Hyperintense Plaques Research Articles

Dilated lenticulostriate artery on whole-brain vessel wall imaging differentiates pathogenesis and predicts clinical outcomes in single subcortical infarction.

This study aimed to investigate the dilation of lenticulostriate artery (LSA) identified by whole-brain vessel wall imaging (WB-VWI) in differentiating the etiologic subtypes of single subcortical infarction (SSI) and to determine whether the appearance of dilated LSA was associated with 90-day clinical outcomes in parental atherosclerotic disease (PAD)-related SSI. Patients with acute SSI were prospectively enrolled and categorized into PAD-related SSI and cerebral small-vessel disease (CSVD)-related SSI groups. The imaging features of LSA morphology (branches, length, dilation, and tortuosity), plaques (burden, remodeling index, enhancement degree, and hyperintense plaque), and CSVD (white matter hyperintensity, lacunes, cerebral microbleed, and enlarged perivascular space) were evaluated. The logistic regression was performed to determine the association of dilated LSA with PAD-related SSI and 90-day clinical outcomes. In total, 131 patients (mean age, 52.2 ± 13.2 years; 99 men) were included. The multivariate logistic regression analysis revealed that the presence of dilated LSAs (odds ratio (OR), 7.40; 95% confidence interval (CI): 1.88-29.17; p = 0.004)) was significantly associated with PAD-related SSI. Moreover, after adjusting for confounding factors, the association of poor outcomes with the total length of LSAs (OR, 0.94; 95% CI: 0.90-0.99; p = 0.011), dilated LSAs (OR, 0.001; 95% CI: 0.0001-0.08; p = 0.002), and plaque burden (OR, 1.35; 95% CI: 1.11-1.63; p = 0.002) remained statistically significant. The dilation of LSA visualized on WB-VWI could differentiate various subtypes of SSI within LSA territory and was a prognostic imaging marker for 90-day clinical outcomes for PAD-related SSI. Evaluation of LSA morphology based on WB-VWI can differentiate the pathogenesis and predict clinical outcomes in SSI, providing crucial insights into the etiologic mechanisms, risk stratification, and tailored therapies for these patients. The prognosis of SSIs within lenticulostriate territory depend on the etiology of the disease. LSA dilation on WB-VWI was associated with parental atherosclerosis and better 90-day outcomes. Accurately identifying the etiology of SSIs in lenticulostriate territory assists in treatment decision-making.

Association of Morphology of Lenticulostriate Arteries and Proximal Plaque Characteristics With Single Subcortical Infarction: A Whole-Brain High-Resolution Vessel Wall Imaging Study.

We aimed to investigate the association of characteristics of lenticulostriate artery (LSA) morphology and parental atheromatous disease (PAD) with single subcortical infarction (SSI) and to explore whether the LSA morphology is correlated with proximal plaque features in asymptomatic PAD. Patients with acute SSI were prospectively enrolled and classified as large- and small-SSI groups. The clinical data and imaging features of LSA morphology (branches, length, dilation, and tortuosity) and middle cerebral artery plaques (normalized wall index, remodeling index, enhancement degree, and hyperintense plaques) were evaluated. Logistic regression was performed to determine the association of large SSIs with morphologic features of LSAs and plaques. The Spearman correlation between the morphologic characteristics of LSAs and plaque features in asymptomatic PAD was analyzed. Of the 121 patients recruited with symptomatic PAD, 102 had coexisting asymptomatic contralateral PAD. The mean length of LSAs (odds ratio, 0.84 [95% CI, 0.73-0.95]; P=0.007), mean tortuosity of LSAs (odds ratio, 1.13 [95% CI, 1.05-1.22]; P=0.002), dilated LSAs (odds ratio, 22.59 [95% CI, 2.46-207.74]; P=0.006), and normalized wall index (odds ratio, 1.08 [95% CI, 1.01-1.15]; P=0.022) were significantly associated with large SSIs. Moreover, the normalized wall index was negatively correlated with the mean length of LSAs (r=-0.348, P<0.001), and the remodeling index was negatively correlated with the mean tortuosity of LSAs (r=-0.348, P<0.001) in asymptomatic PAD. Our findings suggest that mean length of LSAs, mean tortuosity of LSAs, dilated LSAs, and normalized wall index are associated with large SSIs. Moreover, plaque features in asymptomatic PAD are correlated with morphologic features of LSAs.

