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Transcranial Doppler Monitoring in Hypertensive Patients during Physical Exercise
Abstract
To evaluate the diagnostic value of a combined method, i.e. ergometer cycling with continuous bilateral transcranial Doppler monitoring (TCD) to detect cerebral hemodynamic abnormalities in recently diagnosed hypertensive patients.
30 neurologically symptom-free, nontreated patients with essential hypertension and 30 age- and sex-matched controls were studied. Carotid ultrasound, resting ECG and blood parameters were investigated. Cycling ergometry was performed according to the WHO protocol. Blood pressure, heart rate, end-tidal CO2 (etCO2) and bilateral middle cerebral artery (MCA) blood flow velocity (MV) were monitored.
At rest, MV in the MCA did not differ significantly between controls and hypertensive subjects. MV continuously increased in controls until the end of loading whereas a plateau was reached at 4 min in hypertensive subjects. During 6 min of cycling, the time course of absolute values of MV in the MCA and that of the changes in the ratio of mean velocity/end-tidal CO2 (DeltaMV/DeltaetCO2) differed significantly between hypertensive subjects and controls (p = 0.03 and p = 0.02, respectively).
Ergometer cycling combined with TCD revealed altered vasoreactivity, therefore this may be a sensitive method for the detection of early hemodynamic impairment in nontreated hypertensive subjects.
... The middle cerebral artery blood flow velocities measured in the present study correspond to those observed among healthy adolescents by Brouwers et al. [18] . Many previous studies stated that cerebral blood flow and cerebral blood flow velocities are similar in hypertensive and normotensive adults [3,19,20] . Other investigators reported higher cerebral blood flow velocities among hypertensives as compared to healthy individuals [4,21,22] and our results are in accordance with these results. ...
... Other investigators reported higher cerebral blood flow velocities among hypertensives as compared to healthy individuals [4,21,22] and our results are in accordance with these results. To explain the discrepancies between the two sets of observations, we have to note that the study populations were generally different: those who observed similar blood flow velocities among hypertensive and normotensive individuals mainly included middle-aged patients [3,19,20] , while in the other group of reports younger patients were assessed [4,21,22] . It is known that resting cerebral blood flow velocity shows a decreasing tendency over age. ...
... Decreased cerebral vasoreactivity among hypertensive patients as compared to healthy volunteers has been already observed in several studies [4,5,19,29,31] . The majority of these previous studies assessed vasoreactivity during hypercapnic stimuli, such as CO 2 inhalation [5] , intravenous acetazolamide [4] , physical exercise [19] and breath-holding [31] . ...
It is known that cerebral vasoreactivity is altered in adult arterial hypertension but no information is available about cerebral arteriolar function in hypertensive adolescents. Therefore, the aim of the present work was to assess cerebral vasoreactivity responses in adolescent hypertension.
113 hypertensive and 58 normotensive adolescents were assessed with transcranial Doppler sonography by using voluntary hyperventilation (HV) as vasoconstrictory stimulus. Absolute blood flow velocities (systolic, mean and diastolic) and pulsatility indices (PIs) at rest and after HV, as well as percentage change of the blood flow velocities after HV were compared among the groups.
Blood flow velocities at rest were significantly higher in hypertensive individuals, while PIs were similar in the two groups. After HV, all blood flow velocity parameters were higher among hypertensive teenagers than in healthy controls, while PIs did not differ between the two groups. Taking the relative changes after HV into account, it was found that HV induced a more pronounced change of the systolic and mean blood flow velocities of the control subjects than in hypertensive adolescents.
Cerebrovascular reactivity to hypocapnia is decreased in hypertensive adolescents as compared to healthy teenagers. Further studies are needed to clarify the clinical significance of altered cerebral microvascular function in adolescent hypertension.
... [4][5][6] Using TCD technique, some studies reported that velocity at middle cerebral artery (MCA) was significantly and inversely correlated with HD. 7,8 Whereas, some studies showed that hypertension did not alter static and dynamic cerebral autoregulation. [9][10][11][12] The aim of this study is to show how blood pressure, HD and antihypertensive treatment correlate to systolic blood flow velocities (V s ) at common carotid artery (CCA), internal carotid artery (ICA) and MCA in a large population before occurrence of stroke. ...
... Similar results were seen in Korea and Japan's studies, 7,8 although there was also a study showing that the velocity in the MCA did not differ significantly between normal and hypertensive subjects at rest. 11 Our study also clearly showed that it is the blood pressure that influences V s at MCA most, and antihypertensive treatment could modify the V s at MCA towards a normal level by lowering blood pressure. This may suggest that antihypertension 12 which suggested that hypertension results in reduced capability of cerebral vessels to adapt to functional changes, but this can be reversible after treatment. ...
In order to verify the relationship between blood pressure and cerebral blood flow velocity in sub-clinical natural population, 1294 middle-aged and old Beijing rural residents were investigated in autumn 2002. For all subjects, systolic blood flow velocities (V(s)) in common carotid artery (CCA), internal carotid artery (ICA) and middle cerebral artery (MCA) were detected with trans-cranial Doppler. Key factors such as anthropometry, medication use, blood pressure and blood biochemical analysis were investigated at the same time. After controlling for age, gender, diabetes, hypercholesterolaemia, smoking and body mass index, multivariate analysis showed that systolic blood pressure (SBP) correlated positively with V(s) at MCA and slight negatively correlated with at CCA. As blood pressure rose by 10 mm Hg, the V(s) at MCA increased by 1.63 cm/s. Duration of hypertension (HD) negatively correlated with V(s) at MCA (P<0.01). The V(s) at MCA in early-stage and chronic hypertensive patients were 92.9+/-1.9 and 84.1+/-2.3 cm/s, respectively. Antihypertensive treatment could modify the V(s) at MCA towards a normal level by lowering blood pressure. In conclusion, the effect of hypertension on cerebral blood flow is complex. V(s) at MCA positively correlated with SBP, but negatively related to HD. Antihypertensive treatment might be helpful to keep cerebral blood flow at a normal level.
... Conversely, we would not support these data being generalized to diseased populations. Various diseases have been shown to impair cerebral hemodynamics (Benedictus et al., 2017;Magyar et al., 2001). These diseases affect cerebrovascular control differently and speculation of each of these mechanisms is beyond the scope of this study. ...
Although systemic sex-specific differences in cardiovascular responses to exercise are well established, the comparison of sex-specific cerebrovascular responses to exercise has gone under-investigated especially, during high intensity exercise. Therefore, our purpose was to compare cerebrovascular responses in males and females throughout a graded exercise test (GXT). Twenty-six participants (13 Females and 13 Males, 24 ± 4 yrs.) completed a GXT on a recumbent cycle ergometer consisting of 3-min stages. Each sex completed 50W, 75W, 100W stages. Thereafter, power output increased 30W/stage for females and 40W/stage for males until participants were unable to maintain 60-80 RPM. The final stage completed by the participant was considered maximum workload(Wmax ). Respiratory gases (End-tidal CO2 , EtCO2 ), middle cerebral artery blood velocity (MCAv), heart rate (HR), non-invasive mean arterial pressure (MAP), cardiac output (CO), and stroke volume (SV) were continuously recorded on a breath-by-breath or beat-by-beat basis. Cerebral perfusion pressure, CPP = MAP (0. 7,355 distance from heart-level to doppler probe) and cerebral vascular conductance index, CVCi = MCAv/CPP 100mmHg were calculated. The change from baseline (Δ) in MCAv was similar between the sexes during the GXT (p = .091, ωp2 = 0.05). However, ΔCPP (p < .001, ωp2 = 0.25) was greater in males at intensities ≥ 80% Wmax and ΔCVCi (p = .005, ωp2 = 0.15) was greater in females at 100% Wmax . Δ End-tidal CO2 (ΔEtCO2 ) was not different between the sexes during exercise (p = .606, ωp2 = -0.03). These data suggest there are sex-specific differences in cerebrovascular control, and these differences may only be identifiable at high and severe intensity exercise.
