114 research outputs found

    Rivaroxaban 10mg/d in severe renal failure does not prevent ischemic events in premorbid neurologic disease

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    Backgrund The direct oral anticoagulants (DOAC) are increasingly used for primary and secondary stroke prophylaxis in atrial fibrillation, although their use in patients with renal failure is problematic. Case report In an 82-years old female with recurrent strokes and atrial fibrillation, the vitamin-K-antagonist was changed to rivaroxaban because of “unstable international normalized ratio (INR) values”. Because of renal failure with a creatinine clearance of 32ml/min, a dosage of rivaroxaban 10mg/d was chosen. Eleven days after initiation of rivaroxaban, she was re-hospitalized because of acute onset of right-sided weakness of the upper and lower limbs. Conclusions In cases of stroke, renal failure and inadequate anticoagulation it is not useful to change from vitamin-K-antagonists to “low dose” DOAC. Diligent investigations for the cause of INR-instability and continuation of vitamin-K-antagonist therapy seem to be more effective and safer since there is the opportunity of monitoring therapy and to avoid under- as well as over-dosage

    Delayed onset of Takotsubo syndrome after epileptic seizure

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    Diagnostic Problem of LV Hypertrabeculation/Noncompaction?

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    WATCHMAN for Stroke Prevention: An Out-of-Date Procedure

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    Recurrent venous thrombosis under rivaroxaban and carbamazepine for symptomatic epilepsy

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    Background The direct oral anticoagulant (DOAC) rivaroxaban, an oral Factor Xa inhibitor, is increasingly used as an alternative to vitamin-K-antagonists (VKAs). Absorption and elimination of DOACs are dependent on the permeability glycoprotein (P-gp) efflux transporter protein system, and DOACs are substrates of the hepatic cytochrome P 450 3A4 (CYP3A4) enzymes. Therefore, drug-interactions may occur when DOACs are administered with drugs affecting the activity of P-gp or CYP3A4 systems. Several antiepileptic drugs like carbamazepine are known to affect P-gp and CYP3A4-activity. Case report A 55-year-old male was admitted because of pain and swelling of his right leg spontaneously since 2 days. He was under a therapy with 20mg rivaroxaban since 4 months because of an unprovoked venous thrombosis of his right leg. He had a history of poliomyelitis at age 6 months, structural epilepsy due to poly-microgyria with complex partial seizures with secondary generalization since age 6 years, why he was treated with carbamazepine (900mg/d). He reported to be highly adherent to his anticoagulant and antiepileptic medication. Anti-Xa activity was <20ng/ml according to a rivaroxaban calibrated anti-factor Xa assay. Therapy with rivaroxaban was stopped, and low-molecular-weight heparin, followed by phenprocoumon, was started. Conclusion The combination of DOACs with carbamazepine, an inducer of P-gp and CYP3A4-activity, should be avoided since the anticoagulant effect is decreased. There is an urgent need to increase our knowledge and physicians’ awareness about the potential of drug–drug interactions of DOACs

    Presentation, therapy and outcome of patients with ischemic stroke under new oral anticoagulants

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    Background Aim was to describe the clinical spectrum, therapy, and outcome of ischemic strokes under therapy with new oral anticoagulants (NOAC). Methods and results A literature research was carried out in PubMed. Clinical trials as well as case reports were included. Four large trials comparing NOAC with warfarin reported 469 ischemic strokes but neither co-medication, nor comorbidities, location, clinical spectrum, therapy, nor outcome are reported. Eleven cases with ischemic strokes under dabigatran from the literature are reported. Six patients received thrombolytic therapy, in three of them unaware dabigatran therapy. Two patients received mechanical recanalization. Two patients died, one due to cerebral hemorrhage after thrombolysis, the other after partial recanalization of the basilar artery. Conclusions Little is known about ischemic strokes under NOAC. To increase the knowledge, the data of 469 ischemic strokes which occurred in NOAC-investigating trials should be analyzed. Furthermore ischemic and bleeding events under NOAC outside clinical trials should be reported. An international registry, independent from the pharmaceutical industry for collecting these informations is desirable

    Fatal consequences of climbing a ladder under apixaban and drunken

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    Background Apixaban, a factor-Xa-inhibitor, is one of the non-vitamin-K-antagonist oral anticoagulants (NOACs) which are increasingly used in atrial fibrillation (AF). In real life even patients with contraindications to vitamin K antagonists (VKAs) receive NOAC because NOAC are considered as “safer” than VKAs. Case description In a 61-years-old man with hypertension, heart failure and paroxysmal AF apixaban was started. Despite advices from his physicians, he continued alcohol abuse and suffered from recurrent falls. After 9 months he fell from a ladder and suffered from extensive subarachnoidal and intraparenchymal hemorrhages, subdural hematoma, brain edema with midline shift and a left-sided skull fracture. Because of the inability to reverse the anticoagulant therapy, no neurosurgical intervention was carried out and the patient died without regaining consciousness. Conclusions Patients with recurrent falls or chronic alcohol abuse should not be considered as candidates for NOACs. If anticoagulation is deemed necessary, VKA with its potential for prompt reversibility should be favored

    Tako-tsubo cardiomyopathy with transient global amnesia and cerebellar embolic stroke triggered by existential fear

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    Background Embolic stroke is a complication of Tako-Tsubo-cardiomyopathy (TTC), transient left ventricular dysfunction mimicking myocardial infarction without coronary culprit lesion explaining the whole left ventricular dysfunction. Transient global amnesia (TGA) is characterized by sudden onset of anterograde amnesia without compromise of other neurologic functions. Case report A 57 years old female was admitted because of sudden confusion and loss of her memory after emotional stress. TGA was diagnosed. Because of chest pain and laboratory tests indicating myocardial ischemia, she underwent coronary angiography which was normal. Within the following 24h her memory improved. She complained about severe vertigo and cerebral magnetic resonance imaging showed a recent ischemia in the left cerebellum. Conclusions TGA is not a disease for the neurologists exclusively but also cardiac comorbidities have to be considered and cardiologists should be involved in the acute care of these patients in order not to overlook life-threatening diseases
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