Plasma proteomics of patients with non-valvular atrial fibrillation on chronic anti-coagulation with warfarin or a direct factor Xa inhibitor

Chan, Mark Y.; Lin, Muh-Shi; Lucas, Javier; Moseley, Alex; Thompson, J. W.; Cyr, Derek D.; Ueda, Hitoshi; Kajikawa, Mariko; Ortel, Thomas L.; Becker, Rüdiger

doi:10.1160/th12-05-0310

Cited by 35 publications

(30 citation statements)

References 24 publications

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“…Thus, plasma fibulin-1 appears as a new biomarker for vascular damage, which is in line with the results from four subsequent studies, where plasma fibulin-1 was found to be associated with diabetes, hypertension, and kidney damage (19)(20)(21). Interestingly, two of these studies used non-hypothesisdriven proteomic approaches to search for new markers (20,21). In the current study, we could confirm the previously observed associations between plasma fibulin-1 and age, glycemic status, and pulse pressure, although the correlations were not as strong as previously reported (18).…”

Section: Discussionsupporting

confidence: 82%

“…In addition, plasma fibulin-1 concentrations independently predicted mortality in a 15-year follow-up period (18). Thus, plasma fibulin-1 appears as a new biomarker for vascular damage, which is in line with the results from four subsequent studies, where plasma fibulin-1 was found to be associated with diabetes, hypertension, and kidney damage (19)(20)(21). Interestingly, two of these studies used non-hypothesisdriven proteomic approaches to search for new markers (20,21).…”

Section: Discussionsupporting

confidence: 62%

“…Moreover, we demonstrated an association between increased levels of plasma fibulin-1 and arterial stiffness, blood pressure, and glycemic status in a cohort of 305 welldescribed patients with T2D (18). These results, concerning relations between plasma fibulin-1, glycemic status, and hypertension, have been confirmed in three subsequent studies (19)(20)(21). In the initial paper, we also presented a 15-year follow-up study, showing that high plasma fibulin-1 concentrations among patients with T2D were independently predictive of mortality in T2D with a hazard ratio similar to that of plasma cholesterol (18).…”

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confidence: 72%

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Metformin, but Not Rosiglitazone, Attenuates the Increasing Plasma Levels of a New Cardiovascular Marker, Fibulin-1, in Patients With Type 2 Diabetes

et al. 2014

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OBJECTIVEThe extracellular matrix protein fibulin-1 is upregulated in the arterial wall in type 2 diabetes (T2D) and circulates in increased concentrations in diabetes. Metformin is an antidiabetic drug with beneficial cardiovascular disease effects in diabetes. We hypothesized that metformin would influence the increased level of plasma fibulin-1 in diabetes. RESEARCH DESIGN AND METHODSAfter a 4-week run-in period, 371 eligible patients with T2D were randomized to treatment groups in a factorial design including insulin alone (control), +metfor-min, +rosiglitazone, or +both metformin and rosiglitazone. Plasma fibulin-1 was analyzed at the beginning of the study and after 18 and 24 months. RESULTSPlasma fibulin-1 increased in all groups throughout the 2-year period; however, the increase was strongly attenuated among patients treated with metformin. A highly significant difference was observed when the mean change in plasma fibulin-1 was compared between metformin-and non-metformin-treated individuals both at 18 and 24 months of treatment, but rosiglitazone had no effect. Metformin and rosiglitazone alone reduced the HbA 1c levels to comparable levels and in combination even further. CONCLUSIONSMetformin attenuates the increase in plasma fibulin-1 concentrations in T2D, independently of glycemic effects. Changes in fibulin-1 may reflect an important element in diabetic arteriopathy that can be influenced by metformin. Increased mortality and morbidity owing to a higher incidence of cardiovascular diseases (CVDs) is a major clinical challenge in type 2 diabetes (T2D) (1,2). Several studies have demonstrated that management of hypertension, LDL cholesterol, and other major CVD risk factors have reduced micro-and macrovascular complications in patients with T2D; however, optimal risk reduction is still not achieved when these important risk factors are controlled, indicating that further attempts are needed to control the CVD risk burden (3-5). One assumption is that improvement

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Section: Discussionsupporting

confidence: 82%

Section: Discussionsupporting

confidence: 62%

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confidence: 72%

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Metformin, but Not Rosiglitazone, Attenuates the Increasing Plasma Levels of a New Cardiovascular Marker, Fibulin-1, in Patients With Type 2 Diabetes

et al. 2014

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“…11 Because thrombin activates protein C when it binds thrombomodulin, 12 we preferred to preserve this natural anticoagulant mechanism and administered the direct inhibitor of activated factor X rivaroxaban, which also increases thrombomodulin plasma levels, to our patient. 13 Why does this child require such a high daily dose of rivaroxaban to be free from skin necrosis? The pharmacokinetic profile performed with a daily dose of 30 mg showed a rapid metabolism of the drug, particularly during the day, with a peak of activity reached 1 to 2 hours after oral intake and a mean half-life of 3.5 hours.…”

