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Intracranial atherosclerosis (ICAD) is the main subtype of high recurrence of ischemic stroke.
In the trial of stent-placed and active drug therapy to prevent intracranial stenosis (SAMMPRIS), ICAD patients with multiple vascular risk factors had a 12.6% risk of stroke recurrence or death within 1 year in the Chinese intracranial atherosclerosis study.
Compared to coronary/cervical arterial plaques, established imaging features can predict isocardial or cerebral isoemia events, and the morphology of ICAD lesions is largely unknown after or with stroke symptoms.
In symptomatic ICAD, the only parameter predicting stroke recurrence is "tube cavity stenosis", however, this may mean insufficient far-end perfusion, but does not explain stroke mechanisms such as arterial-arterial thromboembolism, cavity syndrome caused by junction atherosclerosis, or insufficient anterior perfusion.
note that one-third of tube cavity stenosis ICAD lesions are only moderate at the time of stroke, suggesting that factors other than the severity of stenosis may also control the stroke risk in ICAD patients.
, the study of acute symptomatic ICAD plaque morphology can improve our understanding of stroke occurrence/recurrence and provide a basis for treatment strategies.
In this study, we evaluated ICAD plaque morphology through 3D rotating angioconesic (3DRA), a catheter-based technique that can assess vascular construction from almost unlimited planes, and can show plaque morphology, and display the morphological characteristics of plaques and further branch/through smoothness at a higher spatial resolution than traditional digital aberration angiology.
compared the morphological characteristics and smooth, irregular and contouring of plaques, as well as the correlation between plaque morphological characteristics and the load of isoemia damage in the downstream brain.
recruited adult patients with acute ishemotic stroke or transient cerebral isoemia attacks (TIA), which were attributed to the high level of ICAD (60%-99% stenosis) identified in 3DRA within 4 weeks of the onset of symptoms.
short-lived cerebral isoemia attack (TIA) is a brief onset of neurological dysfunction caused by isoemia or retinal isoemia, which disappears completely within 24 hours.
all patients have an MRI.
cause of stroke and its correlation with ICAD are determined by neuroscientists based on clinical syndrome, imaging characteristics, and complications of cardiovascular risk factors.
Excludes patients who may have non-atherosclerotic stenosis (e.g. smoke, vasculitis or mezzanine), signs of cardiac embolism (e.g. atrial fibrillation, valve heart disease, or 6-week infarction of the heart), contraindicated cranial cervical or vertebral artery (VA) stenosis, MRI, and 3DRA contraindications.
Participants recruited before SAMMPRIS received life-long monoantigen therapy (aspirin), while participants recruited after SAMMPRIS took short-term double antiplate plate plates (aspirin plus clopidogrel) immediately after an index stroke, followed by life-long aspirin.
all patients were treated with statins, and their LDL target value was slt;70 mg/dL .lt;1.8 mmol/L.
other targets for cardiovascular risk control, such as glycation of hemoglobin, 6.5 percent, systolic blood pressure, and 140 mmHg.
the length of the lesions, the percentage of tube cavity stenosis, the maximum plaque thickness, and the upper plaque shoulder angle were measured.
the surface profile, adjacent branch atherosclerosis disease (BAD) and axial plaque load distribution were evaluated based on a 360-degree rotating full section of the target lesions.
patients with eligible ICAD lesions who had multiple spatial separations were assessed for the most severe lesions of tube cavity stenosis.
classification and measurement is addressed by consulting a senior neurologist and neurologist with 15 years of experience in neurotransigency (TWL).
each participant under the 1.5 Tesla (Siemens Sonata, Germany) or 3.0 Tesla Magnetic Resonance Scanner (Achievea 3.0T Philips, Netherlands) had an MRI examination of the brain, including axial T1 plus Weighted and T2 weighted imaging, diffusion-weighted imaging (DWI), oscillator diffusion coefficient graph, T2 fluid attenuation reversal recovery, and flight-time magnetic resonance angiography from the indicator stroke/transient cerebral isoemia attack within a week.
