Breath-holding Index Research Articles

Basilar and middle cerebral artery reactivity in patients with migraine.

Migraine has been reported as a possible risk factor for ischemic stroke. The mechanisms underlying this association are unknown. To evaluate cerebrovascular reactivity to hypercapnia in the anterior and posterior circulation of patients with migraine, as reduced cerebrovascular reactivity is associated with a predisposition to stroke in various clinical conditions. Using transcranial Doppler ultrasonography, changes in flow velocity during apnea were measured in both middle cerebral arteries and in the basilar artery of 15 control subjects and 30 patients with migraine (15 with aura and 15 without aura) during an attack-free period. Cerebrovascular reactivity was evaluated using the breath-holding index, which is calculated by dividing the percent increase in mean flow velocity recorded during a breath-holding episode by its duration (in seconds) after a normal inspiration. Vascular reactivity in the middle cerebral arteries was similar in patients and controls and significantly lower in the basilar artery of patients with migraine with aura compared with the other 2 groups (P <.0001). These findings show that in patients with migraine with aura, there is an impairment in the adaptive cerebral hemodynamic mechanisms in the posterior circulation. This fact could have pathogenetic implications since the association between migraine and stroke frequently regards patients with migraine with aura, and cerebral infarcts occur more commonly in the vertebrobasilar district.

Normalization of high interictal cerebrovascular reactivity in migraine without aura by treatment with flunarizine.

Modification of migraine-associated cerebrovascular reactivity may provide insight into the mechanism of action of a given therapeutic intervention. With transcranial Doppler and a breath-holding index, cerebrovascular reactivity to hypercapnia was evaluated in 20 patients with migraine without aura interictally and in 11 healthy controls. Patients were started on prophylactic treatment with flunarizine 10 mg per day, and measurements were repeated at the end of every month for 3 months. Headache status was evaluated clinically via a headache index. Headache index; breath-holding index; systolic, diastolic, and mean blood flow velocities; and pulsatility index measurements were recorded at every session. The baseline breath-holding index was significantly higher in the migraine group compared to the control group (P =.002). No difference in other parameters was found between the groups. The change in the headache index was significant (P<.001), indicating a beneficial effect from flunarizine. The breath-holding index improved significantly after treatment (P<.001), and the baseline difference in the breath-holding index between the pretreatment migraine group and the control group was no longer evident at 3 months. There was no significant change with treatment in the other transcranial Doppler parameters. Our finding of unchanged blood flow velocities but normalized cerebrovascular reactivity after treatment suggests that the mechanism of action of flunarizine in migraine does not involve a vasodilatory effect on cerebral vessels. It may be instead that flunarizine modifies cerebrovascular reactivity through its action on centrally located structures that subserve autonomic vascular control.

Exaggerated Interictal Cerebrovascular Reactivity But Normal Blood Flow Velocities in Migraine Without Aura

Interictal cerebrovascular reactivity and blood flow velocities were tested in 23 patients with migraine without aura and 10 age- and sex-matched healthy controls by using the breath holding index (BHI). The mean systolic, diastolic and mean velocities and pulsatility indices were not different in the controls and patients. The BHI was found to be significantly greater (P=0011) in the patients (1.64 +/- 0.33) compared with the controls (1.26 +/- 0.37), showing an exaggerated reactivity to hypercapnia in migraineurs. Reactivity to pCO2 theoretically depends on pre-existing arteriolar tone and thereby on baseline velocity. Our finding of similar blood flow velocities in controls and patients suggests that the underlying cause for this high reactivity may not be an increased vasotonus but an increased sensitivity to changes in blood CO2 levels.

Effect of collateral blood flow and cerebral vasomotor reactivity on the outcome of carotid artery occlusion.

