The family at increased risk for future coronary heart disease is the family with a member who has 1) had one or more myocardial infarctions before age 55 years; 2) has levels of LDL cholesterol greater than 75th percentile for age; 3) has excessively low levels of HDL2 cholesterol; 4) has hypertension or has had a stroke, or both; 5) has excessive weight at any age and excessive weight gain during adulthood, or 6) smokes in the household.
A variant of cystatin C lacking the first NH2-terminal residues and having one amino acid substitution at position 68 forms amyloid deposits mainly in the walls of brain arteries, causing fatal strokes in Icelandic patients with familial cerebral hemorrhage secondary to a form of an autosomal dominant amyloidosis.
Lipoprotein(a) [Lp(a)] is a macromolecular complex found in human plasma that combines structural elements from the lipoprotein and blood clotting systems and that is associated with premature coronary heart disease and stroke.
Elevated concentrations of von Willebrand factor antigen were found associated with some positive lupus anticoagulant assays, the highest concentrations in the two individuals with stroke.
Although the exact relationship to stroke is unclear, we suggest screening young patients with unexplained stroke for plasminogen defects using commercially available assay systems.
Sac I polymorphic S2 allele frequency was higher in stroke-risk groups, whereas Pst I polymorphic P2 allele frequency was similar in control and stroke-risk groups.
Sac I polymorphic S2 allele frequency was higher in stroke-risk groups, whereas Pst I polymorphic P2 allele frequency was similar in control and stroke-risk groups.
Restriction fragment length polymorphism of the apolipoprotein AI gene, which encodes the most prominent apoproteins in high density lipoprotein (HDL), were investigated using the restriction enzymes Sac I and Pst I in white and black subjects to determine the potential role of genetic variations as stroke risks as determined by carotid stenosis and an atherogenic serum profile, such as elevated total cholesterol and low density lipoprotein (LDL) levels or reduced HDL levels.
Restriction fragment length polymorphism of the apolipoprotein AI gene, which encodes the most prominent apoproteins in high density lipoprotein (HDL), were investigated using the restriction enzymes Sac I and Pst I in white and black subjects to determine the potential role of genetic variations as stroke risks as determined by carotid stenosis and an atherogenic serum profile, such as elevated total cholesterol and low density lipoprotein (LDL) levels or reduced HDL levels.
We report apolipoprotein(a) (apo(a)) phenotypes of 69 myocardial infarction survivors and 56 stroke patients, and compare them with those of 190 healthy Chinese.
Apolipoprotein (a) [Lp(a)] phenotypes of 69 myocardial infarction survivor and 56 stroke patients were reported and compared to those of 190 healthy Chinese.
The response to APC was measured in 30 patients suffering from juvenile or recurrent stroke, in 40 patients suffering from venous thromboembolism and in 50 healthy subjects.
In the case here reported no associated predisposing condition to stroke could be identified but familial PS defect was found.No therapy was administered.
In an effort to identify possible risk factors for stroke in Sickle Cell Anemia (Hb SS), we analyzed the distribution of alpha-globin gene deletions in a group of Hb SS patients with and without stroke.
In an effort to identify possible risk factors for stroke in Sickle Cell Anemia (Hb SS), we analyzed the distribution of alpha-globin gene deletions in a group of Hb SS patients with and without stroke.
Inasmuch as one recent report found that mRNA encoding only the 5-HT1D beta receptor subtype was expressed by vascular smooth muscle of the central nervous system, the present findings suggest the importance of developing selective 5-HT1D alpha receptor agonists as a strategy to reduce the risk of myocardial infarction and possibly stroke that complicates the acute treatment of migraine headache.
The deletion polymorphism in the angiotensin-converting enzyme gene is a new independent risk factor for lacunar stroke but is not a risk factor for stroke associated with carotid stenosis.
Levels of prothrombin fragment F(1 + 2), a marker of thrombin generation, were determined in both acute and convalescent stroke and related to factor V genotype.
In 87 patients (studied on average 1 year after their strokes) and 26 of their first-degree relatives, our specific aim was to assess the prevalence of the following stroke risk factors: hypofibrinolysis, familial hypofibrinolysis, high lipoprotein (a) level, and dyslipidemia.
Explanations for familial stroke aggregation include differential phenotypic expression of apolipoprotein (a) and apolipoprotein E, racial variations in the distribution of vascular disease, identification of the autosomal-dominant disorder cerebral autosomal-dominant arteriopathy with subcortical infarcts and leukoencephalopathy, specific point mutations in the mitochondrial-related disorders, and identification of the clinical significance of hereditable coagulopathies.
The human angiotensin converting enzyme (ACE) gene is a candidate genetic locus for stroke because of the importance of the renin-angiotensin system to the development of cardiovascular disease.