Color Doppler waveforms of maternal cervical internal carotid arteries in normotensive and preeclamptic gravidas.
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The objective of this study was to investigate and determine fitted percentiles of blood flow resistance of cervical internal carotid arteries in normal pregnancies from gestational weeks 20 to 42 and to compare the resistance indices and mean velocities of the these arteries in normotensive and preeclamptic gravidas. A duplex color apparatus with pulsed Doppler ultrasound scanner (7.5 MHz) was used to determine the resistance index and mean velocity values of maternal cervical internal carotid arteries in 310 healthy singleton gravidas (group 1) and 74 singleton preeclamptic gravidas (group 2). The resistance index and mean velocity values of the maternal cervical internal carotid arteries decrease as the gestational age increases in normal gravidas, whereas in preeclamptic pregnancies these values are no different from those in normal gravidas during the second half of the gestational period. (+info)
Mechanisms of retarded apical filling in acute ischemic left ventricular failure.
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BACKGROUND: We examined the hypothesis that retardation of apical filling as measured by color M-mode Doppler echocardiography in the diseased left ventricle (LV) reflects a decrease in the intraventricular mitral-to-apical pressure gradient. METHODS AND RESULTS: In 9 open-chest anesthetized dogs, micromanometers were placed near the mitral tip and in the apical region. From the color M-mode Doppler images, the time delay (TD) between peak velocity at the mitral tip and the apical region was determined as an index of LV flow propagation. Acute ischemic LV failure was induced by coronary microembolization. Induction of ischemia caused a marked increase in LV end-diastolic pressure and a decrease in LV ejection fraction. The time constant of LV isovolumic apical pressure decay (tau) increased from 31+/-8 to 49+/-16 ms (P<0.001). The peak early diastolic mitral-to-apical pressure gradient (DeltaPLVmitral-apex) decreased from 1.9+/-0.9 to 0.7+/-0.5 mm Hg (P<0.01), and TD increased from 5+/-3 to 57+/-26 ms (P<0.001). The slowing of flow propagation was limited to the apical portion of the LV cavity. The TD correlated with DeltaPLVmitral-apex (r=-0.94, P<0.01) and with tau (r=0.92, P<0.01). Before ischemia, the mitral-to-apical flow propagation velocity far exceeded the velocity of the individual blood cells, whereas during ischemia, flow propagation velocity approximated the blood velocity. CONCLUSIONS: Retardation of apical filling in acute ischemic failure was attributed to a decrease in the mitral-to-apical driving pressure, reflecting slowing of LV relaxation. The slowing of flow propagation appeared to represent a shift in apical filling from a pattern of column motion to a pattern dominated by convection. (+info)
Effect of acute intraocular pressure changes on short posterior ciliary artery haemodynamics.
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BACKGROUND/AIMS: Vascular insufficiency due to abnormal autoregulation has been proposed as a major factor in the development of glaucoma. The anterior optic nerve is primarily perfused by the short posterior ciliary arteries. The autoregulatory capacity of these vessels in response to acutely elevated intraocular pressure (IOP) was examined in normal human subjects. METHODS: Colour Doppler imaging was performed on the short posterior ciliary arteries of 10 normal subjects at baseline and during four incremental IOP elevations. Using a scleral suction cup placed temporally, IOP was elevated to approximately 25, 30, 40, and 50 mm Hg. Additional measurements were performed immediately after pressure release. Systolic and diastolic flow velocities were measured and Pourcelot's resistivity index was calculated. RESULTS: Systolic and diastolic flow velocities decreased linearly with each incremental increase in IOP (p < 0.001). Pourcelot's resistivity index increased linearly with each incremental increase in IOP (p < 0.001). Changes in end diastolic velocity, peak systolic velocity, and Pourcelot's resistivity index were linearly related to changes in IOP. CONCLUSION: The normal healthy eye is not able to autoregulate to maintain PCA blood flow velocities in response to acute large elevations in IOP. (+info)
Arterial blood flow characteristics in central retinal vein occlusion and effects of panretinal photocoagulation treatment: an investigation by colour Doppler imaging.
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AIMS: To determine whether an increase in vascular resistance in the central retinal and ophthalmic arterial circulations contributes to the development of central retinal vein occlusion (CRVO), or haemodynamic alterations in central retinal and ophthalmic arteries occur secondary to the vein occlusion as increased intravascular pressure is transferred through the capillary bed to the arterial side and the effect of panretinal photocoagulation treatment on these circulations in ischaemic cases. METHODS: The ophthalmic and central retinal arteries of the affected and non-affected eyes of 20 patients with non-ischaemic CRVO, 13 patients with ischaemic CRVO, and 22 control subjects were investigated by colour Doppler imaging. Panretinal photocoagulation (PRP) treatment was applied to the eyes with ischaemic CRVO. Maximum and minimum blood flow velocities, and resistivity indexes were calculated in the affected and healthy eyes of patients and in the control eyes. RESULTS: Average blood flow velocity in the central retinal and ophthalmic arteries of patients with non-ischaemic CRVO did not differ from their fellow eyes, but a significantly lower average blood flow velocity was found in the ophthalmic and central retinal arteries of the patients with ischaemic CRVO compared with their fellow eyes. Patients with ischaemic CRVO had significantly lower blood flow velocities in their ophthalmic and central retinal arteries than non-ischaemic cases that were further reduced following PRP treatment. CONCLUSION: This study suggests that impaired arterial blood flow observed in patients with CRVO may be partly related to secondary changes in the retrobulbar arterial circulation as a result of enhanced arterial resistance following CRVO. These data also demonstrate that PRP treatment decreases retinal and ophthalmic blood flow velocities in patients with ischaemic CRVO. (+info)
Augmented alpha-adrenergic constriction of atherosclerotic human coronary arteries.
