Blood flow reactivity to hypercapnia in strictly unilateral carotid disease: preliminary results.

Levine, Ross L.; Dobkin, Jeffrey A.; Rozental, Jack M.; Satter, Martin; Nickles, Robert J.

doi:10.1136/jnnp.54.3.204

Cited by 34 publications

(30 citation statements)

References 21 publications

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“…38,[61][62][63][64][65][66][67][68][69][70][71][72][73] In 1 study only 70 did the authors explicitly state that associated IWS infarcts were excluded, which is, however, partly explained by the fact that interest in IWS infarcts is relatively recent. For instance, in 1 early PET study, 67 all symptomatic patients had IWS infarcts as well.…”

Section: Studies That Specifically Assessed the Pathophysiology Of Cwmentioning

confidence: 99%

“…The observed hemodynamic abnormalities were reported to predominantly affect the anterior watershed (AWS) 63,64,66,68,69,72 more frequently than the posterior watershed (PWS). 38,67 Four studies assessed the CWS hemodynamics before and after successful revascularization, either extracranial-intracranial bypass 38,62 or carotid endarterectomy, 66,72 and each reported complete or partial resolution of the previously observed perfusion abnormalities.…”

Section: Studies That Specifically Assessed the Pathophysiology Of Cwmentioning

confidence: 99%

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The Pathophysiology of Watershed Infarction in Internal Carotid Artery Disease

Momjian-Mayor

Baron

2005

Stroke

310

224

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Background and Purpose-In carotid disease, infarcts can occur in the cortical as well as internal watershed (WS), or both.Better understanding the pathophysiology of WS infarcts would guide treatment. Two distinct hypotheses, namely low-flow and micro-embolism, are equally supported by neuropathological and physiological studies. Here we review the evidence regarding the mechanisms for WS stroke in carotid disease and whether they differ between cortical and internal WS infarcts. Summary of Review-After a brief account of the anatomy of the WS and the cerebrovascular physiology in circumstances of low perfusion pressure, the literature concerning the mechanisms of WS infarction in carotid disease is reviewed and discussed with emphasis on imaging and ultrasound studies of the cerebral hemodynamics. Conclusion-The evidence strongly favors a hemodynamic mechanism for internal WS infarction, especially regarding the so-called rosary-like pattern in the centrum semiovale. However, the relationships between cortical WS infarction and hemodynamic compromise appear more complicated. Thus, although severe hemodynamic compromise appears to underlie combined cortical and internal WS infarction, artery-to-artery embolism may play an important role in isolated cortical WS infarcts. Based on the high prevalence of microembolic signals documented by ultrasound in symptomatic carotid disease, a recent hypothesis postulates that embolism and hypoperfusion play a synergetic role, according to which small embolic material prone to lodge in distal field arterioles would be more likely to result in cortical micro-infarcts when chronic hypoperfusion prevails. Future studies combining imaging of brain perfusion, diffusion-weighted imaging, and ultrasound detection of microembolic signals should help resolve these issues. (Stroke. 2005;36:567-577.)

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Section: Studies That Specifically Assessed the Pathophysiology Of Cwmentioning

confidence: 99%

Section: Studies That Specifically Assessed the Pathophysiology Of Cwmentioning

confidence: 99%

The Pathophysiology of Watershed Infarction in Internal Carotid Artery Disease

Momjian-Mayor

Baron

2005

Stroke

310

224

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“…Because the vascular responsiveness to vasodilator in the brain with insufficient cerebral perfusion pressure is reduced by autoregulatory vasodilation , hypercapnia can be used to estimate cerebral perfusion reserve in occlusive cerebrovascular disease (Herold et al, 1988;Levine et al, 1991;Kuwabara et al, 1997).…”

mentioning

confidence: 99%

Changes in Human Cerebral Blood Flow and Cerebral Blood Volume during Hypercapnia and Hypocapnia Measured by Positron Emission Tomography

Ito

Kanno

Ibaraki

et al. 2003

J Cereb Blood Flow Metab

215

183

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Summary:Hypercapnia induces cerebral vasodilation and increases cerebral blood flow (CBF), and hypocapnia induces cerebral vasoconstriction and decreases CBF. The relation between changes in CBF and cerebral blood volume (CBV) during hypercapnia and hypocapnia in humans, however, is not clear. Both CBF and CBV were measured at rest and during hypercapnia and hypocapnia in nine healthy subjects by positron emission tomography. The vascular responses to hypercapnia in terms of CBF and CBV were 6.0 ± 2.6%/mm Hg and 1.8 ± 1.3%/mm Hg, respectively, and those to hypocapnia were −3.5 ± 0.6%/mm Hg and −1.3 ± 1.0%/mm Hg, respectively. The relation between CBF and CBV was CBV ‫ס‬ 1.09 CBF 0.29 . The increase in CBF was greater than that in CBV during hypercapnia, indicating an increase in vascular blood velocity. The degree of decrease in CBF during hypocapnia was greater than that in CBV, indicating a decrease in vascular blood velocity. The relation between changes in CBF and CBV during hypercapnia was similar to that during neural activation; however, the relation during hypocapnia was different from that during neural deactivation observed in crossed cerebellar diaschisis. This suggests that augmentation of CBF and CBV might be governed by a similar microcirculatory mechanism between neural activation and hypercapnia, but diminution of CBF and CBV might be governed by a different mechanism between neural deactivation and hypocapnia.

