coronary artery disease. 2014

Hallén, Jonas / Atar, Dan / Serebruany, Victor. ·1Division of Cardiology and Faculty of Medicine, Oslo University Hospital, Aker, University of Oslo, Oslo, Norway; and 2HeartDrug™ Research Laboratories, Johns Hopkins University, Baltimore, MD. ·Am J Ther · Pubmed #19770797.

ABSTRACT: FX06 is a naturally occurring fibrin-derived peptide demonstrated to confer cytoprotection in the setting of primary percutaneous coronary intervention. Because the effect of FX06 on human platelet, coagulation, and fibrinolysis biomarkers (PCFB) is unknown but is important for further clinical development, we evaluated how FX06 affects PCFB. The in vitro effects of the whole-blood pre-incubation with escalating concentrations of FX06 (4, 25, and 75 μg/mL) were assessed in aspirin-naïve healthy volunteers (n = 10), those with multiple risk factors for vascular disease (n = 10), and patients with documented coronary artery disease (n = 10). The last two groups were treated with aspirin (81 mg/daily). Thirty-two variables of PCFB were measured with the vehicle and for each chosen FX06 dose. Pretreatment of blood samples with FX06 resulted in a moderate but significant and mostly dose-dependent increases of platelet aggregation induced by adenosine diphosphate and collagen. Similarly, the closure time was reduced, suggesting share-induced activation, PECAM-1, GP Ib, GP IIb/IIIa activity, and vitronectin receptors, which were also up-regulated. In contrast, P-selectin and GPIIb antigen expression were reduced after FX06. All other PCFB were predominantly unaffected by FX06, with the exception of the increased plasminogen, decreased protein C activity, and activated von Willebrand factor. We conclude that in the therapeutic range, FX06 in vitro mildly affects hemostasis by way of mostly activating platelets. Applying moderate concomitant antiplatelet strategies should be considered for the adequate protection from vascular thrombotic events in patients treated with FX06. Similar ex vivo study in patients receiving aspirin and clopidogrel is warranted.

5 Article Cost effectiveness of drug-eluting stents as compared with bare metal stents in patients with coronary artery disease. 2013

Wisløff, Torbjørn / Atar, Dan / Sønbø Kristiansen, Ivar. ·1Health Economics and Drug Unit, Norwegian Knowledge Centre for the Health Services; 2Department of Health Management and Health Economics, Institute of Health and Society, University of Oslo, Norway; 3Department of Cardiology B, Oslo University Hospital Ullevål; and 4Faculty of Medicine, Institute of Clinical Medicine, University of Oslo, Norway. ·Am J Ther · Pubmed #21822114.

ABSTRACT: The aim of this study was to estimate the incremental cost effectiveness of replacing bare metal stents (BMS) by drug-eluting stents (DES) when using trial data and registry data. We developed a Markov model (model of cost effectiveness of coronary artery disease) in which 60-year-old patients started by undergoing percutaneous coronary intervention for acute or subacute coronary artery disease. The patients are followed until death or 100 years of age. Data on the occurrence of events (revascularization, acute myocardial infarction, and death) were based on Scandinavian registry data. Separate analyses were conducted with data on effectiveness based on randomized controlled trials and patient registries. On using trial data, it was found that sirolimus-eluting stents (SES) yield 0.003 greater life expectancy and $3300 lower costs than do BMS (dominant strategy). Paclitaxel-eluting stents (PES) yield 0.148 more life years than do SES at additional lifetime costs of $2800 ($21,400 per life year gained). On using registry data, the cost per life year gained was found to be $4900 when replacing BMS with DES. Probabilistic sensitivity analyses, on the other hand, indicate that PES only has a 50%-75% probability of being cost effective, regardless of the type of effectiveness data. DESs are cost effective with current willingness to pay for life year gains. Whether PES or SES is the most effective DES remains uncertain.

6 Article Early impact of prescription Omega-3 fatty acids on platelet biomarkers in patients with coronary artery disease and hypertriglyceridemia. 2011

Serebruany, Victor L / Miller, Michael / Pokov, Alex N / Lynch, Donald / Jensen, Jesper K / Hallén, Jonas / Atar, Dan. ·HeartDrug™ Research LLC, Johns Hopkins University, Towson, Md., USA. Heartdrug @ aol.com ·Cardiology · Pubmed #21701167.