Edge-Type Hyperintense Intracranial Artery Plaque: A Potential MRI Biomarker of Stroke Recurrence.

Identifying patients at high risk of stroke recurrence is important for stroke prevention and treatment. To explore the characteristics of T1 hyperintense plaques (HIP) and their relationship with stroke recurrence in patients with symptomatic intracranial atherosclerotic stenosis (sICAS). Retrospective. One hundred fifty-seven patients with moderate-to-severe (≥50%) nonocclusive sICAS and MRI studies (42 females and 115 males, mean age 58.69 ± 10.68 years). 3D higher-resolution black-blood T1-weighted fast-spin-echo sequence at 3.0 T. HIP (signal intensity [SI] of plaque-to-adjacent gray matter >1.0 on non-contrast T1-weighted images) and non-HIP plaques were identified. HIP plaques were categorized as edge type (high SI adjacent to lumen) and non-edge type (high SI within plaque). Clinical and imaging features of different plaque types were compared. Stroke recurrence was assessed through telephone or medical records at 3 and 6 months, and then once a year post-MRI. The relationship between edge type and non-edge types HIP with stroke recurrence was analyzed. Student's t test, Mann-Whitney U-test, chi square test and Fisher's exact test to compare features between plaque types. Kaplan-Meier curves (with log-rank tests) and Cox proportional hazards regression to assess relationship between stroke recurrence and different plaque types. A two-tailed P-value of <0.05 was considered statistically significant. Of 157 culprit lesions, 87 (55%) were HIPs (43 edge type, 44 non-edge type) and 70 (45%) were non-HIPs. Plaque thickness, area, and volume were significantly higher for HIPs than for non-HIPs. Among patients with HIPs, edge type was significantly more likely in the posterior circulation (53.5% vs. 27.3%), and had significantly higher plaque thickness, length, area, volume, plaque burden, and remodeling index than non-edge type. Edge-type HIP was significantly more common than non-edge HIP in patients with diabetes mellitus (51.2% vs. 29.5%) and dyslipidemia (79.1% vs. 54.5%). During median follow-up of 27 months, 33 patients experienced stroke recurrence. Recurrence was associated with edge-type HIP (adjusted hazard ratio = 2.83; 95% confidence interval: 1.40-5.69), both in the overall cohort (34.9% vs. 15.8%) and in patients with HIP (34.9% vs. 9.0%). Age ≥60 years and edge-type HIP had a significant interaction. Hyperintense plaque may be categorized as edge type or non-edge type. Edge-type HIP may be a potential MRI biomarker of stroke recurrence. 3 TECHNICAL EFFICACY: Stage 2.

Clinical features and long-term outcomes of symptomatic low-grade carotid stenosis

ObjectiveIn symptomatic low-grade stenosis, most of the reports did not clarify the long-term outcome. This study aims to clarify the clinical features and long-term outcomes of symptomatic low-grade stenosis cases. Materials and methodsWe included 123 symptomatic patients with low-grade (<50%) carotid stenosis. The relative plaque signal intensity (rSI) and expansive remodeling rate (ERR) were measured using carotid magnetic resonance imaging (MRI). Antiplatelet therapy and treatment for atherosclerosis risk factors were administered in all cases. Carotid endarterectomy (CEA) was performed when ischemic symptoms appeared, or the percent stenosis progressed despite medical treatment. ResultsThe mean percent stenosis, rSI, and ERR on admission were 22.3, 1.70, and 2.01, respectively. The mean volume of the hyperintense plaque on carotid MRI was 641.4± 540 mm3. Sixty percent of cases involved intraplaque hemorrhage and expansive remodeling. During a mean follow-up of 52 months, recurrence of ischemic events was confirmed in 45 cases (36.6%). Of the 67 cases performed follow-up MRI, 34 cases (50%) had an increased volume of T1-hyperintense plaque. CEA or carotid artery stenting was performed in 49 cases. During a mean follow-up of 57.8 months after CEA, two cases of death (fatal intracerebral hemorrhage and asphyxia) and one case of brain stem lacunar infarction were observed, but ipsilateral ischemic events were not. ConclusionMost of the symptomatic patients with low-grade stenosis had both intraplaque hemorrhage and expansive remodeling and presented a high risk of recurrence and stenosis progression. CEA may have preventive effects against ischemic events in low-grade stenosis.