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“…12, 13 Nishimura et al found that CBF did not decrease during trimethaphan-induced hypotension (mean systemic arterial BP reduction 15 mm Hg) when CPR was Ϸ5%, whereas CBF was reduced by 0% to 5% and 5% to 10% when CPR was Ϸ4% and 3%, respectively. 18 Although vasoreactivity to PaCO 2 may not fully reflect the autoregulatory perfusion reserve in response to changes of perfusion pressure, the improved CPR from 3.7% to 4.8%/ mm Hg during chronic ACE inhibitor therapy seems to represent the recovery of autoregulatory protection against hypotension, as observed in experimental [2][3][4] and clinical studies.…”

Section: Hatazawa Et Al Perindopril Improves Cerebral Perfusion Resermentioning

confidence: 99%

“…Two arterial blood samples were taken, 1 at the beginning and 1 at the end of scanning, for measurement of PaCO 2 . The cerebral perfusion reserve (CPR) was defined as the percent CBF response to hypercapnia and hypocapnia, which was calculated as follows: [11][12][13] CPR (%CBF/mmHg)ϭ100ϫ(CBF hyper ϪCBF hypo )/CBF rest ϫ1/(PaCO 2hyper ϪPaCO 2hypo ), where "hyper," "hypo," and "rest" denote measurement during hypercapnia, hypocapnia, and under resting conditions.…”

Section: Cerebral Perfusion Reservementioning

confidence: 99%

Long-Term Angiotensin-Converting Enzyme Inhibitor Perindopril Therapy Improves Cerebral Perfusion Reserve in Patients With Previous Minor Stroke

Hatazawa

Shimosegawa

Osaki

et al. 2004

Stroke

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Background and Purpose-Angiotensin-converting enzyme (ACE) inhibitor-based therapy reduces the recurrence of stroke. The present study assessed the effects of long-term ACE inhibitor therapy on cerebral circulation in patients with previous minor stroke. Methods-After a run-in period, 19 patients were randomized to ACE inhibitor therapy (nϭ9; 4 mg of perindopril daily; mean age, 64Ϯ8 years; mean systolic/diastolic blood pressure [BP]ϮSD, 133Ϯ12/77Ϯ9 mm Hg) or placebo therapy (nϭ10; mean age, 66Ϯ9 years; mean BP, 139Ϯ10/78Ϯ8 mm Hg). Cerebral blood flow (CBF) was measured during hypercapnia, normocapnia, and hypocapnia using a positron emission tomography with H 2 15 O at entry into the study and after 3 to 12 months. Cerebral perfusion reserve (CPR) was defined as percent CBF response to a 1 mm Hg change in arterial partial pressure of CO 2 between hypercapnia and hypocapnia. Results-Systolic/diastolic BP and CBF during normocapnia showed no significant changes between entry and completion of the trial in the perindopril and placebo groups. Mean value of CPR showed a significant increase in the perindopril group (from 3.7Ϯ1.7%/mm Hg to 4.8Ϯ1.7%/mm Hg; PϽ0.05) but not in the placebo group (from 4.1Ϯ0.8%/mm Hg to 4.2Ϯ0.6%/mm Hg; NS). Statistical parametric mapping analysis also showed global and significant increase (PϽ0.01, uncorrected) in CPR in the perindopril group alone. Conclusions-Long-term ACE inhibitor-based therapy had a beneficial effect on the cerebral circulation by improving CPR in patients with previous minor stroke.

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Blood flow reactivity to hypercapnia in strictly unilateral carotid disease: preliminary results.

Cited by 34 publications

References 21 publications

The Pathophysiology of Watershed Infarction in Internal Carotid Artery Disease

The Pathophysiology of Watershed Infarction in Internal Carotid Artery Disease

Changes in Human Cerebral Blood Flow and Cerebral Blood Volume during Hypercapnia and Hypocapnia Measured by Positron Emission Tomography

Long-Term Angiotensin-Converting Enzyme Inhibitor Perindopril Therapy Improves Cerebral Perfusion Reserve in Patients With Previous Minor Stroke

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