Abstract
Acute ischemic strokes (AIS) and hemorrhagic strokes lead to disabling neuropsychiatric and cognitive deficits. A serious and fatal complication of AIS is the occurrence of hemorrhagic transformation (HT). HT is cerebral bleeding that occurs after an ischemic event in the infarcted areas. This review summarises how specific risk factors such as demographic factors like age, gender, and race/ethnicity, comorbidities including essential hypertension, atrial fibrillation, diabetes mellitus, congestive heart failure, and ischemic heart disease along with predictors like higher NIHSS score, larger infarction size, cardioembolic strokes, systolic blood pressure/pulse pressure variability, higher plasma glucose levels, and higher body temperature during ischemic event, lower low-density lipoprotein and total cholesterol, early ischemic changes on imaging modalities, and some rare causes make an individual more susceptible to developing HT. We also discuss few other risk factors such as the role of blood-brain barrier, increased arterial stiffness, and globulin levels in patients postreperfusion using thrombolysis and mechanical thrombectomy. In addition, we discuss the implications of dual antiplatelet therapy and the length of treatment in reference to the incidence of developing HT. Current research into inflammatory mediators and biomarkers such as Cyclooxygenase-2, matrix metalloproteinases, and soluble ST2 and their potential role as treatment options for HT is also briefly discussed. Finally, this review calls for more research into use of dual antiplatelet and the timing of antiplatelet and anticoagulant use in reference to hemorrhagic transformation.
Highlights
Strokes are the second leading cause of death worldwide and the fifth leading cause of death in the United States [1,2,3,4]
Elevated systolic blood pressure increases the risk of hemorrhagic transformation (HT) via multiple mechanisms, similar to chronic hypertension, such as its effects on the vasculature and vascular remodeling affecting collateral circulation, autoregulation, and inflammatory response leading to disruption in blood-brain barrier (BBB) [13, 58, 59]
Researchers examined the extent of infarct growth and levels of Matrix metalloproteinase (MMP)-9 in Acute ischemic strokes (AIS) patients, and the study suggests that high levels of MMP-9 (p = 0:02) and delayed reperfusion were associated with increased infarct growth [80]
Summary
Strokes are the second leading cause of death worldwide and the fifth leading cause of death in the United States [1,2,3,4]. Ischemic strokes arise from severe occlusion and reduction in cerebral perfusion, which results in cerebral hypoxia, irreversible damage, and necrosis of brain tissue [4]. Hemorrhagic strokes have limited treatment options as profuse cerebral bleeding may lead to various complications including herniation and fatalities. HT can occur spontaneously after physiologic reperfusion as the natural course of AIS but can occur after thrombolytic therapy such as tissue plasminogen activator (tPA or rtPA) and/or mechanical reperfusion therapies such as thrombectomy [27] It affects 10-40% of people who have had an ischemic stroke. In a prospective study that consisted of 407 patients with ischemic strokes, researchers analyzed the frequency of spontaneous HT occurrence in relation to the infarcted area using CT and MRI techniques. HT can present as asymptomatic or symptomatic, with severe neurological deficits due to profuse bleeding in the infarcted areas
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