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PubMed2003

Heritability of blood pressure and hemodynamics in African- and European-American youth.

Hypertension prevalence is much higher in African-Americans (AAs) than in European-Americans (EAs). It is unknown whether this difference is related to potential ethnic differences in the relative contribution of genes and environment to population variation in blood pressure and underlying hemodynamics. We studied 308 EA and 226 AA twin pairs, including monozygotic and dizygotic twins, of the same as well as the opposite sex (mean+/-SD age, 14.7+/-3.1 years). Supine resting systolic blood pressure (SBP), diastolic blood pressure (DBP), pulse pressure, and heart rate (HR) were measured by a Dinamap instrument and hemodynamics (stroke volume, cardiac index, and total peripheral resistance [TPR] index) by impedance cardiography. Ethnic and sex effects on genetic and environmental contributions to resting blood pressure and hemodynamics were estimated by genetic model fitting. For most measures, the best-fitting model showed no differences in heritability between AAs and EAs or between males and females, with heritabilities of 0.50 for cardiac index, of 0.64 for HR, and of SBP, pulse pressure, and stroke volume in between. Heritability of DBP was 0.45 in EAs and 0.58 in AAs with no effect of sex. For TPR index in EAs, 46% of the variance could be attributed to familial effects, but no significant distinction could be made between shared environmental and genetic factors. Heritability of TPR index in AAs was 0.51. Adjustment for obesity yielded virtually identical heritabilities. In summary, relative influences of genetic and environmental factors on blood pressure and hemodynamics in AA and EA youth are similar and independent of (genes for) obesity.

Adolescent↗
PubMedDate not supplied

Central hemodynamics in the developmental stage of spontaneous hypertension in the unanesthetized rat.

The hemodynamic alterations associated with the developmental phase of high blood pressure were investigated in the spontaneously hypertensive rat (SHR). All hemodynamic measurements were made in unanesthetized, unrestrained SHR and Wistar-Kyoto (WKY) rats instrumented with chronic electromagnetic flow probes on the ascending aorta and arterial pressure catheters. Rats were studied at 30-41 days, 80 days, and 120 days of age. Hemodynamics of SHRs and WKYs in the 30-41 day group were monitored daily. Spontaneously hypertensive rats demonstrated a higher cardiac index than WKYs (p less than 0.05) from 32 through 41 days of age. Total peripheral resistance (TPR) was not elevated in SHRs at this time. Heart rate and stroke index were elevated in SHRs (p less than 0.05) from 34 through 41 days, however, stroke volume was not. At 80 and 120 days SHRs had higher mean arterial pressure (MAP) and TPR than WKYs (p less than 0.05), although cardiac index was not significantly different. This hemodynamic pattern of a hyperkinetic circulation prior to the development of hypertension supports the theory of total body autoregulation. A transient increase in cardiac index precedes an increase in TPR, which then normalizes cardiac index while elevating MAP.

Aging↗
PubMed1990

A reevaluation of the hemodynamics of pheochromocytoma.

We examined the hemodynamic features of 24 untreated patients with surgically proven pheochromocytoma during steady-state periods and compared them with 24 untreated essential hypertensive patients individually matched for sex, age, body surface area, and arterial blood pressure. We found that, despite having 10-fold higher levels of circulating catecholamines, pheochromocytoma patients have hemodynamic characteristics similar to patients with essential hypertension and that, in individual patients, the ratio of circulating norepinephrine to epinephrine had no relation to the hemodynamic profile. In both groups, increased total peripheral resistance is primarily responsible for maintenance of hypertension. These results suggest that, unlike the acute administration of catecholamines, long-term exposure to high levels of circulating catecholamines does not produce hemodynamic responses characteristic of this group of compounds. This might be due in part to desensitization of the cardiovascular system to catecholamines and might explain the clinical observation that some patients can be completely asymptomatic despite harboring an actively catecholamine-secreting pheochromocytoma.

Adrenal Gland Neoplasms↗
PubMed1991

Central hemodynamic observations in untreated preeclamptic patients.

