Successful intravenous thrombolysis in ischemic stroke caused by infective endocarditis

Introduction  Infective endocarditis can lead to serious neurological complications including ischemic stroke and intracranial hemorrhage. Treatment with intravenous thrombolysis within 3 h of symptom onset has become the standard of care in acute ischemic stroke, but the safety and efficacy of this intervention in patients with infective endocarditis is unknown. Summary of Case  We report the case of a patient with ischemic stroke who experienced substantial neurological improvement after being treated with intravenous thrombolysis (NIH stroke scale score of 15 on admission and 4 after treatment) and was subsequently found to have acute infective mitral endocarditis. Conclusion  Favorable response to thrombolysis may occur in patients with stroke due to infectious endocarditis. The safety of this therapy remains to be established.     

2例感染性心内膜炎并发脑梗死临床分析

目的 分析以脑梗死为首发症状的感染性心内膜炎的发病特点,提高临床认识.方法 对2例感染性心内膜炎并发脑梗死患者的临床特征、辅助检查及相关文献进行分析.结果 两例患者均首诊于综合医院的神经内科,均未能及时确定病因,存在不同程度的临床误诊.结论 感染性心内膜炎是青年性卒中的一个重要原因,应注意早期诊断和治疗.     

D-dimer level predicts in-hospital mortality in patients with infective endocarditis: A prospective single-centre study

Background

Increased circulating D-dimer levels have been correlated with adverse outcomes in various clinical conditions. To our knowledge, the association of on-admission D-dimer and in-hospital mortality in infective endocarditis (IE) has not been investigated. We hypothesized that increased on-admission D-dimer levels would correlate with adverse outcomes when prospectively studied in patients with IE.

Methods

In this prospective study, a total of 157 consecutive patients with the definite IE diagnosis met the inclusion criteria and underwent testing for on-admission D-dimer and CRP assays. The outcome measure was in-hospital death from any cause.

Results

In-hospital mortality occurred in 40 (26%) patients. Increased levels of plasma D-dimer (5.1 ± 1.7 vs 1.9 ± 0.8, p < 0.001), CRP [45(13-98) vs 12(5–28), p < 0.001] were found in dead patients compared with those survived. In addition to S. aureus infection, increased leukocyte count, end-stage renal disease, LVEF < 50%, vegetation size of > 10 mm, perivalvular abscess, on-admission D-dimer (HR: 1.32; 95% CI: 1.24-1.40; p < 0.001) and CRP (HR: 1.18; 95% CI: 1.09-1.36; p = 0.001) levels were significantly associated with in-hospital mortality. Furthermore, the sensitivity and specificity of D-dimer ≥ 4.2 mg/L in predicting in-hospital death in IE were 86% and 85%, respectively. Moreover, the sensitivity and specificity of CRP levels ≥ 13.6 mg/L were 72% and 69%, respectively.

Conclusion

Our findings suggest that on-admission D-dimer level may be a simple, available and valuable biomarker that allows us to identify high-risk IE patients for in-hospital mortality. D-dimer ≥ 4.2 mg/L, CRP ≥ 13.6 mg/L were independently associated with IE related in-hospital death.     

Cardioembolic stroke secondary to non-bacterial endocarditis in wegener disease

Wegener granulomatosis is a systemic vasculitis that mainly affects the upper and lower respiratory tract and the kidneys. The presence of an ischemic stroke in this disease is very rare. A 40-year-old man, smoker with cavitated lesions in both lungs, and inflammation in the nasal mucosa and vocal cords developed an ischemic stroke in the left middle cerebral artery, with the etiological study showing non-bacterial endocarditis. Non-bacterial endocarditis can appear in patients with Wegener granulomatosis, with this being the first case of this cardioembolism reported in this disease.     

Significance of the T2*-weighted gradient echo brain imaging in patients with infective endocarditis

Background

Although aneurysm formation accompanying parenchymal hemorrhage is one of devastating complications in the central nerves system (CNS), imaging studies of the brain are not routinely warranted in patients with infective endocarditis (IE). To assess the clinical importance for detecting silent lesions in the central nervous system, we investigated hypointense signal spots detected on the brain T2*-weighted MR imaging in patients with IE.

Methods and results

Eleven patients with IE were retrospectively reviewed. Seven patients (63.6%) showed hypointense signal spots on T2*-weighted MR images. The number of hypointense signal spots increased within only a few weeks in five patients.

Conclusion

The brain T2*-weighted MR imaging in patients with IE may have a potential role to detect CNS lesions with clinical significance of potentially high risk of intracranial hemorrhage. T2*-weighted hypointense signal spots may be specific to brain involvement, and be quite useful in monitoring CNS lesions associated with IE, even if they are asymptomatic.     