Plaque modification and stabilization after drug-coated balloon angioplasty for intracranial atherosclerotic lesions.

A drug-coated balloon (DCB) has potential applications in the treatment of intracranial atherosclerotic disease (ICAD). We aimed to evaluate changes of vessel wall features of ICAD lesions after DCB treatment by using vessel wall MRI (VWMRI). We retrospectively included patients with symptomatic ICAD who underwent DCB angioplasty alone. The incidences of stenosis of the lumen area, vessel wall thickening, hyperintense plaques, and prominent wall enhancement were compared between the baseline and follow-up VWMRI. There were 29 ICAD lesions from 29 patients, of which 22 were stenosis and 7 were occlusion. The median interval between DCB treatment and follow-up VWMRI was 4.1 [3.3, 6.7] months. After DCB treatment, follow-up VWMRI showed a significant decrease in the stenosis degree of the lumen area (83% [71%, 96%] vs 15% [3%, 41%], p < 0.001). Thirty-eight percent (11/29) of the patients observed normal appearance of the target vessel wall on follow-up VWMRI. In the stenosis group, the prevalence of hyperintense plaques decreased from 66.7% (14/21) at baseline to 23.8% (5/21) at follow-up, and prominent wall enhancement decreased from 66.7% (14/21) at baseline to 19.0%(4/21) at follow-up. The incidence of hyperintense plaques (p = 0.028) and vessel wall thickening (p = 0.018) tended to decrease with follow-up time. Although not significant (p = 0.106), a similar trend was observed between the incidence of prominent wall enhancement and follow-up time. Vascular healing with plaque modification and stabilization occurred following DCB treatment of ICAD lesions. • A drug-coated balloon (DCB) has potential applications in the treatment of intracranial atherosclerotic disease (ICAD). • Vascular healing with plaque modification and stabilization occurred following DCB treatment of ICAD lesions.

Relationship between coronary hyper-intensive plaques identified by cardiovascular magnetic resonance and clinical severity of acute coronary syndrome

BackgroundCoronary hyper-intense plaque (CHIP) detected on T1-weighted cardiovascular magnetic resonance (CMR) has been shown to associate with vulnerable plaque features and worse outcomes in low- and intermediate-risk populations. However, the prevalence of CHIP and its clinical significance in the higher-risk acute coronary syndrome (ACS) population have not been systematically studied. This study aims to assess the relationship between CHIP and ACS clinical severity using intracoronary optical coherence tomography (OCT) as the reference.MethodsA total of 62 patients with known or suspected coronary artery disease were prospectively enrolled including a clinically diagnosed ACS group (n = 50) and a control group with stable angina pectoris (n = 12). The ACS group consisted of consecutive patients including unstable angina pectoris (n = 27), non-ST-segment-elevation myocardial infarction (non-STEMI) (n = 8), and ST-segment-elevation myocardial infarction (STEMI) (n = 15), respectively. All patients underwent non-contrast coronary CMR to determine the plaque-to-myocardium signal intensity ratio (PMR).ResultsAmong the four groups of patients, a progressive increase in the prevalence of CHIPs (stable angina, 8%; unstable angina, 26%; non-STEMI, 38%; STEMI, 67%; p = 0.009), and PMR values (stable angina, 1.1; unstable angina, 1.2; non-STEMI, 1.3; STEMI, 1.6; median values, P = 0.004) were observed. Thrombus (7/8, 88% vs. 4/22, 18%, p = 0.001) and plaque rupture (5/8, 63% vs. 2/22, 9%, p = 0.007) were significantly more prevalent in CHIPs than in plaques without hyper-intensity. Elevated PMR was associated with high-risk plaque features including plaque rupture, thrombus, and intimal vasculature. A positive correlation was observed between PMR and the number of high-risk plaque features identified by OCT (r = 0.44, p = 0.015).ConclusionsThe prevalence of CHIPs and PMR are positively associated with the disease severity and high-risk plaque morphology in ACS.