Evidence suggests that an alteration in cerebral hemodynamics plays a relevant role in the occurrence of stroke in patients with carotid occlusion. The purpose of the present study was to evaluate the relationships among baseline characteristics, type and number of collateral pathways, cerebral vasomotor reactivity (VMR), and outcome of patients with carotid occlusion. One hundred four patients with symptomatic or asymptomatic internal carotid artery occlusion were followed up prospectively for a median period of 24 months. Cerebral VMR to apnea was calculated with transcranial Doppler ultrasonography by means of the breath-holding index (BHI) in the middle cerebral arteries. The patency of the 3 major intracranial collateral vessels was also evaluated. During the follow-up period, 18 patients experienced an ischemic stroke ipsilateral to internal carotid artery occlusion. Among factors considered, only older age, number of collateral pathways, and BHI values in the middle cerebral artery ipsilateral to the occluded side were significantly associated with the risk of ipsilateral stroke (P<0.001, P=0.008, and P<0.001, respectively; multiple Cox regression analysis). A normal VMR and favorable prognosis characterized patients with full collateral development; in this group, no patient experienced an ischemic event. On the other hand, an impaired VMR and increased probability of experiencing a stroke were found in patients without collateral pathways; the annual risk of ipsilateral stroke in this group was 32.7%. Patients with 1 or 2 collateral pathways showed a different VMR ranging from normal to strongly reduced BHI values. The ipsilateral stroke event risk was 17.5% in patients with 1 collateral vessel and 2.7% in patients with 2 collateral pathways. In this case, the risk of cerebrovascular events occurring during the follow-up period was significantly related to VMR. These data suggest that cerebral hemodynamic status in patients with carotid occlusive disease is influenced by both individual anatomic and functional characteristics. The planning of strategies to define the risk profile and any attempt to influence patients' outcome should be based on the evaluation of the intracranial hemodynamic adaptive status, with particular attention to the number of collateral vessels and the related VMR.

Cerebral hemodynamics in patients with carotid artery occlusion and contralateral moderate or severe internal carotid artery stenosis.

The purpose of this study was to evaluate cerebral hemodynamics in patients suffering from occlusion of the carotid artery (CA) and contralateral CA stenosis. Using transcranial Doppler ultrasonography, the cerebrovascular reactivity to hypercapnia in the middle cerebral arteries was evaluated by calculating the breath-holding index (BHI) of 69 symptomatic patients suffering from internal CA (ICA) occlusion and moderate or severe contralateral ICA stenosis. To evaluate which variables influenced BHIs ipsilateral to the site of ICA occlusion, a multiple stepwise linear regression analysis was performed that included the following factors: patient age, percentage of contralateral ICA stenosis, contralateral BHI, number of collateral pathways, and presence of hypertension, diabetes, smoking, and hyperlipidemia. An analysis of variance was conducted to evaluate the impact of the type of collateral vessels on the BHI. A regression analysis showed that the BHI ipsilateral to the site of ICA occlusion could be accounted for by the contralateral BHI (which was entered at the first step of the analysis, p < 0.001) and by the number of collateral pathways (which was entered at the second step, p = 0.033). Neither the degree of contralateral ICA stenosis nor the other variables could be added to improve the model. The analysis demonstrated that the absence of collateral pathways and the presence of the anterior communicating artery (ACoA) alone were associated with lower BHI values than those found in the presence of two or three collateral vessels, regardless of the presence of an anterior collateral pathway. On the basis of these data one can infer that the cerebral hemodynamic status of patients with occlusive disease of the CA is influenced by individual anatomical and functional characteristics. Because improvement in contralateral hemodynamics after surgical correction of an ICA stenosis can only be expected in the presence of an ACoA, the planning of strategies for influencing cerebral blood flow distal to an ICA occlusion and, in particular, the consideration of a contralateral carotid endarterectomy, should be preceded by a careful evaluation of the intracranial hemodynamic adaptive status of the patient. Particular attention should be paid to cerebrovascular reactivity and the number and type of collateral vessels that are present.

Cerebrovascular reactivity and subcortical infarctions.