ABSTRACT: BACKGROUND: Prescription omega-3-acid ethyl esters (PO-3A) have been tested for outcome benefits in patients with coronary artery disease (CAD), arrhythmias and heart failure. Some evidence suggests that PO-3A may exert their benefit via inhibiting platelets. We tested the hypothesis that PO-3A may inhibit platelet activity in patients with documented stable CAD, beyond the antiplatelet properties of aspirin and statins. METHODS: Thirty patients with documented CAD and triglycerides over 250 mg/dl treated with aspirin (70-160 mg/daily) and statins (simvastatin equivalence dose: 5-40 mg/daily) were randomized 1:1:1 to Omacor™ 1 g/day (DHA/EPA ratio 1.25:1.0), Omacor 2 g/day, or a placebo for 2 weeks. Platelet tests including aggregometry and flow cytometry and cartridge analyzer readings were performed at baseline and at 1 and 2 weeks following PO-3A therapy. RESULTS: ADP-induced platelet aggregation (p = 0.037), GP IIb/IIIa antigen (p = 0.031) and activity (p = 0.024), and P-selectin (p = 0.041) were significantly reduced after PO-3A, while platelet/endothelial cell adhesion molecule (p = 0.09), vitronectin receptor (p = 0.16), formation of platelet-monocyte microparticles (p = 0.19) and the VerifyNow IIb/IIIa test (p = 0.27) only exhibited nonsignificant trends suggestive of reduced platelet activity. Finally, collagen- and arachidonic acid-induced aggregation, closure time with the PFA-100 device and expression of thrombospondin (CD36), GP Ib (CD42b), LAMP-3 (CD63), LAMP-1 (CD107a), CD40-ligand (CD154), GP37 (CD165), and PAR-1 receptor intact (SPAN 12) and cleaved (WEDE-15) epitopes were not affected by 2 weeks of PO-3A. CONCLUSION: Independently of the dose and already at 1 week, short-term therapy with PO-3A provided a modest reduction of platelet activity biomarkers, despite concomitant aspirin and statin therapy, when compared to a placebo. The effect of PO-3A is unique, differs from other known antiplatelet agents and suggests potential pleiotropism. These preliminary randomized data call for confirmation in prospective studies.

7 Article A window into your heart: taking cardiac troponin to the next level. 2010

Hallén, Jonas / Atar, Dan. ·Department of Cardiology, Oslo University Hospital, Aker & Ullevål, Oslo, Norway. jonashallen@gmail.com ·Biomark Med · Pubmed #21133709.

ABSTRACT: The cardiac troponins are important cardiovascular biomarkers for myocardial necrosis and are measured in thousands of patients daily. In parallel with the widespread adoption of troponin testing for the diagnosis of myocardial infarction during the last two decades, the analytical sensitivity of assays has progressively improved, which has allowed the identification of more acute coronary syndrome patients at risk of future cardiac events. In addition, using novel high-sensitivity assays, circulating troponin can be observed not only in acute settings, but also in many patients suffering from chronic diseases such as coronary artery disease, heart failure and diabetes. We believe that these findings provide a compelling case for exploring whether troponin levels may be a useful tool for guiding clinical decision-making directly in the management of some of these chronic conditions. Sampling of troponin in such patient populations may allow for more refined risk stratification and, importantly, help clinicians individualize care beyond what is currently possible.

8 Article Correlation of inhibition of platelet aggregation after clopidogrel with post discharge bleeding events: assessment by different bleeding classifications. 2010

Serebruany, Victor / Rao, Sunil V / Silva, Matthew A / Donovan, Jennifer L / Kannan, Abir O / Makarov, Leonid / Goto, Shinya / Atar, Dan. ·HeartDrug Research Laboratories, Johns Hopkins University Towson, 7600 Osler Drive, Towson, MD 21204, USA. heartdrug@aol.com ·Eur Heart J · Pubmed #19854728.

