Combined functional and viability cardiac MR imaging in a single breathhold

The combination of cardiac viability and functional information enhances the identification of different heart tissues in the setting of ischemic heart disease. A method has recently been proposed for obtaining black-blood delayed-enhancement (DE) viability images using the stimulated-echo acquisition mode (STEAM) MRI pulse sequence in a single short breathhold. The method was validated against conventional inversion-recovery (IR) DE images for identifying regions of myocardial infarction (MI). The method was based on the acquisition of three consecutive images of the same anatomical slice. One image has T(1)-weighted contrast in which infarction appears bright. The two other images are used to construct an anatomical image of the heart, which is combined with the first image to produce a black-blood viability image. However, using appropriate modulation and demodulation frequencies, the latter two images bear useful information about myocardial deformation that results in a cardiac strain-encoding (SENC) functional image. In this work, a method is proposed for obtaining three consecutive SENC images in a single acquisition that can be combined to produce a composite image of the heart, which shows both functional and viability information. The proposed technique reduces scan time by one-half, compared with separate acquisitions of functional and viability images, and alleviates misregistration problems caused by separate breathholds.

Pure monoparesis: a particular stroke subgroup?

BACKGROUND: Acute stroke presenting as monoparesis is rare, with a pure motor deficit in the arm or leg extending to an isolated facial paresis. OBJECTIVE: To raise the question if acute stroke presenting as monoparesis is a different entity from stroke with a more extensive motor deficit. PATIENTS: In the Lausanne Stroke Registry (1979-2000), 195 (4.1%) of 4802 patients met the clinical criteria for pure monoparesis involving the face (22%), arm (63%), or leg (15%). RESULTS: In the vast majority of cases (> 95%), monoparesis corresponded to ischemic stroke with a favorable outcome, with initial computed tomography scans or magnetic resonance images showing no signs of hemorrhage. The lesion for a facial deficit was most frequently located subcortically (internal capsule); for an arm deficit, in the superficial middle cerebral artery; and for a leg deficit, in the anterior cerebral artery territory. In pure monoparesis, only 17% of the patients had more than 1 risk factor as compared with 26% of those with bimodal and trimodal hemiparesis and with 46% of all patients with stroke other than those with pure motor stroke. The only frequent risk factor was hypertension (53%); however, this frequency was no different from that in other patients with stroke. No major stroke etiology could be identified in any of the 3 subgroups of monoparesis. CONCLUSION: Our finding of a wide range of stroke localization and etiology in monoparesis without any particular subgroup suggests that no specific plan of investigation can be recommended for these patients.

Hand-arm vibration syndrome with proximal ulnar artery occlusion.

The case of a man exposed during 25 years to vibration while maneuvering a heavy earth moving tractor is reported. The first clinical manifestation of hand-arm vibration syndrome was a bilateral Raynaud's phenomenon followed five years later by digital necrosis. The arteriography revealed a proximal and bilateral ulnar artery occlusion. Bilateral median nerve conduction abnormalities were also present. Vibration exposure level was much higher than the threshold level proposed by the European Commission. Laboratory examinations for vasculitis and other vascular diseases were all negative. The purpose of this report is to show that vibration can be responsible for proximal occlusion of a medium sized artery and severe neurovascular abnormalities which must be distinguished from the usual vasospastic Raynaud's phenomenon and the classical hypothenar hammer syndrome. An early and correct diagnosis is crucial because continued repetitive trauma can result in irreversible ischemic injury and loss of digits.

Glibenclamide enhances neurogenesis and improves long-term functional recovery after transient focal cerebral ischemia

Glibenclamide is neuroprotective against cerebral ischemia in rats. We studied whether glibenclamide enhances long-term brain repair and improves behavioral recovery after stroke. Adult male Wistar rats were subjected to transient middle cerebral artery occlusion (MCAO) for 90 minutes. A low dose of glibenclamide (total 0.6mg) was administered intravenously 6, 12, and 24 hours after reperfusion. We assessed behavioral outcome during a 30-day follow-up and animals were perfused for histological evaluation. In vitro specific binding of glibenclamide to microglia increased after pro-inflammatory stimuli. In vivo glibenclamide was associated with increased migration of doublecortin-positive cells in the striatum toward the ischemic lesion 72 hours after MCAO, and reactive microglia expressed sulfonylurea receptor 1 (SUR1) and Kir6.2 in the medial striatum. One month after MCAO, glibenclamide was also associated with increased number of NeuN-positive and 5-bromo-2-deoxyuridine-positive neurons in the cortex and hippocampus, and enhanced angiogenesis in the hippocampus. Consequently, glibenclamide-treated MCAO rats showed improved performance in the limb-placing test on postoperative days 22 to 29, and in the cylinder and water-maze test on postoperative day 29. Therefore, acute blockade of SUR1 by glibenclamide enhanced long-term brain repair in MCAO rats, which was associated with improved behavioral outcome.