To investigate the association between different kinds of ischemic lesions and cerebrovascular reactivity (CR) and to evaluate their relationships with the major risk factors for stroke. We evaluated CR using the breath-holding index technique during bilateral transcranial Doppler monitoring of flow velocity in the middle cerebral arteries of 41 consecutive patients attending our clinic for a recent, first-ever, ischemic stroke and in 15 control subjects. Based on the location of the lesion determined by computed tomography, the following 3 types of infarctions were identified: cortical (or territorial), single subcortical, and subcortical with multiple silent subcortical infarctions. Patients with a condition of severe carotid artery stenosis or occlusion, which in itself could account for altered CR, were excluded from this study. All physiological and pathologic conditions that could possibly cause an impairment in CR were recorded. The breath-holding index was significantly lower in the multiple subcortical infarctions group than in the control subjects (P < .001), single subcortical infarctions group (P < .01), and cortical infarctions group (P < .01). In all of the groups male sex (P < .05) and a history of hypertension (P < .05), regardless of whether hypertension was treated, correlated with low CR. The multiple regression analysis indicated that the only significant factor able to influence the breath-holding index was the type of lesion. Nonstenotic patients with first-ever stroke who had a recent symptomatic subcortical infarction associated with multiple silent infarctions seem to have an impaired cerebrovascular reserve capacity. The strong association of subcortical infarctions with multiple silent infarctions with low CR indicates the role of small vessel vasculopathy and hypoperfusion as possible pathogenetic mechanisms of subcortical infarctions with multiple silent infarctions.

Influence of physiologic oscillation of estrogens on cerebral hemodynamics

The interactions between estrogens and the cerebrovascular system are complex and not fully understood. There are evidences suggesting that the hormones confer protection against cerebral ischemia. Our aim in this study was to investigate the effects of physiological variations of estradiol plasmatic concentration on cerebral hemodynamics. We investigated cerebrovascular reactivity to hypercapnia with transcranial Doppler ultrasonography and the breath-holding index method in the right middle cerebral artery of 20 young women during the menstrual and the ovulatory phase. Data were compared with those of 20 men matched for age. The mean value of the breath-holding index was significantly higher ( p<0.001) in females during the ovulatory phase than in the menstrual phase. In men, values were similar to those of women during the menstrual phase. These results suggest that estrogens influence the adaptation capacity of the cerebrovascular system. The possible pathophysiological implications of the relationships between sex hormones and cerebral hemodynamics deserve further investigation.

Impaired cerebral vasoreactivity correlates with recent symptomaticity in severe carotid artery disease

P62 OBJECTIVE: Impaired cerebral vasomotor reactivity has been proposed as a measure of exhausted vascular reserve in patients with carotid artery stenosis or occlusion. We tested this hypothesis by measuring vasoreactivity in patients with asymptomatic or recently symptomatic severe carotid artery disease. METHODS: Fourteen patients with severe carotid artery disease (5 with occlusion, 9 with stenosis 80–99%, 8 symptomatic, 6 asymptomatic within 2 years) and 7 healthy controls had continuous bilateral monitoring of mean flow velocity (MFV) in the MCAs by transcranial Doppler (TCD). End-tidal CO2 was measured continuously with an in-line capnometer connected via snorkel mouthpiece, nasal airway occluded by noseclip. After baseline measurements, subjects held their breath for 30 seconds. A breath holding index (BHI) was calculated (% change in MFV/seconds held). After return to baseline MFV, subjects breathed a 5% CO2 gas mixture for 2 minutes. CO2 reactivity was calculated as percent rise in MFV per mmHg PCO2 once the MFV curve plateaued. ANOVA was used to calculate differences between symptomatic, asymptomatic and control groups for CO2 reactivity and BHI. RESULTS: There was a highly significant difference in vasoreactivity by CO2 inhalation in the symptomatic group (2.02±.80 %/mmHg) versus the asymptomatic group (4.45±1.9 %/mmHg) and controls (3.69±.95 %/mmHg) (F 2,18 =7.85, p=.004). A linear relationship was seen between MFV and PCO2, taking multiple MFV measurements at various PCO2 levels throughout the study period (average r 2 =.60 for patients, .77 for controls). BHI did not distinguish between the groups (p=.37). CONCLUSIONS: Measuring cerebral vasoreactivity by CO2 inhalation with continuous TCD monitoring provides an important physiological index of the clinical status of patients with carotid artery disease which may help guide treatment algorithms. The linear relationship between MCA MFV and end-tidal CO2 enables confirmation of the baseline and maximum measurements used to calculate CO2 reactivity, and provides the opportunity to investigate further the link between physiology and clinical state.