Neuro-ophthalmological manifestations as complication of an infection with Mycoplasma pneumoniae and subsequent development of disseminated acute encephalitis

The purpose of this article is to describe two pediatric neuro-ophthalmological clinical cases caused by a systemic infection due to Mycoplasma pneumoniae (M. pneumoniae). The cases are two girls aged 14 and 12 seen in the Emergency Department: The first one had internuclear ophthalmoplegia and second with loss of vision and headache. They had no other neurological foci. Magnetic resonance imaging showed hyperintense plaques in both, suggestive of a demyelinating disease. One month later, the neuro-ophthalmological symptoms resolved, with normal follow-up magnetic resonance imagings. The diagnosis was acute disseminated encephalitis secondary to M. pneumoniae. The diagnosis was made using PCR (gold standard) and/or IgM in serology. It is important to think about this possible etiology in cases of suggestive demyelinating disease. There is controversy about the role of antibiotics and on whether corticosteroids are contemplated. In conclusion, M. pneumoniae must be a differential diagnosis in acute neuro-ophthalmological disorders in children.

Manifestaciones neuroftalmológicas como complicación de una infección por Mycoplasma pneumoniae y desarrollo posterior de una encefalitis aguda diseminada

The purpose of this article is to describe two paediatric neuro-ophthalmological clinical cases caused by a systemic infection due to Mycoplasma pneumoniae (M. pneumoniae). The cases are two girls aged 14 and 12 seen in the Emergency Department: The first one had internuclear ophthalmoplegia and second with loss of vision and headache. They had no other neurological foci. Magnetic resonance imaging showed hyperintense plaques in both, suggestive of a demyelinating disease. One month later, the neuro-ophthalmological symptoms resolved, with normal follow-up magnetic resonance imagings. The diagnosis was acute disseminated encephalitis secondary to M. pneumoniae. The diagnosis was made using PCR (gold standard) and/or IgM in serology. It is important to think about this possible aetiology in cases of suggestive demyelinating disease. There is controversy about the role of antibiotics and on whether corticosteroids are contemplated. In conclusion, M. pneumoniae must be a differential diagnosis in acute neuro-ophthalmological disorders in children.

Hyperintense Plaque on Intracranial Vessel Wall Magnetic Resonance Imaging as a Predictor of Artery-to-Artery Embolic Infarction.

The aim of the present study was to investigate atherosclerotic plaque characteristics in patients with artery-to-artery (A-to-A) embolic infarction by whole-brain high-resolution magnetic resonance imaging. Seventy-four patients (mean age, 54.7±12.1 years; 59 men) with recent stroke in the territory of middle cerebral artery because of intracranial atherosclerotic disease were prospectively enrolled. Whole-brain high-resolution magnetic resonance imaging was performed in all the patients both precontrast and postcontrast administration by using a 3-dimensional T1-weighted vessel wall magnetic resonance imaging technique known as inversion-recovery prepared sampling perfection with application-optimized contrast using different flip angle evolutions. Patients were divided into A-to-A embolic infarction and non-A-to-A embolic infarction groups based on diffusion-weighted imaging findings. The characteristics of the intracranial atherosclerotic plaques were compared between groups. A total of 74 intracranial atherosclerotic plaques were analyzed (36 in A-to-A embolism group and 38 in non-A-to-A embolism group). Hyperintense plaques (HIPs) were more frequently observed in A-to-A embolism group (75.0% versus 21.1%; P<0.001). Eighteen of the 27 HIPs (66.7%) demonstrated hyperintense spots or areas located adjacent to the lumen versus 9 HIPs (33.3%) located within the plaque in A-to-A embolism group. Furthermore, a higher prevalence of plaque surface irregularity was also observed in A-to-A embolism group (41.7% versus 18.4%; P=0.029). Logistic regression analysis showed that HIP was the most powerful independent predictor of A-to-A embolic infarction (P<0.001), with the odds ratio of 11.2 (95% confidence interval, 3.5-36.2). A-to-A embolic infarction has distinct vulnerable plaque characteristics compared with non-A-to-A embolic infarction. HIP and plaque surface irregularity may predict A-to-A embolic infarction.

Abstract WP135: Is Hyperintense Carotid Plaque on T1-weighted Images an Independent Risk Factor for Symptomatic Carotid Stenosis?