(XL) assessed the load of cerebral isoemia damage in the corresponding area of the lesions intracranial arteries.
the MR image at least 1 month after the 3DRA assessment, the examiner knew nothing about the morphological characteristics of the plaque except the location of the ICAD lesions.
acute cerebral infarction is defined by DWI high signal, superficial dispersion coefficient graph low signal definition, chronic infarction is characterized by T2 fluid attenuation reversal recovery imaging high signal and surface dispersion coefficient graph and other strong or high signals.
we divide the infarction load of the corresponding area into: (A) no infarction, (B) only acute infarction or only chronic infarction or (C) acute and chronic infarction coexist.
is is blood damage load was associated with clinical and 3DRA results.
between a stroke attack and 3DRA is 23 days (IQR 13-32).
132 of the 180 lesions are located at the end of the ICA, 6 are at the end of the ICA, 6 are across the end of the ICA and 14 are located in BA and 2 are in the VA.
the average tube cavity stenosis is 75% (IQR 71-84).
the plaque profile is smooth (n=51;28.3%), irregular (n=101;56.1%), or ulcerative (n=28;15.6%).
30 of the 28 ulcerative plaques in the world.
these indicate that surface ulcers with ruptured fiber caps are most common at the near end of the plaque (n=13;46.4%) and one third (n=10;35.7%), with relatively few at the far end (n=7;25.0%).
, however, the tube cavity plaque load is unevenly tilted toward the far end, where half of the plaques (n-89,49.4%) have a maximum thickness (and maximum narrowness) that exceeds one-third of the far end. Of the 132 MCA-M1 plaques, 47 lesions (35.6%) were most prominent in the lower vascular wall, 32 (24.2%) at the upper wall, 32 (24.2%) at the abdominal wall and 21 (15.9%) at the back wall.
of the 14 BA plaques, 7 lesions (50.0%) protruded from the sidewall, 4 (28.6%) protruded from the abdominal wall and 3 (21.4%) protruded from the back wall. Of the 146 MCA-M1 or BA plaques, 88 lesions (60.3 per cent; 80 MCA-M1 and 8 BA lesions) found adjacent BAD, blocked bean arteries (n=66), precrystopathic arteries (n=29), early M2 (n=7), lower cereotr brain arteries (n=7) and small brain arteries (n=3).
study has the following limitations: First, the interval between an indicator stroke/transient istemia attack and a 3DRA examination is 23 days.
the shape of plaques may change during this period under the treatment of antiplate plate plates and statins.
second, 3DRA's vascular turbidity depends on blood flow.
Thus, in our study, small blood vessels that were completely blocked, severely low perfusion, or small caliber (such as substrate artery infleters) may not be noticeable, leading to misjudgment of the position of the branch/perforation opening.
, some plaque morphological assessments are susceptible to subjective judgment.
In summary, smooth plaques, irregular plaques, and ulcerative plaques have different morphological characteristics: ulcerative ICAD plaques have more fragile morphological characteristics, are adjacent to BAD, and are associated with a high incidence of acute and chronic infarction downstream.
further study of the dynamic evolution of plaque morphology, composition and holistic/locally fluidized features will deepen the understanding of the stroke mechanism when ICAD exists.
Leung TW, Wang L, Zou X, et al Plaque morphology in acute symptomatic intracranial atherosclerotic disease Journal of Neurology, Neurosurgery and Psython Published Online First: 25 November 2020. doi: 10.1136/jnnp-2020-325 027 MedSci Original Source: MedSci Original Copyright Notice: All text, images and audio and video materials on this website that indicate "Source: Mets Medicine" or "Source: MedSci Originals" are owned by Mets Medicine and are not authorized to be reproduced by any media, website or individual, and are authorized to be reproduced with the words "Source: Mets Medicine".
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