Acute infantile encephalopathy predominantly affecting the frontal lobe (AIEF): A European case.

Acute infantile encephalopathy predominantly affecting the frontal lobes (AIEF) has been described as a new entity, based on MRI findings (acute abnormal diffusion-weighted imaging signals in the frontal lobes followed by atrophy) and exclusion of other acute encephalopathies. Patients present with acute onset of fever, status epilepticus, and coma. Different causal mechanisms have been suggested such as localized viral infection, toxic insult due to cytokines, or postictal damage. Only children of Japanese descent have been described. We report the case of a Caucasian girl whose history and MRI findings were similar to the Japanese cases. She had a massive regression with verbal apraxia, while cognitive development was less affected; she initially presented with a cluster of complex partial seizures (and not convulsive status epilepticus), making epileptic or post anoxic-ischemic sequelae highly unlikely. The place of this proposed entity among other recently described acute encephalopathies with abnormal diffusion on MRI is discussed.

Treatment of central retinal vein occlusion-related macular edema with intravitreal bevacizumab (Avastin): preliminary results.

PURPOSE: To assess the safety and efficacy of treatment of macular edema secondary to central retinal vein occlusion (CRVO) with intravitreal bevacizumab. PATIENTS AND METHOD: The ongoing prospective study included 8 consecutive patients (8 eyes) with macular edema secondary to CRVO (6 non ischemic and 2 ischemic), treated with intravitreal injection of 1.25 mg (0.05 mL) of bevacizumab. Main outcome was best corrected visual acuity (BCVA) and central foveal thickness (CFT) measured by optical coherence tomography monthly during one year. Retreatment criteria include decrease of BCVA, persistence of macular edema on angiograms and increase of CFT. RESULTS: Mean age of the eight patients was 68 years (range: 50-82 years). Mean duration of symptoms before injection was 98 days (range: 3-289). Mean follow-up was 3.25 months. At baseline, mean BCVA was 0.84 logMar and mean baseline CFT was 771 microm. Mean BCVA was 0.36 and mean CFT thickness was 275 microm (n = 8) at month 1, 0.41 and 411 microm at month 2 (n = 7), 0.3 and 344 microm at month 3 (n = 6), 0.3 and 397 microm at month 4 (n = 5), respectively. In 75 % of patients, a single injection was not sufficient, and retreatment needed. No serious adverse events were observed. CONCLUSIONS: Treatment of macular edema secondary to CRVO with intravitreal bevacizumab injection of 1.25 mg was well tolerated and associated with marked macular thickness reduction and BCVA improvement in all patients. A trend towards reduction of foveal thickness and improvement of visual acuity was observed in both acute and chronic CRVO.