Autophagy induction does not protect retina against apoptosis in ischemia/reperfusion model.

The role played by autophagy after ischemia/reperfusion (I/R) in the retina remains unknown. Our study investigated whether ischemic injury in the retina, which causes an energy crisis, would induce autophagy. Retinal ischemia was induced by elevation of the intraocular pressure and modulation of autophagic markers was analyzed at the protein levels in an early and late phase of recovery. Following retinal ischemia an increase in LC3BII was first observed in the early phase of recovery but did not stay until the late phase of recovery. Post-ischemic induction of autophagy by intravitreal rapamycin administration did not provide protection against the lesion induced by the ischemic stress. On the contrary, an increase in the number of apoptotic cells was observed following I/R in the rapamycin treated retinas.

Artérite á cellules géantes et vitesse de sédimentation normale: plus qu'une exception [Giant cell arteritis and normal sedimentation rate: more than an exception!]

BACKGROUND: Giant cell arteritis (GCA) is a systemic segmental vasculitis of unknown etiology, typically affecting elderly patients. Elevated erythrocyte-sedimentation rate (ESR) is usually found in such patients. PATIENTS AND METHODS: One hundred and twenty three patients underwent temporal artery biopsy in our institution between 1977 and 1995. Among them, 66 (53.7%) biopsies were positive (i.e. histologic findings were very suggestive of GCA). The clinical charts from all patients with positive biopsies were retrieved and 47 were eligible for our study (inadequate data in 19 cases). RESULTS: Seven of the 47 patients with positive biopsies (15%) had a normal ESR and 70% (33/47 cases) had neuro-ophthalmic complications including anterior ischemic optic neuropathy, central retinal artery occlusion, choroidal ischemia and extraocular muscle and/or cranial nerve palsy (III, IV, VI). No differences were found between the groups with normal or elevated ESR as 87.5% (6/7 cases) of the group with normal ESR exhibited neuro-ophthalmic complications. CONCLUSIONS: ESR was normal in 15% of our GCA patients and these patients had the same frequency of neuro-ophthalmic complications as the GCA patients with elevated ESR. Thus, our study does not support the previous concept that patients with higher ESR are more at risk for neuro-ophthalmic complications. GCA with normal ESR is not rare and such patients should be investigated with other blood studies (C-reactive protein) and with fluorescein angiography.

A prospective study of predictors of poststroke depression.

OBJECTIVE: To investigate the association between early depressive behavior after stroke onset and occurrence of poststroke depression (PSD) at 3- and 12-month follow-up evaluations. METHODS: The study prospectively included 273 patients with first-ever single uncomplicated ischemic stroke. In the stroke unit, nurses scored crying, overt sadness, and apathy daily using an observational method to include patients with comprehension deficits. The Barthel Index was used to assess disability. Follow-up evaluation at months 3 and 12 included psychiatric assessment based on the Diagnostic and Statistical Manual of Mental Disorders, 4th edition. RESULTS: Crying (19.8%), overt sadness (50.5%), and apathy (47.6%) were observed. Of the patients observed crying, 4 showed pathologic crying, 19 emotionalism, and 12 catastrophic reactions. Crying and overt sadness, but not apathy, were associated with a subjective experience of depression (p < 0.05). Thirty of 52 (58%) patients observed crying, 12 of 19 (63%) patients with emotionalism, and 5 of 12 (41%) patients with catastrophic reactions developed PSD within the first year. Multiple logistic regression analysis showed that only severe functional disability (odds ratio [OR], 4.31; 95% CI, 2.41 to 7.69), crying behaviors (OR, 2.66; 95% CI, 1.35 to 5.27), and an age <68 years (OR, 2.32; 95% CI, 1.30 to 4.13) were (p < 0.05) predictors of late PSD development (13% of the variance). CONCLUSIONS: In the stroke unit, crying and overt sadness are more reliable indicators of depressed mood than apathy. In patients with first-ever stroke, crying behaviors soon after stroke, a younger age, and severe disability are predictors of poststroke depression occurrence within the first year after stroke onset.

Strokes and TIAs during and after Carotid Artery Doppler: Cause or Coincidence?

The aim of the present study was to explore the prevalence of acute cerebrovascular symptoms temporally related to carotid Doppler examination (DEx), in order to increase the awareness and recording of such events and to discuss possible mechanisms. All adult patients who complained of acute onset neurologic symptoms during or shortly after a carotid DEx, between 01/2003 and 12/2011 in the University Hospital of Lausanne were prospectively collected. We identified four consecutive patients with acute onset neurologic symptoms during or shortly after a carotid DEx among approximately 13,500 patients who underwent carotid DEx in our facility during the nine-year period (0.015% of all examined carotids). Clinical data, imaging reports and CTA (CT angiography) or/and ultrasound images are presented for each patient. Ischemic cerebrovascular events during or immediately after cervical Doppler could be due to chance or to several physical factors. They should be promptly recognized by Doppler personnel and properly treated, but do not put into question the overwhelming benefits of Doppler in cerebrovascular patients.

