Non–Vitamin K Antagonist Oral Anticoagulants in Coronary Artery Disease

2021 ◽  
Author(s):  
Samer Al Said ◽  
Michael Ellscheid ◽  
Eleftherios T. Beltsios ◽  
Norbert Frey

AbstractThe prevention of atherothrombotic events is the primary goal in the treatment of patients with arteriosclerotic disorders. Despite recent improvements in the management of coronary artery disease (CAD) with revascularization techniques and antiplatelet therapy, some patients remain at risk of recurrent cardiovascular events. This could be related to additional thrombin generation. As a result, there has been interest in developing novel therapies to prevent thromboembolic events, targeting thrombin-mediated pathways. These include non–vitamin K antagonist oral anticoagulants (NOACs). This article aims to summarize the recent clinical studies that investigated the role of NOACs in CAD.

Life ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 737
Author(s):  
Marko Kumric ◽  
Josip A. Borovac ◽  
Tina Ticinovic Kurir ◽  
Dinko Martinovic ◽  
Ivan Frka Separovic ◽  
...  

Coronary artery disease (CAD) is widely recognized as one of the most important clinical entities. In recent years, a large body of accumulated data suggest that coronary artery calcification, a process highly prevalent in patients with CAD, occurs via well-organized biologic processes, rather than passively, as previously regarded. Matrix Gla protein (MGP), a vitamin K-dependent protein, emerged as an important inhibitor of both intimal and medial vascular calcification. The functionality of MGP hinges on two post-translational modifications: phosphorylation and carboxylation. Depending on the above-noted modifications, various species of MGP may exist in circulation, each with their respective level of functionality. Emerging data suggest that dysfunctional species of MGP, markedly, dephosphorylated-uncarboxylated MGP, might find its application as biomarkers of microvascular health, and assist in clinical decision making with regard to initiation of vitamin K supplementation. Hence, in this review we summarized the current knowledge with respect to the role of MGP in the complex network of vascular calcification with concurrent inferences to CAD. In addition, we discussed the effects of warfarin use on MGP functionality, with concomitant implications to coronary plaque stability.


2007 ◽  
Vol 37 (5) ◽  
pp. 196 ◽  
Author(s):  
Dae-Woo Hyun ◽  
Ki-Hong Kim ◽  
Hyun-Ju Yoon ◽  
Taek-Geun Kwon ◽  
Ki-Young Kim ◽  
...  

2017 ◽  
Vol 117 (03) ◽  
pp. 429-436 ◽  
Author(s):  
Jie Gao ◽  
Xiaojuan Ma ◽  
Ying Zhang ◽  
Ming Guo ◽  
Dazhuo Shi

SummaryThe acute cardiovascular events following thrombus formation is a primary cause of morbidity and mortality of patients with coronary artery disease (CAD). Numerous studies have shown that a prethrombotic status, which can be defined as an imbalance between the procoagulant and anticoagulant conditions, would exist for a period of time before thrombogenesis. Therefore, early diagnosis and intervention of prethrombotic status are important for reducing acute cardiovascular events. However, none of prethrombotic indicators have been identified as golden standard for diagnosis of prethrombotic status to date. MicroRNAs (miRNAs), a class of short non-coding RNAs, have been shown to be involved in pathophysiologic processes related to prethrombotic status, such as endothelial dysfunction, platelet activation, impaired fibrinolysis and elevated procoagulant factors, etc. Owing to their multiple and fine-tuning impacts on gene expression, miRNAs raise a novel understanding in the underlying mechanism of prethrombotic status. This review aims to discuss the role of miRNAs in prethrombotic status, especially the differently expressed miRNAs in CAD, which may be meaningful for developing promising diagnostic biomarkers and therapeutic strategies for CAD patients in future.


2013 ◽  
Vol 11 (9) ◽  
pp. 1259-1267 ◽  
Author(s):  
Vijay A Doraiswamy ◽  
Marvin J Slepian ◽  
Martin G Gesheff ◽  
Udaya S Tantry ◽  
Paul A Gurbel

2021 ◽  
Author(s):  
Theodoros Michailidis ◽  
Asterios Karakanas ◽  
Nikolaos Schizas ◽  
Petros Keryttopoulos

Nowadays cardiovascular disease remain globally the leading cause of mortality. Coronary artery disease is the predominant clinical entity related to fatal cardiovascular events, while its development is mostly associated with progressive atherosclerosis of the vessels combined with gradual vascular calcification. It is well described and understood that vascular calcification is strongly associated with the occurrence of CVD and increased mortality rates. Therefore, it is essential to understand the metabolic pathways leading to its formation in order to develop effective therapies. A group of vitamin-k dependent proteins seems to play a significant role on the prevention of the arterial wall. Several past studies have shown that in cases of vitamin-k deficiency the process of vessel calcification is accelerated. Vitamin-k depletion and high levels of uncarboxylated and dephosphorylated forms of the aforementioned proteins are considered as important factors that contribute significantly to this rapid progression. Promising studies are giving the stimulus for further research in the field of vitamin-k supplementation and the suspension of vascular calcification.


