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acute_ischemic_stroke

Acute ischemic stroke

Acute ischemic stroke (AIS) AKA cerebral infarction. Obsolete term: cerebrovascular accident (CVA).


Cerebral ischemia due to cerebral vasospasm is a feared complication in patients following aneurysmal subarachnoid hemorrhage (SAH).

A cerebral infarction is a type of ischemic stroke resulting from a blockage in the blood vessels supplying blood to the brain. It can be atherothrombotic or embolic.

Stroke caused by cerebral infarction should be distinguished from two other kinds of stroke: cerebral hemorrhage and subarachnoid hemorrhage.

A cerebral infarction occurs when a blood vessel that supplies a part of the brain becomes blocked or leakage occurs outside the vessel walls. This loss of blood supply results in the death of that area of tissue. Cerebral infarctions vary in their severity with one third of the cases resulting in death.

Etiology

see Posttraumatic cerebral infarction.

see Malignant middle cerebral artery infarction.

Brain infarction results from a focal decrease in cerebral blood flow.

Outcome

Case series

Cilostazol, an antiplatelet drug that inhibits phosphodiesterase 3, is beneficial for patients with atherothrombosis. In contrast to other anti-platelet drugs such as aspirin and thienopyridines, little information is available on the relationship between platelet responses to cilostazol and clinical outcomes.

Ikeda et al. from the Ehime University Graduate School of Medicine in Japan, conducted a prospective study on patients with cerebral infarction who were treated with cilostazol. The platelet response to cilostazol was assessed with a new assay for the phosphorylation of vasodilator-stimulated phosphoprotein (VASP) subsequent to the pharmacological action of cilostazol. Patients were followed up for 2 years and the relationship between VASP assay results and the recurrence of thrombotic events was examined. We also investigated the effects of CYP3A5 and CYP2C19 genotypes involved in the metabolism of cilostazol on the platelet response to cilostazol.

Among the 142 patients enrolled, 130 completed the 2-year follow-up and the recurrence of thrombotic events was noted in 8 (6.2%). VASP phosphorylation levels were significantly lower in patients with than in those without recurrence. The combined genotype of CYP3A5*1/*3 and CYP2C19*1/*1 was associated with a low level of VASP phosphorylation, while either genotype was not. A multivariate analysis showed that high residual platelet reactivity during the cilostazol treatment, which was defined by a low response of platelet VASP phosphorylation to cilostazol, was an independent risk factor for the recurrence of thrombotic events.

A low platelet response to cilostazol determined by a new platelet assay was associated with the recurrence of thrombotic events in patients with cerebral infarction 1).

Epidemiology

Of the approximately 795 000 strokes in the United States annually, 87% are from ischemia and result in significant morbidity and mortality.

Clinical Features

Early neurological deterioration (END) is a common condition associated with poor outcome after acute ischemic stroke.

Diagnosis

Treatment

Outcome

Early neurological deterioration (END) is a common condition associated with poor outcome after acute ischemic stroke.

The majority of victims must endure life-long disabilities that not only affect their livelihood, but also have an enormous societal economic impact.

Blood pressure (BP) variability is independently and linearly associated with the development of neurologic deterioration in acute stage of ischemic stroke 2).

For Nozoe et al. no significant differences in blood pressure, heart rate, and parasympathetic nerve activity were observed. In patients with acute ischemic stroke, it is likely that the increase in sympathetic nervous activity during mobilization is associated with ND 3).

Case series

1)
Ikeda Y, Yamanouchi J, Kumon Y, Yasukawa M, Hato T. Association of platelet response to cilostazol with clinical outcome and CYP genotype in patients with cerebral infarction. Thromb Res. 2018 Oct 10;172:14-20. doi: 10.1016/j.thromres.2018.10.003. [Epub ahead of print] PubMed PMID: 30342278.
2)
Chung JW, Kim N, Kang J, Park SH, Kim WJ, Ko Y, Park JH, Lee JS, Lee J, Yang MH, Jang MS, Oh CW, Kwon OK, Jung C, Kim BJ, Han MK, Gorelick PB, Bae HJ. Blood pressure variability and the development of early neurological deterioration following acute ischemic stroke. J Hypertens. 2015 Jul 31. [Epub ahead of print] PubMed PMID: 26237556.
3)
Nozoe M, Yamamoto M, Kobayashi M, Kanai M, Kubo H, Shimada S, Mase K. Heart Rate Variability During Early Mobilization in Patients with Acute Ischemic Stroke. Eur Neurol. 2018 Sep 11;80(1-2):50-54. doi: 10.1159/000492794. [Epub ahead of print] PubMed PMID: 30205405.
acute_ischemic_stroke.txt · Last modified: 2019/12/15 11:15 by administrador