Risk of New-Diagnosed Atrial Fibrillation After Transient Ischemic Attack.

Background: Transient ischemic attack (TIA) provides a unique opportunity to optimize secondary preventive treatments to avoid subsequent ischemic stroke (SIS). Although atrial fibrillation (AF) is the leading cause of cardioembolism in IS and anticoagulation prevents stroke recurrence (SR), limited data exists about the risk of new-diagnosed AF (NDAF) after TIA and the consequences of the diagnostic delay. The aim of our study was to determine this risk in a cohort of TIA patients with long-term follow-up. Methods: We carried out a prospective cohort study of 723 consecutive TIA patients from January 2006 to June 2010. Median follow-up was 6.5 (5.0-9.6) years. In a subgroup of 204 (28.2%) consecutive patients, a panel of biomarkers was assessed during the first 24 h of the onset of symptoms. Multivariate analyses were performed to find out the associated factors of NDAF. Kaplan-Meier analysis was also performed to analyzed risk of SIS. Results: NDAF was indentified in 116 (16.0%) patients: 42 (36.2%) during admission, 18 (15.5%) within first year, 29 (25%) between one and five years and 27 (23.3%) beyond 5 years. NDAF was associated with sex (female) [hazard ratio (HR) 1.61 (95% CI, 1.07- 2.41)], age [[HR 1.05 (95% CI, 1.03-1.07)], previous ischemic heart disease (IHD) [HR 1.84, (95% CI 1.15-2.97)] and cortical DWI pattern [HR 2.81 (95% CI, 1.87-4.21)]. In the Kaplan-Meier analysis, NT-proBNP ≥ 218.2 pg/ml (log-rank test P < 0.001) was associated with significant risk of NDAF during the first 5 years of follow-up. Patients with NDAF after admission and before 5 years of follow-up had the highest risk of SIS (P = 0.002). Conclusion: The risk of NDAF after TIA is clinically relevant. We identified clinical and neuroimaging factors of NDAF. In addition, NT-proBNP was related to NDAF. Our results can be used to evaluate the benefit of long-term cardiac monitoring in selected patients.

Sex-Related Differences in Clinical Features, Neuroimaging, and Long-Term Prognosis After Transient Ischemic Attack.

BACKGROUND AND PURPOSE: Differences in sex in the incidence, presentation, and outcome of events after ischemic stroke have been studied in depth. In contrast, only limited data are available after transient ischemic attack (TIA). We aim to assess sex-related differences in the presentation, cause, neuroimaging features, and predictors of long-term prognosis in patients with TIA. METHODS: We carried out a prospective cohort study of consecutive patients with TIA from January 2006 to June 2010. Nondefinitive TIA events were defined by the presence of isolated atypical symptoms. The risk of stroke recurrence (SR) and composite of major vascular events were stratified by sex after a median follow-up time of 6.5 (interquartile range, 5.0-9.6) years. RESULTS: Among the 723 patients studied, 302 (41.8%) were female and 79 (10.9%) suffered a nondefinitive TIA event. Vascular territory diffusion-weighted imaging patterns (odds ratio, 1.61 [95% CI, 0.94-2.77]), and nondefinitive TIA events (odds ratio, 2.66 [95% CI, 1.55-4.59]) were associated with women, whereas active smoking (odds ratio, 0.30 [95% CI, 0.15-0.58]) and large artery atherosclerosis causes (odds ratio, 0.50 [95% CI, 0.29-0.83]) were related to men. The risk of SR was similar in both sexes (12.6% [95% CI, 8.9-16.3] for women versus 14.3% [95% CI, 11.0-17.6] for men). In contrast, the risk of major vascular events was significantly lower in women than in men (17.5% [95% CI, 13.2-21.8] versus 23.8% [95% CI, 19.7-27.9]). In both sexes, after adjusting for age, large artery atherosclerosis was associated with SR (hazard ratio, 3.22 [95% CI, 1.42-7.24] and hazard ratio, 2.00 [95% CI, 1.14-3.51]). In a Kaplan-Meier analysis, females with positive diffusion-weighted imaging (P=0.014) and definitive TIA (log-rank test P=0.022) had a significantly higher risk of SR. CONCLUSIONS: Despite similar risks of SR, there were sex-related differences in baseline characteristics, presenting symptoms, patterns of acute ischemic lesions, cause, and outcomes. These findings encourage further research into optimal preventive strategies that take into account these differences.

Metabolomics Predicts Neuroimaging Characteristics of Transient Ischemic Attack Patients.