... [29,30] Results from clinical and experimental studies have suggested that activation of the RAAS may contribute to the development of arterial stiffness, and RAAS blockade in patients with hypertension has more pronounced effects on arterial stiffness than other antihypertensive drugs. [31,32] Mallareddy et al performed a meta-analysis of clinical trials investigating the effects of ACE inhibitors on arterial stiffness measured by PWV or AIx, and concluded that ACEI have modest beneficial effects in reducing arterial stiffness, and this effect is at least partly independent of blood pressure changes. [33] In this study, ACE inhibitor treatment for 3 months did not result in a significant decrease in arterial stiffness parameters. ...
The importance of optimal blood pressure control for preventing or reducing the impairment of vascular and cognitive functions is well known. However, the reversibility of early alterations in vascular and cognitive functions through antihypertensive agents is under-investigated. In this study, we evaluated the influence of 3 months of angiotensin-converting enzyme (ACE) inhibition treatment on the morphological and functional arterial wall and cognitive performance changes in 30 newly diagnosed primary hypertensive patients.
Common carotid intima-media thickness (IMT) and brachial artery flow-mediated dilatation (FMD) were detected by ultrasonography. Arterial stiffness indicated by augmentation index (AIx) and pulse wave velocity (PWV) was assessed by arteriography. Cognitive functions were assessed by neuropsychological examination.
The executive function overall score was significantly higher at 3-month follow-up than at baseline (median, 0.233 (IQR, 0.447) vs –0.038 (0.936); P = .001). Three-month ACE inhibition did not produce significant improvement in IMT, FMD, AIx and PWV values. Significant negative associations were revealed between IMT and complex attention (r = –0.598, P = .0008), executive function (r = –0.617, P = .0005), and immediate memory (r = –0.420, P = .026) overall scores at follow-up. AIx had significant negative correlations with complex attention (r = –0.568, P = .001), executive function (r = –0.374, P = .046), and immediate memory (r = –0.507, P = .005). PWV correlated significantly and negatively with complex attention (r = –0.490, P = .007).
Timely and effective antihypertensive therapy with ACE inhibitors has significant beneficial effects on cognitive performance in as few as 3 months. Early ACE inhibition may have an important role in the reversal of initial impairments of cognitive function associated with hypertension-induced vascular alterations.
... This observation may agree with previous report that shows a reduction in arterial blood flow in high BMI subjects. In line with above argument, is the report that high BMI is associated with a reduction in cerebral blood flow velocity and increases cardiovascular resistance [24]. ...
... However, how hypertension compromises cognition remains speculative. It has been proposed that the increased risk of cognitive decline and Alzheimer disease relates to endothelial dysfunction and subsequent changes in cerebral hemodynamics including decreased cerebral blood flow at rest [9,10], impaired cerebrovascular reactivity [11][12][13] and abnormal neurovascular coupling [14]. More recently, animal studies related hypertension-associated impaired cognition to decreased levels of brain-derived neurotrophic factor (BDNF) in the hippocampus [4][5][6]15], a brain region largely involved in learning and memory [16]. ...
Objective:
Decreased brain-derived neurotrophic factor (BDNF) level has been reported in the hippocampus of hypertensive rats. The present study explored whether brain neurons and/or endothelial cells are targeted by hypertension with respect to BDNF expression and the potential of physical exercise to cope with hypertension.
Methods:
Physical exercise was induced in spontaneously hypertensive rats (SHR) and Wistar Kyoto (WKY) rats. The hippocampus of sedentary and exercised rats (n = 6 for each group) were used for western blots to assess proBDNF, mature BDNF (mBDNF), tropomyosin-related kinase B (TrkB), P-TrkB (TrkB phosphorylated at tyrosine 816), synaptophysin, endothelial nitric oxide synthase (eNOS) and eNOS phosphorylated at serine 1177 protein levels. BDNF and proBDNF localization in the hippocampus was studied in WKY rats, SHR and exercised SHR (n = 5 each). mBDNF and proBDNF protein levels were also assessed in hippocampal slices prepared from SHR (n = 10) that were incubated for 24 h with the nitric oxide (NO) donor glyceryl trinitrate. SBP was measured by the tail-cuff method.
Results:
Exercise modified blood pressure neither in SHR nor WKY. As compared with WKY rats, SHR displayed decreased levels of mBDNF, P-TrkB, synaptophysin, eNOS and eNOS phosphorylated at serine 1177 but no change in proBDNF and TrkB levels. These effects coincided with low BDNF staining in both endothelial cells and neurons. Exercise improved the endothelium-derived NO system and the BDNF pathway in both strains. The NO donor increased mBDNF but decreased proBDNF levels.
Conclusion:
Our results revealed that endothelial and neuronal BDNF expressions were both impaired in hypertension and that physical exercise improved hippocampal mBDNF levels and signaling through blood pressure-independent mechanisms.
... There are few data on the characteristics of cerebral circulatory reactions to physical exercise of different types and intensities, which is partly due to technical difficulties in studying intracranial blood flow. A number of investigators have observed a positive linear relationship between the blood flow rate in the arteries of the base of the brain and the level of exercise [16,20,21]. Other studies have demonstrated that performance of maximal and submaximal levels of exercise produced either no increase or a decrease in the linear blood flow rate in the brain [9,11,15]. ...
The aim of this research was to study the cerebral hemodynamics reaction to step increase of physical exercises intensity during bicycle ergometer test in young healthy male subjects. Hemodynamics parameters were registered with the transcranial Doppler ultrasonography of middle cerebral artery (MCA) prior to the study and during the last seconds of every step of physical exercise. Cerebral hemodynamics response to physical exercise was characterized by a significant increase of peak systolic blood velocity in the MCA up to 0.25 W/kg of the body weight (90 rpm with regard to 0 W/kg) without further increase of blood velocity in the same physical exercise becoming more intensive up to 0.5 W/kg of the body weight. The stabilization mechanism of blood velocity in cerebral arteries in case of physical exercise increase and, hence, the autoregulation mechanism of cerebral circulation means that the increase of regional cerebral vascular resistance depends on the value of arterial pressure. The autoregulation mechanism of cerebral circulation starts working with he exercise intensity of 0.25 W/kg and the value of systolic blood pressure about 140-145 mm Hg.
... Although insulin resistance, type 2 diabetes and hypertension have been associated with impaired cerebrovascular function in non-pregnant populations [52][53][54], abnormalities of the cerebrovascular function are not always detected at rest. Indeed, Magyar et al. [186] showed impaired cerebral haemodynamics in response to exercise in newly diagnosed hypertensive patients, compared with age-and sex-matched controls, whereas at rest, MCA velocity did not differ between groups. Recently, impaired CBF during progressive exercise has also been shown in diabetic patients without signs of cardiovascular autonomic neuropathy [187]. ...