Introduction: Carotid plaque showing hyperintensity on T1-weighted magnetic resonance imaging reflects unstable plaque consisting of lipid/necrosis and/or hemorrhage and has been reported as a risk factor for embolic complications during carotid endarterectomy (CEA) or stenting. However, it remains unclear whether hyperintense plaque is related to stroke events. Thus, we evaluated the difference in the intraplaque signal between asymptomatic and symptomatic patients with carotid stenosis. Methods: We prospectively collected and retrospectively analyzed 68 patients who underwent CEA (age, 53-79 years; 61 men and 7 women; 52 symptomatic and 16 asymptomatic). Using a fast spin-echo technique at 1.5 T, the contrast ratio (CR) of carotid plaque to adjacent muscle was calculated on axial images based on maximum plaque size. Differences in patient characteristics (age, sex, hypertension, dyslipidemia, diabetic mellitus, and degree of stenosis) as well as CRs between symptomatic and asymptomatic patients were examined using Fisher’s exact test, the Mann-Whitney test, and multivariable logistic regression analysis. Results: The CRs of the carotid plaque were significantly higher in the symptomatic group than in the asymptomatic group (0.97-2.32 [median, 1.55] and 0.95-2.01 [1.32], respectively; p = 0.026). In addition, age, hypertension, and stenosis degree were significantly higher in the former than in the latter (p = 0.013- 0.003). Multivariate logistic regression analysis revealed that only hypertension and CRs of the plaque were independent risks of symptomatic stenosis (odds ratio, 11.0 and 2.7; 95% confidence interval, 2.0-62.0 and 1.1-6.6; p = 0.007 and 0.025; respectively). Conclusion: CRs of the carotid plaque as well as hypertension were significantly and independently related with symptomatic patients, suggesting that hyperintense plaque can be a risk factor of stroke events in patients with carotid stenosis.

Prediction of the filter no-reflow phenomenon in patients with angina pectoris by using multimodality: Magnetic resonance imaging, optical coherence tomography, and serum biomarkers

BackgroundAlthough the occurrence of no-reflow during percutaneous coronary intervention (PCI) has been shown to be associated with worse short- and long-term clinical outcomes, the clinical relevance of preventing flow deterioration by using the filter-based distal protection devices (DPDs) is controversial. We investigated predictors of the filter no-reflow (FNR) phenomenon during PCI by using multimodality, such as hyperintense plaques (HIPs) in the coronary artery on T1-weighted imaging (T1WI) non-contrast magnetic resonance, plaque composition by using optical coherence tomography (OCT), and serum biomarkers, in patients with angina pectoris. Methods and resultsFifty lesions from 50 patients with angina were examined. All patients underwent T1WI within 24h before invasive coronary angiography was performed, and preinterventional OCT was performed on a native atherosclerotic culprit lesion. The signal intensity of coronary plaque to cardiac muscle ratio (PMR) was calculated on a standard console of the magnetic resonance system. Of the 50 lesions, 20 lesions showed FNR during PCI, while non-FNR was observed in 30 lesions. A cut-off value >1.85 of PMR had a sensitivity of 65%, a specificity of 93%, a positive predictive value of 87%, and a negative predictive value of 80% for identifying lesions with FNR. Multivariate analysis revealed that the presence of HIPs with PMR >1.85 (p=0.008) was the only independent predictor of the FNR phenomenon during PCI. ConclusionsThis study shows that the presence of HIPs with PMR >1.85 on T1WI was a novel independent predictor of the FNR phenomenon during PCI in angina patients. This result may help in identifying high-risk lesions for no-reflow to deploy filter-based DPDs.

Teaching Neuro Images : Cerebral white matter involvement in a patient with Vogt-Koyanagi-Harada syndrome

A 27-year-old man presented with decreased vision bilaterally. Ophthalmologic examination revealed panuveitis with bilateral serous retinal detachments (figure 1) characteristic of Vogt-Koyanagi-Harada (VKH) syndrome. Analysis of CSF revealed mild pleocytosis. No oligoclonal bands were detected. On MRI, there was bilateral abnormal thickening of the choroid with retinal detachment (figure 2, A and B), with hyperintense lesion on fluid-attenuated inversion recovery (FLAIR) image in the periventricular deep white matter (figure 2C). VKH syndrome is one of the causes of uveo-meningeal syndromes. Differential diagnosis of VKH syndrome includes Wegener granulomatosis, sarcoidosis, and Behçet disease.(1) The main disorders showing association with hyperintense plaques on deep white matter FLAIR images are inflammatory, metabolic, vascular, degenerative, autoimmune, and demyelinating diseases. MRI is a helpful tool in diagnosing VKH syndrome; in addition to the typical bilateral ocular findings, scattered periventricular white matter lesions on FLAIR are also described.(2.)

