scholarly journals Rivaroxaban: A New Treatment Paradigm in the Setting of Vascular Protection?

2018 ◽  
Vol 118 (S 01) ◽  
pp. S12-S22 ◽  
Author(s):  
Faiez Zannad ◽  
Rupert Bauersachs
Keyword(s):  
Myocardial Infarction ◽  
Acute Coronary Syndrome ◽  
Plaque Rupture ◽  
Factor Xa ◽  
Coagulation Cascade ◽  
Low Grade ◽  
Limb Ischaemia ◽  
Vascular Protection ◽  
Vessel Occlusion ◽  
Coronary Syndrome

AbstractThe pathophysiology of atherosclerosis involves a diseased endothelium, lipid accumulation and low-grade inflammation. In later stages of coronary artery disease (CAD) and peripheral arterial disease (PAD), plaque rupture may induce atherothrombosis caused by fibrin formation and platelet activation, leading to vessel occlusion with subsequent organ damage such as myocardial infarction, stroke or limb ischaemia. Because of the high disease burden associated with CAD and PAD, there is a need for continuous vascular protection beyond currently available treatments including antiplatelet agents. Due to its central role in the coagulation cascade, inhibition of factor Xa, with the subsequent reduced thrombin formation that impacts not only fibrin but also platelets, may provide additional benefit over using antiplatelets alone. Evidence from Anti-Xa Therapy to Lower Cardiovascular Events in Addition to Standard Therapy in Subjects with Acute Coronary Syndrome-Thrombolysis In Myocardial Infarction-51 (ATLAS-ACS 2-TIMI 51) supports the use of the direct, oral, factor Xa inhibitor rivaroxaban (2.5 mg twice-daily [bid] and 5 mg bid) in reducing mortality and morbidity in patients with acute coronary syndrome, when combined with antiplatelets. Here, we review the role of rivaroxaban in three clinical trials of CAD and/or PAD: Cardiovascular OutcoMes for People using Anticoagulation StrategieS (COMPASS), Vascular Outcomes studY of ASA alonG with rivaroxaban in Endovascular or surgical limb Revascularization for PAD (VOYAGER PAD) and Cardiovascular Outcome Modification, Measurement AND Evaluation of Rivaroxaban in patients with Heart Failure (COMMANDER HF).

scholarly journals Acute Myocardial Infarction In Systemic Mastocytosis: Case Report With Literature Review Of The Role Of Inflammatory Process In Acute Coronary Syndrome

2020 ◽  
Vol 16 ◽  
Author(s):  
Ayman Battisha ◽  
Khalid Sawalha ◽  
Bader Madoukh ◽  
Omar Sheikh ◽  
Karim Doughem ◽  
...  
Keyword(s):  
Risk Factors ◽  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Acute Coronary Syndrome ◽  
Plasma Lipids ◽  
Plaque Rupture ◽  
Systemic Mastocytosis ◽  
Cardiac Risk ◽  
Control Group ◽  
Coronary Syndrome

: Systemic Mastocytosis (SM) is a disorder of excessive mast cell infiltration in multiple organ tissues. Atherosclerosis is a major risk factor for developing acute coronary syndrome [1]. In addition to lipid accumulation in the arterial wall, inflammation plays an important role in the pathogenesis of plaque rupture and activating the thrombosis cascade [2]. The Mast cells contribution to plaque destabilization has been well established in multiple animal and human studies [3]. In a recent study, SM has been proven to be associated with a higher incidence of acute coronary syndrome even with lower plasma lipids level [4]. The study showed that 20% of patients with SM had cardiovascular events compared to only 6% in the control group with adjustment to all cardiac risk factors. Here, we present a case of acute myocardial infarction in a patient with SM with limited risk factors other than age.

scholarly journals Interrogation of the Coagulation Cascade Acute Coronary Syndrome Using Novel Elisa-Based Assays for Single Protease Quantification

Blood ◽  
2018 ◽  
Vol 132 (Supplement 1) ◽  
pp. 5013-5013
Author(s):  
Jens Posma ◽  
Rene van Oerle ◽  
Diane Fens ◽  
Jose govers Riemslag ◽  
Julia Mueller ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Coronary Syndrome ◽  
Angina Pectoris ◽  
Plasma Levels ◽  
Conflicts Of Interest ◽  
Coagulation Cascade ◽  
Thrombotic Complication ◽  
Factor Xii ◽  
Coronary Syndrome ◽  
Healthy Control