Cerebral blood flow (CBF) regulation is an indicator of cerebrovascular health increasingly recognized as being influenced by physical activity. Although regular exercise is recommended during healthy pregnancy, the effects of exercise on CBF regulation during this critical period of important blood flow increase and redistribution remain incompletely understood. Moreover, only a few studies have evaluated the effects of human pregnancy on CBF regulation. The present work summarizes current knowledge on CBF regulation in humans at rest and during aerobic exercise in relation to healthy pregnancy. Important gaps in the literature are highlighted, emphasizing the need to conduct well-designed studies assessing cerebrovascular function before, during and after this crucial life period to evaluate the potential cerebrovascular risks and benefits of exercise during pregnancy.
... Although untreated hypertension, which stimulates cerebrovascular remodeling and endothelial damage, [36] has been linked to reduced cerebral VR in the general population, [37][38][39][40] we did not observe a statistically significant association between hypertension and lower cerebral VR in our cohort. This may be at least partially accounted for by near universal use of anti-hypertensive therapy among individuals with hypertension in our cohort. ...
Objective:
To compare cerebral vasoreactivity, a measure of cerebrovascular endothelial function, between treated, virally suppressed HIV-infected individuals and HIV-uninfected controls and to evaluate the effect of HIV-specific factors on cerebral vasoreactivity.
Methods:
Cross-sectional study of 65 antiretroviral therapy-treated, virally suppressed HIV-infected individuals and 28 HIV-uninfected controls. Participants underwent noninvasive assessment of cerebral vasoreactivity using transcranial Doppler ultrasound and inhaled carbon dioxide (CO2). We used mixed effects multivariable linear regression to determine the association of HIV infection and HIV-specific factors with cerebral vasoreactivity.
Results:
Mean age was 57.2 years for HIV-infected participants and 53.5 years for HIV-uninfected controls. Most participants (95%) were men. Twenty-six per cent of HIV-infected participants were nonwhite compared to 32% of controls. Among HIV-infected participants, mean CD4 cell count was 596 cells/μl, and mean duration of viral suppression was 7.8 years. Cerebral vasoreactivity in response to hypercapnia (cerebral VRhyper) was lower in HIV-infected individuals compared to uninfected controls (3.23 versus 3.81%, P = 0.010). After adjusting for demographic and vascular risk factors, HIV infection was independently associated with lower cerebral vasoreactivity (-0.86%, 95% CI -1.30 to -0.42%, P < 0.001). We did not find a statistically significant effect of recent or nadir CD4 cell count on cerebral vasoreactivity. There was a trend toward higher cerebral vasoreactivity for each additional year of viral suppression.
Conclusion:
Treated, virally suppressed HIV infection negatively impacted cerebral vasoreactivity even after adjustment for traditional vascular risk factors. These data highlight the potential contribution of cerebrovascular endothelial dysfunction to the elevated risk of stroke observed in HIV-infected individuals.
Purpose of review:
Summarize the methods used for measurement of cerebral blood flow and oxygenation; describe the effects of hypertension on cerebral blood flow and oxygenation.
Recent findings:
Information regarding the effects of hypertension on cerebrovascular circulation during exercise is very limited, despite a plethora of methods to help with its assessment. In normotensive individuals performing incremental exercise testing, total blood flow to the brain increases. In contrast, the few studies performed in hypertensive patients suggest a smaller increase in cerebral blood flow, despite higher blood pressure levels. Endothelial dysfunction and increased vasoconstrictor concentration, as well as large vessel atherosclerosis and decreased small vessel number, have been proposed as the underlying mechanisms. Hypertension may adversely impact oxygen and blood delivery to the brain, both at rest and during exercise. Future studies should utilize the newer, noninvasive techniques to better characterize the interplay between the brain and exercise in hypertension.
The prevalence of dementia worldwide is growing at an alarming rate. A number of studies and meta-analyses have provided evidence for increased risk of dementia in patients with metabolic syndrome (MS) as compared to persons without MS. However, there are some reports demonstrating a lack of association between MS and increased dementia risk. In this review, taking into account the potential role of individual MS components in the pathogenesis of MS-related cognitive dysfunction, we considered the underlying mechanisms in arterial hypertension, diabetes mellitus, dyslipidemia, and obesity. The pathogenesis of dementia in MS is multifactorial, involving both vascular injury and non-ischemic neuronal death due to neurodegeneration. Neurodegenerative and ischemic lesions do not simply coexist in the brain due to independent evolution, but rather exacerbate each other, leading to more severe consequences for cognition than would either pathology alone. In addition to universal mechanisms of cognitive dysfunction shared by all MS components, other pathogenetic pathways leading to cognitive deficits and dementia, which are specific for each component, also play a role. Examples of such component-specific pathogenetic pathways include central insulin resistance and hypoglycemia in diabetes, neuroinflammation and adipokine imbalance in obesity, as well as arteriolosclerosis and lipohyalinosis in arterial hypertension. A more detailed understanding of cognitive disorders based on the recognition of underlying molecular mechanisms will aid in the development of new methods for prevention and treatment of devastating cognitive problems in MS.
Background. Adolescent hypertension predicts hypertension and increased cardiovascular morbidity in adulthood. The aim of the present work was to test whether cerebrovascular reactivity to CO2 is altered among hypertensive adolescents. Methods. From the population-based cohort of the Debrecen Hypertension Study, 113 hypertensive and 58 normotensive adolescents underwent transcranial Doppler measurements at rest and after 30 seconds of breath holding. Results. Systolic, mean, and diastolic blood flow velocities were higher among hypertensive individuals at rest. Taking the absolute blood flow velocity parameters into account, after breath holding, only the pulsatility index was significantly higher in the hypertensive group. The percentage change of the different blood flow parameters showed less intensive change in hypertensive teenagers. Conclusion. Cerebral vasoreactivity is decreased among hypertensive individuals as compared to healthy controls.
Cerebral hemodynamic reactions to light physical exercise increasing stepwise on a bicycle ergometer were studied in healthy young male subjects. Hemodynamic parameters were measured by transcranial Doppler ultrasonography from the middle cerebral artery (MCA) before the start of the study and during the last few seconds of each exercise step. Cerebral hemodynamic reactions to physical exercise were characterized by a significant increase in systolic blood flow rate in the middle cerebral artery only at exercise levels of about 0.25 W/kg body weight (90 rpm at 0 W/kg) with no further increase in the blood flow rate with increases in loading to 0.5 W/kg body weight. The mechanism stabilizing blood flow rate in the cerebral arteries as physical exercise increased and, thus, the mechanism of cerebral circulatory autoregulation consisted of a arterial pressure-dependent increase in regional cerebral vascular resistance. The threshold at which the cerebral blood flow rate autoregulatory mechanism was triggered in normal subjects corresponded to a loading of about 0.25 W/kg and a systolic arterial pressure of about 140-145 mmHg.
Adolescent hypertension predicts hypertension and increased cardiovascular morbidity in adulthood. The aim of the present work was to test whether cerebrovascular reactivity to CO2 is altered among hypertensive adolescents.
From the population-based cohort of the Debrecen Hypertension Study, 113 hypertensive and 58 normotensive adolescents underwent transcranial Doppler measurements at rest and after 30 seconds of breath holding.
Systolic, mean, and diastolic blood flow velocities were higher among hypertensive individuals at rest. Taking the absolute blood flow velocity parameters into account, after breath holding, only the pulsatility index was significantly higher in the hypertensive group. The percentage change of the different blood flow parameters showed less intensive change in hypertensive teenagers.