Reported central hemodynamics obtained with a Swan-Ganz pulmonary artery thermodilution catheter in preeclamptic patients show marked disparity, which has been interpreted to indicate a variable hemodynamic expression of the disease. However, the variability also may be due, at least in part, to the pharmacological treatment that most of the women studied received during Swan-Ganz measurements. To evaluate the effects of treatment on hemodynamics, we compared the results of Swan-Ganz measurements in 87 preeclamptic women who had received no treatment at all with those obtained in 47 preeclamptic women who had received various drugs and intravenous fluids. Control values were obtained in 10 normotensive pregnant volunteers. Measurements were performed between 25 and 34 weeks of gestation. The median (range) cardiac index in the untreated patients of 3.3 (2.0-5.3) l.min-1.m-2 was significantly lower than that in the treated patients of 4.3 (2.4-7.6) l.min-1.m-2 and in the normotensive pregnant women of 4.2 (3.5-4.6) l.min-1.m-2. The systemic vascular resistance index in the untreated group of 3,003 (1,771-5,225) dyne.sec.cm-5.m2 was significantly higher than that of 2,212 (1,057-3,688) in the treated and of 1,560 (1,430-2,019) dyne.sec.cm-5.m2 in the normotensive control group. The median (range) pulmonary capillary wedge pressure in the untreated group was 7 (-1-20) mm Hg and did not differ from that of 7 (0-25) mm Hg in the treated group. Variability of all hemodynamic variables was much lower in untreated than in treated patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Output↗
PubMed1993

Arterial hemodynamics in human hypertension. Effects of angiotensin converting enzyme inhibition.

Previous studies have shown some distinct hemodynamic alterations in essential hypertension, including increased resistance, wave reflections, and pulse wave velocity and decreased systemic compliance. These abnormalities are completely normalized by nonspecific smooth muscle dilation with nitroprusside but not by combined alpha- and beta-adrenergic blockade. The renin-angiotensin system, acting possibly via both circulating and local tissue effects, is thought to play an important role in essential hypertension, so its role in the altered hemodynamics deserves careful investigation. A hypertensive patient group was compared with a normotensive group similar in age, body size, and proportion of men and women. During diagnostic cardiac catheterization, ascending aortic micromanometer pressures and electromagnetic flows were measured in the baseline state. Intravenous captopril of a sufficient dosage (11 mg) to normalize blood pressure then was given to the hypertensive patients while measurements were repeated. From the pressures and flows, aortic input impedance, wave reflection magnitude, and compliance were computed. In the hypertensive group, the important hemodynamic alterations consisted of increased peripheral resistance, first zero crossing of aortic impedance phase angle, and wave reflections and decreased systemic compliance. Captopril had a pronounced hemodynamic effect. It normalized blood pressure, resistance, and impedance phase angle zero crossing. Compliance, although increased substantially by captopril, was still slightly lower than normotensive levels. The magnitude of wave reflections, although substantially lowered by angiotensin converting enzyme inhibition, was still persistently greater than normal. The present results, together with those previously reported, demonstrate that a complex interplay of factors underlies the increased smooth muscle tone in essential hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1996

Correlates of the hemodynamic determinants of blood pressure.

The purpose of this study was to investigate the association of sex, race, lean body mass, and fat mass with the hemodynamic determinants of blood pressure, including stroke volume, heart rate, and total peripheral vascular resistance. The study included 201 subjects aged 6 to 17 years, 105 of whom were male and 98 of whom were black. Lean body mass and fat mass were both significant (P < .05) independent determinants of stroke volume, cardiac output, and total peripheral vascular resistance. However, the direction of the effect of lean body mass was opposite for stroke volume and cardiac output compared with that of total peripheral vascular resistance. The direct relationship of lean body mass with systolic blood pressure (SBP) and diastolic blood pressure (DBP) (regression coefficients, 0.55 +/- 0.05 for SBP and 0.47 +/- 0.05 for DBP) indicates that the effect of lean body mass on cardiac output may predominate. Lean body mass explained substantially more of the variance of the hemodynamic variables than did fat mass. After control for the effects of body size, male subjects had higher heart rate and cardiac output, and female subjects had higher vascular resistance. White subjects had higher stroke volume and cardiac output, and black subjects had higher peripheral vascular resistance. This study demonstrates that lean body mass is a more important correlate of the hemodynamic determinants of blood pressure than is fat mass and that sex and race have significant independent relationships with the hemodynamic determinants of blood pressure in children and adolescents.

