Hemorrhagic Stroke

There is a noted increased prevalence of hemorrhagic stroke in patients with ACT-TT genotype polymorphism. The strongest association is noted in patients who have intracranial bleeds despite normal blood pressure values. The role of proteolytic enzymes in the pathophysiology of cerebral bleeding has been suggested very recently. ACT is a protease inhibitor that regulates the activity of serine proteases such as neutrophil cathepsin G. Release of this enzyme may lead to degradation of the vascular matrix proteins and coagulation factors.

A study of association of incidence of parenchymal intracerebral hemorrhage and alfa-1 antichymotrypsin genetic polymorphism may indicate a marker for parenchymal intracerebral hemorrhagic stroke to lead to possible interventions in this disabling and fatal disease. Introduction: Most cerebrovascular diseases present as an abrupt onset of a focal neurological deficit that is referred to as a stroke. In the United States, the term stroke is generally used specifically to mean cerebral infarction.

The term hemorrhagic stroke is used to indicate cerebrovascular accident due to intracerebral hemorrhage. This happens due to bleeding within the brain parenchyma, subarachnoid space, or the subdural or epidural space. The majority of the intracerebral hemorrhages are associated with hypertension; however, spontaneous hemorrhage, arteriovenous malformations, and other causes are less common (Vila, N. , Obach, V. , Revilla, M. , Oliva, R. ,and Chamorro, A. , 2000). Aims and Objectives: Generally, within 10 s after cerebral blood flow ceases, metabolic failure of cerebral brain tissue occurs.

The electroencephalogram done at that point in time would demonstrate slowing of electrical activity, and the brain dysfunction would be clinically manifest. If the circulation is restored immediately, there is abrupt and complete recovery of function. If the perfusion abnormality persists for a few minutes, neuronal injury results. With restoration of flow, the recovery of function takes several minutes or hours and may be incomplete. In addition to this, pathologically, there might be a no-reflow phenomenon.

This means during the circulatory failure, the blood elements may sludge, and the capillary endothelium may swell. Even if the primary cause of the flow failure is corrected, the blood flow may not re-establish itself (Pawlikowska, L. et al. , 2004). More prolonged period of ischemia may result in frank tissue necrosis. This would initiate cerebral edema, and typically this would progress over 3 to 4 days. By far, this is the most common type of nontraumatic intracranial hemorrhage. Hypertension and cerebral myloid angiopathy cause the majority of these hemorrhages. Background and Significance:

Hypertensive Intracerebral Hemorrhage: In these patients, intracerebral hemorrhage usually results from spontaneous rupture of a small penetrating artery deep in the brain. The small arteries in certain specific areas, such as, the basal ganglia, the deep cerebellum, and the pons seem more prone to hypertension-induced vascular injury. The leak may be small, or a large clot may form and compress the adjacent tissue. Despite recent advances in acute stroke therapy, hemorrhagic stroke remains the leading cause of severe disability and the third leading cause of death after heart disease and cancer in the Western countries (Li, S.

et al. , 2003). Given the importance of prevention as a strategy to reduce the overall burden of stroke, the identification of markers of stroke risk is the key for both risk prediction and for potential proactive intervention to avert future events. Although genetic epidemiological studies have implicated several genetic variants as risk factors for hemorrhagic stroke, the genetic determinants of this condition remain largely unknown. Although genetic epidemiological studies have implicated several variants as risk factors for ischemic or hemorrhagic stroke, the genetic determinants of these conditions remain largely unknown.

An association study of genetic polymorphisms of a specific candidate gene and hemorrhagic stroke in population can be done in order to identify a gene polymorphism that confers susceptibility to hemorrhagic stroke and thereby contribute to the primary and personalized prevention of these events (O’Donell, H. C. et al. , 2000). A role of proteolytic enzymes has been suggested in the pathogenesis of stroke. In search for a new genetic factor that can be implicated in genesis of stroke, this work aims to examine and investigate the gene polymorphism of the serine protease inhibitor, alfa-1 antichymotrypsin in patients with stroke.

Hemorrhagic stroke is a complex disease, a large proportion of which may become fatal or complicated. Advancing age and hypertension are the most important risk factors for hemorrhagic stroke. Although hypertension is the principal modifiable factor, abnormal blood pressure is an association with up to 80% of these patients. Therefore, additional nonhemodynamic factors intervene in the process of arterial rupture. It can now be recognized as a result of strong interaction between environmental and genetic factors.

Evidence has accumulated to suggest the role of genetic factors in the pathogenesis of ischemic stroke, but very little is known about the role of genetic predisposition to hemorrhagic stroke. Recently several gene polymorphisms have been associated with hemorrhagic stroke. Identification of new potential genes that may increase the risk of stroke independently or by modulating the effect of known vascular risk factors is a matter of great interest (Lapchak PA, Chapman DF, and Zivin JA. , 2000).

A role of proteolytic enzymes has been suggested in the pathophysiology of ischemic or hemorrhagic stroke. Release of neutrophil cathepsin G, a proteolytic enzyme may lead to vascular matrix degradation, platelet aggregation, and coagulation disorders. These effects are generally prevented …

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