Low-Dose Endotoxin Reduces Human Cerebrovascular Reactivity and Produces Procoagulant State

P118 Stroke risk is increased in the presence of some infections. We studied potential mechanisms linking infections and stroke risk. We used endotoxin, a component of gram negative bacteria, as a standardized inflammatory stimulus. We infused low-dose endotoxin (1ng/kg) as a bolus in four healthy men, and analyzed cerebrovascular and hemostatic effects over 24 hours. We measured cerebral vasomotor reactivity, using transcranial Doppler ultrasonography to calculate breath-holding index (BHI); the latter consists of the percent change of middle cerebral artery blood flow velocity over time during breath holding. We also measured thrombin-antithrombin complexes (TAT, an index of thrombin generation), and soluble e-selectin (a marker of endothelial activation). Following infusion of endotoxin, there were substantial physiological changes primarily at three to six hours post-infusion. Temperature peaked at 100 °F (p&lt;.05), with no significant change in mean arterial pressure. BHI showed maximum decline from 1.55 ± 0.88 to 0.33 ± 0.35 %/sec (p&lt;.05). TAT levels increased from 3.0 ± 0.9 to 41.0 ± 21.1 ug/ml (p&lt;.05). Soluble e-selectin levels increased from 66.6 ± 35.2 to 207.4 ± 78.9 ug/ml (p&lt;.05). These findings indicate that a standardized low-dose inflammatory stimulus produces a marked decline in human cerebrovascular reactivity while simultaneously inducing a procoagulant state with endothelial activation . The reduction in cerebrovascular reactivity combined with a procoagulant state may contribute to increased stroke risk in this setting.

Impaired cerebral vasoreactivity and risk of stroke in patients with asymptomatic carotid artery stenosis.

Standards for treating patients with asymptomatic carotid artery stenosis have been difficult to establish because of the lack of evidence for factors influencing these patients' prognoses. However, preliminary evidence suggests that an alteration in cerebral hemodynamic function may play a relevant role in the occurrence of stroke in patients with carotid artery disease. To investigate the relationship between cerebrovascular reactivity to hypercapnia and cerebrovascular events in patients with severe unilateral asymptomatic carotid artery stenosis. Prospective, blinded longitudinal study conducted in an outpatient neurovascular department in Italy between June 1996 and April 1998, with a median follow-up of 28.5 months. Ninety-four patients with asymptomatic carotid artery stenosis of at least 70% (74 men; mean age, 71 years). Subsequent occurrence of cerebral ischemic events (transient ischemic attack or stroke) or death, analyzed by cerebrovascular reactivity to hypercapnia (measured by transcranial Doppler ultrasonography and calculated by the breath-holding index values in the middle cerebral arteries). The overall annual rate for all ischemic events was 7.9%. Seventeen patients (18%) had ischemic events, all but 1 of which were ipsilateral to the carotid artery stenosis. Among factors considered, only lower breath-holding index values in the middle cerebral artery ipsilateral to carotid artery stenosis were significantly associated with the risk of an event (hazard ratio, 0.09; 95% confidence interval, 0.02-0.38; P=.001, by multivariate analysis). Based on data from previously studied healthy subjects, the cutoff of the breath-holding index for distinguishing between impaired and normal cerebrovascular reactivity was determined to be 0.69. Using this cutoff, the annual ipsilateral ischemic event risk was 4.1% in patients with normal and 13.9% in those with impaired breath-holding index values. These results suggest a link between impaired cerebrovascular reactivity and the risk of ischemic events ipsilateral to severe asymptomatic carotid stenosis.

Impaired cerebral vasoreactivity correlates with recent symptomaticity in severe carotid artery disease

