Rare complication of circumflex artery occlusion during transfemoral aortic valve replacement (TAVR)

Circumflex artery occlusion is an unusual but grave complication that can be intra-operatively challenging to identify. Various modalities of imaging are possible during transfemoral aortic valve replacement (TAVR). Fluoroscopy and/or trans-esophageal echocardiography maybe used for assessment during and after TAVR. Imaging dilemma can cause delay or alter diagnosis. We report a case of an imaging complication during TAVR which might have modified the outcome of the procedure.     

Effects of hypoglycaemia on working memory and regional cerebral blood flow in type 1 diabetes: a randomised,crossover trial

Aims/hypothesis

The aim of this randomised, crossover trial was to compare cognitive functioning and associated brain activation patterns during hypoglycaemia (plasma glucose [PG] just below 3.1 mmol/l) and euglycaemia in individuals with type 1 diabetes mellitus.

Methods

In this patient-blinded, crossover study, 26 participants with type 1 diabetes mellitus attended two randomised experimental visits: one hypoglycaemic clamp (PG 2.8?±?0.2 mmol/l, approximate duration 55 min) and one euglycaemic clamp (PG 5.5 mmol/l?±?10%). PG levels were maintained by hyperinsulinaemic glucose clamping. Cognitive functioning was assessed during hypoglycaemia and euglycaemia conditions using a modified version of the digit symbol substitution test (mDSST) and control DSST (cDSST). Simultaneously, regional cerebral blood flow (rCBF) was measured in pre-specified brain regions by six H₂ ¹⁵O-positron emission tomographies (PET) per session.

Results

Working memory was impaired during hypoglycaemia as indicated by a statistically significantly lower mDSST score (estimated treatment difference [ETD] ?0.63 [95% CI ?1.13, ?0.14], p?=?0.014) and a statistically significantly longer response time (ETD 2.86 s [7%] [95% CI 0.67, 5.05], p?=?0.013) compared with euglycaemia. During hypoglycaemia, mDSST task performance was associated with increased activity in the frontal lobe regions, superior parietal lobe and thalamus, and decreased activity in the temporal lobe regions (p?<?0.05). Working memory activation (mDSST ? cDSST) statistically significantly increased blood flow in the striatum during hypoglycaemia (ETD 0.0374% [95% CI 0.0157, 0.0590], p?=?0.002).

Conclusions/interpretation

During hypoglycaemia (mean PG 2.9 mmol/l), working memory performance was impaired. Altered performance was associated with significantly increased blood flow in the striatum, a part of the basal ganglia implicated in regulating motor functions, memory, language and emotion.

Trial registration

NCT01789593, clinicaltrials.gov

Funding

This study was funded by Novo Nordisk.

     

Relationship between hepatocellular injury and transfusional iron overload prior to and during iron chelation with desferrioxamine: a study in adult patients with acquired anemias

The role of iron overload as cause of liver dysfunction has never been studied in detail in patients without concomitant hepatotropic infections who receive multiple transfusions. We therefore investigated the relationship between the extent of hepatocellular injury as reflected by serum levels of aminotransferases (alanine aminotransferase [ALT] and aspartate aminotransferase [AST]) and several iron status indices in 39 anti-hepatitis C virus-negative (HCV(-)) nonthalassemic patients with transfusional iron overload owing to acquired anemias. In 12 patients, we monitored aminotransferase levels and indices of iron status during iron chelation treatment. Before treatment, elevated aminotransferase activity was seen only at liver iron concentrations more than 300 microM/g. During treatment all aminotransferase values were normal if the liver iron concentration returned below 350 microM/g. At the start of treatment, ALT (R(2) = 0.64, P =.006) and AST activity (R(2) = 0.57, P =.01) were closely related to urinary iron excretion, reflecting the size of the chelatable or the labile iron pool. During treatment, a comparable pattern was seen and the urinary iron excretion was also directly related to the liver iron concentration at concentrations above approximately 400 microM/g. All elevated ALT values were associated with a urinary iron excretion more than 15 mg/24 h. In conclusion, our data suggest the existence of a critical liver iron concentration range, above which hepatocellular injury is seen. The extent of the injury seems to be determined mainly by the size of the chelatable or labile iron pool, supporting the concept of the labile iron pool as the compartment directly involved in iron toxicity. Our findings may be helpful in establishing criteria for safety from complications of transfusional iron overload.     

