Rivaroxaban Case Study

Introduction
The development of thrombus is an important part of the transition of the coronary lesions from a stable to an unstable state which is considered the substrate for acute coronary syndromes (ACS). Angiographic and post-mortem findings confirm this (1, 2). The above consists the pathophysiological background of recent studies that had as an objective to prove the efficacy of rivaroxaban in recent ACS (3). Rivaroxaban is an anti-Xa antithrombotic factor that was firstly studied for the prevention of stroke and embolism in patients with non-valvular atrial fibrillation with positive results (4, 5, 6). Factor Xa initiates the final pathway of the coagulation cascade and results in the formation of thrombin (3, 4).
In the aforementioned
This is in contrast with the aforementioned result of the angiography exam (Table IV). 0/11 (0%) of the S group had recent thrombus compared to 4/11(36,4) in the U group, a difference which was not quite significant (p=0,09).The difference of the frequency of organized thrombus was insignificant [2/11(18,2%) in S and 1/11(9,1) in U, p=1] harmonizing with the comparison of the frequencies of recent and organized thrombus in the same lesion [2/11(18,2) in S and 5/11(46%) in U, p=0,35] (Figure 3)
The cellular analysis revealed that the number of lesions infiltrated with MC was significantly different between the two groups. In contrast, there was no association between the frequency of SMC, CMC and LY (Table V). Specifically all the patients in each group had SMC, the frequency of MC between the S and the U was 9.1% and 63.6% (p=0,02), of LY 9.1% and 27.2% (p=0.65) and of CHC 9,1% and 36,4% (p=0,35)
This is an unexpected result. Previous studies have shown that the instability of the atheromatic plaques comes with higher cellularity (22, 23). Tracy et al proved that higher cellularity is associated with instable lesions and Gordon et al that acute thrombosis was associated with higher proliferation rate (22, 23). Lastly, Moreno et al focused on the thrombogenicity of SMC and tissue factor’s expressed by MC (24). The small number of patients included in our study may explain these contradicting results. A reluctant interpretation of the result could be that not only inflammation factors (that are strongly associated with the rupture of the atheromatic plaque) are responsible for the thrombotic lumen obstruction.
Conclusion: The results of our study demonstate 1) that the presence of thrombus is the rule in the unstable angina syndrome , but it is also present in what appears to be a stable angina period, 2) the presence of thrombus in distinct stages of organization in the same lesion suggests the episodic thrombotic nature of lesion evolution over a long period of time and 3) the presence of thrombus is not always associated with an inflammatory cellular infiltrate, which suggests that other mechanisms may be responsible