P62 OBJECTIVE: Impaired cerebral vasomotor reactivity has been proposed as a measure of exhausted vascular reserve in patients with carotid artery stenosis or occlusion. We tested this hypothesis by measuring vasoreactivity in patients with asymptomatic or recently symptomatic severe carotid artery disease. METHODS: Fourteen patients with severe carotid artery disease (5 with occlusion, 9 with stenosis 80–99%, 8 symptomatic, 6 asymptomatic within 2 years) and 7 healthy controls had continuous bilateral monitoring of mean flow velocity (MFV) in the MCAs by transcranial Doppler (TCD). End-tidal CO2 was measured continuously with an in-line capnometer connected via snorkel mouthpiece, nasal airway occluded by noseclip. After baseline measurements, subjects held their breath for 30 seconds. A breath holding index (BHI) was calculated (% change in MFV/seconds held). After return to baseline MFV, subjects breathed a 5% CO2 gas mixture for 2 minutes. CO2 reactivity was calculated as percent rise in MFV per mmHg PCO2 once the MFV curve plateaued. ANOVA was used to calculate differences between symptomatic, asymptomatic and control groups for CO2 reactivity and BHI. RESULTS: There was a highly significant difference in vasoreactivity by CO2 inhalation in the symptomatic group (2.02±.80 %/mmHg) versus the asymptomatic group (4.45±1.9 %/mmHg) and controls (3.69±.95 %/mmHg) (F 2,18 =7.85, p=.004). A linear relationship was seen between MFV and PCO2, taking multiple MFV measurements at various PCO2 levels throughout the study period (average r 2 =.60 for patients, .77 for controls). BHI did not distinguish between the groups (p=.37). CONCLUSIONS: Measuring cerebral vasoreactivity by CO2 inhalation with continuous TCD monitoring provides an important physiological index of the clinical status of patients with carotid artery disease which may help guide treatment algorithms. The linear relationship between MCA MFV and end-tidal CO2 enables confirmation of the baseline and maximum measurements used to calculate CO2 reactivity, and provides the opportunity to investigate further the link between physiology and clinical state.

Reactividad cerebrovascular mediante el índice breath holding (Apnea voluntaria): fiabilidad de la repetición precoz

The Breath Holding Index (BHI) is a non-invasive method for evaluation of cerebrovascular reactivity, the results of which correlate with those obtained by using intravenous acetazolomide and CO2 inhalation, so that it can be used as an alternative method to these in cooperative patients. However, the technique is not completely defined. Therefore Markus et al make a second measurement of the BHI 2-3 minutes later and take the arithmetical mean of the two readings as the final result. To assess the intra-observer concordance between two BHI obtained with less than two minutes difference, and therefore whether the second index obtained may be used as an indicator of cerebrovascular reactivity. Our study included 18 patients (7 men and 11 women; average age: 28.8 years; limits 17-50 years) with primary headache and no known cerebrovascular disease, diabetes mellitus or arterial hypertension. Using transcranial Doppler 28 measurements of the BHI (BHI1) were made in the middle cerebral arteries (right and/or left) in a similar way to that described by Markus. Once the average arterial velocity returned to basal levels the procedure was repeated in the first two minutes (BHI2) after the first index. Statistical analysis was done using the Student's t test and the kappa index between the two BHI after taking 0.8 as the cut-off point. The BHI2 (average +/- DT: 0.79 +/- 0.34) was significantly lower than that of BHI1 (average +/- DT: 1.04 +/- 0.44) (p < 0.005, t = 3.683). The kappa index between the two indices was very low: 0.058 +/- 0.158. The BHI2 is not a reliable index of cerebrovascular reactivity since it under-estimates it in relation to the previous index, even when the average arterial velocity has returned to basal levels.

Influencia de la presión arterial en el estudio de la reactividad cerebrovascular en oclusiones carotídeas

Cerebrovascular reactivity (CVR) is the capacity of the cerebral microcirculation to increase cerebral blood flow on vasodilator stimulation. This is reduced in patients with carotid obstruction. The changes in arterial pressure produced whilst carrying out different tests for estimation of the CVR may affect its measurement by transcranial Doppler. To evaluate the concordance between the different methods for estimation of the CVR by transcranial Doppler in patients with carotid obstruction and to evaluate the importance of monitoring the arterial pressure during CVR tests. We evaluated 17 patients with internal carotid artery obstruction confirmed on arteriography. The CVR was determined by three different methods: apnea test. Breath-Holding Index (BHI) and intravenous acetazolamide test. During the tests of RCV the arterial pressure was monitored. We found that there was a reduction in the average basal rate of flow and of the pulsatile index on the obstructed side, with a statistically significant association in relation to the contralateral side (p < 0.001). There was good concordance between the different tests of CVR, with reduced CVR seen on the obstructed side as compared to the contralateral side (p < 0.001) for the different tests. However, this correlation was not seen in stenosis < 70%. During the apnea test changes in blood pressure occurred, with a tendency to increase in the systolic pressure. However, there were no significant changes in blood pressure during the acetazolamide test. There is good concordance in the CVR between the apnea, BHI and acetazolamide tests in carotid obstruction. Changes in arterial pressure occurred during the apnea and BHI tests. However, the acetazolamide test caused no change in arterial pressure.

