Echocardiographic diagnosis, management and monitoring of pulmonary embolism with right heart thrombus in a patient with myotonic dystrophy: a case report

Acute pulmonary embolism (PE) is a common disease which frequently results in life-threatening right ventricular (RV) failure. High-risk PE, presenting with hypotension, shock, RV dysfunction or right heart thrombus is associated with a high mortality, particularly during the first few hours. Accordingly, it is important to commence effective therapy as soon as possible. In the case described in this report, a 49-year-old woman with myotonic dystrophy type 1 presented with acute respiratory failure and hypotension. Transthoracic echocardiography showed signs of right heart failure and a mobile right heart mass highly suspicious of a thrombus. Based on echocardiographic findings, acute thrombolysis was performed resulting in hemodynamic stabilization of the patient and complete resolution of the right heart thrombus. This case underscores the important role of transthoracic echocardiography for the diagnosis, management and monitoring of PE and underlines the efficacy and safety of thrombolysis in the treatment of PE associated with right heart thrombus

The role of the inducible nitric oxide synthase (iNOS) in infilrating leukocytes in a rodent model of cerebral ischemia

Die vorliegende Arbeit diente der Untersuchung der iNOS-Expression in einwandernden Leukozyten sowie ortständiger Mikroglia nach transienter zerebraler Ischämie. Der iNOS wird eine wichtige Rolle in der Vermittlung des späten ischämischen Schadens durch Produktion toxischer Mengen an NO zugeschrieben. Der Expressionsort des iNOS-Proteins ist jedoch bisher ungeklärt. Es gibt Hinweise darauf, dass während und nach dem ischämischen Ereignis einwandernde Leukozyten iNOS exprimieren und somit zu einer Vergrößerung des Infarkts führen. Jedoch ist auch eine Expression der iNOS in residenten Gliazellen beschrieben worden. Zur Beantwortung dieser Fragestellung wurde in der vorliegenden Arbeit ein GFP-Chimären-Modell verwendet, welches eine Unterscheidung zwischen einwandernden Zellen und residenter Glia zulässt. Durch die Transplantation von Knochenmark aus iNOS- defizienten (iNOS-/-) Mäusen in Wildtyp(wt)-Tiere und umgekehrt wurden Chimären geschaffen, die entweder nur in Zellen des peripheren Blutes oder nur in Zellen des ZNS iNOS exprimierten. Zwischen den vier untersuchten Transplantationsgruppen (wt→wt, iNOS-/-→iNOS-/-, iNOS-/-→wt, wt→iNOS-/-) war kein Unterschied in der Infarktgröße nach 45-minütiger transienter fokaler zerebraler Ischämie festzustellen. Es war keine Expression der iNOS in den Wildtyp-Mäusen und auch keine Protektion der drei verwendeten unterschiedlichen iNOS-Knock-out-Mäuse gegenüber ihren Wildtypen im verwendeten Modell der transienten Ischämie nachzuweisen. Nach den gewonnenen Daten muss die Rolle der iNOS nach zerebraler Ischämie kritisch betrachtet werden. Die Ergebnisse der vorliegenden Arbeit und die verschiedener anderer Studien weisen darauf hin, dass die iNOS nicht generell als Mediator der schadensvergrößernden Inflammationsreaktion nach zerebraler Ischämie zu sehen ist.The present study set out to examine the expression of iNOS in CNS- infiltrating leukocytes and resident micoglia after transient cerebral ischemia. iNOS is thought to play an important role in the mediation of late ischemic damage by producing toxic amounts of NO. Yet the site of iNOS expression is still unclear. It has been reported that infiltrating leukocytes express iNOS after cerebral ischemia and thereby can lead to enlargement of the infarcted area. However, an expression of iNOS has also been reported in resident microglia . In order to further clarify this discrepancy we used a rodent gfp-chimera which allows the differentiation of infiltrating cells from resident glia. By transplanting bone marrow from iNOS-deficient mice into wildtypes and vice versa chimera were generated that either expressed iNOS in peripheral blood cells or in resident CNS cells. No difference in infarct size could be detected between the four transplantation groups (wt→wt, iNOS-/-→iNOS-/-, iNOS-/-→wt, wt→iNOS-/-) after 45 min of transient focal cerebral ischemia. Based on this data the role of iNOS in the post-ischemic setting has to be reevaluated. The findings of this study suggest that iNOS may not be a general mediator of the inflammatory reaction after cerebral ischemia