A prospective natural-history study of coronary hyper-intense plaques detected by non-contrast T1-weighted magnetic resonance imaging

Background: We previously showed that coronary hyperintense plaques (HIPs) detected with noncontrast T1-weighted imaging (T1WI) are strongly associated with positive coronary remodeling, remarkably lower Hounsfield units, and ultrasound attenuation. It remains unclear, however, whether the presence of coronary HIPs is associated with an increased risk of coronary events. Methods: We examined the signal intensity of coronary plaques using noncontrast T1WI in 568 high-risk patients 55 years of age or older who had evidence of coronary artery disease (CAD) or diabetes plus one other cardiovascular risk factor. A coronary HIP was defined as a signal that is ≥140% of the adjacent myocardium. All patients were divided into 4 groups according to the presence or absence of HIPs and CAD, i.e., HIP-positive + CAD (n=90), HIP-positive + no CAD (n=46), HIP-negative + CAD (n=111), and HIP-negative + no CAD (n=321). The median follow-up duration was 3.9 years. The primary end point was a composite of cardiac death, myocardial infarction, cardiac troponin T-positive unstable angina, and percutaneous coronary intervention due to progressive angina. Results: Compared to the non-HIP group, patients with HIPs were significantly more likely to experience a cardiovascular event (log-rank p<0.001, Figure). Multivariate Cox regression analysis identified the presence of HIPs as the strongest independent predictor of cardiovascular events (hazard ratio, 3.35; 95% confidence interval, 1.77–6.36; p < 0.001), compared to a history of CAD (hazard ratio, 2.03; 95% confidence interval, 1.15–3.59; p=0.01) and other coronary risk factors. ![Figure][1] Figure 1 Conclusions: Compared with patients without HIPs, patients with coronary HIPs are at a higher risk of cardiovascular events developing over time. [1]: pending:yes

Hyperintense plaque identified by magnetic resonance imaging relates to intracoronary thrombus as detected by optical coherence tomography in patients with angina pectoris

AimsMany investigators have speculated that hyperintense plaques (HIPs) of the carotid artery on non-contrast T1-weighted imaging (T1WI) in magnetic resonance indicate the presence of mural or intraplaque haemorrhage containing methemoglobin. Coronary plaque imaging with T1WI is challenging, and the clinical significance of coronary HIP on T1WI remains unknown. The aim of this study was to compare HIPs on T1WI with coronary plaque morphology assessed by optical coherence tomography (OCT), which allows us to identify not only plaque rupture, but also fibrous cap thickness and intracoronary thrombus in vivo, in patients with angina pectoris.Methods and resultsTwenty-six lesions from 26 patients with either stable or unstable angina pectoris were examined in this study. All patients underwent T1WI within 24 h before the day on which invasive coronary angiography was performed, and pre-interventional OCT was performed on a native atherosclerotic lesion, considered to be the culprit lesion. Of the 26 lesions studied, 16 (62%) were HIPs and 10 (38%) were non-HIPs. The signal intensity of the coronary plaque to cardiac muscle ratio in HIPs was significantly higher than that in non-HIPs. There were no significant differences in the frequency of lipid-rich plaque, thin-cap fibroatheroma, plaque rupture, and calcification between HIPs and non-HIPs. In contrast, the frequency of thrombus was significantly higher in HIPs than in non-HIPs (P = 0.004).ConclusionThis study shows that the HIPs on T1WI in angina patients relate to the presence of intracoronary thrombus as detected by OCT imaging.