Naloxone reversal and morphine exacerbation of neurologic deficits secondary to focal cerebral ischemia in baboons

The effects of an opiate agonist (morphine) and antagonist (naloxone) on neurologic function in conditions of acute and subacute focal cerebral ischemia were tested in a baboon model. Fourteen baboons (Papio papio) underwent unilateral transorbital microsurgical occlusion of the middle cerebral artery (MCA). Blood pressure, heart rate and core temperature were monitored continuously; frequent arterial blood gas measurements were made. Cardiac output, cardiac filling pressures, and regional cerebral blood cross-flow were measured in selected baboons. Naloxone administered intravenously consistently reversed hemiparesis and hemiplegia in all baboons for as long as they lived (4 h to 8 days postocclusion). Morphine administered intravenously converted hemiparesis to hemiplegia; this effect was naloxone-reversible. There were no significant changes in any parameter measured after the administration of either drug. Phenylephrine (used to elevate mean arterial pressure to 20 mm higher than the highest pressure measured after naloxone administration) and isoproterenol (used to elevate cardiac output to 1 l/min higher than the highest value measured after naloxone administration) produced no change in neurologic function. It appears that naloxone can reverse, and morphine exacerbate, focal ischemic neurologic deficits produced in baboons by MCA occlusion. The observed changes in neurologic function are not associated with or mediated by alterations in core temperature or cardiopulmonary functions.     

Acute enlargement,morphological changes,and rupture of intracranial infectious aneurysm in infective endocarditis. Serial imaging

A 72-year-old man received a transcatheter aortic valve implantation (TAVI) 2 years ago for leakage of the degenerative bioprosthesis with Corevalve n°31 implantation, presented infective endocarditis (IE) (streptococcus sanguinis) of the bioprosthetic aortic valve. One month after antibiotic treatment was initiated, he presented a left-sided hemiplegia, a right frontal hematoma. MRI/contrast-enhanced magnetic resonance angiography (CE-MRA) revealed 2 infectious intracranial aneurysms (IIAs) of the right (10 mm) and left middle cerebral artery (MCA) (M2 segment, 5 mm). The right MCA IIA was treated within 1 day by glue-embolization. Seven days later, the patient acutely developed motor aphasia. CE-MRA showed significant enlargement (15 mm) and morphologic change of the ruptured left MCA IIA. This IIA was treated with Onyx-embolization.This case adds additional evidence that IIAs, during IE, can show rapid growth and morphological change over a 7 day course and emphasizes the imperative need of close imaging follow-up when IIAs are managed by antibiotic therapy.     

Macrophage migration inhibitory factor promotes cell death and aggravates neurologic deficits after experimental stroke

Multiple mechanisms contribute to tissue demise and functional recovery after stroke. We studied the involvement of macrophage migration inhibitory factor (MIF) in cell death and development of neurologic deficits after experimental stroke. Macrophage migration inhibitory factor is upregulated in the brain after cerebral ischemia, and disruption of the Mif gene in mice leads to a smaller infarct volume and better sensory-motor function after transient middle cerebral artery occlusion (tMCAo). In mice subjected to tMCAo, we found that MIF accumulates in neurons of the peri-infarct region, particularly in cortical parvalbumin-positive interneurons. Likewise, in cultured cortical neurons exposed to oxygen and glucose deprivation, MIF levels increase, and inhibition of MIF by (S,R)-3-(4-hydroxyphenyl)-4,5-dihydro-5-isoxazole acetic acid methyl ester (ISO-1) protects against cell death. Deletion of MIF in Mif^−/− mice does not affect interleukin-1β protein levels in the brain and serum after tMCAo. Furthermore, disruption of the Mif gene in mice does not affect CD68, but it is associated with higher galectin-3 immunoreactivity in the brain after tMCAo, suggesting that MIF affects the molecular/cellular composition of the macrophages/microglia response after experimental stroke. We conclude that MIF promotes neuronal death and aggravates neurologic deficits after experimental stroke, which implicates MIF in the pathogenesis of neuronal injury after stroke.     