Adolescent↗
PubMedDate not supplied

Hypertension in obese patients: hemodynamic and volume studies.

Distinct hemodynamic and volume characteristics have been suggested for established hypertension in severe obesity, namely, a high cardiac output, and expanded blood volume, and a normal peripheral resistance. To evaluate whether hypertension in moderately obese patients represents a separate entity that can be defined by hemodynamic and volume profiles, we studied these in 50 such patients and compared results with those obtained in 59 nonobese essential hypertensives and 25 normal subjects. Both obese and nonobese hypertensives had a normal cardiac index (men, 2.8 +/- 0.1 vs 2.8 +/- 0.09 liter/min/m2; women, 2.9 +/- 0.1 vs 2.8 +/- 0.1 liter/min/m2, respectively) and similarly elevated total peripheral resistance (men, 47.1 +/- 2.3 vs 46.5 +/- 1.9 U . m2; women, 45.0 +/- 2.4 vs 44.0 +/- 1.3 U . m2, respectively) as compared to normals (cardiac index: men, 2.9 +/- 0.09 liter/min/m2, women, 3.4 +/- 0.2 liter/min/m2; total peripheral resistance: men, 29.4 +/- 1.0 U . m2, women, 28.3 +/- 2.8 U. m2). Volume measurements corrected to body surface area showed that both obese and nonobese hypertensive patients had lower blood volume (men, 2.6 +/- 0.05 vs 2.5 +/- 0.05 liter/m2; women, 2.2 +/- 0.05 vs 2.3 +/- 0.05 liter/m2, respectively) than normals (men, 2.9 +/- 0.08 liter/m2; women, 2.5 +/- 0.08 liter/m2). The results of this study suggest that hypertension in moderately obese subjects is similar in its hemodynamic and volume profiles to hypertension in the nonobese and that the presence of obesity does not alter the hemodynamic characteristics of established essential hypertension.

Adult↗
PubMedDate not supplied

Cardiovascular hemodynamics and vasopressin blockade in DOCA-salt hypertensive rats.

In conscious rats with near-malignant phases of DOCA-salt (DS) hypertension, hemodynamics were studied with microspheres before and after administration of a vasopressin (VP) vasopressor antagonist in relation to plasma VP levels (pVP). Compared to the controls, the DS rats showed significant elevations in mean arterial pressure (MAP), total vascular resistance (TVR), and pVP, and a flow redistribution from kidney and spleen to skeletal muscles and heart, with increased vascular resistance in almost all organs. The antagonist elicited no significant systemic hemodynamic effects in DS rats as a whole; however, two subgroups, responders vs nonresponders, were identified according to the effects on MAP. In responders with a pVP of 29.2 +/- 2.7 (SE) pg/ml, the antagonist lowered MAP (-24.9 +/- 5.9 mm Hg) and TVR significantly, while in nonresponders with a pVP of 15.2 +/- 3.4 pg/ml, there were no effects. The major antagonist-induced regional responses were increased flow and decreased vascular resistance in skeletal muscles and skin in whole DS rats, and additionally in the gastrointestinal tract, portal organs, and testes in the responders. Significant correlations were observed between pVP, MAP, TVR, and depressor responses to the antagonist only when all data for DS and control rats were pooled. Thus, the systemic hemodynamic effects of VP are important only in responders with exceedingly elevated pVP. VP contributes significantly to the regional hemodynamic abnormalities in skeletal muscles and skin in whole DS rats, and also in several other organs in the responders.

Animals↗
PubMed1987

Red blood cell Li+-Na+ countertransport, Na+-K+ cotransport, and the hemodynamics of hypertension.