Acute aphasia after right hemisphere stroke

Abstract Right hemispheric stroke aphasia (RHSA) rarely occurs in right- or left-handed patients with their language representation in right hemisphere (RH). For right-handers, the term crossed aphasia is used. Single cases, multiple cases reports, and reviews suggest more variable anatomo-clinical correlations. We included retrospectively from our stroke data bank 16 patients (right- and left-handed, and ambidextrous) with aphasia after a single first-ever ischemic RH stroke. A control group was composed of 25 successive patients with left hemispheric stroke and aphasia (LHSA). For each patient, we analyzed four modalities of language (spontaneous fluency, naming, repetition, and comprehension) and recorded eventual impairment: (1) on admission (hyperacute) and (2) between day 3 and 14 (acute). Lesion volume and location as measured on computed tomography (CT) and magnetic resonance imaging (MRI) were transformed into Talairach stereotaxic space. Nonparametric statistics were used to compare impaired/nonimpaired patients. Comprehension and repetition were less frequently impaired after RHSA (respectively, 56% and 50%) than after LHSA (respectively, 84% and 80%, P = 0.05 and 0.04) only at hyperacute phase. Among RHSA, fewer left-handers/ambidextrous than right-handers had comprehension disorders at second evaluation (P = 0.013). Mean infarct size was similar in RHSA and LHSA with less posterior RHSA lesions (caudal to the posterior commissure). Comprehension and repetition impairments were more often associated with anterior lesions in RHSA (Fisher's exact test, P < 0.05). Despite the small size of the cohort, our findings suggest increased atypical anatomo-functional correlations of RH language representation, particularly in non-right-handed patients. Rapport de synthèse : Des aphasies secondaires à un accident vasculaire ischémique cérébral (AVC) hémisphérique droit sont rarement rencontrées chez des patients droitiers ou gauchers avec une représentation du langage dans l'hémisphère droit. Chez les droitiers, on parle d'aphasie croisée. Plusieurs études sur le sujet ont suggéré des corrélations anatomocliniques plus variables. Dans notre étude, nous avons inclus rétrospectivement, à partir d'une base de données de patients avec un AVC, seize patients (droitiers, gauchers et ambidextres) souffrant d'une aphasie suite à un premier et unique AVC ischémique hémisphérique droit. Un groupe contrôle est composé de vingt-cinq patients successifs avec une aphasie suite à un AVC ischémique hémisphérique gauche. Pour chaque patient, nous avons analysé quatre modalités de langage, à savoir la fluence spontanée, la dénomination, la répétition et la compréhension et leur éventuelle atteinte à deux moments distincts : 1) à l'admission (phase hyperaiguë) et 2) entre le 3e et le 14e jour (phase aiguë). Le volume et la localisation de la lésion mesurés, soit sur un CT-scanner soit sur une imagerie par résonance magnétique cérébrale, ont été analysés à l'aide de l'échelle stéréotaxique de Talairach. Des statistiques non paramétriques ont été utilisées pour comparer les patients atteints et non atteints. . La compréhension et la répétition étaient moins souvent atteintes, seulement en phase hyperaiguë, après une aphasie suite à un AVC hémisphérique droit (resp. 56% et 50%) plutôt que gauche (resp. 84 % et 80%, p= 0.05 et 0.04). Parmi les aphasies suite à un AVC ischémique hémisphérique droit, moins de gauchers et d'ambidextres que de droitiers avaient des troubles de la compréhension lors de la seconde évaluation (p=0.013}. La .taille moyenne de la zone infarcie était semblable entre les aphasies droites et gauches, avec moins de lésions postérieures (caudale à la commissure postérieure) lors des aphasies droites. Les troubles de la répétition et de la compréhension étaient plus souvent associés à des lésions antérieures lors d'aphasie droite. (Fischer's exact test, p>0.05). Malgré la petite taille de notre cohorte de patients, ces résultats suggèrent une augmentation des corrélations anatomocliniques atypiques lors d'une représentation du langage dans l'hémisphère droit, surtout chez les patients non droitiers.

Impact of preoperative central neurologic dysfunction on patients undergoing emergency surgery for type a dissection.

BACKGROUND: Preoperative central neurologic deficits in the context of acute type A dissection are a complex comorbidity and difficult to handle. The aim this study was to analyze this subgroup of patients by comparing them with neurologically asymptomatic patients with type A dissection. Results may help the surgeon in preoperative risk assessment and thereby aid in the decision-making process. METHODS: We reviewed the data of patients admitted for acute type A dissection during the period from 1999 to 2010. Associated risk factors, time to surgery from admission, extension of the dissection, localization of central nervous ischemic lesions, and the influence of perioperative brain protective strategies were analyzed in a comparison of preoperative neurologically deficient to nondeficient patients. RESULTS: Forty-seven (24.5%) of a total of 192 patients had new-onset central neurologic symptoms prior to surgery. Concomitant myocardial infarction (OR 4.9, 95% CI 1.6-15.3, P = 0.006), renal failure (OR 5.9, 95% CI 1.1-32.8, P = 0.04), dissected carotid arteries (OR 9.2, 95% CI 2.4-34.7, P = 0.001), and late admission to surgery at >6 hours after symptom onset (OR 2.7, 95% CI 1.1-6.8, P = 0.04) were observed more frequently in neurologically deficient patients. These patients had a higher 30-day in-hospital mortality on univariate analysis (P = 0.01) and a higher rate of new postoperative neurologic deficits (OR 9.2, 95% CI 2.4-34.7, P = 0.02). Neurologic survivors had an equal hospital stay, and 67% of them had improved symptoms. CONCLUSIONS: The predominance of neurologic symptoms at admission may be responsible for an initial misdiagnosis. The concurrent central nervous system ischemia and myocardial infarction explains a higher mortality rate and a more extensive "character" of the disease. Neurologically deficient patients are at higher risk of developing new postoperative neurologic symptoms, but prognosis for the neurologic evolution of survivors is generally favorable.

Hypoxia/hypoglycemia preconditioning prevents the loss of functional electrical activity in organotypic slice cultures.