In Reply:

We would like to express our gratitude to the authors for their thoughtful comments about our article.1 In our study, we indicated that patients with intraplaque hemorrhage, as detected by hyperintense plaque on black-blood T1-weighted imaging regardless of degree of stenosis, have a higher risk of subsequent ipsilateral ischemic events. However, the reason we did not include anything regarding the risk of recurrence for all patients with intraplaque hemorrhage, compared with those without T1-weighted hyperintense plaques, was that our study lacked the necessary data concerning the mild to moderate stenosis group without intraplaque hemorrhage. The recurrence event rates were 16.7% in the black-blood T1-weighted imaging–positive group and 3% in the negative group with severe stenosis. A Kaplan-Meier analysis showed a trend toward a lower event-free survival rate in the black-blood T1-weighted imaging–positive group (log-rank test = 2.94, P = .09), but there was no significant difference in the recurrence event rates. The small number of patients may account for the lack of a statistically significant difference. We are in complete agreement with the authors that further studies of asymptomatic patients with moderate stenosis are necessary. As we mentioned in our Discussion, our study was a retrospective evaluation and targeted symptomatic patients who probably already had fibrous cap rupture, one of the most important risk factors in cerebral ischemic events.2 We are in the process of undertaking research on asymptomatic patients with moderate stenosis. Yoshitaka Kurosaki Osaka, Japan Kazumichi Yoshida Sen Yamagata Okayama, Japan

T1-weighted MRI for the detection of coronary artery plaque haemorrhage

Hyperintense areas in atherosclerotic plaques on pre-contrast T1-weighted MRI have been shown to correlate with intraplaque haemorrhage. We evaluated the presence of T1 hyperintensity in coronary artery plaques in coronary artery disease (CAD) patients and correlated results with multi-detector computed tomography (MDCT) findings. Fifteen patients with CAD were included. Plaques detected by MDCT were categorised based on their Hounsfield number. T1-weighted inversion recovery (IR) MRI prepared coronary MRI for the detection of plaque and steady-state free-precession coronary MR-angiography for anatomical correlation was performed. After registration of MDCT and MRI, regions of interest were defined on MDCT-visible plaques and in corresponding vessel segments acquired with MRI. MDCT density and MR signal measurement were performed in each plaque. Forty-three plaques were identified with MDCT. With IR-MRI 5/43 (12%) plaques were hyperintense, 2 of which were non-calcified and 3 mixed. Average signal-to-noise and contrast-to-noise ratios of hyperintense plaques were 15.7 and 9.1, compared with 5.6 and 1.2 for hypointense plaques. Hyperintense plaques exhibited a significantly lower CT density than hypointense plaques (63.6 vs. 140.8). There was no correlation of plaque signal intensity with degree of stenosis. T1-weighted IR-MRI may be useful for non-invasive detection and characterisation of intraplaque haemorrhage in coronary artery plaques.

Hyperintense Carotid Plaque on T1-Weighted Turbo-Field Echo MRI in Symptomatic Patients with Low-Grade Carotid Stenosis and Carotid Occlusion

Background: In addition to stenosis grading, magnetic resonance imaging (MRI) may provide valuable information about plaque ‘status’, e.g. hyperintense vulnerable carotid plaque, associated with higher morbidity and mortality. In the present study, we investigated the prevalence, clinical and radiological correlates of hyperintense carotid plaques on T₁-weighted turbo-field echo (T₁w-TFE) MRI in patients with ischemic symptoms. Methods: A total of 153 patients presenting with transient ischemic attack or ischemic infarct, studied with contrast-enhanced magnetic resonance angiography (CEMRA), were retrospectively examined. Stenosis grade was obtained from CEMRA images, presence or absence of hyperintense carotid plaque from T₁w-TFE MRI. Stenosis grade and baseline characteristics were compared between patients with and without a hyperintense plaque. Results: Twenty-eight patients (18%) showed one or more hyperintense internal carotid (ICA) plaques. Hyperintense plaques were found in patients with <50% stenosis (6 of 158 ICAs), 50–70% stenosis (4 of 11), >70% stenosis (14 of 74) and carotid occlusion (4 of 28). Presence of hyperintense plaque was associated with older age (70 vs. 62 years; p < 0.05), higher prevalence of cardiac disease (61 vs. 28%; p < 0.01), ischemic infarct as presenting symptom (37 vs. 14%; p < 0.01), ischemic cerebral lesions on MRI (63 vs. 32%; p < 0.01), and the ICA on the patients’ symptomatic side (70 vs. 42%; p < 0.01). Conclusions: More than one third of patients with 50–70% stenosis present with a hyperintense plaque. This subgroup of patients could in the future possibly benefit from more aggressive medicinal therapy or revascularization.