Red blood cell Li+-Na+ countertransport and Na+-K+ cotransport activities, home blood pressure, invasive systemic hemodynamics, and limb venous compliance were measured in 65 white men (23 normotensive, 22 borderline hypertensive, and 20 mild essential hypertensive subjects). Li+-Na+ countertransport activity was positively and significantly correlated with subject-determined home systolic blood pressure (r = 0.31, p less than 0.02) and with directly measured systolic (r = 0.29, p less than 0.02) and diastolic (r = 0.27, p less than 0.03) blood pressures in the hemodynamic laboratory, independent of potential confounding variables. Analysis of the hemodynamic determinants of blood pressure revealed a significant positive correlation of countertransport with vascular resistance (r = 0.30, p less than 0.02) but not with cardiac output or cardiac index. High red blood cell Na+-K+ cotransport activity was not independently associated with hypertension or with a characteristic hemodynamic pattern but was related to decreased venous compliance. Red blood cell Li+-Na+ countertransport deserves further study as a marker for the genetic substrate of human essential hypertension. Red cell Na+-K+ cotransport may be altered secondarily by factors related to high blood pressure and seems to be a valid marker for abnormalities of the venous system in hypertension.

Adult↗
PubMed1975

Calculations of pulsatile flow through a branch: implications for the hemodynamics of atherogenesis.

Numerical simulations of pulsatile blood flow through a symmetrical branch modeling the aortic bifurcation were carried out to assess several hemodynamic theories of atherogenesis by comparing the distribution of hemodynamic variables with that of early lesions in arterial branches. Considerable spatial and temporal variations in wall shear were found when the flow was pulsatile; the highest values occurred at the convex corner on the outer wall of the branch and in the neighborhood of the flow divider tip, and the lowest shears were experienced by the outer wall of the daughter vessel a short distance distal to the corner. Transient flow reversal occurred almost everywhere in the branch, and a transient separated region was found corresponding to the low-shear region in the daughter vessel. The shear profiles and the calculated separated region were influenced to some degree by the extent of flow development at the branch inlet and markedly by the branch area ratio. All of the proposed hemodynamic promoters of atherosclerosis that were examined--high shear, low shear, and separation--were found at sites in the branch where lesions commonly develop. Comparisons with a steady-flow calculation at the same mean flow rate showed that the severity of all of these proposed hemodynamic determinants was increased by pulsatility.

Arteries↗
PubMed1989

Opiate receptor antagonism in right-sided congestive heart failure. Naloxone exerts salutary hemodynamic effects through its action on the central nervous system.

Opiate receptor inhibition causes adrenergic receptor-mediated increases in aortic pressure, cardiac output, and left ventricular contractile function in right heart failure. To study whether the effects of opiate receptor inhibition are mediated by means of an action on the central opiate system, we administered equimolar doses of naloxone hydrochloride and naloxone methobromide (MeBr) and normal saline to heart failure dogs. Chronic stable right heart failure was produced by progressive pulmonary artery constriction and tricuspid valve avulsion. Naloxone hydrochloride caused an increase in mean aortic pressure, cardiac output, left ventricular dP/dt and dP/dt/P, plasma catecholamines, and regional blood flows to the myocardium, quadriceps muscle, kidneys, and splanchnic beds. Plasma beta-endorphin and adrenocorticotropin also increased. In contrast, neither normal saline nor naloxone MeBr (which does not cross the blood-brain barrier) affected the systemic or regional hemodynamics or neurohormones. Naloxone hydrochloride was also administered to anesthetized heart failure dogs. Pentobarbital anesthesia removed cortical perception of nociceptive stimulation, reduced the increase in plasma epinephrine, and abolished vasodilation in skeletal muscle that occurred in conscious dogs after naloxone hydrochloride administration but had no major effects on responses of plasma norepinephrine, systemic hemodynamics, or other regional blood flows to opiate receptor inhibition. Naloxone hydrochloride had no effect in sham-operated dogs. The results indicate that the hemodynamic effects of naloxone are mediated by an action within the central nervous system. Furthermore, since pentobarbital anesthesia did not markedly alter the hemodynamic responses to naloxone hydrochloride, the acute salutary effects of opiate receptor inhibition probably are not caused by removal of the antinociceptive effect of endogenous opioids in heart failure.