Procalcitonin versus C-reactive protein for predicting pneumonia in adults with lower respiratory tract infection in primary care

BACKGROUND: The role of procalcitonin in diagnosing bacterial infection has mainly been studied in patients with severe infections. There is no study on the value of procalcitonin measurements in adults with lower respiratory tract infection (LRTI) treated in primary care. AIM: To evaluate the accuracy of plasma procalcitonin in predicting radiographic pneumonia, bacterial infection, and adverse outcome in a population of adults with LRTI treated in primary care. DESIGN OF STUDY: Prospective, observational study. SETTING: Forty-two general practices and an outpatient clinic at the Department of Infectious Diseases, Odense University Hospital, Denmark. METHOD: A total of 364 patients with LRTI were prospectively enrolled from 42 general practices. Patients were examined with chest radiography, microbiological analyses, and measurements of C-reactive protein (CRP) and procalcitonin. The outcome measure was hospitalisation within 4 weeks of enrollment. RESULTS: Median procalcitonin was 0.05 ng/ml, which was below the functional sensitivity of the assay (0.06 ng/ml). In predicting radiographic pneumonia, bacterial infection, and hospitalisation, the sensitivities of procalcitonin >0.06 ng/ml were 0.70, 0.51, and 0.67, and of CRP were > or =20 mg/l, 0.73, 0.56, and 0.74 respectively. Corresponding positive predictive values were between 0.09 and 0.28. CONCLUSION: Both procalcitonin >0.06 ng/ml and CRP > or =20 mg/l were associated with radiographic pneumonia, bacterial infection, and subsequent hospitalisation, but positive predictive values were too low for any of the two inflammatory markers to be of use in clinical practice. To measure procalcitonin values accurately in the primary care setting, a more sensitive method is needed, but there was no indication that procalcitonin is superior to CRP in identifying patients with pneumonia, bacterial aetiology, or adverse outcome.     

A Model of the Ventilatory Depressant Potency of Remifentanil in the Non-steady State

Background: The C50 of remifentanil for ventilatory depression has been previously determined using inspired carbon dioxide and stimulated ventilation, which may not describe the clinically relevant situation in which ventilatory depression occurs in the absence of inspired carbon dioxide. The authors applied indirect effect modeling to non-steady state Paco2 data in the absence of inspired carbon dioxide during and after administration of remifentanil.

Methods: Ten volunteers underwent determination of carbon dioxide responsiveness using a rebreathing design, and a model was fit to the end-expiratory carbon dioxide and minute ventilation. Afterwards, the volunteers received remifentanil in a stepwise ascending pattern using a computer-controlled infusion pump until significant ventilatory depression occurred (end-tidal carbon dioxide [Peco2] > 65 mmHg and/or imminent apnea). Thereafter, the concentration was reduced to 1 ng/ml. Remifentanil pharmacokinetics and Paco2 were determined from frequent arterial blood samples. An indirect response model was used to describe the Paco2 time course as a function of remifentanil concentration.

Results: The time course of hypercarbia after administration of remifentanil was well described by the following pharmacodynamic parameters: F (gain of the carbon dioxide response), 4.30; ke0 carbon dioxide, 0.92 min-1; baseline Paco2, 42.4 mmHg; baseline minute ventilation, 7.06 l/min; kel,CO2, 0.08 min-1; C50 for ventilatory depression, 0.92 ng/ml; Hill coefficient, 1.25.     