Cerebral vasoreactivity is decreased among hypertensive individuals as compared to healthy controls.
Background:
Relatively little is known about physiological cerebrovascular haemodynamics during physical stress in elderly healthy individuals. The aim of this study was to determine the effect of ergometer stress on cerebrovascular haemodynamics in elderly healthy individuals in comparison with young healthy individuals, using non-invasive methods.
Methods:
Continuous middle cerebral artery blood flow velocity (CBFV; transcranial Doppler ultrasound), beat-to-beat blood pressure, heart rate and transcutaneous pCO(2) were measured in response to 3 min ergometer exercise stress in 18 elderly healthy subjects (mean age +/- SD 66.5 +/- 5.8 years) and 18 healthy young subjects (mean age +/- SD 29.4 +/- 4.7 years). Pulsatility index (PI) was used as a parameter for cerebrovascular resistance. The subjects were in a supine position with an elevated trunk and performed exercise by pedalling on an ergometer, generating 75-100 W. Statistical analysis was carried out using MANOVA, a general linear model with repeated measures.
Results:
In both groups, blood pressure increased significantly (p < 0.001) with time during exercise, with no significant differences between the groups or regarding interaction (time sequence/group factor). Heart rate increased significantly with time during exercise (p < 0.001) and was significantly more prominent (p = 0.002) and prolonged (p < 0.001) in the young group. pCO(2) did not differ with time or between the groups and with regard to interaction. Mean CBFV (MFV) increased significantly during time (p < 0.001). Between the groups, there was no significant difference (p = 0.836), but with regard to interaction (time sequence/group factor), there was a significant delay in MFV increase in the group of young subjects (p = 0.002). The PI, a measure of cerebrovascular resistance, increased significantly with time without significant differences between the groups (p = 0.061), but was significantly delayed in the elderly regarding the interaction time sequence/group factor (p < 0.001).
Conclusion:
The cerebrovascular changes during ergometer exercise may reflect the combined activation of the cerebrovascular autoregulative mechanisms (predominantly neurogenic and myogenic). In healthy normotensive elderly subjects, cerebral autoregulatory capacity is retained but delayed in response to ergometer stress compared with young healthy subjects. We speculate that these findings may contribute to a higher risk of cerebral hypoperfusion in the elderly.
Previously, 30 untreated hypertensive patients were investigated by transcranial Doppler (TCD) monitoring during physical exercise, and changes of hemodynamic parameters were compared with those of age matched healthy subjects. After 3-year antihypertensive (AHT) treatment, these hypertensives were investigated again. The aim of this study was to compare the cerebral hemodynamic changes in the regularly treated and noncompliant (untreated) hypertensives during ergometer cycling.
Nineteen of 30 previously untreated hypertensive patients could be investigated again using the same method as before. Eleven were regularly treated (treated hypertensive [T-HT] group), and 8 did not take their AHT medications due to lack of compliance (noncompliant hypertensive [NC-HT] group). Blood pressure, heart rate, end-tidal CO2 (etCO2; Capnogard capnograph), and bilateral middle cerebral artery mean blood flow velocity (MV) were continuously monitored during ergometer cycling according to the World Health Organization protocol. Values of 2-minute loading were analyzed.
Median loading time did not differ significantly between the T-HT and NC-HT groups. After 2 minutes of cycling in treated patients, the ratio of MV and etCO changes (DeltaMV/DeltaetCO2) showed similar values as before therapy (P = .38), whereas in noncompliant patients, a further worsening of the ratio of DeltaMV/DeltaetCO2 could be observed (P = .04).
The decrease of arteriolar vasodilation (ie, the ratio of DeltaMV/DeltaetCO2) could be demonstrated in the NC-HT group after 3 years. TCD combined with ergometer cycling is a useful method for evaluation of cerebral hemodynamic changes after AHT therapy.
Cerebrosvascular reserve capacity can be estimated by Doppler CO2 or acetazolamide (Diamox) stimulation. These two methods were compared in 18 normal subjects. The variability of CO2 reactivity (mean 27.4 ± 3.8%/ vol% CO2) was markedly lower than that of Diamox reactivity (mean 41.2 ± 21.3%), which was partly caused by reactive hyperventilation. Unexpectedly, there was no positive correlation between CO2 and acetazolamide challenge (r = –0.14). A maximum dilation of the cerebral arterioles after acetazolamide administration could not be achieved as demonstrated by a diminished, but still existing CO2 reactivity during Diamox testing. Compared to CO2 stimulation, Diamox testing was more time-consuming and caused numerous, though reversible side effects. Thus, using transcranial Doppler sonography for assessing cerebrovascular reserve capacity, CO2 stimulation seems preferable to acetazolamide administration in most cases.
The aim of our study was to evaluate by transcranial Doppler ultrasonography the dynamics of blood flow velocity changes in the middle cerebral artery during and after hypocapnia-induced vasoconstriction in untreated essential hypertensive patients.
Sixteen hypertensive patients (10 men and six women, 29-62 years of age) and 10 healthy control subjects (six men and four women, 30-62 years of age) were studied. Patients with mild-to-moderate essential hypertension (mean +/- SE blood pressure, 171/106 +/- 3/2 mm Hg) belonged to stage I or II of the World Health Organization classification. Mean blood flow velocity in the middle cerebral artery, arterial blood pressure, and end-tidal CO2 partial pressure were recorded at baseline, during 2-minute hyperventilation, and every 30 seconds up to 5 minutes after hyperventilation.
End-tidal CO2 partial pressure values overlapped in the two groups throughout the study. Baseline values of mean blood flow velocity in hypertensive patients were similar to those in normotensive subjects (mean +/- SE values, 64.7 +/- 3.9 cm/sec versus 58.6 +/- 3.7 cm/sec). A similar fall in mean blood flow velocity was observed in hypertensive patients and normotensive subjects (43.2 +/- 2.8% versus 46.7 +/- 3.6%). Mean blood flow velocity reverted to baseline more quickly in hypertensive patients: 1.5 minutes after hyperventilation, mean blood flow velocity was 60.7 +/- 3.1% and 84.9 +/- 1.8% of control in normotensive subjects and hypertensive patients, respectively. No changes in arterial blood pressure were observed in either group throughout the study.
This study demonstrates that the recovery of blood flow velocity in the middle cerebral artery after hyperventilation is faster in hypertensive patients than in normal subjects, thus providing further evidence that chronic hypertension is associated with changes in the dynamics of cerebral blood vessel reactivity.
Transcranial Doppler ultrasound-determined middle (MCA) and anterior (ACA) cerebral artery mean flow velocities (Vmean) and pulsatility indexes (PI) were measured during "no-load" [21, 60, and 102 revolutions/min (rpm)] and loaded cycling (30, 60, and 149 W) at approximately 60 rpm. At rest Vmean MCA was 51 (36-55) cm/s (median and range; n = 10) and Vmean ACA was 41 (36-49) cm/s (n = 7; P < 0.05). With no load on the cycle Vmean MCA increased 4 (2-36), 10 (0-47), and 27% (4-58) (P < 0.05) at the three pedaling frequencies, respectively; arterial PCO2 (PaCO2) remained constant. During loaded cycling the increases were 19 (6-42), 25 (2-45), and 32% (12-67) (P < 0.01), respectively, with only a minimal change in PaCO2. No significant changes were observed in Vmean ACA. Changes in Vmean MCA were similar to those recorded by the initial slope index (ISI) of the 133Xe clearance method (n = 11), which in turn were smaller than increases recorded by the fast-compartment flow. PI ACA followed PI MCA during no-load as well as loaded exercise and increased with work rate, perhaps reflecting an increase in pulse pressure from 56 (48-63) mmHg at rest to 109 (88-123) mmHg at 149 W (P < 0.01). Data demonstrate a graded increase in regional cerebral perfusion during dynamic exercise corresponding to the MCA territory.