Panic disorder as presenting symptoms of multiple sclerosis

Materials and methods A 47 years old female patient admitted to psychiatry clinic with attacs of palpitation, sweating, dispnea with a feeling of heart attack. These symptoms were present for 3 months,3-4 times a week and the patient started to have expectation anxiety. She was diagnosed as panic disorder and started paroxetine 20 mg/day. After one month her symptoms were not beter, and because of reference delusions as if people were looking at her, olanzapine 10 mg/day was added. After another month of medication, because she was not better, she was sent to neurology and she had a cerebral magnetic resonance imaging(MRI).In her neurologic examination her deep tendon reflexes were found to be increased. In her MRI a right frontal 10 × 5 mm periventricular deep white matter plaque and multiple subcorticle white matter hyperintense plaques were seen. In her serebrospinal oligoclonal band was positive. She was diagnosed as multiple sclerosis and after 5 day treatment of methylprednisolone 1000 mg/day, her psychiatric symptoms disappeared.

Hyperintense Plaque With Noncontrast T1-Weighted Magnetic Resonance Coronary Plaque Imaging Leading to Acute Coronary Syndrome

A 73-year-old diabetic man underwent multislice computed tomography (MSCT) and noncontrast T1-weighted (T1W) magnetic resonance imaging (MRI) for the evaluation of atypical chest discomfort after an exercise ECG was nondiagnostic. The MSCT demonstrated a low-density positive remodeling plaque and spotty calcification without significant stenosis in the proximal segment of the right coronary artery (Figure 1A and 1B). Noncontrast T1W MRI, using a 1.5-T MR system (Intera, Philips Medical Systems, Best, the Netherlands), revealed a hyperintense plaque (HIP) in the right coronary artery in an area corresponding to …

Development of Carotid Intraplaque Hemorrhage Demonstrated by Serial Magnetic Resonance Imaging

68-year-old man presented with a sudden onset of weakness and paresthesia of the left arm. He had a history of myocardial infarction 4 years earlier and a known renal artery stenosis. A nonenhanced computed tomographic scan of the brain showed no signs of hemorrhage or infarction. The patient underwent intravenous thrombolysis with alteplase (0.9 mg/kg body wt, 10% initial bolus dose over 1 minute, followed by infusion of the remaining 90% of the dose over 60 minutes). Soon after, the symptoms completely disappeared except for the persistence of a slight paresthesia of the left arm. Doppler ultrasonography revealed a hypoechoic plaque proximally in the right internal carotid artery causing a 50% to 69% stenosis. ECG showed sinus rhythm with complete right bundle-branch block without ST-segment or T-wave abnormalities. Transcranial Doppler imaging revealed no stenosis of the right middle cerebral artery. Serum lipid profile was within normal limits. In addition to the aspirin (100 mg once per day) and atorvastatin (40 mg once per day) he was already using, the patient was prescribed dipyridamole (200 mg twice per day) for secondary stroke prevention. Fifteen days after the initial onset of symptoms, the patient was enrolled in a clinical study investigating the natural history of carotid artery plaques. Magnetic resonance imaging scans of the brain and right carotid artery plaque were obtained, which revealed a recent discrete infarction of the right sensory region (Figure 1A and 1B) and a plaque with a large lipid-rich necrotic core with no or little hemorrhage (Figure 2A through 2D), respectively. Three months after the initial event, the patient once more presented with sudden onset of weakness and a numb feeling of the left arm. The patient again underwent intravenous thrombolysis with alteplase. However, the symptoms persisted. A nonenhanced computed tomographic scan, performed 24 hours after thrombolysis, revealed a hypodense area in the right motor region. Repeated Doppler ultrasonography showed no change in carotid plaque echogenicity and degree of luminal narrowing of the right internal carotid artery. Ten days after the onset of the second event, the patient underwent repeated magnetic resonance imaging scans of the brain and right internal carotid artery plaque. These scans confirmed recent infarction in the right motor region (Figure 1C and 1D) and revealed recent intraplaque hemorrhage (Figure 2E through 2H). Because of recurrent symptoms, the patient underwent carotid endarterectomy 20 days after the onset of the second event. Histological analysis of the excised plaque demonstrated large intraplaque hemorrhage (Figure 3A and 3B), confirming the magnetic resonance imaging findings. According to the American Heart Association, it was a type VI plaque (complex plaque with possible surface defect, hemorrhage, or thrombus). 1