The aim of this updated guideline is to provide comprehensive and timely evidence-based recommendations on the prevention of future stroke among survivors of ischemic stroke or transient ischemic attack. The guideline is addressed to all clinicians who manage secondary prevention for these patients. Evidence-based recommendations are provided for control of risk factors, intervention for vascular obstruction, antithrombotic therapy for cardioembolism, and antiplatelet therapy for noncardioembolic stroke. Recommendations are also provided for the prevention of recurrent stroke in a variety of specific circumstances, including aortic arch atherosclerosis, arterial dissection, patent foramen ovale, hyperhomocysteinemia, hypercoagulable states, antiphospholipid antibody syndrome, sickle cell disease, cerebral venous sinus thrombosis, and pregnancy. Special sections address use of antithrombotic and anticoagulation therapy after an intracranial hemorrhage and implementation of guidelines.

/pdf/guidelines-for-the-prevention-of-stroke-in-patients-with-4s66xf1dte.pdf

Guidelines for the prevention of stroke in patients with stroke and transient ischemic attack: a guideline for healthcare professionals from the American Heart Association/American Stroke Association

http://xoomer.virgilio.it/lusebra/NuoviFile/PrevenzioneTVP.pdf

Prevention of venous thromboembolism

https://scholarlypublications.universiteitleiden.nl/access/item%3A3138188/view

A common genetic variation in the 3'-untranslated region of the prothrombin gene is associated with elevated plasma prothrombin levels and an increase in venous thrombosis.

The aim of this updated statement is to provide comprehensive and timely evidence-based recommendations on the prevention of stroke among individuals who have not previously experienced a stroke or transient ischemic attack. Evidence-based recommendations are included for the control of risk factors, interventional approaches to atherosclerotic disease of the cervicocephalic circulation, and antithrombotic treatments for preventing thrombotic and thromboembolic stroke. Further recommendations are provided for genetic and pharmacogenetic testing and for the prevention of stroke in a variety of other specific circumstances, including sickle cell disease and patent foramen ovale.

Guidelines for the Primary Prevention of Stroke A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association

The aim of this new statement is to provide comprehensive and timely evidence-based recommendations on the prevention of ischemic stroke among survivors of ischemic stroke or transient ischemic attack Evidence-based recommendations are included for the control of risk factors, interventional approaches for atherosclerotic disease, antithrombotic treatments for cardioembolism, and the use of antiplatelet agents for noncardioembolic stroke Further recommendations are provided for the prevention of recurrent stroke in a variety of other specific circumstances, including arterial dissections; patent foramen ovale; hyperhomocysteinemia; hypercoagulable states; sickle cell disease; cerebral venous sinus thrombosis; stroke among women, particularly with regard to pregnancy and the use of postmenopausal hormones; the use of anticoagulation after cerebral hemorrhage; and special approaches for the implementation of guidelines and their use in high-risk populations

https://www.ahajournals.org/doi/pdf/10.1161/01.str.0000199147.30016.74?ijkey=567b368d4e69985fc2c1c99723b3d8de8e39c28a

Guidelines for prevention of stroke in patients with ischemic stroke or transient ischemic Attack : A statement for healthcare professionals from the American Heart Association/American Stroke Association Council on Stroke : Co-sponsored by the Council on Cardiovascular Radiology and Intervention : The American Academy of Neurology affirms the value of this guideline

Activated protein C (APC) is a serine protease with potent anticoagulant properties, which is formed in blood on the endothelium from an inactive precursor During normal haemostasis, APC limits clot formation by proteolytic inactivation of factors Va and VIIIa (ref 2) To do this efficiently the enzyme needs a nonenzymatic cofactor, protein S (ref 3) Recently it was found that the anticoagulant response to APC (APC resistance) was very weak in the plasma of 21% of unselected consecutive patients with thrombosis and about 50% of selected patients with a personal or family history of thrombosis; moreover, 5% of healthy individuals show APC resistance, which is associated with a sevenfold increase in the risk for deep vein thrombosis Here we demonstrate that the phenotype of APC resistance is associated with heterozygosity or homozygosity for a single point mutation in the factor V gene (at nucleotide position 1,691, G-->A substitution) which predicts the synthesis of a factor V molecule (FV Q506, or FV Leiden) that is not properly inactivated by APC The allelic frequency of the mutation in the Dutch population is approximately 2% and is at least tenfold higher than that of all other known genetic risk factors for thrombosis (protein C (ref 8), protein S (ref 9), antithrombin10 deficiency) together

/pdf/mutation-in-blood-coagulation-factor-v-associated-with-33avp1ullq.pdf

Mutation in blood coagulation factor V associated with resistance to activated protein C

Amino acid dimorphism in IL1A is detectable by PCR amplification.

The von Willebrand factor gene contains a highly polymorphic variable number tandem repeat sequence (VNTR) in intron 40. We observed the spontaneous mutation to a new length allele. Sequence analysis revealed that the change in length corresponds to one tetranucleotide repeat unit. This observation emphasizes the risk of errors in family studies and prenatal diagnosis due to VNTR instability.

Pieter A. van der Velden

Papers

Mutation in blood coagulation factor V associated with resistance to activated protein C

Amino acid dimorphism in IL1A is detectable by PCR amplification.

Instability of repeats of the von Willebrand factor gene variable number tandem repeat sequence in intron 40.