Abstract Background: Acute coronary syndrome (ACS), the main contributor to myocardial infarction, is a thrombotic complication of atherosclerosis. Growing evidence supports a role for the intrinsic coagulation cascade in various thrombotic diseases. To gain more inside in the contribution of the intrinsic coagulation cascade in an ACS, we developed novel, ELISA-based assays for the quantification of Kallikrein, activated factor XII (FXIIa), FXIa, FXa, FIXa, and thrombin in complex with a physiological inhibitor. Methods: During this prospective cohort study, blood from patients with a first ACS (n=61) was collected upon admission (before heparin injection(t=0), and after 1(t=1) and 6 (t=2) months. Plasma levels of Kallikrein-C1inhibitor (K-C1inh), FXIIa-C1inh, FXIa-C1inh, FXIa-α1 anti trypsin, FXIa-antithrombin (AT), FIXa-AT, FXa-AT, and thrombin-AT(TAT) were measured using newly developed ELISA's and compared to apparently healthy controls (n=60). Methods were validated according to the EP5-protocol for within- and -between run variability. Results: The inter coefficients of variability for K-C1inh is 11.9%, FXIa-α1-AT 14.4%, FXIa-AT 13.7%, FIXa-AT 4.9%, FXa-AT 2.6% and TAT 8.6 %. Levels of FXIa-α1-AT, FXI- ΑΤ, FIXa-AT and TAT were all significantly elevated in plasma from ACS patients at time of the acute event compared to healthy control: FXIa-α1 anti trypsin respectively 202.8 (IQR 156.6 - 283.4) vs 29.0 pM (IQR 0.00 - 101.0); FXIa-AT levels were respectively 35.9 pM (IQR 23.9 - 43.4) vs 28.0 pM (IQR 23.3 - 34.0); FIXa-AT respectively 102.0pM (IQR 87.4 - 123.0) vs 90.5 pM (IQR 83.2 - 104.3); TAT respectively 5.59 (IQR 3.91 - 9.85) vs 2.26 pM (IQR 1.78 - 2.71)(Fig1). Plasma levels of FXIa-α1-AT, FXIa-AT FIXa-AT, and TAT decreased during follow up. Additionally, FXIa-α1-AT, FXIa-AT FIXa-AT, and TAT were higher in patients with ST-elevated myocardial infarction (STEMI) compared to subjects with non-STEMI or angina pectoris. Conclusion: Elisa based profiling of the coagulation proteases provide a highly sensitive and reproducible method used to distinguish the different activation states of single proteases in the coagulation cascade. With these novel assays we show that FXIa-α1-AT, FXIa-AT FIXa-AT, and TAT are significantly elevated in patients with ACS. Additionally, patients with STEMI have a more pronounced hypercoagulable state than non-STEMI and angina pectoris patients. Figure 1. Figure 1. Disclosures No relevant conflicts of interest to declare.

Anti-Platelet and Anti-Thrombotic Therapy Post-AMI

2011 ◽  
Author(s):  
Dana Dawson ◽  
Keith Fox
Keyword(s):  
Myocardial Infarction ◽  
Acute Coronary Syndrome ◽  
Coronary Artery ◽  
Acute Coronary Syndromes ◽  
Myocardial Reperfusion ◽  
St Elevation Myocardial Infarction ◽  
Coagulation Cascade ◽  
Coronary Syndrome ◽  
Coronary Syndromes ◽  
St Elevation

• Acute coronary syndromes (ACS) encompass a spectrum of presentations which include unstable angina, non-ST-elevation myocardial infarction (NSTEMI or NSTE-ACS), and ST-elevation myocardial infarction (STEMI or STE-ACS)• Anti-platelet and anti-thrombotic agents are administered as ancillary therapy to myocardial reperfusion in patients presenting with an acute coronary syndrome, to maintain the patency of the infarct-related coronary artery• More specific and potent inhibitors of platelet activation and of the coagulation cascade are emerging with the aim being to further improve clinical outcomes in patients presenting with an acute coronary syndrome, without increasing the risks of major bleeding.

Acute Coronary Syndrome

2019 ◽  
pp. 190-196
Author(s):  
Siva S. Ketha ◽  
Juan Carlos Leoni Moreno
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Acute Coronary Syndrome ◽  
Plaque Rupture ◽  
Clinical Manifestations ◽  
St Segment Elevation ◽  
Coronary Syndrome ◽  
Segment Elevation Myocardial Infarction ◽  
St Segment ◽  
Atherosclerotic Plaque Rupture

Acute coronary syndrome (ACS) encompasses all clinical manifestations caused by active myocardial ischemia and includes 3 entities: unstable angina (UA), acute non–ST-segment elevation myocardial infarction (NSTEMI), and acute ST-segment elevation myocardial infarction (STEMI). Atherosclerotic plaque rupture is the most consistent pathophysiologic event in ACS. After plaque rupture, cardiac myocytes die as a consequence of continued occlusion, thereby causing acute myocardial infarction (MI). Prompt recognition of ACS is crucial because the greatest therapeutic effect is achieved if treatment is performed soon after presentation.

scholarly journals Is Plaque Rupture Always Responsible in Acute Coronary Syndrome?