Changes in middle cerebral artery flow velocity (Vmean), measured by transcranial Doppler ultrasound, were used to determine whether increases in mean arterial pressure (MAP) or brain activation enhance cerebral perfusion during exercise. We also evaluated the role of "central command," mechanoreceptors, and/or muscle "metaboreceptors" on cerebral perfusion. Ten healthy subjects performed two levels of dynamic exercise corresponding to a heart rate of 110 (range 89-134) and 148 (129-170) beats/min, respectively, and exhaustive one-legged static knee extension. Measurements were continued during 2-2.5 min of muscle ischemia. MAP increased similarly during static [114 (102-133) mmHg] and heavy dynamic exercise [121 (104-136) mmHg] and increased during muscle ischemia after dynamic exercise. During heavy dynamic exercise, Vmean increased 24% (10-47%; P less than 0.01) over approximately 3 min despite constant arterial carbon dioxide tension. In contrast, static exercise with a higher rate of perceived exertion [18 (13-20) vs. 15 (12-18) units; P less than 0.01] was associated with no significant change in Vmean. Muscle ischemia after exercise was not associated with an elevation in Vmean, and it did not provoke an increase in Vmean after static exercise. Changes in Vmean during exercise were similar to those recorded with the initial slope index of the 133Xe clearance method. The data show that middle cerebral artery mean flow velocity reflects changes in cerebral perfusion during exercise. Furthermore, they support the hypothesis that cerebral perfusion during exercise reflects an increase in brain activation that is independent of MAP, central command, and muscle metaboreceptors but is likely to depend on influence of mechanoreceptors.
A proportion of individuals with carotid artery stenosis show a reduced cerebrovascular reserve as measured by a reduced cerebral arterial vasodilatory response to carbon dioxide. Two methods of quantifying this vasodilatory response, using transcranial Doppler ultrasonography, have been in general use: the total range of vasodilation between hypocapnia, induced by hyperventilation, and hypercapnia induced by breathing carbon dioxide, and the response to breathing a fixed concentration of 5% carbon dioxide. We studied whether it is possible to use the rise in carbon dioxide occurring during breath-holding as the vasodilatory stimulus.
Using transcranial Doppler, cerebral reactivity to carbon dioxide was measured in 23 subjects undergoing intravenous digital subtraction angiography of their carotid arteries for symptoms of cerebrovascular disease. A breath-holding method was compared with the two previous methods, which required administration of carbon dioxide.
All three methods gave results that correlated highly significantly with the degree of carotid stenosis, although the correlation was highest when the full vasodilatory range was measured. This method was adopted as the gold standard, and the other methods were compared with it. The breath-holding method correlated at least as well (rho = 0.67) as the 5% CO2 method (rho = 0.64). It identified a similar group of low reactors to our gold standard method, whereas the 5% CO2 method gave some discrepant results.
The breath-holding method offers potential as a convenient, well-tolerated screening method of assessing carbon dioxide reactivity not requiring the administration of carbon dioxide, although further validation against more established methods of measuring cerebrovascular reserve is first required.
The aim of this study was to determine the ability of transcranial Doppler ultrasonography when used to assess cerebral vasoreactivity. The results of this method were compared with regional cerebral blood flow measurements.
Forty-three patients with symptoms suggesting cerebrovascular disease took part. Transcranial Doppler findings in the middle cerebral arteries were compared with regional cerebral blood flow in the corresponding perfusion territories before and after acetazolamide administration.
There was a significant positive correlation between the absolute increase in cerebral blood flow in milliliters per 100 g per minute and the percent increase in velocity (r = 0.63). The right-left, side-to-side difference of the acetazolamide response obtained by the two methods also showed a positive correlation (r = 0.80). Control limits obtained from healthy subjects were used for both the blood flow increase (absolute values and asymmetry in absolute values) and the velocity increase (percent increase and asymmetry in percent increase). The two methods then agreed in their evaluation of vasoreactivity in 74 (86%) of the 86 middle cerebral artery perfusion territories; 20 (23%) were assessed by both methods as having a reduced vasodilatory reserve. Eleven hemispheres with a slightly reduced regional cerebral blood flow response to acetazolamide were not detected by transcranial Doppler, whereas all territories with a marked reduction were identified by Doppler. Only one hemisphere with a normal cerebral blood flow increase after acetazolamide administration was assessed by Doppler as having reduced vasoreactivity.
Transcranial Doppler and the acetazolamide test may be used in clinical situations to assess cerebral vasoreactivity.
Analysis of the blood flow velocities in the middle cerebral artery by transcranial Doppler ultrasonography was performed in 158 healthy volunteers (aged 14-70 years; 82 men and 76 women). In a subgroup of 38 men and 21 women the end-tidal [CO2] was also measured. The influence of biological factors such as age, sex, end-tidal [CO2], and pulsatility and resistance indices on the mean blood flow velocity in normal ageing was investigated by multiple regression analysis. In both sex groups the measured mean blood flow velocity decreased significantly with age (P values less than 0.0003 for women and less than 0.0001 for men). Women had significantly higher blood flow velocities than men (P = 0.008) and the age-corrected sex difference of 5.2 cm s-1 did not significantly depend on age (P = 0.93). The age-related linear decline of the mean blood flow velocity could not be explained by a concomitant decrease of the end-tidal [CO2]. In a group of subjects older than 50 years, the decrease of the mean blood flow velocity was significantly related to the increase of the pulsatility or resistance index.
Until recently, both the diagnosis of intracranial occlusive disease of the large brain arteries, as well as intracranial flow abnormalities due to extracranial arterial lesions, have been a "blind spot" for ultrasound techniques. With the advent of transcranial Doppler sonography (TCD), however, a broad spectrum of potential clinical and scientific applications of TCD to the intracranial vasculature has been advocated. In order to achieve an informative insonation of vessels and a correct interpretation of findings, knowledge of both anatomical landmarks within the skull and flow characteristics of distinct vessel segments are necessary. This paper presents such data elaborated from 64 carotid and 42 vertebral angiograms, 40 contrast-medium enhanced CT scans demonstrating the circle of Willis, 122 normal sagittal MRI scans of the brainstem, 40 cadaver skulls, 38 fresh cadavers, 106 normal volunteers and 59 patients with subclavian steal mechanisms. The main findings were as follows: The inner internal carotid artery bifurcation, the M1-segment of the middle cerebral artery, the C3-segment of the carotid siphon, the vertebral artery junction and the top of the basilar artery were found at insonation depths of 60.4 +/- 7, 40 +/- 8 to 60.4 +/- 7, 62 +/- 4, 84 +/- 8 and 108 +/- 8 mm, respectively. Normal mean flow velocities within the M1-segment, the posterior cerebral artery, the carotid siphon and the basilar trunk were 58 +/- 15.6, 39 +/- 9.9, 47 +/- 13.8 and 41 +/- 10 cm/s, respectively, and revealed a marked decrease with age. Intraindividual side-to-side differences were low. Vertebrobasilar data from measurements of neuroradiological material closely met in vivo findings in normals and patients. Criteria for the identification of various vessel segments are provided. On the basis of these findings, a topographical orientation within the skull should be possible in order that beginners commence TCD accurately. Normative velocity data are helpful for differentiating normal and pathological flow conditions at different ages.
