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A patient is presented with a postpartum hepatic artery thrombosis in association with presumed fibromuscular hyperplasia. Massive hepatic infarction developed characterized clinically by fever, coma, ascites, ileus, jaundice, and renal failure; and biochemically by markedly elevated SGOT and SGPT, alkaline phosphatase, total bilirubin levels, and decreased thromboplastin time. The diagnosis was made in vivo by computed tomography (CT). Angiography revealed thrombotic occlusion of the hepatic artery in association with presumed fibromuscular hyperplasia. Laparoscopy and biopsy confirmed the diagnosis.

Exploration des spezifischen Reizleitungssystems des Herzens durch Aktivitätsableitung vom Hisschen Bündel Die heute routinemäßig angewendete klinische Elektrokardiographie ist nicht in der Lage, direkte Information iiber die Ausbreitung der elektrischen Aktivität im spezifischen Reizleitungssystem der Ventrikel zu liefern. Sogar bei Abnahme des Elektrogramms vom Epikard gelingt es nicht, Auskunft über die Impulsübermittlung während des PQ-Intervalls zu bekommen. Während des isoelektrischen Teils dieser Strecke erfolgt aber die Obermittlung der Erregung durch den Atrioventrikularknoten, das Hissche Bündel, die Schenkel und die Purkinje-Fasern (Abbildung 1). Giraud und Mitarbeitern (1) gelang es 1960 zum ersten Mal während der Herzkatheteruntersuchung eines Patienten mit Fallotscher Trilogie, elektrische Aktivität vom Hisschen Bündel abzuleiten. Watson und Mitarbeiter (2) beschrieben die gleiche biphasische Bewegung bei einem l4jährigen Mädchen mit Ebsteinscher Anomalie. Scherlag und Mitarbeiter (3) konnten bei Hunden die elektrische Aktivität vom Hisschen Bündel registrieren. Narula und Mitarbeiter (4) sowie Scherlag und Mitarbeiter (S) erhoben diese Methode zu einer Routineuntersuchung zur Exploration des spezifischen Reizleitungssystems des menschlichen Herzens.

Two patients with a history of paroxysmal supraventricular tachycardia were analysed by His bundle and intra-atrial recordings. The electrocardiogram showed sinus bradycardia in I patient and sinus bradycardia with sino-atrial Wenckebach in the other. The conduction times through the A V node and His Purkinje system were normal in both cases. The intra-atrial conduction time was slightly prolonged (55 msec) in one and normal (40 msec) in the other during normal sinus rhythm. In both cases with atrial pacing from high right atrium, the conduction time from the pacing impulse (PI) to atrial activation in the area of the A Vjunction (PI-A) progressively lengthened with increase in atrial pacing rate and finally classical second-degree Wenckebach type of block was manifested at cycle lengths of 460 and 465 msec. The pacing impulse to QRS interval (PI-R) showed a progressive increase before the blocked stimulus. The lengthening of the PI-R interval was due to progressive increase in the intra-atrial (PI-A) conduction time. In the dropped beats, thepacing impulse was notfollowed by an A deflection. This observation indicated Type I block within the atrium. Similarly, during induced premature atrial beats, the PI-A time progressively lengthened as the coupling interval was shortened. These findings were reproducible and were seen despite a fourfold increase in stimulus strength and changes in electrodes and site of stimulation along the lateral right atrial border. This study (I) shows second-degree Wenckebach block within the atrium; (2) supports the existence of sinoatrial Wenckebach; and (3) suggests the atrium as another possible site for re-entry and a cause for supraventricular tachycardia because of the degree of delay and block exhibited within the atrium.

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