Hemorrhagic infarct of the brain without a reopening of the occluded arteries in cardioembolic stroke.

Abstract

We examined the brains of 14 patients (four men and 10 women, mean age 68.9 years) who died from brain herniation after cardioembolic stroke with persistent occlusion of the internal carotid-middle cerebral arterial axis. Our examination showed hemorrhagic infarct in seven patients and pale infarct in the other seven, contradicting the commonly proposed pathophysiologic mechanism for the development of hemorrhagic infarct that the opening of previously occluded vessels makes an infarct hemorrhagic. Analysis of blood pressure after stroke revealed one or more surges of arterial hypertension or rapid rise of blood pressure in patients with hemorrhagic infarct without a reopening of the occluded artery. Such arterial hypertension was not always present in patients with pale infarct. Hemorrhage into an infarct with persisting occlusion of the proximal artery is assumed to occur when the involved blood vessels are exposed to the force of arterial blood pressure from the leptomeningeal collaterals. This occurs when arterial blood pressure rises after stroke in the presence of efficient leptomeningeal collaterals and before occlusion of these collaterals by a swollen cerebral hemisphere containing a large infarct. (Stroke 1989;20:876-883)

Matrix Metalloproteinase Expression Is Related to Hemorrhagic Transformation After Cardioembolic Stroke

“…19 Occasionally, delayed hemorrhage occurs without reperfusion, and in these cases, the source of the hemorrhage is postulated to be collateral circulation to the damaged area. 20 An interesting association also occurs between time to artery reopening and presence of HT in our series. Most patients with early HI recanalized within 12 hours, but all patients who developed late HI had an absence of early spontaneous recanalization.…”

Effects of 24-Hour Blood Pressure and Heart Rate Recorded With Ambulatory Blood Pressure Monitoring on Recovery From Acute Ischemic Stroke

“…Brain edema and hemorrhagic transformation are key factors to link acute high BP and poor outcomes. 4,[17][18][19] The spontaneous decline in BP during the initial hours sometimes reflects the recanalization of occluded cerebral arteries, which often results in favorable outcomes. 20,21 Mental stress of hospital admission contributes to elevated BP 11 ; release from the stress can lower BP and possibly improve clinical conditions.…”

Treatment and Outcome of Hemorrhagic Transformation After Intravenous Alteplase in Acute Ischemic Stroke: A Scientific Statement for Healthcare Professionals From the American Heart Association/American Stroke Association

“…4 It has been suggested that hemorrhagic infarction is a result of multifocal red blood cell extravasation, whereas parenchymal hematoma is the a result of a single bleeding site in the blood vessel damaged by ischemia and reperfusion. 51 Reperfusion of injured brain tissue, related to recanalization of the affected artery, 52 provides the impetus for the development of hemorrhagic transformation. Recanalization of the affected artery, however, is not the only determinant of the risk of hemorrhagic transformation, which can also occur with persistent occlusion, as noted in autopsy and imaging studies.…”

“…Recanalization of the affected artery, however, is not the only determinant of the risk of hemorrhagic transformation, which can also occur with persistent occlusion, as noted in autopsy and imaging studies. 52,53 Reperfusion injury may be exacerbated by or lead to elevated blood pressure. 54,55 In addition, postthrombolytic hemorrhage can occur in areas remote from the infarcted tissue, 56 lending support to the notion that thrombolytics can contribute to hemorrhage by mechanisms other than reperfusion.…”