Early onset of obsessive–compulsive disorder and associated comorbidity

Background: Previous studies have aimed to identify subtypes of obsessive–compulsive disorder (OCD) based on their age of onset (AOO). Obsessive–compulsive spectrum disorders (OCS disorders) such as tic disorders have been particularly associated with an early onset in some studies. However, subtypes of early‐ and late‐onset OCD are unevenly determined, and the biological and the clinical validity of these subtypes are unknown. This study was undertaken to discriminate the subtypes of OCD in different AOO levels and to test the hypothesis that different AOO bands are associated with a differential pattern of comorbidity. Methods: Two hundred fifty‐two patients with OCD were interviewed directly with the German version of the Schedule for Affective Disorders and Schizophrenia—Lifetime Anxiety Version, which provides DSM‐IV diagnosis. Subgroups with different ages of onset were investigated (cut‐off levels of 10, 15, and 18 years). Results: Subjects with an early AOO (onset ≤10 years) were significantly more likely to have OCS disorders (odds ratio [OR]=3.46; P =.001; 95% confidence interval [CI]: 1.72–6.96), in particular tic/Tourette's disorders (OR=4.63; P =.002; 95% CI: 1.78–12.05), than were late‐onset subjects. Conclusions: For most mental disorders (e.g., anxiety and mood disorders), no associations with AOO of OCD were identified. However, subjects in the early‐onset group (≤10 years) had a significant increase in comorbid tic and Tourette's disorders. Future research should examine potential neurobiological features associated with early‐onset presentations of OCD. Early detection and management of comorbidities may offset impairments later in life. Depression and Anxiety 26:1012–1017, 2009. © 2009 Wiley‐Liss, Inc.     

Alexithymia in obsessive-compulsive disorder - results from a family study

BACKGROUND: Previous studies have suggested an association between alexithymia and obsessive-compulsive disorder (OCD). However, it is unclear to which extent alexithymic traits in OCD patients reflect familial deficits in cognitively processing and communicating feelings that are also present in their first-degree relatives. This study investigates the hypotheses of an elevated level of alexithymia in subjects with OCD and their first-degree relatives compared to controls and their first-degree relatives. METHODS: 82 cases with OCD and 169 first-degree relatives were compared to 76 controls and 144 first-degree relatives from a German family study on OCD (GENOS). All subjects completed the 20-item Toronto Alexithymia Scale (TAS-20). Direct or family informant interviews were carried out with the German version of the Schedule for Affective Disorders and Schizophrenia - lifetime version for anxiety disorders (DSM-IV). RESULTS: OCD was associated with significantly higher scores of alexithymia. However, first-degree relatives of OCD cases and of controls did not differ in TAS-20 scores. In linear regression analyses, the TAS-20 total score showed significant intrafamilial associations within the families of control subjects but not within families of OCD cases. CONCLUSION: OCD is a severe mental disorder that is associated independently from other current comorbid axis I disorders with deficits in identifying and expressing feelings. However, alexithymia does not represent a familial risk factor for OCD.     

Silver-induced lipid peroxidation in mice: interactions with selenium and nickel

Lipid peroxidation in silver-treated mice was assayed by measuring the malondialdehyde (MDA) content of liver, kidney and brain tissue. After a single intraperitoneal injection of 20 mg/kg silver lactate, lipid peroxidation was significantly increased in the liver 3, 12 and 48 h after exposure whereas MDA levels in kidney and brain were not significantly affected. Pretreatment with 2 mg/kg sodium selenite i.p. for 2 days resulted in an increase in silver-induced lipid peroxidation in the liver. Liver from mice treated with 20 mg/kg silver lactate followed by an injection of 35 micrograms/kg nickel chloride had significantly higher contents of MDA than did livers from mice treated with either silver or nickel alone, suggesting a synergism between silver and other lipid peroxidation-inducing compounds.