Background Myocardial haemorrhage after myocardial infarction (MI) frequently goes undetected. Since the paramagnetic effects of oxidised iron may result in signal loss on T2* and T2-weighted MRI, we investigated the diagnostic accuracy of T2-weighted MRI in experimental MI. Methods Acute MI was created in swine (43±9.5 kg) by occluding the left anterior descending coronary artery (n=10) or circumflex (n=5) for 90 min followed by reperfusion for ≤3 days (n=2), 10 days (n=7) or 60 days (n=6). Cardiac MRI was performed at 1.5 T using T2-prepared steady-state free-precession (T2P-SSFP) and gadolinium enhanced (CE) MRI. Left ventricular (LV) sections were visually inspected, photographed and stained for histology. Gross images and histology were scored for myocardial haemorrhage by an experienced cardiac pathologist blinded to all other data. Regions of low signal intensity on T2-weighted and CE-MRI were independently determined by three cardiologists blinded to the pathology results. Results Eighty ventricular slices of pathology were matched with MRI (n=68 for first pass CE-CMR). All sections exhibited hyperintense zones consistent with oedema on T2-weighted, scar on CE-MRI and pathologic evidence of MI. Myocardial haemorrhage occurred in 49 LV sections (61%) and corresponded with signal voids on 48 T2-weighted (98%) and 26 CE-MRI (53%). Alternatively, signal voids occurred in the absence of haemorrhage in three T2-weighted (90% specificity) and five CE-MRI (84% specificity). On first pass CE-MRI, 27/43 perfusion defects corresponded with haemorrhage (63% sensitivity) while 5/25 defects occurred in the absence of haemorrhage (80% specificity). The positive and negative predictive values for pathological evidence of haemorrhage were 94% & 96% for T2-weighted, 84% & 53% for CE-MRI, and 84% & 56% for first pass perfusion. Conclusions T2-weighted MRI has high diagnostic accuracy for myocardial haemorrhage. Heterogeneity of signal intensity associated with acute MI on T2-weighted MRI is partially due to intramyocardial haemorrhage.

Summary.  Background: Endothelial membrane microparticles (EMP) in plasma are elevated in several vascular diseases. Objectives: To test the hypothesis that EMP would be increased in patients with acute ischemic stroke and would correlate with stroke severity, brain lesion volume and outcome. Patients and methods: Forty‐one patients were studied and divided into two groups based on the National Institutes of Health Stroke Scale (NIHSS) score: 20 patients with mild stroke (NIHSS score < 5) and 21 patients with moderate–severe stroke (NIHSS score ≥ 5). Lesion volume was measured using diffusion‐weighted magnetic resonance imaging and discharge outcome was based on the discharge Barthel and Rankin scores. Twenty‐three age‐matched control subjects were also studied. Using flow cytometry, endoglin‐positive EMP: CD105+ CD41a−CD45− (E+EMP), specific endothelial EMP expressing VE‐cadherin and endoglin: CD105+CD144+ (C+EMP), EMP expressing phosphatidylserine: CD105+PS+ CD41a− (PS+EMP) and EMP expressing ICAM‐1: CD105+CD54+ CD45− (I+EMP) were analyzed. Results: Significantly higher PS+EMP counts were observed in the group of acute ischemic stroke patients [median 59 (25th–75th percentile: 28–86) MP μL−1] relative to the controls [28 (14–36) MP μL−1] (P = 0.002). All four EMP phenotypes studied were elevated in the subgroup of moderate–severe stroke patients relative to the controls (all P < 0.05). In the patients with acute ischemic stroke three EMP phenotypes (E+EMP, PS+EMP and I+EMP) correlated significantly with brain lesion volume, with I+EMP (P = 0.002) showing the strongest correlation. Admission counts of C+EMP (P = 0.0003) and E+EMP (P = 0.003) correlated significantly with discharge clinical outcome. Conclusions: Certain circulating EMP phenotypes may be associated with severity, lesion volume and outcome of acute ischemic stroke. EMP analysis shows promising contribution to understanding stroke pathophysiology.

The regional distribution of skeletal muscle blood flow was measured during postischemic reactive hyperemia using GdDTPA contrast-enhanced (CE) MRI. The release of an occlusive thigh cuff was used to deliver a step-input of contrast concentration that was coincident with the onset of reactive hyperemia. A first-order tracer kinetic equation was used to estimate the unidirectional influx constant, K-i, (ml/100 g/min), and the distribution volume of Gd-DTPA in the tissue, v(e), from T-1-weighted images acquired with saturation recovery (SR) steady-state free precession (SSFP) and spoiled gradient-echo (SPGR) protocols. The capillary permeability surface [PS) area increased significantly during reactive hyperemia, which facilitated rapid extraction of Gd-DTPA during the first pass. Regional muscle group studies from 11 normal volunteers yielded blood flow (K-i) values of 108.3 +/- 34.1 ml/100 g/min in the gastrocnemius, 184.3 +/- 41.3 ml/100 g/min in the soleus, and 122.4 +/- 34.4 ml/100 g/min in the tibialis anterior. The distribution volumes (Ve) in the corresponding muscle groups were respectively 8.3% +/- 2.1%,9.3% +/- 1.9%, and 7.9% +/- 1.8% from the kinetic model, and 8.8% +/- 2.4%, 9.1 % +/- 1.9%, and 7.2% +/- 1.4% from tissue relaxometry studies. Bulk blood flow studies in the same volunteers using phase-contrast velocimetry (popliteal artery) yielded significantly lower flow values, but with a correlation coefficient R-2 = 0.62 and P = 0.004.