The goal of this study was the development of a simple bedside test to assess cerebrovascular reserve capacity using transcranial Doppler sonography. We studied 33 normal persons at rest and after stimulation of cerebral blood flow with 1 g acetazolamide. Their mean +/- SD increase in blood flow velocity in 54 middle cerebral arteries 10 minutes after stimulation was 24.4 +/- 9.2 cm/sec. We tried to validate the increase in blood flow velocity as cerebrovascular reserve capacity in 21 patients with obstructive carotid artery disease and symptoms of cerebral ischemia. The patients were studied using transcranial Doppler sonography and xenon-133 dynamic single-photon emission computed tomography after acetazolamide stimulation. Their increases in blood flow velocity (delta FV) and increases in cerebral blood flow (delta CBF) correlated significantly in both hemispheres (asymptomatic: Y = 0.32X + 10.65, r = 0.45, p = 0.04; symptomatic: Y = 0.36X + 2.28, r = 0.59, p = 0.004). There was no significant difference between the slopes of the regression lines. Blood flow velocity and cerebral blood flow at rest were not correlated. The increase in blood flow velocity after acetazolamide stimulation offers a simple and reliable method for assessing cerebrovascular reserve capacity.
We used positron emission tomography to examine retrospectively the effects of blood pressure on regional cerebral blood flow and oxygen metabolism in seven normotensive and eight hypertensive patients with a history of transient neurologic deficits. In the hypertensive patients, a decrease in regional cerebral blood flow was closely related to blood pressure; these changes were most pronounced in the supratentorial structures, especially the striatum and thalamus. In contrast, the regional cerebral metabolic rate for oxygen was less related to blood pressure. Consequently, the regional oxygen extraction fraction was increased in the hypertensive patients, while regional cerebral blood volume and the regional cerebral blood flow volume ratio were unchanged. Multivariate regression analysis confirmed that hypertension was an independent factor affecting regional cerebral blood flow. The analysis also disclosed that age, sex, hematocrit, smoking, and PaCO2 affected regional cerebral blood flow. These findings suggest that the hemodynamic reserve in hypertensive individuals is reduced, which may predispose them to cerebral ischemia and perhaps stroke, even during small decreases in cerebral perfusion pressure.
Using the 133Xe-DSPECT technique, quantitative measurements of regional cerebral blood flow (rCBF) were performed before and after provocation with acetazolamide (Diamox) i.v. in 32 patients without evidence of brain disease (normals). In 6 cases, additional studies were carried out to establish the time of maximal rCBF increase which was found to be approximately 15 min p.i. 1 g of Diamox increases the rCBF from 58 +/- 8 at rest to 73 +/- 5 ml/100 g/min. A Diamox dose of 2 g (9 cases) causes no further rCBF increase. After plotting the rCBF before provocation (rCBFR) and the Diamox-induced rCBF increase (reserve capacity, delta rCBF) the regression line was delta rCBF = -0,6XrCBFR + 50 (correlation coefficient: r = -0,77). In normals with relatively low rCBF values at rest, Diamox increases the reserve capacity much more than in normals with high rCBF values before provocation. It can be expected that this concept of measuring rCBF at rest and the reserve capacity will increase the sensitivity of distinguishing patients with reversible cerebrovascular disease (even bilateral) from normals.
Regional cerebral blood flow was studied by means of the 133Xe inhalation method in 26 untreated and 10 treated patients with essential hypertension. The untreated subjects were divided into newly and previously diagnosed groups to assess the relation between regional cerebral blood flow and the duration of hypertension. The overall flow reduction was more marked in the frontal and temporal regions in the previously diagnosed group, and this was attributed to pathological changes in the district served by the middle cerebral artery. Regional temporal lobe impairment was also noted in the newly diagnosed and treated subjects. A significant correlation was found between regional cerebral blood flow and mean arterial blood pressure.
By providing a non-invasive method for continuous display of mean flow velocity (Vmean) in the cerebral arteries, transcranial Doppler (TCD) ultrasound supplements evaluation of cerebral perfusion. Dynamic exercise increases middle cerebral artery (MCA) Vmean from approximately 55 to 65 cm s-1 dependent on work rate, and even more when corrected for changes of the arterial carbon dioxide tension. Evaluation of Vmean corresponds to that of cerebral blood flow as determined with the 133Xenon clearance technique, and reflects regional cortical regulation of the active muscles with important afferent nervous influence. Concomitant increases of mean arterial pressure (MAP) and heart rate is only of minor importance as illustrated during static exercise and post-exercise muscle ischaemia, where Vmean is not significantly elevated. During sustained head-up tilt, the Vmean remained unchanged at a MAP approximately 83 mmHg. Below this level, it decreased in parallel with MAP until MAP reached 50 mmHg. At an even lower MAP, Vmean seemed to approach a lower limit approximately 25 cm s-1, but at a diastolic pressure of 21 mmHg there was no flow in the MCA. Conversely, during post-exercise muscle ischemia, an increase in MAP to 140 mmHg did not influence Vmean. This is in contrast to patients operated for carotid artery stenosis and who develop ipsilateral headache. In these patients the ipsilateral MCA Vmean changed in parallel with MAP, and autoregulation was re-established only after one to two weeks. In patients with severe carotid stenosis and poor collateral circulation, the CO2-reactivity as expressed by Vmean was the lowest, and could be negative on the ipsilateral side. During carotid endarterectomy, a Vmean clamp/Vmean pre-clamp ratio below 0.6 identified patients with a cerebral blood flow below 20 ml 100 g-1 min-1. Furthermore, when the ratio was below 0.4 pathological electroenchephalographic changes developed. Thus, Vmean of the large basal cerebral arteries reflects cerebral perfusion with respect to regional flow distribution, autoregulatory response, and CO2-reactivity in normal man and patients with limited cerebral flow.
Dynamic exercise enhances regional cerebral artery mean flow velocity. J. Appl. Physiol. 78(1): 12-16, 1995.--Anterior (ACA) and middle (MCA) cerebral artery mean flow velocities (Vmean) and pulsatility indexes were determined using transcranial Doppler in 14 subjects during dynamic exercise after assessment of the carbon dioxide reactivity for both arteries. Right hand contractions provoked an elevation in left MCA Vmean [19% (12-28); P < 0.01], whereas the pulsatility decreased in all four arteries (P < 0.05). During right foot movement, left ACA Vmean increased by 23% (11-37; P < 0.01) with lesser (approximately 10%; P < 0.05) increases in the other arteries, and pulsatility index decreased (P < 0.05). During cycling, ACA and MCA Vmean increased bilaterally by 23% (10-49) and 18% (5-32), respectively (P < 0.01), and the pulsatility was also elevated (P < 0.05). Cerebral artery pulsatility did not demonstrate a focal response but depended did not demonstrate a focal response but depended on the muscle mass involved during exercise. The data demonstrate a significant increase in Vmean for the artery supplying the cortical projection of the exercising limb. Insignificant and marginally significant increases in Vmean may be related to sympathetically mediated vasoconstriction and/or coactivation of untargeted muscle groups.