BACKGROUND: Neuroimaging is essential for the diagnosis and prognosis of transient ischemic attack (TIA). The discovery of a plasmatic biomarker related to neuroimaging findings is of enormous interest because, despite its relevance, magnetic resonance diffusion weighted imaging (DWI) is not always available in all hospitals that attend to TIA patients. METHODS: Metabolomic analyses were performed by liquid chromatography coupled to mass spectrometry in order to establish the metabolomic patterns of positive DWI, DWI patterns and acute ischemic lesion volumes. We used these methods with an initial TIA cohort of 129 patients and validated them with a 2nd independent cohort of 152 patients. FINDINGS: Positive DWI was observed in 115 (40.9%) subjects and scattered pearls in one arterial territory was the most frequent lesion pattern (35.7%). The median acute ischemic lesion volume was 0.33 (0.15-1.90)cm3. We detected a specific metabolomic profile common to both cohorts for positive DWI (11 molecules including creatinine, threoninyl-threonine, N-acetyl-glucosamine, lyso phosphatidic acid and cholesterol-related molecules) and ischemic lesion volume (10 molecules including lysophosphatidylcholine, hypoxanthine/threonate, and leucines). Moreover lysophospholipids and creatinine clearly differed the subcortical DWI pattern from other patterns. INTERPRETATION: There are specific metabolomic profiles associated with representative neuroimaging features in TIA patients. Our findings could allow the development of serum biomarkers related to acute ischemic lesions and specific acute ischemic patterns.

Contribution of high-b-value diffusion-weighted imaging in determination of brain ischemia in transient ischemic attack patients.

BACKGROUND AND PURPOSE: High-b-value diffusion-weighted imaging (DWI) (b = 2,000 and b = 3,000 second/mm(2)) offers theoretical advantages over DWI examinations at b = 1,000 second/mm(2) for detection of acute ischemic stroke. The purpose of this study was to determine whether high-b-value DWI are better than b = 1,000 images in TIA patients. METHODS: We compared DWI obtained with 3 different b-values (1,000, 2,000, and 3,000 second/mm(2)) and fluid-attenuated inversion recovery (FLAIR) sequences in 75 consecutive TIA patients. DWI examinations were performed within 3.25 ± 1.5 days after the onset of symptoms. Presence of ischemic lesion, volume, lesion conspicuity, and lesion distinction were determined. RESULTS: A total of 40 (53.3%) patients revealed ischemic acute lesions with b = 1,000 while 34 (45.3%) were positive on FLAIR. High-b-value DWI did not increase the sensitivity for the detection of acute brain ischemia. The median lesion value increased as the b-value did: .17 mL (interquartile range [IQR] .12-.78) at b = 1,000; .19 mL (IQR .13-1.00) at b = 2,000; .29 mL (IQR .14-1.02) at b = 3,000; and .12 mL (IQR .04-.62 mL) on FLAIR (P < .001). As b-value increased, we observed hyperintensities in white matter that could erroneously be considered as acute ischemia. CONCLUSION: High-b-value DWI did not improve the conspicuity and distinction of the ischemic lesions.

Higher carotid intima media thickness predicts extracranial vascular events and not stroke recurrence among transient ischemic attack patients.

BACKGROUND: Increased common carotid artery intima-media thickness has been associated with an increased risk of vascular ischemic events. We investigated the relationship between common carotid artery intima-media thickness and extracranial vascular events (coronary heart disease and peripheral arterial disease) or stroke recurrence in a cohort of transient ischemic attack patients from the REGITELL registry. METHODS: High-resolution B-mode ultrasonographic measurements of the common carotid artery intima-media thickness were performed in a series of 283 consecutive transient ischemic attack patients. Clinical, neuroimaging, ultrasonographic, and etiological data were collected. Patients were followed prospectively for six-months or more. Extracranial vascular events and stroke recurrence were recorded. RESULTS: Fifteen extracranial vascular events (12 coronary heart disease and three peripheral arterial disease) and 29 recurrent strokes occurred during a median follow-up period of 12.3 months. Patients who experienced extracranial vascular events had significantly (P < 0.001) higher common carotid artery intima-media thickness values (1.087 (standard deviation 0.189) mm) than subjects who were free of extracranial vascular events (0.887 (standard deviation 0.195) mm). Nevertheless, common carotid artery intima-media thickness was not found to correlate with stroke recurrence. Cox proportional hazards multivariate analyses identified hypercholesterolemia (hazard ratio 6.87, 95% confidence interval: 1.93-24.39, P = 0.003) and common carotid artery intima-media thickness > 0.939 mm (hazard ratio 8.90, 95% confidence interval: 2.00-39.49, P = 0.004) as independent predictors of extracranial vascular events after transient ischemic attack. Almost one of every three patients with hypercholesterolemia and high common carotid artery intima-media thickness had extracranial vascular events. CONCLUSIONS: An elevated common carotid artery intima-media thickness value was associated with a higher long-term risk of extracranial vascular events but no with stroke recurrence. Hypercholesterolemia was the main risk factor for extracranial vascular events. The combination of hypercholesterolemia and common carotid artery intima-media thickness > 0.939 mm justify the establishment of aggressive therapies and the study of subclinical coronary heart disease and peripheral arterial disease.

