Direct oral anticoagulation

Direct oral anticoagulants (DOA) – compares favourably to warfarin

08/31/2015

Ref. circulation 2015 

http://www.ncbi.nlm.nih.gov/m/pubmed/25995317/
This is very useful article on the newest addition to well known meds:

Efficacy and Harms of Direct Oral Anticoagulants in the Elderly for Stroke Prevention in Atrial Fibrillation and Secondary Prevention of Venous Thromboembolism: Systematic Review and Meta-Analysis.

Sharma M, et al. Circulation. 2015.

Abstract

BACKGROUND: Evidence regarding the use of direct oral anticoagulants (DOACs) in the elderly, particularly bleeding risks, is unclear despite the presence of greater comorbidities, polypharmacy, and altered pharmacokinetics in this age group.

METHODS AND RESULTS: We performed a systematic review and meta-analysis of randomized trials of DOACs (dabigatran, apixaban, rivaroxaban, and edoxaban) for efficacy and bleeding outcomes in comparison with vitamin K antagonists (VKA) in elderly participants (aged ≥75 years) treated for acute venous thromboembolism or stroke prevention in atrial fibrillation. Nineteen studies were eligible for inclusion, but only 11 reported data specifically for elderly participants. The efficacy in managing thrombotic risks for each DOAC was similar or superior to VKA in elderly patients. A nonsignificantly higher risk of major bleeding than with VKA was observed with dabigatran 150 mg (odds ratio, 1.18; 95% confidence interval, 0.97-1.44) but not with the 110-mg dose. Significantly higher gastrointestinal bleeding risks with dabigatran 150 mg (1.78, 1.35-2.35) and dabigatran 110 mg (1.40, 1.04-1.90) and lower intracranial bleeding risks than VKA for dabigatran 150 mg (0.43, 0.26-0.72) and dabigatran 110 mg (0.36, 0.22-0.61) were also observed. A significantly lower major bleeding risk in comparison with VKA was observed for apixaban (0.63, 0.51-0.77), edoxaban 60 mg (0.81, 0.67-0.98), and 30 mg (0.46, 0.38-0.57), whereas rivaroxaban showed similar risks.

CONCLUSIONS: DOACs demonstrated at least equal efficacy to VKA in managing thrombotic risks in the elderly, but bleeding patterns were distinct. In particular, dabigatran was associated with a higher risk of gastrointestinal bleeding than VKA. Insufficient published data for apixaban, edoxaban, and rivaroxaban indicate that further work is needed to clarify the bleeding risks of these DOACs in the elderly.

SYSTEMATIC REVIEW REGISTRATION: http://www.crd.york.ac.uk/PROSPERO. Unique identifier: PROSPERO CRD42014007171/.

© 2015 American Heart Association, Inc.

familial AAA;

Should you ‘mark’ your AAA patient as ‘FAMILIAL’

08/18/2015
Sources: EJVES Aug 2015

Many definitions exist, the easiest is when at least one first-degree relative (parent, sibling, offspring) is diagnosed with an aortic aneurysm. Based upon family history review, the proportion of patients with AAA with familial AAA is around 13% (range 6–36%).2 Ultrasound screening of the relatives of those with AAAs suggests a prevalence of 17% (range 9–29%) in men and 4% (range 0–11%) in women.

Clinical phenotypes – Studies suggest that patients with familial AAA are significantly more likely to be female, younger, have fewer cardiovascular risk factors (e.g., hypertension and diabetes mellitus), and possibly have a lower carotid intima-media thickness. Studies also show a high rate of thoracic aortic aneurysms and an increased rate of bilateral iliac aneurysms in patients with familial AAA. Relatives of patients with familial AAA also appear to have increased aortic diameters. 

In any case, additional environmental effects, such as smoking, hypertension and hypercholester- olemia could enhance the risk of aneurysm formation and therefore explain the variability in expression of the disease. 

Most accepted genetic aortic aneurysm syndromes are caused by defects in genes involved in the transforming growth factor-b pathway,8 and are associated with syn- dromes like Marfan disease and LoeyseDietz syndrome. 

Until now, family studies have detected a linkage with the 19q13 and 4q31 regions in the genome but without identifying specific genes in these regions. A genome- wide single nucleotide polymorphism with AAA include DAB2IP, LRP1, LDLR, ANRIl, and SORT1.10 Having one of these alleles results in an additional `20% risk for devel- oping AAA; however, the causal relationship of these poly- morphisms still needs to be elucidated.

ACTION PLAN – 

The present American College of Cardiology/American Heart Association guidelines recom- mend ultrasound screening for male relatives aged 60 years or older, while the European Society for Vascular Surgery guidelines recommend ultrasound screening of both male and female relatives aged >50 years who have a family history of AAA. 
It is not known whether endovascular aneurysm repair (EVAR) or open repair (OR) is the optimal treatment for patients with familial AAA. Only very limited data are available; however, as patients with familial AAA tend to be younger, they may benefit from OR, which carries a lower secondary intervention risk with time.