In cerebral ischemic preconditioning (IPC), a first sublethal ischemia increases the resistance of neurons to a subsequent severe ischemia. Despite numerous studies, the mechanisms are not yet fully understood. Our goal is to develop an in vitro model of IPC on hippocampal organotypic slice cultures. Instead of anoxia, we chose to apply varying degrees of hypoxia that allows us various levels of insult graded from mild to severe. Cultures are exposed to combined oxygen and glucose deprivation (OGD) of varying intensities, ranging from mild to severe, assessing both the electrical activity and cell death. IPC was accomplished by exposure to the mildest ischemia condition (10% of O2 for 15 min) 24 h before the severe deprivation (5% of O2 for 30 min). Interestingly, IPC not only prevented delayed ischemic cell death 6 days after insult but also the transient loss of evoked potential response. The major interest and advantage of this system over both the acute slice preparation and primary cell cultures is the ability to simultaneously measure the delayed neuronal damage and neuronal function.

A web-based pilot study of inter-pathologist reproducibility using the ISHLT 2004 working formulation for biopsy diagnosis of cardiac allograft rejection: The European experience.

BACKGROUND: The aim of this study was to assess, at the European level and using digital technology, the inter-pathologist reproducibility of the ISHLT 2004 system and to compare it with the 1990 system We also assessed the reproducibility of the morphologic criteria for diagnosis of antibody-mediated rejection detailed in the 2004 grading system. METHODS: The hematoxylin-eosin-stained sections of 20 sets of endomyocardial biopsies were pre-selected and graded by two pathologists (A.A. and M.B.) and digitized using a telepathology digital pathology system (Aperio ImageScope System; for details refer to http://aperio.com/). Their diagnoses were considered the index diagnoses, which covered all grades of acute cellular rejection (ACR), early ischemic lesions, Quilty lesions, late ischemic lesions and (in the 2005 system) antibody-mediated rejection (AMR). Eighteen pathologists from 16 heart transplant centers in 7 European countries participated in the study. Inter-observer reproducibility was assessed using Fleiss's kappa and Krippendorff's alpha statistics. RESULTS: The combined kappa value of all grades diagnosed by all 18 pathologists was 0.31 for the 1990 grading system and 0.39 for the 2005 grading system, with alpha statistics at 0.57 and 0.55, respectively. Kappa values by grade for 1990/2005, respectively, were: 0 = 0.52/0.51; 1A/1R = 0.24/0.36; 1B = 0.15; 2 = 0.13; 3A/2R = 0.29/0.29; 3B/3R = 0.13/0.23; and 4 = 0.18. For the 2 cases of AMR, 6 of 18 pathologists correctly suspected AMR on the hematoxylin-eosin slides, whereas, in each of 17 of the 18 AMR-negative cases a small percentage of pathologists (range 5% to 33%) overinterpreted the findings as suggestive for AMR. CONCLUSIONS: Reproducibility studies of cardiac biopsies by pathologists in different centers at the international level were feasible using digitized slides rather than conventional histology glass slides. There was a small improvement in interobserver agreement between pathologists of different European centers when moving from the 1990 ISHLT classification to the "new" 2005 ISHLT classification. Morphologic suspicion of AMR in the 2004 system on hematoxylin-eosin-stained slides only was poor, highlighting the need for better standardization of morphologic criteria for AMR. Ongoing educational programs are needed to ensure standardization of diagnosis of both acute cellular and antibody-mediated rejection.

The L-Type Ca+ and KATP channels may contribute to pacing-induced protection against anoxia-reoxygenation in the embryonic heart model.

L-Type Ca(2+) and K(ATP) Channels in Pacing-Induced Cardioprotection. AIMS: The L-type Ca(2+) channel, the sarcolemmal (sarcK(ATP)), and mitochondrial K(ATP) (mitoK(ATP)) channels are involved in myocardial preconditioning. We aimed at determining to what extent these channels can also participate in pacing-induced cardioprotection. METHODS: Hearts of 4-day-old chick embryos were paced in ovo during 12 hour using asynchronous intermittent ventricular stimulation at 110% of the intrinsic rate. Sham operated and paced hearts were then submitted in vitro to anoxia (30 minutes) and reoxygenation (60 minutes). These hearts were exposed to L-type Ca(2+) channel agonist Bay-K-8644 (BAY-K) or blocker verapamil, nonselective K(ATP) channel antagonist glibenclamide (GLIB), mitoK(ATP) channel agonist diazoxide (DIAZO), or antagonist 5-hydroxydecanoate. Electrocardiogram, electromechanical delay (EMD) reflecting excitation-contraction (E-C) coupling, and contractility were determined. RESULTS: Under normoxia, heart rate, QT duration, conduction, EMD, and ventricular shortening were similar in sham and paced hearts. During reoxygenation, arrhythmias ceased earlier and ventricular EMD recovered faster in paced hearts than in sham hearts. In sham hearts, BAY-K (but not verapamil), DIAZO (but not 5-hydroxydecanoate) or GLIB accelerated recovery of ventricular EMD, reproducing the pacing-induced protection. By contrast, none of these agents further ameliorated recovery of the paced hearts. CONCLUSION: The protective effect of chronic asynchronous pacing at near physiological rate on ventricular E-C coupling appears to be associated with subtle activation of L-type Ca(2+) channel, inhibition of sarcK(ATP) channel, and/or opening of mitoK(ATP) channel.