The present study was designed to examine cerebral hemodynamics in early and chronic stages of hypertension using transcranial Doppler sonography.
Our study population consisted of 16 chronic hypertensive patients with chronic and small deep brain infarction, 10 young early-stage hypertensive subjects, and 16 young normotensive healthy volunteers. Using three-dimensional mapping techniques, we identified the M1 portion of the middle cerebral arteries and measured mean blood flow velocity, and we calculated the Gosling pulsatility index (PI), Fourier PI of the first harmonic (Fourier PI1), and cerebrovascular resistance.
Mean blood flow velocity in the young hypertensive group was statistically higher (71.7 +/- 11.7 cm/s [mean +/- SD]) than among chronic hypertensive subjects (56.9 +/- 21.4 cm/s, P < .01) and normotensive subjects (63.2 +/- 11.8 cm/s, P < .05). Gosling PI presented a mirror image of mean blood flow velocity in both hypertensive and normotensive subjects. Chronic hypertensive subjects showed significantly higher Fourier PI1 (0.32 +/- 0.05) and cerebrovascular resistance (2.08 +/- 0.82 mm Hg/cm per second) than normotensive subjects (0.25 +/- 0.03 and 1.31 +/- 0.23 mm Hg/cm per second [P < .005], respectively) or early-stage hypertensive subjects (0.25 +/- 0.04 and 1.44 +/- 0.26 mm Hg/cm per second [P < .02], respectively).
Early-stage hypertensive subjects demonstrated higher velocity, normal Fourier PI1, and near normal vascular resistance, whereas chronic hypertensive subjects showed near normal velocity, higher Fourier PI, and greater vascular resistance. Results may indicate different degrees of cerebral arteriopathy and arteriolopathy between early and late stages of hypertension.
Spontaneously hypertensive rats (SHR) are hypertensive, hyperactive, and hydrocephalic; furthermore SHR have smaller brain volume and weight than age-matched, normotensive Wistar-Kyoto rats (WKY). At 6-7 months of age, local cerebral glucose is sizably lower in SHR than WKY. The hypothesis that these several abnormalities of SHR lead to variations in cerebral microvascular bed morphology was tested in 6-7-month-old SHR and WKY by quantitating various parameters of small, intermediate, and large parenchymal microvessels (grouped by luminal diameter) in 21 brain areas. Within each rat strain, the microvascular bed properties such as vessel profile frequency (density) varied considerably among the 21 brain areas. In opposition to the hypothesis, mean luminal diameter as well as profile frequency, surface area, and luminal volume of the microvascular beds per unit tissue mass were virtually identical in each brain area of SHR and WKY for the three groups of microvessels. These findings coupled with the reports of less tissue per structure but similar density of neurons throughout the brain of SHR and WKY indicate that there are fewer neurons and less vascular tissue per brain structure in 6-7-month-old SHR than WKY; in addition, they suggest a linkage between the size of parenchymal microvascular beds and the surrounding nervous tissue.
Cerebral blood flow has been reported to increase during dynamic exercise, but whether this occurs in proportion to the intensity remains unsettled. We measured middle cerebral artery blood flow velocity (νm) by transcranial Doppler ultrasound in 14 healthy young adults, at rest and during dynamic exercise performed on a cycle ergometer at a intensity progressively increasing, by 50 W every 4 min until exhaustion. Arterial blood pressure, heart rate, end-tidal, partial pressure of carbon dioxide (P
ETCO2), oxygen uptake (\(\dot V\)O2) and carbon dioxide output were determined at exercise intensity. Mean vM increased from 53 (SEM 2) cm · s−1 at rest to a maximum of 75 (SEM 4) cm · s−1 at 57% of the maximal attained \(\dot V\)O2(\(\dot V\)O2max), and thereafter progressively decreased to 59 (SEM 4) cm · s−1 at \(\dot V\)O2max. The respiratory exchange ratio (R) was 0.97 (SEM 0.01) at 57% of \(\dot V\)O2maxand 1.10 (SEM 0.01) at \(\dot V\)O2max. The P
ETCO2 increased from 5.9 (SEM 0.2) kPa at rest to 7.4 (SEM 0.2) kPa at 57% of \(\dot V\)O2maxand thereafter decreased to 5.9 (SEM 0.2) kPa at \(\dot V\)O2max. Mean arterial pressure increased from 98 (SEM 1) mmHg (13.1 kPa) at rest to 116 (SEM 1) mmHg (15.5 kPa) at 90% of \(\dot V\)O2max, and decreased slightly to 108 (SEM 1) mmHg (14.4 kPa) at \(\dot V\)O2max. In all the subjects, the maximal value of v
m was recorded at the highest attained exercise intensity below the anaerobic threshold (defined by R greater than 1). We concluded that cerebral blood flow as evaluated by middle cerebral artery flow velocity increased during dynamic exercise as a function of exercise intensity below the anaerobic threshold. At higher intensities, cerebral blood flow decreased, without however a complete return to baseline values, and it is suggested that this may have been at least in part explained by concomitant changes in arterial PCO2.
Forty-five measurements of diameters of 12 human cerebral arteries were performed during 10 craniotomies under moderate changes in mean blood pressure and end tidal CO2. The mean change in blood pressure was 30 +/- 16 mm Hg (standard deviation) and that of end tidal CO2 was 14 +/- 6 mm Hg (standard deviation). These changes were induced with nitroprusside, phenylephrine, and adjustment of ventilator rate. Measurements were made through the operating microscope focused at the highest power, with meticulous attention to constant angle and distance from the artery. The mean diameter change in the large cerebral arteries (carotid, middle cerebral artery, vertebral artery) was less than 4%, but the smaller arteries (anterior cerebral artery, M2 segment of middle cerebral artery) showed diameter changes as large as 29% and 21% to end tidal CO2 and blood pressure changes, respectively. These data suggest that at the time of craniotomy, diameters of the large cerebral vessels do not significantly change during moderate variations in blood pressure and CO2, but that larger changes may occur in smaller vessels. This constancy of diameter suggests that the transcranial Doppler velocities obtained during intraoperative monitoring of craniotomies may closely reflect blood flow through the insonated artery.
Changes in the diameter of intracranial arteries might have a major role in the pathophysiology of migraine. Though several studies have found alterations in velocity of blood flow and in cerebral vasomotor reactivity of intracranial arteries in migraineurs in headache-free periods, as well as during migraine attacks, the results are inconclusive. To determine if intracranial hemodynamic characteristics of patients with migraine differ from those of controls, we measured baseline velocity of blood flow by transcranial Doppler in the middle cerebral arteries in headache-free periods in 51 migraine patients and in 101 age-matched controls. Cerebrovascular reactivity was measured after intravenous administration of acetazolamide in 12 migrainous patients and in 19 controls. Baseline mean velocity was significantly higher in the migraine group (70 versus 65 and 72 versus 65 cm/s with P = 0.02 and P = 0.0007 on the left and right sides, respectively). The difference stayed significant during acetazolamide stimulation, but the course of response did not differ between controls and migraineurs. Despite statistical significance, absolute differences were small. Therefore, middle cerebral artery velocity measurements and the acetazolamide test are not useful for the diagnosis of migraine in the interictal period.