2019 ◽  
Vol 5 (1 (P)) ◽  
pp. 39
Author(s):  
Putrika Prastuti Ratna Gharini
Keyword(s):  
Myocardial Infarction ◽  
Acute Coronary Syndrome ◽  
20Th Century ◽  
Plaque Rupture ◽  
Coronary Syndrome ◽  
Atherothrombotic Event ◽  
Universal Definition ◽  
Definition Of

The majority cause of myocardial infarction is the atherothrombotic event, mainly cause by plaque rupture. Since the 20th century, it was found that the plaque rupture was not the solely condition responsible for the acute coronary syndrome. With the invention of more sensitive myocardial biomarker, a series of guideline was written as guideline for the definition of myocardial infarction. This review discuss about the consensus in the Universal Definition of  Myocardial Infarction.

scholarly journals GAMBARAN PROFIL LIPID PADA PENDERITA SINDROM KORONER AKUT DI RSUP. PROF. DR. R. D. KANDOU PERIODE JANUARI – SEPTEMBER 2015

e-CliniC ◽  
2016 ◽  
Vol 4 (1) ◽  
Author(s):  
Eva Nur Faridah ◽  
Janry A. Pangemanan ◽  
Starry H. Rampengan
Keyword(s):  
Myocardial Infarction ◽  
Acute Coronary Syndrome ◽  
Ldl Cholesterol ◽  
Plaque Rupture ◽  
Hdl Cholesterol ◽  
St Elevation Myocardial Infarction ◽  
Coronary Syndrome ◽  
Cholesterol Levels ◽  
Low Hdl ◽  
St Elevation

Abstract: Acute coronary syndrome (ACS) is due to plaque rupture or erosion of atherosklerosis, including unstable angina pectoris, non-ST elevation myocardial infarction, and ST-elevation myocardial infarction. In indonesia, ACS is still regarded as the highest death contributor. One of the risk factors of ACS is dyslipidemia, that is abnormality condition of lipid in blood. Objective: This study aims to determine description of lipid profile in patients with acute coronary syndrome. Methods: This was a descriptive observational method, based on the secondary data from patients in CVBC Prof. Dr. R. D. Kandou Hospital during January to September 2015. Result: The result showed that from 80 patients of ACS were 37 patients (46,25%) with high total cholsterol levels (≥ 200 mg/dL), 70 patients (87,5%) with low HDL cholesterol levels (≤ 40 - 50 mg/dL), there are 58 patients (72,5%) with high LDL cholesterol levels (> 100 mg/dL) and 32 patients (40%) with high triglycerides levels (≥ 150 mg/dL). Conclusion: Most of ACS patients in this research had high LDL cholesterol levels and low HDL cholesterol levels.Keywords: Acute coronary syndrome, dyslipidemia, lipid profileAbstrak: Sindrom koroner Akut ( SKA ) terjadi karena adanya ruptur atau erosi dari plak aterosklerosis, termasuk angina pektoris tidak stabil, non-ST elevasi miokard infark, dan ST elevasi miokard infark. Di Indonesia, SKA masih di anggap sebagai penyumbang angka kematian tertinggi. Salah satu faktor risiko SKA adalah dislipidemia, yaitu berupa gangguan metabolisme lipid. Tujuan: Penelitian ini bertujuan untuk mengetahui gambaran profil lipid pada penderita sindrom koroner akut. Metode: Penelitian ini bersifat deskriptif observasional dengan menggunakan data sekunder dari penderita SKA di CVBC RSUP. Prof. Dr. R. D. Kandou periode januari – september 2015. Hasil: Hasil penelitian ini menunjukkan dari 80 penderita SKA didapatkan 37 orang (46,25%) adalah penderita yang memiliki kadar kolesterol total tinggi (≥ 200 mg/dL), sebanyak 70 orang (87,5%) memiliki kadar HDL rendah (≤ 40 – 50 mg/dL), adapun yang memiliki kadar LDL tinggi (> 100 mg/dL) yaitu 58 orang (72,5%) dan 32 orang (40%) adalah penderita yang memiliki kadar trigliserida tinggi (≥ 150 mg/dL). Kesimpulan: Penderita sindrom koroner akut dalam penelitian ini sebagian besar memiliki kadar kolesterol LDL yang tinggi dan kadar kolesterol HDL yang rendah.Kata kunci: Sindrom koroner akut, dislipidemia, profil lipid

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