Abstract Background Statin prevents occurrence and recurrence of atherosclerotic events. With regard to venous thromboembolism (VTE), a randomized controlled trial suggested that statin reduced occurrence of VTE, whereas its usefulness as secondary prevention of VTE remains to be elucidated. Purpose This study aimed to assess the association between statin prescription, recurrent VTE and bleeding events in patients with VTE. Methods The COMMAND VTE Registry is a multicentre registry enrolling consecutive 3027 patients with acute symptomatic VTE among 29 centres in Japan. We divided the cohort into the patients who were prescribed statin (N=437) and those not (N=2590), and compared the two groups. We assessed hazard ratios (HRs) of those with statin relative to those without for long-term clinical outcomes (recurrent symptomatic VTE and International Society of Thrombosis and Hemostasis [ISTH] major bleeding). Because the durations of anticoagulation therapy were widely different between the two groups, we constructed Cox's proportional hazard model incorporating status of anticoagulation during the follow-up period as a time-varying covariate. Also, because the incidences of death were strikingly different between the two groups due to the difference in the prevalence of active cancer, we used Fine-Gray's subdistribution hazard model in the presence of competing risks. We incorporated clinically relevant factors into these two models as covariates (10 factors for recurrent VTE and 11 for major bleeding). Results The statin group was significantly older than the non-statin group (statin 71.2±11.8 vs. non-statin 66.5±15.8, P<0.001). The prevalence of active cancer in the statin group was less than one-half of that in the non-statin group (12% vs. 25%, P<0.001), and the cumulative 3-year incidence of death was significantly lower in the statin group than in the non-statin group (12.8% vs. 26.1%, log-rank P<0.001). The table shows the adjusted HRs of the statin group relative to the non-statin group. The HRs of the statin group relative to non-statin group for recurrent VTE were significantly low, but those for major bleeding were insignificant. Adjusted hazard ratios Outcome measures Model 1 P value Model 2 P value Adjusted HR [95% CI] Adjusted HR [95% CI] Recurrent VTE 0.59 [0.36–0.98] 0.042 0.53 [0.32–0.89] 0.02 Major bleeding 0.87 [0.60–1.24] 0.43 0.997 [0.69–1.43] 0.99 Model 1 derived from Cox's model with time-varying covariate of anticoagulation status. Model 2 derived from Fine-Gray's model. Study flowchart Conclusions Prescription of satin was associated with significantly low risks for recurrent VTE, whereas that was not for major bleeding events. Statin could be a potential treatment option for secondary prevention of VTE.
A relationship between serum polyunsaturated fatty acids (PUFAs) and cardiovascular disease has been reported; however, the existence of a relationship between serum PUFAs and extent of vessel disease (VD) in patients with ST elevation myocardial infarction (STEMI) remains unclear.
as 1 day and 5 days after valve replacement.Post-interventional blood sampling was performed before administration of maintenance doses of clopidogrel. Results:The study cohort comprised 144 patients.One hundred patients received a loading dose of 300 mg clopidogrel which was administered at a median of 18.7 [16.6 -21.9] hours before intervention.Patients on chronic treatment with clopidogrel (75mg daily dose; n=44) received no additional loading.In the loading group, ADP-induced platelet reactivity immediately before TAVI was 157 [80-295], at day 1 after TAVI 86 and at day 5 after TAVI 116 [59-182] AU*min.This corresponded to 12% non-responders at a cut-off of 468 AU*min before TAVI, whereas there were no non-responders after TAVI procedure.Similar results were obtained in the chronic treatment group.After TAVI, there was a stronger correlation between ADP-induced platelet reactivity and IPC.Expression of P-Selectin and PAC-1 as markers of platelet activation showed a decrease after TAVI.Figure 1 Conclusion: On treatment ADP-induced platelet reactivity is significantly affected by TAVI.Non-Responder status to clopidogrel is absent after TAVI.This may be explained by consumption of highly reactive platelets during the procedure and caution the use of more potent P2Y12 inhibitors such as prasugrel or ticagrelor after TAVI.