Anesthesia↗
PubMed1990

Hemodynamic resistance as a measure of functional impairment in aortic valvular stenosis.

Calculated valve area depicts anatomical stenosis but does not quantify hemodynamic impairment. We propose that hemodynamic resistance, defined as the mean pressure gradient across the valve divided by mean flow rate during systolic ejection, gives a better indication of hemodynamic obstruction. This index was compared with Gorlin valve area in 40 patients with aortic stenosis. Calculated area ranged from 0.22 to 1.26 cm2, and mean transvalvular resistance ranged from 117 to 1,244 dyne.sec.cm-5. In general, resistance varied inversely with calculated area, but there was substantial variation about the mean relation. All of the variation could be accounted for by variations in the pressure gradients at each value of calculated area. Resistance was higher in proportion to area when flow and pressure gradient were high. Analysis of five published studies of a total of 83 valves showed that calculated area changed at least three times more than resistance when pressure gradient was varied. The utility of resistance as an index of stenosis is demonstrated by example calculations that show how during exercise a stenotic valve increases the ventricular work rate out of proportion to the work done on the peripheral resistance. These calculations are possible because hemodynamic resistance defines functional impairment in units commonly used for quantification of opposition to flow. Furthermore, resistance appears to be less dependent than area on conditions of measurement and does not require an empirical constant.

Aortic Valve↗
PubMed1997

Hemodynamic regulation of tumor necrosis factor-alpha gene and protein expression in adult feline myocardium.

Tumor necrosis factor-alpha (TNF-alpha) mRNA and protein biosynthesis were examined in adult feline myocardium in the presence and absence of superimposed hemodynamic pressure overloading. A brief period of hemodynamic pressure overloading ex vivo resulted in de novo TNF-alpha mRNA expression within 30 minutes and de novo TNF-alpha protein production within 60 minutes; neither TNF-alpha mRNA nor protein was detected in hearts perfused at normal perfusion pressures. Moreover, TNF-alpha mRNA and protein biosynthesis were observed in myocyte and nonmyocyte cell types in the pressure-overloaded hearts. To determine whether a simple passive stretch of the myocardium was a sufficient stimulus for TNF-alpha biosynthesis, we examined TNF-alpha mRNA expression in stretched and unstretched papillary muscles. This study showed that myocardial stretch was a sufficient stimulus for the induction of TNF-alpha mRNA biosynthesis. The functional significance of the intramyocardial production of TNF-alpha was determined by examining cell motion in isolated contracting cardiac myocytes treated with superfusates from pressure-overloaded and control hearts. These studies showed that cell motion was depressed in myocytes treated with superfusates from the pressure-overloaded hearts but was normal with the superfusates from the control hearts. Finally, hemodynamic pressure overloading in vivo under physiological conditions was also shown to result in de novo intramyocardial TNF-alpha mRNA biosynthesis. In conclusion, this study constitutes the initial demonstration that the adult mammalian myocardium elaborates biologically active TNF-alpha, both ex vivo and in vivo, in response to hemodynamic pressure overloading.

Animals↗
PubMed2005

Quantitative assessment of cerebral hemodynamics using perfusion-weighted MRI in patients with major cerebral artery occlusive disease: comparison with positron emission tomography.