Neuroprotection in cerebral ischemia : an effect of c-Jun N-terminal kinase inhibition on the inflammatory response

RESUMESuite à un accident vasculaire cérébral (AVC) ischémique, les cellules gliales ducerveau deviennent activées, de nombreuses cellules inflammatoires pénètrent dans letissu lésé et sécrètent une grande variété de cytokines et chémokines. Aujourd'hui, ilexiste des interrogations sur les effets bénéfiques ou délétères de cette inflammation surla taille de la lésion et le pronostic neurologique.Ce projet vise à évaluer l'effet d'un peptide neuroprotecteur, D-JNKI1, inhibiteur de lavoie pro-apoptotique de signalisation intracellulaire c-Jun N-terminal kinase (JNK), surl'inflammation post-ischémique.Nous montrons d'abord que la microglie est largement activée dans toute la région lésée48 h après l'induction d'une ischémie chez la souris. Cependant, malgré l'inhibition dela mort neuronale par D-JNKI1 évaluée à 48 h, nous n'observons de modification ni del'activation de la microglie, ni de son nombre. Ensuite, nous montrons que le cerveaupeut être protégé même s'il y a une augmentation massive de la sécrétion de médiateursinflammatoires dans la circulation systémique très tôt après induction d'un AVCischémique. De plus, nous notons que la sécrétion de molécules inflammatoires dans lecerveau n'est pas différente entre les animaux traités par D-JNKI1 ou une solutionsaline, bien que nous ayons obtenu une neuroprotection significative chez les animauxtraités.En conclusion, nous montrons que l'inhibition de la voie de JNK par D-JNKI1n'influence pas directement l'inflammation post-ischémique. Ceci suggère quel'inhibition de l'inflammation n'est pas forcément nécessaire pour obtenir en hautdegré de neuroprotection du parenchyme lésé après ischémie cérébrale, et que lesmécanismes inflammatoires déclenchés lors d'une ischémie cérébrale ne sont pasforcément délétères pour la récupération du tissu endommagé.SUMMARYAfter cerebral ischemia, glial cells become activated and numerous inflammatory cellsinfiltrate the site of the lesion, secreting a large variety of cytokines and chemokines. Itis controversial whether this brain inflammation is detrimental or beneficial and how itinfluences lesion size and neurological outcome.This project was aimed at critically evaluating whether the neuroprotective peptide DJNKI,an inhibitor of the pro-apopotic c-Jun N-terminal kinase (JNK) pathway,modulates post-ischemic inflammation in animal models of stroke. Specifically, it wasasked whether JNK inhibition prevents microglial activation and the release ofinflammatory mediators.In the first part of this study, we showed that microglia was activated throughout thelesion 48 h after experimental stroke. However, the activation and accumulation ofmicroglia was not reduced by D-JNKI1, despite a significant reduction of the lesionsize. In the second part of this project, we demonstrated that neuroprotection measuredat 48 h occurs even though inflammatory mediators are released in the plasma veryearly after the onset of cerebral ischemia. Furthermore, we found that secretion ofinflammatory mediators in the brain was not different in groups treated with D-JNKI1or not, despite a significant reduction of the lesion size in the treated group.Altogether, we show that inhibition of the JNK pathway using D-JNKI1 does notinfluence directly post-stroke inflammation. Inhibition of inflammation is therefore notnecessarily required for neuroprotection after cerebral ischemia. Thus, post-strokeinflammation might not be detrimental for the tissue recovery.

Infusion of atrial natriuretic peptide to patients with congestive heart failure.

