Benefits of left atrial appendage occlusion for stroke prevention.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to Josef Finsterer.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
In a 48-year-old immunocompetent man with recurrent fever since 21 months, endocarditis of the native aortic valve due to Staphylococcus warneri was diagnosed. Twenty-six months before, a prosthetic lumbar disc had been implanted in L 4/5. The lack of typical other infectious sources favours the hypothesis of a disc-prosthesis-induced bacteraemia.
Explore the source record for details and available documents.
Tako-tsubo-like left ventricular dysfunction phenomenon (TTP) is characterized by transient left ventricular apical ballooning associated with symptoms, electrocardiographic changes and minimal cardiac enzyme release in the absence of coronary artery disease. Initially described in Japan, TTP occurs worldwide, predominantly in women and frequently after emotional or physical stress. Symptoms include anginal chest pain, dyspnea and syncope. Electrocardiographic ST elevations may be present only for several hours, and are followed by negative T waves that persist for months. Arterial hypertension is found in up to 76% of TTP patients, hyperlipidemia in up to 57% and diabetes mellitus in up to 12%. Potential pathophysiological mechanisms for TTP include catecholamine-induced myocardial stunning or hyperkinesis of the basal left ventricular segments, coronary vasospasm, plaque rupture, myocarditis and genetic factors. TTP patients should be monitored similarly to myocardial infarction patients because organ failure, cardiogenic shock, ventricular fibrillation or rupture may occur. Beta-blockers are indicated, whereas catecholamines and nitrates should be avoided. The long-term prognosis is unknown.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Diagnosing mitochondrial disorder remains a challenge. In a 75-year-old women, with short stature, muscle cramps, ptosis, fasciculations and progressive, proximal limb weakness and wasting, hyponatriemia, abnormal lactate-stress-test, and slightly abnormal electromyography, muscle biopsy suggested granulomatous myositis. Corticosteroids and azathioprin were ineffective. After a second work-up amyotrophic-lateral-sclerosis was diagnosed. Riluzole was started, without effect. She developed respiratory insufficiency, requiring mechanical ventilation. Apical ballooning was found. After switching to non-invasive positive pressure ventilation and physiotherapy, she markedly improved. After a third diagnostic work-up, mitochondrial disorder was suspected. Unfortunately, she died suddenly from a cardiac arrhythmia at home. Mitochondrial disorder may mimic motor neuron disease, muscle biopsy may mimic myositis, and may show only little evidence for respiratory chain disorder.
Explore the source record for details and available documents.
Although there are indications that beta-blockers affect the skeletal muscle in therapeutic dosages, their influence on mitochondrial disorders is unknown. A 52-year-old woman developed double vision, myalgias, muscle cramps, and hip and thigh muscle stiffness. Clinical neurologic examination revealed ptosis, dysarthria, sore neck muscles, weakness and wasting of the thighs, and generally brisk tendon reflexes. Lactate stress testing was significantly abnormal. Needle electromyography was nonspecifically abnormal and myopathic. Muscle biopsy showed mild myopathic changes, target fibers, and a single COX-negative fiber. Probable mitochondrial disorder was diagnosed. The patient had been on 30 mg of propranolol during 7 years for arterial hypertension. Shortly after discontinuation of the drug, her double vision gradually disappeared, myalgias and muscle cramps gradually resolved, and the patient reported an increase in muscle mass on repeated follow-ups. Long-term administration of propranolol may aggravate a mitochondrial disorder. Discontinuation of propranolol may result in a gradual resolution of these adverse reactions.
A 35-year-old Chinese woman presented with a 26-year history of persistent headache, relieved only by diuretics. Characteristic CT findings, peripheral eosinophilia, lymphocytic CSF pleocytosis, elevated CSF IgG, positive oligoclonal bands, antibody-positive ELISA, and Western blot results with Taenia solium antigen, and a favorable response to albendazole led to the diagnosis of neurocysticercosis.
OBJECTIVES: Creutzfeldt-Jakob disease (CJD) is not only a disorder of the central nervous system but also affects the skeletal muscle. Subclinical skeletal muscle involvement, manifesting as hyper-creatine-kinase (CK)-emia, is rare. CASE REPORT: The patient, a 60-year-old male, developed progressive dementia, accompanied by dysphagia and bursts of aggression, disorientation and optic hallucinations. Five months after onset of the cognitive decline, hyper-CK-emia of 117 U/l (normal: <81 U/l) was noted for the first time. During 12 months until decease, hyper-CK-emia was permanently present and reached a maximum of 354 U/l. Hyper-CK-emia was attributed to subclinical involvement of the skeletal muscle in CJD. Hyper-CK-emia due to progressive brain damage, double trouble of an additional primary myopathy or due to excessive myoclonic jerking was excluded. CONCLUSIONS: This case shows that CJD may be present with mild hyper-CK-emia in individual patients, most likely due to concomitant undiagnosed involvement of the skeletal muscle in the primary disease.
Ebstein's malformation (EM) is characterized by dysplasia and displacement of the tricuspid inferior and septal leaflets from the true atrioventricular (AV) junction. Left ventricular hypertrabeculation/non-compaction (LVHT) including the 'atrialized' portion in EM has not been described. A 42-year-old man with a history of radiofrequency ablation of a Mahaim-like bundle suffered from chest pain. Coronary angiography was normal, but echocardiography showed a septal tricuspid leaflet inserting 3.5-cm apically beyond the AV junction, deep recesses of the atrialized interventricular septum, and a heavily trabeculated left ventricle; these were confirmed by cardiac magnetic resonance imaging. Neurologically, hypoacusis, positive pyramidal signs, postural tremor and brisk tendon reflexes were identified.