Section: Discussionmentioning

confidence: 99%

Anticoagulant Treatment With Rivaroxaban in Severe Protein S Deficiency

et al. 2013

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We report a case of a 6-year-old girl with severe protein S deficiency due to a homozygous mutation and recurrent episodes of skin necrosis. She developed purpura fulminans at birth and a catheter-related venous thrombosis complicated by massive pulmonary embolism at the sixth day of life. Long-term oral anticoagulant therapy with a vitamin K-antagonist was started with a therapeutic range of the international normalized ratio of prothrombin time between 2.0 and 3.0. Unfortunately, this common range was not sufficient because recurrent episodes of warfarin-induced skin necrosis developed if the international normalized ratio was ,4.0. Vitamin K antagonists decrease plasma level of vitamin K-dependent coagulation proteins, including the natural anticoagulant protein C. In our patient, the hypercoagulable state due to warfarin-induced reduction of protein C, other than severe protein S deficiency, outweighed the anticoagulant efficacy of the inhibition of procoagulant factors II, VII, IX, and X. The switch of anticoagulant therapy from warfarin to rivaroxaban, a direct inhibitor of activated factor X that does not inhibit other vitamin K-dependent proteins, resulted in the disappearance of skin necrosis at 1 year of follow-up. Rivaroxaban may be considered as a valid anticoagulant alternative in patients with severe inherited protein S deficiency and warfarin-induced skin necrosis.

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“…Reduced arterial barorefl ex sensitivity was reported in patients suffering from vasovagal syncope in some studies (1,3,4), whereas another studies did not found differences in barorefl ex sensitivity in these subjects (5). In some reports, an increased baroreceptor refl ex gain was observed in fainting subjects (6, 7).…”

Section: Introductionmentioning

confidence: 98%

Reduced baroreflex sensitivity in patients with vasovagal syncope

Mitro¹,

Šimurda²,

Evin³

et al. 2015

BLL

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OBJECTIVES: The evidence is confl icting regarding the role of barorefl ex in patients with vasovagal syncope. The aim of the study was to measure barorefl ex sensitivity (BRS) and hemodynamic parameters during head up tilt test (HUT) with nitroglycerine stimulation. METHODS: Nitroglycerine stimulated HUT was performed in 51 patients with the history of recurrent syncope (mean age 46± 19 years, 18 men, 23 women). Cardiac output (CO), stroke volume (SV), left-ventricular ejection time (LVET) and total peripheral resistance (TPR) were assessed during HUT by volume-clamp method using a beat-to-beat photopletysmography. Spontaneous BRS sensitivity was computed using a sequential BRS calculation. RESULTS: HUT was positive after nitroglycerine administration in 28 patients and negative in 23 patients. BRS was lower at the time of syncope in HUT positive group compared to end-test values in HUT negative group (0.54±0.27 vs 0.72±0.35, p = 0. 03). At the time of syncope, CO was signifi cantly lower in HUT positive patients compared to HUT negative patients (2.6±1.4 vs 4.3±1.4 l/min, p < 0.0001), similarly as SV (34.7±14.7 vs 49.2±19 ml, p=0.005 ). LVET was signifi cantly higher in syncopal patients (282.27±26.2 vs 240.5±58.8 ms, p=0.002) and TPR did not differ between two groups. CONCLUSIONS: Reduced BRS may contribute to the development of the vasovagal syncope by inability to adequately counteract hypotension resulting from decreased cardiac output at the time of syncope (Tab. 3, Ref. 18). Text in PDF www.elis.sk.

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Plasma proteomics of patients with non-valvular atrial fibrillation on chronic anti-coagulation with warfarin or a direct factor Xa inhibitor

Cited by 35 publications

References 24 publications

Metformin, but Not Rosiglitazone, Attenuates the Increasing Plasma Levels of a New Cardiovascular Marker, Fibulin-1, in Patients With Type 2 Diabetes

Metformin, but Not Rosiglitazone, Attenuates the Increasing Plasma Levels of a New Cardiovascular Marker, Fibulin-1, in Patients With Type 2 Diabetes

Anticoagulant Treatment With Rivaroxaban in Severe Protein S Deficiency

Reduced baroreflex sensitivity in patients with vasovagal syncope

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