Indications à la coronarographie en urgence. Partie II: syndromes coronariens aigus sans élévation du segment ST [Indications for urgent coronary angiography. Part II: Acute coronary syndromes without ST-segment elevation]

The optimal treatment strategy for patients presenting with an acute coronary syndrome without ST elevation is controversial and different therapeutic approaches are recognized. Currently, given the literature available, it is not possible to recommend a universal systematic invasive approach. It is essential to individually risk stratify patients in order to identify those high risk patients that have been shown to benefit from an invasive strategy. Compared to conservative medical treatment, patients at low risk have not been shown to benefit from an invasive strategy. Urgent coronary angiography remains recommended for those patients with persistent or recurrent ischemic symptoms under optimal medical treatment.

Local transient myocardial liposomal gene transfer of inducible nitric oxide synthase does not aggravate myocardial function and fibrosis and leads to moderate neovascularization in chronic myocardial ischemia in pigs.

Microcirculation (2010) 17, 69-78. doi: 10.1111/j.1549-8719.2010.00002.x Abstract Background: This study was designed to explore the effect of transient inducible nitric oxide synthase (iNOS) overexpression via cationic liposome-mediated gene transfer on cardiac function, fibrosis, and microvascular perfusion in a porcine model of chronic ischemia. Methods and Results: Chronic myocardial ischemia was induced using a minimally invasive model in 23 landrace pigs. Upon demonstration of heart failure, 10 animals were treated with liposome-mediated iNOS-gene-transfer by local intramyocardial injection and 13 animals received a sham procedure to serve as control. The efficacy of this iNOS-gene-transfer was demonstrated for up to 7 days by reverse transcriptase-polymerase chain reaction in preliminary studies. Four weeks after iNOS transfer, magnetic resonance imaging showed no effect of iNOS overexpression on cardiac contractility at rest and during dobutamine stress (resting ejection fraction: control 27%, iNOS 26%; P = ns). Late enhancement, infarct size, and the amount of fibrosis were similar between groups. Although perfusion and perfusion reserve in response to adenosine and dobutamine were not significantly modified by iNOS-transfer, both vessel number and diameter were significantly increased in the ischemic area in the iNOS-treated group versus control (point score: control 15.3, iNOS 34.7; P < 0.05). Conclusions: Our findings demonstrate that transient iNOS overexpression does not aggravate cardiac dysfunction or postischemic fibrosis, while potentially contributing to neovascularization in the chronically ischemic heart.

Rupture of a concealed aneurysm after intravenous thrombolysis of a thrombus in the parent middle cerebral artery.

BACKGROUND: Management of ischemic stroke in the presence of aneurysmal brain disease is controversial. Recent retrospective evidence suggests that in selected patients, intravenous thrombolysis (IVT) remains a safe approach for reperfusion. METHODS: We document a case of post-thrombolysis aneurysmal rupture. Supported by additional scientific literature we postulate that acute aneurysmal thrombosis leading to stroke in the culprit artery may be an ominous sign of rupture and should be considered separately from fortuitously discovered distant aneurysmal disease. RESULTS: A 71-year-old female presented with an acute right middle cerebral artery stroke syndrome. IVT allowed vessel reperfusion and revealed a previously concealed, juxtaposed non-giant M1 segment saccular aneurysm. Secondary aneurysmal rupture ensued. The aneurysm was secured by surgical clipping. Postoperative course was uneventful. CONCLUSIONS: This case shows that despite reports of thrombolysis safety in the presence of brain aneurysms, thrombolysis remains potentially hazardous and hints toward an increased risk when the stroke arises on the parent vessel itself.

Diffusion tensor imaging shows structural remodeling of stroke mirror region: results from a pilot study.

Background: The role of the non-injured hemisphere in stroke recovery is poorly understood. In this pilot study, we sought to explore the presence of structural changes detectable by diffusion tensor imaging (DTI) in the contralesional hemispheres of patients who recovered well from ischemic stroke. Methods: We analyzed serial DTI data from 16 stroke patients who had moderate initial neurological deficits (NIHSS scores 3-12) and good functional outcome at 3-6 months (NIHSS score 0 or modified Rankin Score ≤1). We segmented the brain tissue in gray and white matter (GM and WM) and measured the apparent diffusion coefficient (ADC) and fractional anisotropy in the infarct, in the contralesional infarct mirror region as well as in concentrically expanding regions around them. Results: We found that GM and WM ADC significantly increased in the infarct region (p < 0.01) from acute to chronic time points, whereas in the infarct mirror region, GM and WM ADC increased (p < 0.01) and WM fractional anisotropy decreased (p < 0.05). No significant changes were detected in other regions. Conclusion: DTI-based metrics are sensitive to regional structural changes in the contralesional hemisphere during stroke recovery. Prospective studies in larger cohorts with varying levels of recovery are needed to confirm our findings.