Atrial natriuretic peptides (ANP) exert vasodilating and natriuretic actions. The present study was undertaken to test the effect of low dose infusions of synthetic ANP on hemodynamic and humoral variables of patients with severe heart failure. Eight patients, aged 26 to 71 years, with severe congestive heart failure due to ischemic heart disease or idiopathic dilated cardiomyopathy were included in the study. Synthetic human (3-28) ANP was infused at doses ranging from 0.5 to 2 micrograms/min for up to 3 h. Pulmonary capillary wedge pressure fell from 24 +/- 1 to 16 +/- 2 mm Hg (mean +/- SEM) (p less than 0.01) and cardiac index tended to rise from 2 +/- 0.2 to 2.3 +/- 0.2 L/min/m2 (NS), while blood pressure and heart rate did not change. One patient experienced a marked drop in pulmonary capillary wedge and arterial blood pressure that necessitated the administration of saline. ANP infusion did not alter plasma renin activity or plasma aldosterone, norepinephrine, or vasopressin levels. It decreased plasma epinephrine levels from 0.472 +/- 0.077 to 0.267 +/- 0.024 nmol/L (p less than 0.05). Plasma ANP levels were markedly elevated in all patients before initiating the infusion. They had no predictive value for the hemodynamic response to exogenous ANP. No correlation was observed between the hemodynamic effects of ANP and those induced by the subsequently administered converting enzyme inhibitor captopril, which seemed to improve cardiac function more consistently.(ABSTRACT TRUNCATED AT 250 WORDS)

Enhancement of autophagic flux after neonatal cerebral hypoxia-ischemia and its region-specific relationship to apoptotic mechanisms.

The multiplicity of cell death mechanisms induced by neonatal hypoxia-ischemia makes neuroprotective treatment against neonatal asphyxia more difficult to achieve. Whereas the roles of apoptosis and necrosis in such conditions have been studied intensively, the implication of autophagic cell death has only recently been considered. Here, we used the most clinically relevant rodent model of perinatal asphyxia to investigate the involvement of autophagy in hypoxic-ischemic brain injury. Seven-day-old rats underwent permanent ligation of the right common carotid artery, followed by 2 hours of hypoxia. This condition not only increased autophagosomal abundance (increase in microtubule-associated protein 1 light chain 3-11 level and punctuate labeling) but also lysosomal activities (cathepsin D, acid phosphatase, and beta-N-acetylhexosaminidase) in cortical and hippocampal CA3-damaged neurons at 6 and 24 hours, demonstrating an increase in the autophagic flux. In the cortex, this enhanced autophagy may be related to apoptosis since some neurons presenting a high level of autophagy also expressed apoptotic features, including cleaved caspase-3. On the other hand, enhanced autophagy in CA3 was associated with a more purely autophagic cell death phenotype. In striking contrast to CA3 neurons, those in CA1 presented only a minimal increase in autophagy but strong apoptotic characteristics. These results suggest a role of enhanced autophagy in delayed neuronal death after severe hypoxia-ischemia that is differentially linked to apoptosis according to the cerebral region.

Stroke Aphasia: 1,500 Consecutive Cases.

Background: To study the characteristics of vascular aphasia in a cohort of patients with a first-ever stroke. Methods: All patients admitted to the Lausanne neurology department for a first-ever stroke between 1979 and 2004 were included. Neurological examination including language was performed on admission. Stroke risk factors, stroke origin and location, associated symptoms and Rankin scale scores were recorded for each patient. The influence of these factors on aphasia frequency and subtypes was analyzed using logistic regression models. Results: 1,541 (26%) of patients included in this study had aphasia. The more frequent clinical presentations were expressive-receptive aphasia (38%) and mainly expressive aphasia (37%), whereas mainly receptive aphasia was less frequently observed (25%). In ischemic stroke, the frequency of aphasia increased with age (55% of nonaphasic vs. 61% of aphasic patients were more than 65 years old), female sex (40% of women in the nonaphasia group vs. 44% in the aphasia group) and risk factors for cardioembolic origin (coronary heart disease 20 vs. 26% and atrial fibrillation 15 vs. 24%). Stroke aphasia was more likely associated with superficial middle cerebral artery (MCA) stroke and leads to relevant disability. Clinical subtypes depended on stroke location and associated symptoms. Exceptions to the classic clinical-topographic correlations were not rare (26%). Finally, significant differences were found for patients with crossed aphasia in terms of stroke origin and aphasia subtypes. Conclusions: Risk factors for stroke aphasia are age, cardioembolic origin and superficial MCA stroke. Exceptions to classic clinical-topographic correlations are not rare. Stroke aphasia is associated with relevant disability. Stroke location and associated symptoms strongly influence aphasia subtypes.