Background— Direct brain biopsy is rarely indicated during acute stroke. This study uses peripheral blood mononuclear cells (PBMCs) to determine whether a systemic gene expression profile could be demonstrated in patients with acute ischemic stroke. Methods and Results— Using oligonucleotide microarrays, we compared the gene expression profile of an index cohort of 20 patients with confirmed ischemic stroke on neuroimaging studies with that of 20 referent subjects. Validation studies used quantitative real-time polymerase chain reaction to measure the levels of 9 upregulated genes in the index cohort, and an independent cohort of 9 patients and 10 referent subjects was prospectively studied to determine the accuracy of the Prediction Analysis for Microarrays list to classify stroke. After correction for multiple comparisons with the Bonferroni technique, 190 genes were significantly different between the stroke and referent groups. Broad classes of genes included white blood cell activation and differentiation (≈60%), genes associated with hypoxia and vascular repair, and genes potentially associated with an altered cerebral microenvironment. Real-time polymerase chain reaction confirmed increased mRNA expression in 9 of 9 upregulated stroke-associated genes in the index cohort. A panel of 22 genes derived from the Prediction Analysis for Microarrays algorithm in the index cohort classified stroke in the validation cohort with a sensitivity of 78% and a specificity of 80%. Control for the Framingham stroke risk score revealed only a partial dependence of the stroke gene expression profile in PBMCs on vascular risk. Conclusions— This study demonstrated an altered gene expression profile in PBMCs during acute ischemic stroke. Some genes with altered expression were consistent with an adaptive response to central nervous system ischemia.

Objective: To determine if the CD4(+) CD28(-) T-cell subset is expanded in patients with recurrent stroke or death after acute ischemic stroke. This subset of the peripheral blood T-cell lymphocyte population has a strong pro-inflammatory and tissue-damaging potential. Methods: Consecutive patients within the first 48 hours of ischemic stroke were prospectively studied. Peripheral blood CD4(+) CD28(-) cells were quantified by flow cytometry. The study endpoint was recurrent stroke or death from any cause during 1 year of follow-up. Results: One hundred six patients (mean age 75.0 +/- 13.5 years; 50 women) were studied. The median CD4(+)CD28(-) cell count was 4.5% (range 0.2 to 72.2%). Twenty-seven endpoints (10 recurrent strokes and 17 deaths) occurred during follow-up. Stroke recurrence/death rates were significantly associated with increasing CD4(+)CD28(-) counts, rising from 14.2% in patients with CD4(+)CD28(-) levels of <1.0 to 48.1% for those with CD4(+)CD28(-) counts of <8.0% (p = 0.003, Cochran linear test of trend). Higher CD4(+)CD28(-) counts were also present in patients with a history of prior stroke (p = 0.03). After adjustment for age, admission NIH Stroke Scale score, prior stroke, and atrial fibrillation, CD4(+)CD28(-) counts of <8.0% were associated with a cumulative hazard ratio of 5.81 (95% CI: 1.58 to 21.32) for stroke recurrence or death. Conclusions: Rising counts of circulating CD4(+)CD28(-) cells are associated with an increasing risk of stroke recurrence and death, in addition to an observed association with prior stroke. Expansion of this T-cell subset presumably represents a biomarker and possibly a contributory pathogenic mechanism of recurrent stroke and death after ischemic stroke.

Aortic dissection is an uncommon, life-threatening, and treatable emergency that typically presents with tearing chest and back pain.1 With use of the Stanford classification, aortic dissections can be divided into type A (involving the ascending aorta) and type B (involving the aorta distal to the origin of the left subclavian artery).2 Type A dissections may cause ischemic stroke in up to 5 to 10% of patients3 through extension of the dissection into the common carotid arteries or through thromboembolism or cerebral hypoperfusion. A 64-year-old man was referred to the neurologist for evaluation of acute stroke. He had a history of hypertension. He was reversing his car when he suddenly grasped his hands to his chest and “blacked out.” He was briefly unresponsive but began to speak with garbled speech and had a Wernicke aphasia. He arrived at the hospital within 30 minutes of onset. His blood pressure was 180/120 mm Hg …