Regional cerebral blood flow in familial hypercholesterolemia.

Rodriguez, Guido; Bertolini, Stefano; Nobili, Flavio; Arrigo, Alessandro; Masturzo, P; Elicio, N; Gambaro, M.; Rosadini, G

doi:10.1161/01.str.25.4.831

Cited by 18 publications

(8 citation statements)

References 39 publications

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“…This finding is consistent with the nonsignificant relationship between reduced cerebral blood flow and elevated cholesterol level in healthy subjects (48). Another study revealed that even long-lasting hypercholesterolemia was not associated with alterations in cerebral blood flow (24).…”

Section: Discussionsupporting

confidence: 84%

“…Thus far, methods to measure rCBF, such as positron emission tomography (PET) and single photon emission computed tomography (SPECT), have involved the use of radiation or the administration of intravenous contrast agents (22)(23)(24)(25). Consequently, related studies typically involve small sample sizes and thus have limited value in revealing relationships between cerebrovascular risk factors and rCBF.…”

mentioning

confidence: 99%

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Effect of Cerebrovascular Risk Factors on Regional Cerebral Blood Flow

Laar

Graaf²,

Mali³

et al. 2008

Radiology

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Section: Discussionsupporting

confidence: 84%

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confidence: 99%

Effect of Cerebrovascular Risk Factors on Regional Cerebral Blood Flow

Laar

Graaf²,

Mali³

et al. 2008

Radiology

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“…To our knowledge, this is the first transcranial Doppler-acetazolamide study that investigated cerebral hemodynamics in hyperlipidemic patients. The results are in agreement with earlier acetazolamide-133 Xe inhalation method measurements in which basal mean cerebral blood flow and global cerebral blood flow changes after administration of acetazolamide (CVR) did not differ between controls and hypercholesterolemic patients: Rodriguez et al 19 found normal CVR in 13 of 15 patients with long-lasting, severe familial hypercholesterolemia.…”

Section: Discussionsupporting

confidence: 91%

“…However, to our knowledge, only 1 study has investigated the impact of hyperlipidemia on CRC. 19 Decreased CRC refers to a decreased ability of cerebral arterioles to adapt in critical conditions (eg, sudden falls in systemic blood pressure or orthostatic conditions) and probably predicts a higher risk of stroke. 13 It is suspected that patients hypercholesterolemia, with a potential risk factor for stroke, may have a lower CRC.…”

mentioning

confidence: 99%

Cerebrovascular reserve capacity in patients with hyperlipidemia

Kerényi

Fülesdi

Ficzere

et al. 2000

J. Clin. Ultrasound

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Purpose. Because recent data are conflicting, it is not certain whether hyperlipidemia is an independent risk factor for cerebrovascular diseases. Decreased cerebrovascular reserve capacity refers to the decreased ability of the cerebral arterioles to adapt in critical conditions and probably predicts a higher risk of stroke. The aim of this study was to compare cerebrovascular reserve capacity in hyperlipidemic patients and healthy controls using transcranial Doppler sonography.Methods. Thirty-four hyperlipidemic patients and 21 healthy controls were examined. With transcranial Doppler sonography, the mean blood flow velocity in the middle cerebral artery was registered at rest and at 5, 10, 15, and 20 minutes after intravenous administration of 1,000 mg acetazolamide. Cerebrovascular reactivity and reserve capacity were calculated from mean blood flow velocities. Various laboratory measurements were also made and assessed for correlation with resting cerebral blood flow velocity and cerebrovascular reserve capacity.Results. No significant differences could be observed between controls and hyperlipidemic patients in cerebrovascular reactivity or cerebrovascular reserve capacity. No correlation was found between various laboratory measurements and resting cerebral blood flow velocity or cerebrovascular reserve capacity.Conclusions. We could not demonstrate any differences in cerebrovascular reserve capacity between hyperlipidemic patients and healthy controls. Thus, the vasodilatory ability of the cerebral arterioles seems to remain unchanged in this patient group and is not correlated with the severity of hyperlipidemia.

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“…Also, cerebral perfusion is lowered during paroxysms of atrial fibrillation ( Totaro et al ., 1993 ) and during tachycardia in patients with coronary artery disease ( Hagendorff et al ., 1994 ), and both cerebral blood flow and cognitive function increase following pacemaker implantation in patients with bradycardia ( Koide et al ., 1994 ). Arterial hypertension, diabetes ( Kastrup et al ., 1990 ) and familial hypercholesterolaemia ( Rodriguez et al ., 1994 ) influence regulation of cerebral blood flow, and cerebral auto‐regulation is impaired in patients resuscitated after cardiac arrest ( Nishizawa & Kudoh, 1996). In the heart failure patient with cerebral symptoms, cerebral hypoxia can be expected even in the face of near normal blood pressure and blood gas variables, and in this study, some patients presented with a critically lowered ScO 2 despite near‐normal MAP, SaO 2 and PaCO 2 .…”

Section: Discussionmentioning

confidence: 99%

Well‐being and cerebral oxygen saturation during acute heart failure in humans

Madsen

Nielsen

Christiansen

2000

Clinical Physiology

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Cerebral symptoms and near-infrared spectrophotometry-determined cerebral oxygen saturation (ScO2) were followed in patients treated for normotensive acute congestive heart failure. The reproducibility and normal range for ScO2 were established from 39 resting subjects without cardio-respiratory disease: the ScO2 ranged from 55 to 78% with a coefficient of variation for triple determination of 6%. Patients rated cerebral symptoms on a scale with end-points of 0 (best) and 10 (worst). In eight patients with acute heart failure, arterial oxygen tension increased during decongestive treatment, from 9.1 (4.9-10) to 10.4 kPa (7.3-17); median with range, as did arterial oxygen saturation, from 94 (48-97) to 97% (87-99) (P<0.02), whereas the mean arterial pressure, heart rate and arterial carbon dioxide tension remained unchanged. The cerebral symptom score improved from 8 (3-10) to 1 (1-9) and the ScO2 increased from 34 (20-58) to 50% (19-91) (P<0.02). A ninth patient presented with a silent but massive myocardial infarction: she was cerebrally obtunded with a ScO2 of 18% and soon died. In patients with normotensive acute heart failure and cerebral symptoms, cerebral oxygen saturation is low, and during successful treatment ScO2 increases with the well-being of the patient.

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Regional cerebral blood flow in familial hypercholesterolemia.

Cited by 18 publications

References 39 publications

Effect of Cerebrovascular Risk Factors on Regional Cerebral Blood Flow

Effect of Cerebrovascular Risk Factors on Regional Cerebral Blood Flow

Cerebrovascular reserve capacity in patients with hyperlipidemia

Well‐being and cerebral oxygen saturation during acute heart failure in humans

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