Intracranial arterial and arteriovenous malformations presenting with infarction. Lausanne Stroke Registry study.

Cerebral aneurysms and arteriovenous malformations (AVMs) are well-known sources of intracranial hemorrhage, but can also manifest as other clinical symptoms or remain clinically asymptomatic. The aim was to document and analyze cases of aneurysm or AVM with brain infarction. Survey on 4804 stroke patients treated at the Department of Neurology, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland between 1978 and 2000 using the Lausanne Stroke Registry. Twenty patients presented with cerebral aneurysm and 21 with cerebral AVM. Hemorrhage was present in 100% of the AVM and in 75% of the aneurysm patients; in one (5%) of the remaining aneurysm patients, aneurysm and infarction were located in different territories. Infarction associated with Sylvian artery aneurysm was found in three (15%), vertebrobasilar ischemia because of fusiform left vertebral artery aneurysm in one (5%), and dural fistula draining to the distal transversal and left sigmoid sinus associated with a stroke in the territory of the left anterior inferior cerebellar artery in one patient. Ischemic stroke is infrequent, but important, complication in unruptured intracranial aneurysms and AVMs. The early recognition and therapy of these vascular malformations in selected patients can avoid a major neurological deficit or death caused by their rupture.

c-Jun N-terminal kinase pathway inhibition in intracerebral hemorrhage.

Background: Inhibition of the c-Jun N-terminal kinase (JNK) pathway by the TAT-coupled peptide XG-102 (formerly D-JNKI1) induces strong neuroprotection in ischemic stroke in rodents. We investigated the effect of JNK inhibition in intracerebral hemorrhage (ICH). Methods: Three hours after induction of ICH by intrastriatal collagenase injection in mice, the animals received an intravenous injection of 100 mu g/kg of XG-102. The neurological outcome was assessed daily and the mice were sacrificed at 6 h, 1, 2 or 5 days after ICH. Results: XG-102 administration significantly improved the neurological outcome at 1 day (p < 0.01). The lesion volume was significantly decreased after 2 days (29 +/- 11 vs. 39 +/- 5 mm(3) in vehicle-treated animals, p < 0.05). There was also a decreased hemispheric swelling (14 +/- 13 vs. 26 +/- 9% in vehicle-treated animals, p < 0.05) correlating with increased aquaporin 4 expression. Conclusions: XG-102 attenuates cerebral edema in ICH and functional impairment at early time points. The beneficial effects observed with XG-102 in ICH, as well as in ischemic stroke, open the possibility to rapidly treat stroke patients before imaging, thereby saving precious time.

Dietary fish oil is antihypertrophic but does not enhance postischemic myocardial function in female mice.

Clinically and experimentally, a case for omega-3 polyunsaturated fatty acid (PUFA) cardioprotection in females has not been clearly established. The goal of this study was to investigate whether dietary omega-3 PUFA supplementation could provide ischemic protection in female mice with an underlying genetic predisposition to cardiac hypertrophy. Mature female transgenic mice (TG) with cardiac-specific overexpression of angiotensinogen that develop normotensive cardiac hypertrophy and littermate wild-type (WT) mice were fed a fish oil-derived diet (FO) or PUFA-matched control diet (CTR) for 4 wk. Myocardial membrane lipids, ex vivo cardiac performance (intraventricular balloon) after global no-flow ischemia and reperfusion (15/30 min), and reperfusion arrhythmia incidence were assessed. FO diet suppressed cardiac growth by 5% and 10% in WT and TG, respectively (P < 0.001). The extent of mechanical recovery [rate-pressure product (RPP) = beats/min x mmHg] of FO-fed WT and TG hearts was similar (50 +/- 7% vs. 45 +/- 12%, 30 min reperfusion), and this was not significantly different from CTR-fed WT or TG. To evaluate whether systemic estrogen was masking a protective effect of the FO diet, the responses of ovariectomized (OVX) WT and TG mice to FO dietary intervention were assessed. The extent of mechanical recovery of FO-fed OVX WT and TG (RPP, 50 +/- 4% vs. 64 +/- 8%) was not enhanced compared with CTR-fed mice (RPP, 60 +/- 11% vs. 80 +/- 8%, P = 0.335). Dietary FO did not suppress the incidence of reperfusion arrhythmias in WT or TG hearts (ovary-intact mice or OVX). Our findings indicate a lack of cardioprotective effect of dietary FO in females, determined by assessment of mechanical and arrhythmic activity postischemia in a murine ex vivo heart model.