Temporal distribution and magnitude of the vulnerability period around stroke depend on stroke subtype.

Background: We aimed to analyze the rate and time distribution of pre- and post-morbid cerebrovascular events in a single ischemic stroke population, and whether these depend on the etiology of the index stroke. Methods: In 2,203 consecutive patients admitted to a single stroke center registry (ASTRAL), the ischemic stroke that led to admission was considered the index event. Frequency distribution and cumulative relative distribution graphs of the most recent and first recurrent event (ischemic stroke, transient ischemic attack, intracranial or subarachnoid hemorrhage) were drawn in weekly and daily intervals for all strokes and for all stroke types. Results: The frequency of events at identical time points before and after the index stroke was mostly reduced in the first week after (vs. before) stroke (1.0 vs. 4.2%, p < 0.001) and the first month (2.7 vs. 7.4%, p < 0.001), and then ebbed over the first year (8.4 vs. 13.1%, p < 0.001). On daily basis, the peak frequency was noticed at day -1 (1.6%) with a reduction to 0.7% on the index day and 0.17% 24 h after. The event rate in patients with atherosclerotic stroke was particularly high around the index event, but 1-year cumulative recurrence rate was similar in all stroke types. Conclusions: We confirm a short window of increased vulnerability in ischemic stroke and show a 4-, 3- and 2-fold reduction in post-stroke events at 1 week, 1 month and 1 year, respectively, compared to identical pre-stroke periods. This break in the 'stroke wave' is particularly striking after atherosclerotic and lacunar strokes.

A tennis player with hand claudication.

The case of a professional tennis player presenting exercise-induced hand pain with late appearance of digital blanching is reported. A bilateral hypothenar hammer syndrome and stenosis of the common palmar digital arteries close to the head of the metacarpals where the racket handle exerts its maximal force was observed with arteriography. As the patient decided to stop tennis practice, the condition improved without any medication. Six months after stopping tennis he was symptom free. Three conclusions can be drawn from this case report: 1) arteries of both hands can be injured by intense tennis practice, 2) pain in the dominant hand during tennis practice can be due to arterial insufficiency even in the absence of digital blanching which is a sign of severity, 3) hypothenar hammer syndrome is the main cause but stenosis of the common palmar digital arteries can possibly contribute to the ischemic phenomenon. Early recognition is important to avoid ineffective treatment and permanent symptoms. Therefore, we recommend an arterial examination in tennis players suffering from exercise-induced hand pain even in the absence of digital blanching which can be only a late manifestation.

Oxygen tension controls the expression of the monocarboxylate transporter MCT4 in cultured mouse cortical astrocytes via a hypoxia-inducible factor-1α-mediated transcriptional regulation.

The monocarboxylate transporter MCT4 is a high capacity carrier important for lactate release from highly glycolytic cells. In the central nervous system, MCT4 is predominantly expressed by astrocytes. Surprisingly, MCT4 expression in cultured astrocytes is low, suggesting that a physiological characteristic, not met in culture conditions, is necessary. Here we demonstrate that reducing oxygen concentration from 21% to either 1 or 0% restored in a concentration-dependent manner the expression of MCT4 at the mRNA and protein levels in cultured astrocytes. This effect was specific for MCT4 since the expression of MCT1, the other astrocytic monocarboxylate transporter present in vitro, was not altered in such conditions. MCT4 expression was shown to be controlled by the transcription factor hypoxia-inducible factor-1α (HIF-1α) since under low oxygen levels, transfecting astrocyte cultures with a siRNA targeting HIF-1α largely prevented MCT4 induction. Moreover, the prolyl hydroxylase inhibitor dimethyloxalylglycine (DMOG) induced MCT4 expression in astrocytes cultured in presence of 21% oxygen. In parallel, glycolytic activity was enhanced by exposure to 1% oxygen as demonstrated by the increased lactate release, an effect dependent on MCT4 expression. Finally, MCT4 expression was found to be necessary for astrocyte survival when exposed for a prolonged period to 1% oxygen. These data suggest that a major determinant of astrocyte MCT4 expression in vivo is likely the oxygen tension. This could be relevant in areas of high neuronal activity and oxygen consumption, favouring astrocytic lactate supply to neurons. Moreover, it could also play an important role for neuronal recovery after an ischemic episode.