Identification of the subgroup of asymptomatic patients with severe internal carotid artery stenosis and high risk of stroke has important clinical implications. Cerebral vasomotor reactivity provides information regarding intracranial hemodynamic features and might have a prognostic value in predicting cerebrovascular ischemic events, especially in patients with carotid stenosis. The aim of our study was to assess the cerebral vasomotor reactivity in asymptomatic patients with carotid stenosis and evaluate its role in stroke occurrence.
Cerebral vasomotor reactivity was assessed using transcranial Doppler ultrasonology and the Diamox test (intravenous administration of 1.0 g acetazolamide) in 44 asymptomatic patients with severe (> 70%) internal carotid artery stenosis. Patients were followed up prospectively (mean, 2 years).
Cerebral vasomotor reactivity was estimated as good (> 40% increase of blood flow velocity in the middle cerebral artery ipsilateral to the carotid stenosis after undergoing the Diamox test) in 23 patients; it was impaired in the other 21. During the follow-up period, the overall annual rate for ipsilateral stokes was 2.3%; it was 7.9% for all ischemic cerebral events. No strokes or transient ischemic attacks occurred in the former group, but there were 7 cerebral ischemic events (2 strokes [1 fatal] and 5 transient ischemic attacks) in the latter group. There was a statistically significant correlation between cerebral ischemic events and impaired cerebral vasomotor reactivity (P = .009).
The data of this preliminary study suggest an important role of impaired cerebral vasomotor reactivity in predicting ischemic cerebral events. Preventive vascular surgery might be considered in this high-risk subgroup of asymptomatic patients with severe carotid stenosis.
This study was designed to demonstrate cerebral hemodynamic changes related to hypertension using transcranial Doppler ultrasonography. We measured the flow velocities and the Gosling pulsatility index of the middle cerebral artery and the internal carotid artery in 94 stroke-free, hypertensive patients and 81 age- and gender-matched healthy controls. Compared with the control subjects, patients with a longer duration (> or = 5 years) of hypertension showed significantly lower flow velocities of the middle cerebral artery and a higher Gosling pulsatility index of the middle cerebral- and the internal carotid artery. These differences were not observed in patients with a shorter duration of hypertension (<5 years). In the patient group, the mean velocity of the middle cerebral artery was significantly and inversely correlated with the duration of hypertension. Decreased flow velocity with increased pulsatility observed in this study suggest that alterations in the small cerebral vessels and arterioles contribute primarily to cerebral hemodynamic changes occurring in long-standing hypertension and also suggest the possible usefulness of transcranial Doppler in monitoring the progression of cerebral atherogenesis related to hypertension.
We studied the usefulness of transcranial Doppler sonography for assessing changes in vasoreactivity in patients with hypertension and the hemodynamic consequences of hypertension.
The study group comprised 25 patients with chronic severe hypertension and 25 age- and sex-matched healthy subjects. Cerebrovascular reserve capacity was assessed by transcranial Doppler recording of the blood flow velocity in both middle cerebral arteries before and 5, 10, 15, and 20 minutes after intravenous injection of 1 g of acetazolamide (Diamox). Blood pressure, blood gases, and other blood parameters were also measured before and after acetazolamide injection. The sizes of the left atrium, left ventricle, and aortic root were measured by echocardiography and correlated with the vasoreactivity after acetazolamide injection.
After acetazolamide injection, no significant changes in blood pressure were observed in either group. The mean blood flow velocity in the middle cerebral arteries of hypertensive patients (60.8 +/- 2.6 cm/sec) was not significantly different from that of controls (58.8 +/- 1.9 cm/sec) before acetazolamide injection. Ten minutes after acetazolamide injection, the percentage change in blood flow velocity was significantly lower in the hypertensive group (36.2 +/- 4.5%) than in the controls (52.6 +/- 3.7%). A significant negative correlation (p < 0.05) between decreased vasoreactivity and increased size of the left atrium and aortic root was observed.
Vasoreactivity decreases in hypertensive patients without neurologic deficits or computed tomography abnormalities. Enlargement of the left atrium correlates well with the severity of the impairment in vasoreactivity. Transcranial Doppler sonography can be a sensitive tool in the investigation of vascular impairment caused by hypertension and in the follow-up of hypertensive patients.
The early preclinical detection of cerebrovascular complications in individuals with diabetes is one of the goals of care described in the St. Vincent Declaration. In accordance with this goal, the aim of the present work was to investigate whether altered cerebral microvascular function in patients suffering from type 1 diabetes can be detected with a transcranial Doppler probe after the administration of acetazolamide. A total of 72 type 1 diabetic patients and 40 healthy control subjects entered the study. Patients were divided into two groups: those with long-term diabetes (disease duration of >10 years, n = 37) and those with short-term diabetes (disease duration of < or =10 years, n = 35). Mean blood-flow velocity in the middle cerebral artery (MCAV) was measured at rest and at 5, 10, 15, and 20 min after intravenous administration of 1 g acetazolamide with a transcranial Doppler probe and expressed as the percentage change from the pretest measurement. The percentage increase in MCAV (cerebrovascular reactivity) was calculated at each time point and compared between the groups. Cerebrovascular reserve capacity (CRC), expressed as the maximal percentage increase of the MCAV, was compared between the groups. Additionally, a reproducibility study of CRC was performed in 10 patients, using intraclass correlations. Cerebrovascular reactivity in the long-term diabetes group was lower (means +/- SD: 5 min, 23.4 +/- 15.4%; 10 min, 28.8 +/- 17.0%; 15 min, 30.0 +/- 15.6%; 20 min, 24.2 +/- 17.8%) than that of the control subjects (5 min, 43.5 +/- 23.9%; 10 min, 55.3 +/- 24.0%; 15 min, 56.7 +/- 23.8%; 20 min, 54.8 +/- 25.9%) and the short-term diabetic patients (5 min, 43.6 +/- 25.9%; 10 min, 52.2 +/- 27.7%; 15 min, 55.3 +/- 32.2%; 20 min, 45.8 +/- 35.8%). CRC was lower in the long-term diabetes group than in the control group or the short-term diabetes group. Impairment of cerebrovascular reactivity was associated with retino- and nephropathy and increased levels of fibrinogen. In contrast, CRC was independent from actual glucose, insulin, glycosylated hemoglobin, von Willebrand factor antigen, and alpha-2 macroglobulin levels. Transcranial Doppler measurements of the changes in MCAV after stimulation with acetazolamide can detect altered cerebral microvascular function in patients with diabetes. Cerebrovascular reactivity and reserve capacity are reduced in patients with long-term diabetes. Further prospective studies should delineate the clinical significance of our results.
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.
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.
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.
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.
Cerebrovascular reactivity, cerebrovascular reserve capacity, and velocity acceleration can be easily and reliably assessed by measuring acetazolamide-induced changes using transcranial Doppler. The authors' aim was to determine whether there are gender-related differences in these parameters. Fifty-six healthy subjects (27 males, 29 females) were examined using transcranial Doppler. Velocities in the middle cerebral artery on both sides were recorded before and at 5, 10, 15, and 20 minutes after intravenous administration of 1 g acetazolamide. The baseline mean flow velocity in the middle cerebral artery was significantly higher in women than in men (p < 0.02). After acetazolamide administration, significantly higher cerebrovascular reactivity, cerebrovascular reserve capacity, and velocity acceleration were observed in females than in males (p < 0.001 in all cases). Subgroup analysis showed that women before menopause responded with higher cerebrovascular reserve capacity and velocity acceleration than age-matched men (p < 0.01 and p < 0.001, respectively), but no significant difference was found between females after menopause and men of similar age.