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BACKGROUND: Although adrenergic activation plays a major role in the initiation of experimental myocardial ischemia, the significance of alpha-adrenergic coronary constriction in humans has been questioned. The present study assessed the impact of selective alpha-adrenergic receptor activation in patients with normal or atherosclerotic coronary arteries. METHODS AND RESULTS: In 39 patients, coronary blood flow (CBF, mL/min) was determined from combined angiography and Doppler measurements. In 8 patients with normal coronary arteries (group 1) and 9 with single coronary artery stenosis (group 2), doses of 1, 2.5, 5, and 10 mg IC of the alpha1-agonist methoxamine (M) were injected. Identical doses of the alpha2-agonist BHT933 (B) were injected in 8 patients with normal coronary arteries (group 3) and 8 with single stenosis (group 4). In 6 additional patients with single stenosis (group 5), aortocoronary sinus lactate differences were measured in response to M and B. CBF remained unchanged in group 1. In contrast, CBF was decreased dose-dependently in group 2, with a maximum at 10 mg M (39.0+/-9.4 versus 15.2+/-7.0). In groups 3 and 4, CBF was also decreased dose-dependently, with a maximum at 10 mg B (63.3+/-24.8 versus 49. 1+/-27.9 and 41.5+/-19.0 versus 12.7+/-8.0, respectively). In group 5, there was more net lactate production with B than with M (-0. 34+/-0.11 versus -0.04+/-0.09 mmol/L). CONCLUSIONS: In normal coronary arteries, alpha1-adrenergic activation does not reduce CBF, whereas alpha2-adrenergic activation reduces CBF by microvascular constriction. Both alpha1- and alpha2-adrenergic epicardial and microvascular constriction are augmented by atherosclerosis and can induce myocardial ischemia. (+info)
The effect of cold stress on uterine artery blood flow velocity waveforms in late pregnant women with and without preeclampsia.
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Cold stimulus, immersing the hand into ice water, was given to pregnant women with and without preeclampsia. The uterine artery blood flow was observed before, during and after the stimulus by Doppler ultrasound. The pulsatility index in the uterine artery blood flow was significantly increased by the cold exposure in preeclampsia from 1.14 to 1.52, whereas it increased in normal control from 0.95 to 1.25. In two of 11 cases of preeclampsia with fetal growth restriction, cold stimulus to the mother elicited a decrease of variability on fetal heart rate monitoring. Cold stimulus induces the constriction of the uterine artery, leading to a decrease of placental blood flow. (+info)
Transcranial color-coded duplex sonography of intracranial veins and sinuses in adults. Reference data from 130 volunteers.
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BACKGROUND AND PURPOSE: Transcranial color-coded duplex sonography (TCCS) of intracranial veins and sinuses in adults is a new, emerging application of ultrasonographic imaging. This study reports a standardized examination protocol for venous TCCS and provides reference data for clinical application. METHODS: In 130 healthy volunteers (mean age, 45.9+/-16.9 years; range, 14 to 77 years) the intracranial venous system was examined using frequency-based transtemporal TCCS. Identification rate, blood flow velocity, resistance index, and systolic/diastolic ratio were recorded for each examined venous vessel. RESULTS: Intracranial veins and sinuses show a low pulsatile forward flow with maximal systolic blood flow velocity up to 20 cm/s. Significant side differences of blood flow velocity in the paired venous structures could not be detected. Venous flow velocities decreased with age, whereas resistance indices and systolic/diastolic ratios increased. Women showed higher flow velocities than men. Mean identification rates for all age groups ranged from 70% to 90% for the deep middle cerebral vein, the basal cerebral vein, and the great cerebral vein of Galen. The straight sinus, the transverse sinus, and the rostral part of the superior sagittal sinus could be detected in 55% to 70% of cases. Detection rates were dependent on age and decreased as age increased. CONCLUSIONS: Venous TCCS can reliably image a significant part of the cerebral venous system. This method can provide information on venous hemodynamics in normal subjects and pathological cases. (+info)
Usefulness of transcranial color-coded sonography in the diagnosis of cerebral vasospasm.
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BACKGROUND AND PURPOSE: The noninvasive diagnosis of cerebral vasospasm with the use of conventional transcranial Doppler ultrasonography (TCD) is based on a velocity study of the middle cerebral artery (MCA). The authors report a prospective comparative study between transcranial color-coded sonography (TCCS), conventional transcranial Doppler (TCD), and angiography in the diagnosis of cerebral vasospasm after surgical treatment for aneurysm. METHODS: Thirty consecutive patients underwent routine angiography after surgical treatment for intracranial aneurysm. The distribution of vasospasm was determined after a prospective calculation of the angiographic diameter of the MCA, internal carotid artery (ICA), and anterior cerebral artery (ACA). The blood flow velocities (systolic and maximum) of the MCA, ICA, and ACA were evaluated by TCCS and TCD. RESULTS: The correlation between mean maximum velocity and angiographic diameter was significant for the MCA (r=-0.637, P<0.0001), ICA (r=-0.676, P<0.0001), and ACA (r=-0.425, P<0.01). TCCS sensitivity and specificity were higher than those for TCD for MCA (100% and 93%, respectively) and ICA (100% and 96.6%, respectively). For ACA, the sensitivity and specificity were 71.4% and 84.8%, respectively. CONCLUSIONS: The authors suggest that TCCS is useful for accurate monitoring of cerebral vasospasm in the MCA and ICA. In the ACA, TCCS monitors the hemodynamic state of the anterior part of the circle of Willis, which could expose the patient to a delayed ischemic deficit. (+info)