Abstract
BackgroundCurrent recommendations of stroke treatment favour a moderately elevated blood pressure in the acute phase, based on the concept of an improved cerebral perfusion. Here, cerebral blood flow was assessed in a case series of patients with acute hemodynamic stroke by means of transcranial colour-coded sonography (TCCS) to study the effects of pharmacologically induced hypertension.FindingsWe investigated six patients with acute hemodynamic stroke and blood pressure-dependent clinical fluctuation of neurological symptoms. TCCS was performed during the initiation phase of catecholamine-induced controlled hypertension. A blood pressure-dependent increase of flow velocity in the ipsilesional middle and the posterior cerebral artery was found in all patients (mean increase 0.80% and 0.65% per mmHg, respectively).ConclusionsCatecholamine-induced hypertension in severe hemodynamic stroke leads to an ultrasound-detectable rise of cerebral blood flow. This finding gives ‘proof-of-principle’ evidence, supporting active blood pressure management in this selected group of stroke patients. Outcome-related questions of target blood pressure, treatment duration or applicability to other forms of stroke, however, remain to be studied. In this, transcranial ultrasound may be a valuable tool for patient selection and subsequent bedside monitoring.
Highlights
MethodsAcute stroke patients were prospectively included if they fulfilled the following criteria: (1) proximal occlusion or high-grade stenosis of the internal carotid artery (ICA) (>80%, ECST criteria [3]), (2) ultrasound-determined intracranial collateral flow activation (retrograde ipsilesional flow in the A1 segment of the anterior cerebral artery (ACA), activated posterior communicating artery, retrograde ophthalmic artery flow or signs of leptomeningeal collateral activation, i.e. increased flow velocity in the distal ACA or posterior cerebral artery (PCA)), (3) blood pressure (BP)-related worsening of the neurological deficits (NIH-SS ≥1), (4) presumed haemodynamic cause because of marked poststenotic flow patterns in the ipsilesional middle cerebral artery (MCA) and (5) subsequent continuous intra-arterial BP monitoring and need for catecholamine intervention to achieve or keep a BP target of systolic 160 to 190 mmHg.All patients had already completed extracranial colourcoded sonography (ECCS) and transcranial colour-coded sonography (TCCS) studies (Toshiba Powervision 6000, Tokyo, Japan) including detailed intracranial collateral flow assessment during the routine process of acute stroke unit admission
Current recommendations of stroke treatment favour a moderately elevated blood pressure in the acute phase, based on the concept of an improved cerebral perfusion
Catecholamine-induced hypertension in severe hemodynamic stroke leads to an ultrasounddetectable rise of cerebral blood flow
Summary
Acute stroke patients were prospectively included if they fulfilled the following criteria: (1) proximal occlusion or high-grade stenosis of the ICA (>80%, ECST criteria [3]), (2) ultrasound-determined intracranial collateral flow activation (retrograde ipsilesional flow in the A1 segment of the anterior cerebral artery (ACA), activated posterior communicating artery, retrograde ophthalmic artery flow or signs of leptomeningeal collateral activation, i.e. increased flow velocity in the distal ACA or posterior cerebral artery (PCA)), (3) BP-related worsening of the neurological deficits (NIH-SS ≥1), (4) presumed haemodynamic cause because of marked poststenotic flow patterns in the ipsilesional middle cerebral artery (MCA) and (5) subsequent continuous intra-arterial BP monitoring and need for catecholamine intervention to achieve or keep a BP target of systolic 160 to 190 mmHg.All patients had already completed extracranial colourcoded sonography (ECCS) and TCCS studies (Toshiba Powervision 6000, Tokyo, Japan) including detailed intracranial collateral flow assessment during the routine process of acute stroke unit admission. Without interference to clinical decisions and procedures, serial measurements of non-angle-corrected blood flow velocities were performed in the ipsilateral M1-MCA and P2-PCA segments during initiation of continuous catecholamine infusion. Datasets of maximal flow velocities and corresponding systolic BP values were noted, following a stepwise increase of catecholamine dosage and a stabilisation phase of 2 to 3 min. All patients gave informed consent; the study was approved by the local ethics committee
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