Elevation of left-sided diaphragm leading to myocardial infarction by compression of the left circumflex artery.

A previously healthy 46-year-old male presented to our emergency department with severe thoracic pain, dyspnea and vomiting, which had suddenly started 2 hours before. He had no history of unusual features and no cardiovascular risk factors. The 12-lead electrocardiogram indicated a posterolateral myocardial infarction. Immediate coronary catheterization revealed occlusion of the proximal left circumflex artery (LCX). Recanalization and coronary stent implantation were successful. No other coronary lesions were detectable that could have indicated coronary artery disease. During catheterization, superposed intestinal loops in the left thorax were striking. The chest X-ray revealed crass cranial displacement of the left-sided diaphragm with intestinal loops beneath, leading to compression of the ipsilateral lung and to a mediastinal shift to the right. Thoracic computed tomography showed compression by the elevated diaphragm of the posterior atrioventricular groove and the left circumflex (LCX) artery embedded in this. Clinical workup revealed no muscular disorder or central dysfunction responsible for diaphragm elevation; no reason for a phrenic nerve lesion was found. The patient subsequently developed ventilatory failure, necessitating intermittent noninvasive bilevel positive airway pressure. After 5 days of intermittent ventilation, the elevation of the diaphragm reduced noticeably and respiratory assistance could be stopped. The cause of this reversible unilateral diaphragm elevation remained unknown.

[Pharmacological lowering of portal pressure in normal rats and in experimental liver cirrhosis]. / Pharmakologische Pfortaderdrucksenkung bei der gesunden und experimentell leberzirrhotischen Ratte.

Four pharmacons were tested on an acute portal pressure lowering effect in an experimental animal model with 25 normal and 25 rats with Thioacetamide-toxic liver cirrhosis. Invasive measurements of arterial and portal pressure were made under Hexobarbital-Sodium anaesthesia during 30 minutes after pharmacon application. The portal pressure of cirrhotic rats was under basic conditions 9.5 +/- 1.5 mm Hg and significant higher as in normal animals (5.3 +/- 0.9 mm Hg, p less than 0.01). After 10 mg/kg body mass Propranolol the portal pressure decreased in both animal groups small but not significantly over the whole measurement time. 1 mg/kg Verapamil lowered arterial middle pressure significantly, but increased portal pressure at all 15-20% in both animal groups. Application of 0.1 mg/kg Prazosin decreased the arterial middle pressure at all 5-15% and the portal pressure at all 20-30% in both study groups (both significantly). For Canrenoat-Potassium (20 mg/kg) no clear effect could by evaluated on portal pressure. The model of Thioacetamide-toxic cirrhosis of the rat offers conditions like cirrhosis in human medicine in order to study the effects of portal pressure lowering pharmacons. Propranolol and Prazosin decrease portal pressure and should by further investigated.

[Noninvasive determination of viscoelastic properties of human finger arteries under various tonus conditions affecting vascular smooth muscle]. / Nichtinvasive Bestimmung der viskoelastischen Eigenschaften der Fingerarterien bei verschiedenen Tonuszuständen der glatten Gefässmuskulatur.

The amplitude of the volume pulse in relation to transmural pressure and the compliance as a viscoelastic property of the digital arteries were determined noninvasively in 9 male subjects (mean age 16 years). The amplitude of the volume pulse was measured impedance-plethysmographically and the amplitude of the pressure pulse sphygmomanometrically. The registration of the pulses was performed under different conditions (sitting-control), lying, 3-min forearm ischaemia, concentration-performance test, hyperventilation, 0.8 mg Nitrangin sublingual) to provoke different states of the vessel wall. The amplitude of the volume pulse under concentration-performance test (0.054 +/- 0.015 ml), hyperventilation (0.045 +/- 0.015 ml) and Nitrangin (0.142 +/- 0.034 ml) is significantly (p = 0.025) different from control (0.086 +/- 0.016 ml). The amplitude of the volume pulse and the compliance increase with decreasing transmural pressure.