So you have identified a way to find a problem. WHAT THE FUCK IS THE SOLUTION TO REMOVING THAT PLAQUE? Useless research then with no solution.
Factors for Enhancement of Intracranial Atherosclerosis in High Resolution Vessel Wall MRI in Ischemic Stroke Patients
- 1Department of Neurology, Yonsei University College of Medicine, Seoul, South Korea
- 2Department of Radiology, Yonsei University College of Medicine, Seoul, South Korea
- 3Biostatistics Collaboration Unit, Department of Research Affairs, Yonsei University College of Medicine, Seoul, South Korea
Introduction: High resolution vessel
wall MRI (VW-MRI) has enabled to characterize intracranial
atherosclerosis (ICAS). We studied to identify the factors for
enhancement of ICAS in VW-MRI in patients with acute ischemic stroke.
Methods: Consecutive patients with
acute ischemic stroke or TIA who underwent VW-MRI between January 2017
and December 2017 were included. Enhancement on VW-MRI was defined as an
increase in intensity on contrast-enhanced T1-weighted sequence. We
compared the clinical and the radiologic findings between patients with
wall enhancement and those without wall enhancement.
Results: Of the 48 patients with ICAS,
28 patients revealed enhancement on VW-MRI. Patients with enhancement
were more likely to have severe stenotic lesions and higher levels of
total cholesterol, triglycerides, low-density cholesterol, Apo (b), and
Apo (b)/Apo (a) lipoprotein ratio (p < 0.05). Multivariable
analysis demonstrated that total cholesterol (OR: 5.378, 95% CI,
1.779–16.263), triglycerides (OR: 3.362, 95% CI, 1.008–11.209), low
density lipoprotein cholesterol (OR: 4.226, 95% CI, 1.264–14.126), Apo
(b) lipoprotein (OR: 3639.641, 95% CI, 17.854–741954.943) levels, and
Apo (b)/Apo (a) lipoprotein ratio (OR, 65.514; 95% CI, 1.131–3680.239)
were independently associated with enhancement of ICAS. High-density
lipoprotein cholesterol and Apo (a) lipoprotein levels were not
significantly different between the patients with wall enhancement and
those without wall enhancement.
Conclusions: The presence and severity
of enhancement of ICAS was significantly associated with dyslipidemic
conditions. These results suggest that strict lipid modification should
be achieved for the management of ICAS.
Introduction
Ischemic stroke is a major cause of mortality and morbidity worldwide (1).
Atherosclerosis, in particular, intracranial atherosclerosis (ICAS), is
recognized as one of the most common etiological factors of ischemic
stroke accounting for 30–50% of the ischemic cerebrovascular events (2).
Moreover, ischemic stroke attributable to ICAS is known to be
associated with an increased risk of poor functional outcomes after
stroke, cognitive impairment, and vascular death (3).
Precise in vivo characterization of ICAS is crucial, as this knowledge
enables the clinicians to better stratify the stroke risk for individual
patients and to plan therapeutic strategies accordingly.
Conventionally, clinicians have focused primarily on
detection and estimation of the degree of luminal stenosis by using
luminography techniques such as digital subtraction angiography or
magnetic resonance angiography (MRA). However, luminography alone is
insufficient to fully determine the histopathologic composition and
instability of the plaque (4, 5).
Currently, the advent of high resolution vessel wall magnetic resonance
imaging (VW-MRI) has enabled clinicians to differentiate among various
intracranial vasculopathies and to characterize the vulnerability of
ICAS plaque, which is thought to be the culprit lesion of ischemic
events, and the degree of luminal stenosis (6–9).
Among the VW-MRI findings, contrast enhancement of the ICAS plaque is
increasingly being reported as a reliable marker of plaque
vulnerability. It also tends to be predictive of future cerebrovascular
events (4, 10, 11). However, the factors for the presence or extent of arterial wall enhancement on VW-MRI are not fully understood (12, 13).
In the present study, we aimed to identify the factors
for the enhancement of ICAS in VW-MRI in patients with acute ischemic
stroke.
No comments:
Post a Comment