ABSTRACT: AIMS: To correlate inhibition of platelet aggregation (IPA) with bleeding events assessed by TIMI, GUSTO, and BleedScore scales in a large cohort of patients with coronary artery disease (CAD) and ischaemic stroke (IS) treated with chronic low-dose aspirin plus clopidogrel. Data from recent trials and registries suggest a link between increased risk of bleeding and cardiovascular mortality. However, the potential association of bleeding risk and IPA is not established. It may play a critical role for the safety of more aggressive platelet inhibition or/and individual tailoring of antiplatelet strategies. METHODS AND RESULTS: Secondary post hoc analyses of 5 microM ADP-induced IPA and bleeding complications assessed by TIMI, GUSTO, and BleedScore scales in a combined data set consisting of patients with documented CAD (n = 246) and previous IS (n = 117). Demographic characteristics differ substantially depending on the underlying vascular disease; however, IPA and bleeding risks were similar between CAD and IS. All three bleeding scales adequately captured serious haemorrhagic events, where the TIMI scale was the most exclusive, whereas BleedScore was the most inclusive. Over half of all patients experienced superficial event(s), most commonly occurring during two to three distinct bleeding episodes. There was no correlation between IPA and duration of antiplatelet therapy. Inhibition of platelet aggregation >50% strongly correlates with minor (r(2) = 0.58, P < 0.001; c-statistic = 0.92), but not severe (r(2) = 0.11, P = 0.038; c-statistic = 0.57), bleeding events. CONCLUSION: Chronic oral combination antiplatelet regimens are associated with a very high (56.5-60.7%) prevalence of superficial bleeding episodes, which are grossly underestimated in trials and registries. The role of such frequent mild complications for the overall benefit of antiplatelet therapy is entirely unknown, as is their effect on compliance. Although IPA is well suited for defining the risk of minor complications, prediction of more severe bleeding events may be challenging.

9 Article Association of platelet responsiveness with clopidogrel metabolism: role of compliance in the assessment of "resistance". 2009

Serebruany, Victor / Cherala, Ganesh / Williams, Craig / Surigin, Serge / Booze, Christopher / Kuliczkowski, Wiktor / Atar, Dan. ·HeartDrug Research Laboratories, Johns Hopkins University, Towson, MD 21204, USA. heartdrug@aol.com ·Am Heart J · Pubmed #19958858.

ABSTRACT: BACKGROUND: Noncompliance is probably the major cause of clopidogrel "resistance." However, noncompliance is difficult to prove without confirming that the drug has been administered. Therefore, detection of plasma clopidogrel and/or metabolite(s) as the reliable objective method to confirm compliance is important. METHODS: We sought to correlate the inhibition of platelet aggregation (IPA) with plasma levels of unchanged clopidogrel (UC), active thiol metabolite (ATM), and inactive carboxyl metabolite (ICM) in a large cohort of patients with coronary artery disease and ischemic stroke treated with clopidogrel. We conducted secondary post-hoc analyses of IPA and plasma UC, ATM, and ICM in a dataset consisting of presumably compliant patients with coronary disease (n = 422) and post-stroke (n = 209). RESULTS: Overall noncompliance rate was 22% (n = 138), while such risks were significantly higher in stroke survivors (n = 79, or 38%) when compared to patients with coronary disease (14%; n = 59; P = .001). Only ICM (19,154 +/- 7,228 ng/ml) was suitable for detecting compliance, while UC (15.2 +/- 9.4 ng/ml), and ATM (8.1 +/- 3.7 ng/ml) in most cases are barely detectable, and diminish over time in the stored samples. The best correlation with IPA (r2 = 0.847) was observed for active metabolite, followed by unchanged clopidogrel (r2 = 0.602), and finally inactive metabolite (r2 = 0.529). The predictive value for noncompliance was also high for inactive metabolite (c-statistic = 0.911). CONCLUSIONS: Therapy with clopidogrel is associated with double-digit underestimated risks for noncompliance, especially in stroke survivors, supporting the hypothesis that lack of IPA, and clopidogrel "resistance" are attributed to hidden noncompliance. Plasma ICM, but not UC, or ATM is a useful marker to monitor compliance to clopidogrel in registries and clinical trials.

10 Minor Interpreting clinical trials: the 'beautiful' case. 2009

Agewall, Stefan / Atar, Dan. · ·Fundam Clin Pharmacol · Pubmed #19236485.

ABSTRACT: -- No abstract --