BACKGROUND AND PURPOSE: Cerebrovascular reactivity (CVR) to acetazolamide is a key parameter in determining the severity of hemodynamic impairment in patients with major cerebral artery occlusive disease. Perfusion-weighted MRI (PW MRI) can measure the cerebral blood volume (CBV) as an indicator of hemodynamic impairment. CBV measured by PW MRI was compared with CVR measured by positron emission tomography (PET). METHODS: Twelve normal subjects and 17 patients with major cerebral artery occlusive disease underwent PW MRI and PET. The images were coregistered with 3-dimensional spoiled gradient-recalled acquisition images. Quantitative PW MRI-CBV maps were generated using the indicator dilution method with arterial input function. One large cortical region of interest for each unilateral middle cerebral artery territory was determined on each image. PET-CVR was calculated by measuring cerebral blood flow before and after acetazolamide challenge. RESULTS: A significant negative correlation was observed between PW MRI-CBV and PET-CVR (r=-0.713; P<0.0001). PW MRI-CBV higher than the mean +2 SD obtained in normal subjects (15.2 mL/100 g) was defined as elevated and PET-CVR lower than the mean -2 SD obtained in normal subjects (15.1%) was defined as reduced. Assuming the PET-CVR as the true determinant of hemodynamic impairment, PW MRI-CBV provided 80.0% sensitivity and 91.7% specificity, with 80.0% positive predictive value for detecting patients with reduced CVR. CONCLUSIONS: The PW MRI-CBV method can simply and accurately identify patients with hemodynamic impairment without exposure to ionizing radiation.

Adult↗
PubMedDate not supplied

Effect of chronic middle cerebral artery stenosis on the local cerebral hemodynamics.

In 36 patients with angiographically proven middle cerebral artery (MCA) stenosis, local cerebral hemodynamics were studied employing angiography, 133Xe inhalation regional cerebral blood flow (rCBF) measurements and CT scans. They had transient ischemic attacks in 8 and completed stroke in 28. The patients with less than 50% stenosis (n = 16) had no hemodynamic abnormality in angiographical and rCBF examinations. The infarction in this group was small and located in the basal ganglia area. The patients with 50 to 74% stenosis (n = 9) often revealed a delayed filling of MCA branches in the angiography, however, they showed no significant rCBF reduction. The infarction in this group was also small and located in the basal ganglia area. The patients with 75 to 99% stenosis (n = 11) exhibited a significant flow depression both in angiographical and rCBF examinations. Three of them had large cerebral infarction in the watershed zone or the cerebral cortex. The results of the present study suggest that the hemodynamic effect of MCA stenosis begins to manifest at 50% in grade and becomes apparent at 75%. The danger of hemodynamic crisis as well as the risk of large cerebral infarction may increase when MCA stenosis exceeds 75% in grade.

Adult↗
PubMed1996

Effects of isovolemic hemodilution on hemodynamics, cerebral perfusion, and cerebral vascular reactivity.

BACKGROUND AND PURPOSE: To verify the hemorheological effects of isovolemic hemodilution on hemodynamics and cerebral perfusion of normal humans, we tested the efficacy of isovolemic hemodilution in systemic hemodynamics and cerebral bood flow augmentation and its influences in vascular reserve. METHODS: Isovolemic hemodilution was studied in a total of 13 normal healthy subjects. Regional cerebral blood flow was measured by the xenon-enhanced CT method. Cerebral vascular activity was measured by acetazolamide challenge. These measurements, in association with hemorheological and hemodynamic monitoring, were analyzed before and after isovolemic hemodilution with low-molecular-weight dextran. RESULT: Our results showed significant change in hemodynamic parameters after isovolemic hemodilution, including tachycardia, a 24% increase of cardiac index, and decrease of peripheral vascular resistance. Both left and right heart work index increased as a consequence of increased cardiac index. Regional cerebral blood flow increased 35.0 +/- 2.5% at 3 hours after hemodilution and 20.2 +/- 3.9% at 1 week after hemodilution. Cerebral vascular reactivity decreased from 32.1 +/- 4.1% to 25.3 +/- 4.0% after hemodilution, implicating a certain degree of vasodilation in the process of hemodilution. The whole procedure of hemodilution was completed in 52 +/- 6 minutes, and the subjects did not report discomfort during the procedure. CONCLUSIONS: Isovolemic hemodilution in subjects with normal cerebral perfusion can augment cerebral blood flow efficiently in a rapid fashion, and this effect can last for at least a week. The mechanism of flow augmentation may be partially attributed to vasodilation, which could be manifested as tachycardia, increased cardiac output, and decreased cerebral vascular reactivity.