[Diagnostic lessons of recurrence pattern after transient ischemic attacks]. / Implicaciones diagnósticas del perfil de recurrencia tras un ataque isquémico transitorio.

BACKGROUND AND OBJECTIVE: Early stroke recurrence risk alter a transient ischemic attack (TIA) is high. We studied the diagnostic implications of the recurrence pattern after TIA. METHODS: 210 consecutive TIA patients were studied. Ultrasonographic (US), neuroimaging and cardiologic data were collected. RESULTS: At 90 day follow-up, 14 patients (6.7%; 95% CI: 3.3-10.1) among 209 suffered an ischemic infarction (II), 9 (4.3%; 1.5-7.1) a TIA and 6 (2.9%; 0.6-5.1) a cardiac ischemic event. Moreover, 13 patients (6.2%; 2.8-9.6) among 210 with a seven-day follow-up had an II. Multivariate analyses only identified the presence of intracranial stenoses (HR, 23.29; 95% CI, 3.49 to 23.57; p<0.018) as independent predictors of stroke within the first 7 days, and large-artery occlusive disease (HR, 9.07; CI, 3.49 to 23.57; p<0.001) as a predictor of stroke recurrence at 90 day follow-up. A new diagnosis of atrial fibrillation was observed in 21 subjects (10.0%), and it was documented in the baseline ECG in 62% cases. Acute diffusion abnormalities were identified in 81 (44,5%) of 182 patients, and chronic ischemic lesions were observed in 110 (60.4%) on MRI vs 56 (26.7%) among 210 on CT scan. CONCLUSION: Due to very early recurrence, the routine use of ultrasonography within the first hours after an index TIA will be useful to identify those patients at high risk. The prognostic usefulness of diffusion-weighted studies will be only achieved if it is performed early. Routine noninvasive cardiac rhythm monitoring has a low detection rate.

The California, ABCD, and unified ABCD2 risk scores and the presence of acute ischemic lesions on diffusion-weighted imaging in TIA patients.

BACKGROUND AND PURPOSE: Some clinical models, like California ABCD and unified ABCD2 scores, are now available to predict the early risk of stroke after a TIA. Despite the transitivity of symptoms, DWI identified an area of acute brain ischemia in almost half of patients. It would be interesting to know how the presence of DWI abnormalities relates to clinical risk scores to plan other prognostic variables or to recommend the performance of DWI. METHODS: We prospectively studied 135 consecutive TIA patients visited by the neurologists in our institution. All patients underwent DWI (3.8+/-1.7 days after symptoms onset). Clinical risk scores (California, ABCD, and ABCD2) were calculated prospectively for each patient. The identification of acute ischemic lesions (positive DWI) was related to the presence of clinical features and clinical risk scores. RESULTS: DWI were positive in 67 (49.6%) patients. After Bonferroni adjustment, elevated ABCD, ABCD2, and California scores were not associated with a positive DWI. However, some clinical symptoms such as facial palsy and motor weakness were associated with a positive DWI (P<0.001). The logistic regression model identified only facial palsy as an independent predictor of acute ischemic lesions (odds ratio 6.26, 95% CI 2.49 to 15.71, P<0.001). CONCLUSIONS: Clinical symptoms such as motor impairment, but not clinical risk scores, were associated with a positive DWI. Performing a DWI may add prognostic information to clinical risk scales as a predictor of stroke recurrence after TIA in future large studies.

Central nervous system involvement in hereditary neuropathy with liability to pressure palsies: description of a large family with this association.

OBJECTIVE: To describe a large family with hereditary neuropathy with liability to pressure palsies associated with central nervous system demyelination. DESIGN: We examined the 18 members of a pedigree. Genetic analysis was performed on 15 subjects, standard nerve conduction studies on 10 subjects, and brain magnetic resonance imaging studies on 8 subjects. RESULTS: Hereditary neuropathy with liability to pressure palsies was confirmed in 9 patients of the pedigree. Brain magnetic resonance imaging findings showed multiple areas of demyelination in 6 of 6 affected members and were normal in 2 of 2 healthy relatives. Magnetic resonance imaging abnormalities were predominantly located in the subcortical frontal white matter. All patients had acute and recurrent nerve palsies, while clinical features of central nervous system involvement were not a characteristic of this pedigree. CONCLUSIONS: We demonstrate that this association, previously reported in sporadic cases, is not coincidental. Therefore, patients with hereditary neuropathy with liability to pressure palsies can present central nervous system white matter lesions, and the role of the PMP22 (peripheral myelin protein 22) gene deletion in the central nervous system should be further studied.