Antithrombotic therapy in heart failure

Verheugt, Freek W.A.

doi:10.1007/s12471-012-0250-5

Cited by 8 publications

(6 citation statements)

References 8 publications

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“…Early studies and post hoc analyses of large clinical trials have demonstrated a reduction in thromboembolic events, risk of stroke, and mortality. In contrast, recent underpowered prospective controlled studies found no benefit in the use of warfarin in patients with systolic HF and normal sinus rhythm 36,37 . The low to moderate risk of thromboembolism and the questionable benefit of anticoagulation need to be weighed against the potential for hemorrhagic complication.…”

Section: Discussionmentioning

confidence: 98%

The Atrial Fibrillation Paradox of Heart Failure

Shelton

Clark

Kaye

et al. 2010

Congestive Heart Failure

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The prevalence of atrial fibrillation (AF) in patients with heart failure (HF) is high, but longitudinal studies suggest that the incidence of AF is relatively low. The authors investigated this paradox prospectively in an epidemiologically representative population of patients with HF and persistent AF. In all, 891 consecutive patients with HF [mean age, 70+/-10 years; 70% male; left ventricular ejection fraction, 32%+/-9%] were enrolled. The prevalence of persistent AF at baseline was 22%. The incidence of persistent AF at 1 year was 26 per 1000 person-years, ranging from 15 in New York Heart Association class I/II to 44 in class III/IV. AF occurred either at the same time or prior to HF in 76% of patients and following HF in 24%. A risk score was developed to predict the occurrence of persistent AF. The annual risk of persistent AF developing was 0.5% (0%-1.3%) for those in the low-risk group compared with 15% (3.4%-26.6%) in the high-risk group. Despite a high prevalence of persistent AF in patients with HF, the incidence of persistent AF is relatively low. This is predominantly due to AF coinciding with or preceding the development of HF. The annual risk of persistent AF developing can be estimated from clinical variables.

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Section: Discussionmentioning

confidence: 98%

The Atrial Fibrillation Paradox of Heart Failure

Shelton

Clark

Kaye

et al. 2010

Congestive Heart Failure

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“…Over the past years, there is increasing evidence about the brainheart interaction with major potential implications for treatment of cardiovascular diseases. For instance, cerebrovascular accidents (CVAs) and transient ischaemic attacks (TIAs) are frequently caused by cardiac arrhythmias and/or congestive heart failure [5,6]. In particular atrial fibrillation may result in cognitive disorders preceding the occurrence of TIAs or CVAs [7][8][9][10].…”

mentioning

confidence: 99%

Neurocardiology: close interaction between heart and brain

Wall

Gilst

2012

Neth Heart J

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“…2,21,22 BT is the period from broken capillaries to bleeding discontinuation. The process could be either intrinsic or extrinsic coagulation, depending on the pathways of initiating prothrombin activator formation and other factors, which ultimately activate factor X, leading to thrombus formation and coagulation.…”

Section: Discussionmentioning

confidence: 99%

Effects of 6-(4-chlorophenoxy)-tetrazolo[5,1-a]phthalazine on Anticoagulation in Mice and the Inhibition of Experimental Thrombosis in Rats

Zhang

Lan³

et al. 2014

Journal of Cardiovascular Pharmacology

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: Thrombosis is a major complication that could be fatal in acute or chronic cardio-cerebral-vascular diseases. Therefore, the development of novel agents for anticlotting and the prevention of thrombosis and cardiovascular diseases are clinically significant. This study aimed to evaluate the anticoagulant and antithrombotic effects of 6-(4-chlorophenoxy)-tetrazolo[5,1-a]phthalazine (Q808), a new phthalazine tetrazole derivative. Bleeding time, clotting time, and serum calcium ion (Ca) concentration were assessed in mice, whereas arteriovenous thrombus weight and plasma prothrombin time were evaluated in rats, and platelets Ca influx was determined in rabbit. Daily oral administration of Q808 at 25, 50, or 100 mg/kg for 3 days significantly delayed bleeding time and clotting time in mice compared with controls. Q808 administration at 50 mg/kg significantly reduced experimental thrombus weight by 62.6% and delayed plasma prothrombin time by 58.7% in rats, whereas 50 and 100 mg/kg of Q808 daily significantly increased serum Ca concentration in mice. Q808 at 0.2, 0.4, and 0.8 mg/mL significantly inhibited thrombin-induced Ca influx in rabbit platelets. Our results suggest that Q808 at 25-200 mg/kg daily exerts anticoagulant and antithrombotic effects, and its mechanisms of action may involve both the intrinsic and extrinsic coagulation pathways that inhibit certain coagulation factors and platelet functions.

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Antithrombotic therapy in heart failure

Cited by 8 publications

References 8 publications

The Atrial Fibrillation Paradox of Heart Failure

The Atrial Fibrillation Paradox of Heart Failure

Neurocardiology: close interaction between heart and brain

Effects of 6-(4-chlorophenoxy)-tetrazolo[5,1-a]phthalazine on Anticoagulation in Mice and the Inhibition of Experimental Thrombosis in Rats

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