Alcohol Use and Alcohol-Related Seizures in Patients With Epilepsy

Purpose: This study aimed to assess alcohol consumption and the occurrence of alcohol-related seizures in patients with epilepsy within the last 12 months.Methods: In an epilepsy outpatient clinic, a standardized questionnaire was used to collect data retrospectively from consecutive adult epilepsy patients who had been suffering from the disease for at least 1 year. Logistic regression analyses were performed to identify independent predictors.Results: A total of 310 patients with epilepsy were included. Of these, 204 subjects (65.8%) consumed alcohol within the last 12 months. Independent predictors for alcohol use were antiepileptic drug monotherapy (OR 1.901) and physicians' advice that a light alcohol intake is harmless (OR 4.102). Seizure worsening related to alcohol consumption was reported by 37 of the 204 patients (18.1%) who had used alcohol. All 37 subjects had consumed large quantities of alcohol prior to the occurrence of alcohol-related seizures regardless of their usual alcohol-drinking behavior. The amount of alcohol intake prior to alcohol-related seizures was at least 7 standard drinks, which is equivalent to 1.4 L of beer or 0.7 L of wine. In 95% of cases, alcohol-related seizures occurred within 12 h after cessation of alcohol intake. Independent predictors for alcohol-related seizures were generalized genetic epilepsy (OR 5.792) and chronic heavier alcohol use (OR 8.955).Conclusions: Two-thirds of interviewed subjects had consumed alcohol within the last 12 months. This finding may be an underestimate due to patients' self-reporting and recall error. In all cases, the occurrence of alcohol related-seizures was associated with timely consumption of considerably large amounts of alcohol. Thus, a responsible alcohol intake seems to be safe for most patients with epilepsy. However, subjects with epilepsy and especially those with generalized genetic epilepsy should be made aware of an increased risk for seizures related to heavy alcohol consumption. Factors accompanying acute heavy alcohol intake such as altered sleep architecture, impaired adherence to antiepileptic medication, and metabolic disturbances may further facilitate the occurrence of seizures

Data_Sheet_1_Alcohol Use and Alcohol-Related Seizures in Patients With Epilepsy.DOCX

<p>Purpose: This study aimed to assess alcohol consumption and the occurrence of alcohol-related seizures in patients with epilepsy within the last 12 months.</p><p>Methods: In an epilepsy outpatient clinic, a standardized questionnaire was used to collect data retrospectively from consecutive adult epilepsy patients who had been suffering from the disease for at least 1 year. Logistic regression analyses were performed to identify independent predictors.</p><p>Results: A total of 310 patients with epilepsy were included. Of these, 204 subjects (65.8%) consumed alcohol within the last 12 months. Independent predictors for alcohol use were antiepileptic drug monotherapy (OR 1.901) and physicians' advice that a light alcohol intake is harmless (OR 4.102). Seizure worsening related to alcohol consumption was reported by 37 of the 204 patients (18.1%) who had used alcohol. All 37 subjects had consumed large quantities of alcohol prior to the occurrence of alcohol-related seizures regardless of their usual alcohol-drinking behavior. The amount of alcohol intake prior to alcohol-related seizures was at least 7 standard drinks, which is equivalent to 1.4 L of beer or 0.7 L of wine. In 95% of cases, alcohol-related seizures occurred within 12 h after cessation of alcohol intake. Independent predictors for alcohol-related seizures were generalized genetic epilepsy (OR 5.792) and chronic heavier alcohol use (OR 8.955).</p><p>Conclusions: Two-thirds of interviewed subjects had consumed alcohol within the last 12 months. This finding may be an underestimate due to patients' self-reporting and recall error. In all cases, the occurrence of alcohol related-seizures was associated with timely consumption of considerably large amounts of alcohol. Thus, a responsible alcohol intake seems to be safe for most patients with epilepsy. However, subjects with epilepsy and especially those with generalized genetic epilepsy should be made aware of an increased risk for seizures related to heavy alcohol consumption. Factors accompanying acute heavy alcohol intake such as altered sleep architecture, impaired adherence to antiepileptic medication, and metabolic disturbances may further facilitate the occurrence of seizures.</p