Low-Dose Endotoxin Reduces Human Cerebrovascular Reactivity and Produces Procoagulant State

P118 Stroke risk is increased in the presence of some infections. We studied potential mechanisms linking infections and stroke risk. We used endotoxin, a component of gram negative bacteria, as a standardized inflammatory stimulus. We infused low-dose endotoxin (1ng/kg) as a bolus in four healthy men, and analyzed cerebrovascular and hemostatic effects over 24 hours. We measured cerebral vasomotor reactivity, using transcranial Doppler ultrasonography to calculate breath-holding index (BHI); the latter consists of the percent change of middle cerebral artery blood flow velocity over time during breath holding. We also measured thrombin-antithrombin complexes (TAT, an index of thrombin generation), and soluble e-selectin (a marker of endothelial activation). Following infusion of endotoxin, there were substantial physiological changes primarily at three to six hours post-infusion. Temperature peaked at 100 °F (p

Cerebrovascular Reactivity in Internal Carotid Artery Occlusion

To the Editor: Vernieri and colleagues1 concluded in their recent article that treatment options in internal carotid artery occlusion can be differentiated on the basis of cerebral hemodynamic status. Specifically, their results has demonstrated that the breath-holding index (BHI) in the middle cerebral artery detected by transcranial Doppler ultrasonography (TCD) is predictive of cerebrovascular ischemic symptoms ipsilateral to the internal carotid artery occlusion. Finally, the authors suggest the use of BHI in selecting patients for the classic or a new type of surgical extracranial/intracranial bypass study. I would like to raise the following comments. First, “carotid stump syndrome” is a well-known phenomenon: continual episodes of transient ischemic attack (TIA) and/or stroke ipsilateral to an occluded internal carotid artery; embolism has been implicated in the pathogenesis, and border-zone infarction is less common.2 3 The source of emboli includes the ipsilateral internal carotid artery stump, the ipsilateral external carotid artery, the contralateral internal and external carotid arteries, the vertebrobasilar system, and the heart. In the study by Vernieri and colleagues,1 patients with significant stenosis of the contralateral carotid artery system, significant vertebral artery disease, or cardiac source of emboli were excluded. These exclusions might have resulted in a lower rate of ischemic stroke, especially on the side contralateral to the carotid artery occlusion, and augmented the importance of hemodynamic mechanisms in producing cerebrovascular ischemia. In addition, I am interested in knowing whether there was any significant stenosis in the external carotid artery ipsilateral to the internal carotid artery occlusion. Second, CT or MRI of the brain was performed at baseline in all the patients with internal carotid artery occlusion, but the neuroimaging findings were not described in the article.1 This information may be important because some “asymptomatic” patients and some symptomatic patients with “TIA only” could have “silent” …

Patterns of cerebrovascular reactivity in patients with carotid artery occlusion and severe contralateral stenosis

There is evidence suggesting that among other factors, an alteration in cerebral hemodynamics plays a relevant role in the occurrence of strokes in patients with carotid disease. The purpose of this study was to investigate patterns of cerebrovascular reactivity in patients with internal carotid occlusion and severe contralateral carotid stenosis and their relationship with symptomatology. Using transcranial Doppler ultrasound, cerebrovascular reactivity to hypercapnia in middle cerebral arteries was evaluated with the breath-holding index (BHI) in 42 patients with internal carotid occlusion and severe contralateral carotid stenosis and in 40 control subjects. A significant decrease of BHI on the occluded side was observed in symptomatic patients with respect to asymptomatic ones (0.12+/-0.1 vs. 0.75+/-0.4, P<0.0001) and with respect to the control group (1.11+/-0.1, P<0.0001). The difference was also significant between asymptomatic patients and controls (P<0.0001). Breath-holding values on the stenotic side were significantly higher (P<0.0001) in asymptomatic patients (1.01+/-0.2) with respect to symptomatic ones (0.39+/-0.1). A significant difference (P<0.0001) was also present between controls and symptomatic patients. The pattern of cerebrovascular reactivity in patients with severe bilateral carotid steno-occlusive disease seems to be strictly dependent on the presence of previous symptoms. Further studies are needed to investigate whether the study of cerebral hemodynamics in patients with bilateral carotid artery disease is important for planning therapeutic strategies.