Analysis of Chlamydia pneumoniae-specific oligoclonal bands in multiple sclerosis and other neurologic diseases

OBJECTIVE: Paired serum and cerebrospinal fluid (CSF) specimens were investigated for Chlamydia pneumoniae-specific oligoclonal bands (OCBs) to determine band specificity in multiple sclerosis (MS). MATERIAL AND METHODS: Serum and CSF samples were collected from patients with relapsing-remitting MS (n = 56), other inflammatory (n = 18) or non-inflammatory (n = 15) neurologic diseases, and from 10 healthy controls. OCBs were determined with affinity immunoblotting of C. pneumoniae-specific IgG onto antigen-coated nitrocellulose paper after protein separation with agarose isoelectric focusing. RESULTS: Chlamydia pneumoniae-specific OCBs were present in 5 of 56 patients with MS, and in 3 of 18 patients with other inflammatory neurologic diseases. CONCLUSIONS: The intrathecal production of C. pneumoniae-specific oligoclonal IgG occurs in a minority of patients with MS. This intrathecal anti-C. pneumoniae reactivity is likely part of a polyspecific humoral immune response in MS.     

Structure, function, property, and role in neurologic diseases and other diseases of the sHsp22

Small heat shock proteins are members of the heat shock proteins family. They share important identical features: 1) they form the conserved structure 'alpha-crystallin domain' with about 80-100 residues in the C-terminal part of the proteins; 2) they have monomeric molecular masses ranging in 12-43 kDa; 3) they associate into large oligomers consisting in many cases of subunits; 4) they increase expression under stress conditions; 5) they exhibit a highly dynamic structure; and 6) they play a chaperone-like role. Hsp22 (also known as HspB8, H11, and E2IG1) retains the structural motif of the 'alpha-crystallin' family of Hsps and is a member of the superfamily of sHsps. Hsp22 displays chaperone activity, autokinase activity, and trigger or block apoptosis activity. It differs from canonical family members existing as a monomer. A decrease in the HspB8 activity may contribute to the development of some neurologic diseases and others.     

Anti-GFAP antibodies in the cerebrospinal fluid of patients with multiple sclerosis and other neurologic diseases

The antibodies against glial fibrillary acidic protein (GFAP) in the CSF of patients with multiple sclerosis and other neurological diseases were determined. It was shown that the binding activity of CSF IgG with GFAP was higher in patients with MS and other organic neurological diseases as compared to control group (neurotics). The results support the idea, that in SM there is a general immune dysregulation, leading to production of a variety of autoantibodies against different antigens, including the presently shown GFAP.     

Immunoblot analysis of circulating antibodies against muscle proteins in amyotrophic lateral sclerosis and other neurologic diseases

Serum from patients with amyotrophic lateral sclerosis (ALS) was tested by immunoblotting for reactivity against three muscle-derived preparations: denervated chick leg muscle extracts, media conditioned by denervated rat hemidiaphragms, and a human muscle extract. For each preparation, multiple bands were present using serum from all patients and controls, and no band was unique to ALS. Against rat muscle-conditioned medium, bands in the 56,000 (56K) molecular weight range were present to an equal degree in ALS and in controls; in addition, different bands near 56K were recognized by serum from different ALS patients. These results fail to confirm a recent report suggesting that anti-56K reactivity is characteristic of ALS.     

The diagnosis and treatment of stroke in a patient with cancer: nonbacterial thrombotic endocarditis (NBTE): a case report and review

Stroke in patients with cancer is different in terms of its etiology from stroke in the general population. Clinicians should be alerted to the possiblity of non-bacterial thrombotic endocarditis (NBTE), associated coagulopathy, and viable treatment options. We review the case of a 42-year-old woman with cerivcal carcinoma and no risk factors for stroke who suddenly developed difficulty with speech and right-sided sensory changes. Her complete work-up and course are addressed.     

Skeletal Muscle wasting and contractile performance in septic rats

We investigated the temporal effects of sepsis on muscle wasting and function in order to study the contribution of wasting to the decline in muscle function; we also studied the fiber-type specificity of this muscle wasting. Sepsis was induced by injecting rats intraperitoneally with a zymosan suspension. At 2 h and at 2, 6, and 11 days after injection, muscle function was measured using in situ electrical stimulation, Zymosan injection induced severe muscle wasting compared to pair-fed and ad libitum fed controls. At 6 days, isometric force-generating capacity was drastically reduced in zymosan-treated rats. We conclude that this was fully accounted fo by the reduction of muscle mas. At day 6, we also observed increased activity of the 20S proteasome in gastrocnemius but not soleus muscle from septic rats. In tibialis anterior but not in soleus, muscle wasting occurred in a fiber-type specific fashion, i.e., the reduction in cross-sectional area was significantly smaller in type 1 than type 2A and 2B/X fibers. These findings suggest that both the inherent function of a muscle and the muscle fiber-type distribution affect the responsiveness to catabolic signals.