We conclude that in subjects attending a metabolic ward, homozygosity for a deletion polymorphism of the ACE gene consistently discriminates subjects with a stroke history.
The preliminary results of the present study failed to confirm our hypothesis that ACE gene polymorphism is a cardiovascular risk factor in children of parents with premature stroke.
We conclude that determination of the carotid IMT and of the ACE I/D polymorphism do not permit discrimination of the cardiovascular risk in children of parents with or without premature stroke.
Many patients who receive intravenous (i.v.) recombinant tissue-plasminogen activator (rt-PA) for acute cerebral ischemia were under angiotensin-converting enzyme inhibitors (ACE-Is) or angiotensin receptor blockers (ARBs) at stroke onset.
The aim of this replication study was to confirm our previous findings of associations between the TNF(-308) G/A, IL4R 503 S/P, and ADRB2 27 Q/E polymorphisms and large vessel stroke risk.
Tumor necrosis factor, which exists both as a soluble (solTNF) and a transmembrane (tmTNF) protein, plays an important role in post-stroke inflammation.
The frequencies of the different genotypes for the Leiden V mutation and ACE I/D polymorphism in the 3 subgroups of stroke were compared with 199 stroke-free control subjects whose MRI findings were normal.
Twelve of 16 studies found that ADD1 polymorphism alone or in combination with that of ACE positively associates with stroke or coronary heart disease or renal or vascular dysfunctions.
These findings indicate the important roles that TNF-α and IL-1β serum levels play regarding the risk of PSD, particularly during the acute phase of stroke and in patients with genetic susceptibility.
These data provide evidence that serum TNF-α and IL-1β concentrations are related to poor long-term outcomes after stroke in the presence of particular alleles.
Up-regulated TNF-α expression has also been found in various neurodegenerative diseases such as cerebral malaria, AIDS dementia, Alzheimer's disease, multiple sclerosis, and stroke, suggesting a potential pathogenic role of TNF-α in these diseases as well.
In regard to clinical studies, treatment with Angiotensin Converting Enzyme (ACE) inhibitors and AT1 receptor antagonists exerts preventive and therapeutic effects on stroke.
Angiotensin-converting enzyme (ACE) polymorphism may play a role in stroke and silent brain infarction (SBI) susceptibility, but the results among the populations studied to date have not been consistent.
Randomized, active controlled parallel group trials were included if they compared CCBs with α-blockers, β-blockers, angiotensin II receptor blockers, angiotensin-converting enzyme inhibitors, or diuretics, had a follow-up of ≥6 months, and had assessments of blood pressure (BP) and CV events [all-cause death, CV death, major CV events (myocardial infarction, MI; congestive heart failure, CHF; stroke; and CV death), MI, stroke, or CHF] in patients with baseline systolic/diastolic BP ≥140/≥90 mm Hg with either concomitant previous stroke and/or CAD.
The aim of this study was to evaluate the association of genetic variants within the genes encoding tumor necrosis factor-α (TNF-α) and matrix metalloproteinase-3 (MMP-3), with stroke.