Acetazolamide↗
PubMed1997

Transcranial Doppler ultrasound criteria for hemodynamically significant internal carotid artery stenosis based on residual lumen diameter calculated from en bloc endarterectomy specimens.

BACKGROUND AND PURPOSE: Transcranial Doppler (TCD) is often used in conjunction with carotid duplex ultrasonography (CDUS) to evaluate the hemodynamic significance of internal carotid artery (ICA) stenosis. We examined the sensitivity and specificity of TCD criteria for detection of a hemodynamically significant stenosis (residual lumen diameter < 1.5 mm) at the origin of the ICA. METHODS: We selected patients who underwent carotid end-arterectomy (CEA) and had preoperative TCD data available. Eighty-one patients underwent transorbital evaluation, 49 of whom also had transtemporal TCD performed. The endarterectomy specimens were removed en bloc and sectioned, and the minimal residual lumen diameter calculated by computer analysis. RESULTS: For the transorbital approach, the strongest indicators of a residual lumen diameter < 1.5 mm were reversed flow in the ipsilateral ophthalmic artery and a > 50% peak systolic velocity difference between the carotid siphons (distal ICAs) in patients with unilateral ICA origin stenosis. They were 100% specific and 31% and 26% sensitive, respectively. For the transtemporal approach in patients with a unilateral stenosis, a > 35% difference in ipsilateral middle cerebral artery (MCA) peak systolic velocity relative to the contralateral MCA or a > 50% difference in contralateral anterior cerebral artery (ACA) peak systolic velocity relative to the ipsilateral ACA were 100% specific for identifying a residual lumen diameter of < 1.5 mm. Sensitivities were 32% and 43%, respectively. Irrespective of contralateral stenosis, a > 35% difference in ipsilateral MCA peak systolic velocity relative to the ipsilateral posterior cerebral artery had a 100% specificity and a 23% sensitivity for detecting a < 1.5 mm minimal residual lumen diameter. CONCLUSIONS: Although the TCD sensitivity for detecting a hemodynamically significant stenosis is relatively low, it can be highly specific (up to 100%). We conclude that TCD enhances the specificity of highly sensitive CDUS criteria for detecting a hemodynamically significant ICA stenosis.

Aged↗
PubMed1998

Posthyperventilatory steal response in chronic cerebral hemodynamic stress: a positron emission tomography study.

BACKGROUND AND PURPOSE: The alteration of regional cerebral blood flow (CBF) during and after hyperventilation was measured using positron emission tomography (PET) to determine the circulatory response induced by daily respiratory changes in the cerebral area under chronic hemodynamic stress. METHODS: Three normal volunteers and 12 patients with an obstruction of major cerebral arteries underwent PET measurements of the CBF after an injection of H2(15)O: (1) in the resting condition, (2) during hyperventilation (HV scan), (3) 1 to 3 minutes after hyperventilation (post-HV scan), (4) during the inhalation of 5% CO2, and (5) after an injection of acetazolamide. Eleven patients also underwent a 15O gas study to measure CBF, oxygen extraction fraction (OEF), and cerebral blood volume (CBV). RESULTS: (1) In 9 patients, the CBF value in the post-HV scan was lower than that in the HV scan in 1 or more regions in the area of the obstructed arteries, although the PaCO2 level during the post-HV scan was higher than that during the HV scan in all patients. All control regions in the patients and in the normal volunteers showed an elevated CBF in the post-HV scan compared with the HV scan. (2) The negative post-HV response (posthyperventilatory steal) was prominent in 4 patients with moyamoya vessels and in another 5 patients with atherosclerotic disease who had PET evidence of hemodynamic stress (elevated CBV or OEF). (3) The regional pre- to post-HV change in CBF was significantly correlated with the CBF responses to acetazolamide and CO2. CONCLUSIONS: Vasodilatation after the termination of hyperventilation in the normal areas induces a steal response in the cerebral area suffering from hemodynamic stress and may cause profound hypoperfusion in everyday situations. This phenomenon may be important to our understanding of the clinical symptoms and the natural course of chronic cerebral occlusive disease bearing hemodynamic stress.

Acetazolamide↗