Cerebrovascular reactivity in carotid artery occlusion: possible implications for surgical management of selected groups of patients.

The aim of this study was to use transcranial Doppler ultrasonography to investigate cerebrovascular reactivity to hypercapnia in the middle cerebral arteries of patients with carotid occlusion with different outcomes. Cerebrovascular reactivity to hypercapnia was calculated with the breath-holding index (BHI). Patients with unilateral carotid occlusion were divided as follows: asymptomatic (20 patients), transient ischemic attack (TIA) (20 patients), minor (20 patients) and major stroke (14 patients). Values of BHI homolateral to the carotid occlusion were compared with those of 25 healthy subjects and 34 stroke patients without significant carotid stenosis. BHI values were comparable in healthy controls, non stenotic stroke patients and asymptomatic occluded patients. BHI values of patients with symptomatic occlusion were significantly lower than those of the above-mentioned groups (P<0.0001). Moreover, the reduction of BHI was significantly associated with the extent of the neurological impairment. In fact, BHI values were significantly higher in TIA than in minor and major stroke (P<0.0001) and in minor than in major stroke patients (P<0.02). Finally, we found that a BHI value homolateral to carotid occlusion of 0.69 can be considered the cut-point for distinguishing between symptomatic and asymptomatic patients. Prospective studies are needed to demonstrate if the presence of this threshold value may help in selecting a subset of patients with asymptomatic carotid occlusion or with transient or mild neurological deficit with the highest probability of benefiting from surgical therapy.

Outcome of carotid artery occlusion is predicted by cerebrovascular reactivity.

The purpose of this study was to investigate the possibility of obtaining prognostic indications in patients with internal carotid occlusion on the basis of intracranial hemodynamic status, presence of previous symptoms of cerebrovascular failure, and baseline characteristics. Cerebral hemodynamics were studied with transcranial Doppler ultrasonography. Cerebrovascular reactivity to apnea was calculated by means of the breath-holding index (BHI) in the middle cerebral arteries. Sixty-five patients with internal carotid artery occlusion were followed-up prospectively (median, 24 months), 23 patients were asymptomatic and 42 symptomatic (20 with transient ischemic attack and 22 with stroke). During the follow-up period, 11 symptomatic patients and 1 asymptomatic patient had another ischemic event ipsilateral to carotid occlusion. Among factors considered, only lower BHI values in the middle cerebral arteries ipsilateral to carotid occlusion and older age were significantly associated with the risk of developing symptoms (P=0.002 and P=0.003, respectively; Cox regression multivariate analysis). Based on our data, a cut point of the BHI value for distinguishing between pathological and normal cerebrovascular reactivity was determined to be 0.69. All patients except one, who developed TIA or stroke during the follow-up period, had BHI values ipsilateral to carotid occlusion of <0.69. These data suggest that impaired cerebrovascular reactivity is predictive for cerebral ischemic events in patients with carotid occlusion.

Abstracts of literature

Abstracts of literature

Impairment of daytime cerebrovascular reactivity in patients with obstructive sleep apnoea syndrome.

Several studies have demonstrated a clear association between snoring, sleep apnoea and increased risk of stroke. However, the possible role of sleep apnoea in the pathophysiogenetic mechanisms of cerebrovascular disease is still unknown. Our aim in this study was to investigate cerebral haemodynamic changes during the waking state in eight patients with sleep apnoea syndrome (OSAS) by means of transcranial Doppler (TCD). In particular, we studied cerebral vascular reactivity (CVR) to hypercapnia calculated by means of the breath holding index (BHI). The investigation was performed in the early morning, soon after awakening, and in the late afternoon. Data were compared with those of eight healthy subjects matched for age and vascular risk factors. OSAS patients showed significantly lower BHI values with respect to controls both in the morning (0.56 vs. 1.36; P < 0.0001) and in the afternoon (1.12 vs. 1.53; P < 0.0001). In patients, BHI values in the afternoon were significantly higher than in the morning (P < 0.0001). These data demonstrate a diminished vasodilator reserve in OSAS patients, particularly evident in the morning. This reduction of the possibility of cerebral vessels to adapt functionally in response to stimulation could be linked to hyposensitivity of cerebrovascular chemoreceptors after the continuous stress caused by nocturnal hypercapnia.