Author(s):  
An Young ◽  
Mariana Garcia ◽  
Samaah M. Sullivan ◽  
Chang Liu ◽  
Kasra Moazzami ◽  
...  

Objective: In patients with stable coronary artery disease (CAD), the risk of major adverse cardiovascular events (MACE) remains elevated despite treatment. The role of microvascular dysfunction on MACE beyond traditional risk indicators and inflammation is not well established. We examined whether peripheral microvascular dysfunction is associated with MACE in patients with CAD. Approach and Results: Microvascular function was measured with the Reactive Hyperemia Index (RHI) using digital peripheral arterial tonometry in 546 patients with CAD, who were followed 7 years for incident MACE. The primary end point included cardiovascular death or myocardial infarction; the secondary end point included cardiovascular death, myocardial infarction, or heart failure hospitalization. Hazard models for competing risk were used to estimate the association between RHI and MACE adjusting for age, sex, race, traditional risk factors, medications, and CAD severity. We also examined the association of baseline interleukin-6, C-reactive protein, monocyte chemoattractant protein-1, and matrix metallopeptidase-9 with RHI. Mean age was 62±9 years. Mean RHI was 2.1±0.63. After adjustment, for each 1-SD decrease in RHI, there was a 40% increase in the primary end point (hazard ratio, 1.4 [95% CI, 1.1–1.9], P =0.01) and a similar increase in the secondary end point (HR, 1.3 [95% CI, 1.1–1.7], P =0.006). Inflammatory biomarker levels were associated with greater RHI impairment ( P <0.05) but did not affect the relationship between RHI and MACE. Conclusions: Peripheral microvascular dysfunction is associated with increased risk of MACE in patients with stable CAD, implicating the role of microvascular disease in the pathogenesis of adverse outcomes in patients with CAD.


2007 ◽  
Vol 117 (1-2) ◽  
pp. 33-40
Author(s):  
Ewa Stępień ◽  
Konstanty Szułdrzyński ◽  
Agnieszka Branicka ◽  
Elżbieta Stankiewicz ◽  
Agnieszka Pazdan ◽  
...  

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Dahlia Banerji ◽  
Yasir Akram ◽  
Sandeep Somalaraju ◽  
Rishi Bajaj ◽  
Luigi Pacifico

Introduction: Statin therapy has been proven to reduce LDL levels and the risk of cardiovascular events. We sought to evaluate the incremental role of Ezetimibe in addition to on-going Statin therapy to assess changes in lipid profile and cardiovascular events. Methods: A comprehensive search in Medline Indexed and Non-indexed was performed to search for randomized controlled trials that examined the role of Ezetimibe plus Statins compared to Statin monotherapy on lipid profile and cardiovascular event rate in patients with coronary artery disease (CAD). We used the mean change for continuous variables and event rates for dichotomous variables for calculating p- values. Results: We included a total of 17 Randomized Control Trials (RCTs) with 22,603 patients, in our meta-analysis. Among these, 15 studies assessed biochemical improvement, whereas 2 RCTs with 18,186 patients evaluated the clinical outcomes. Summary effects were estimated using random effects model. The cumulative estimate showed that addition of Ezetimibe to Statins resulted in an overall mean reduction of total cholesterol (mean change -14.69 mg/dL, 95% CI -18.03, -10.34, p <0.00001), LDL (mean change -12.92 mg/dL, 95% CI -15.5, -12.34, p <0.00001), and triglycerides (mean change -9.94 mg/dL, 95% CI -13.33, -6.55, p <0.00001). However, there was no significant improvement in HDL level. There was also an 11% reduction in mortality with Ezetimibe addition (Odds Ratio 0.89, 95% CI 0.82, 0.96, p =0.002). ConclusioN: In conclusion, addition of Ezetimibe to a Statin in patients with CAD results in a significant reduction in total cholesterol, LDL and triglycerides and also demonstrates a significant mortality benefit.


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