Herz
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Hypoplastic left heart syndrome (HLHS) represents an anatomical spectrum of congenital disease with varying degrees of underdevelopment of the left-sided cardiac structures (Figure 1). The outlook for children born with HLHS, an otherwise highly lethal malformation, has improved with increasing experience with reconstructive techniques. This report represents a detailed analysis of the overall risk and mid-term results for a group of 39 consecutive neonates with HLHS referred to our hospital over a 5-year period between January 1994 and November 1998. ⋯ In 18 out of the 20 survivors neuro-developmental outcome and exercise performance were within the range of normals. Staged surgical palliation represents a realistic therapeutic option for neonates born with HLHS. At this intermediate stage of follow-up exercise performance and quality of life are satisfactory.
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Chest pain can arise from cardiovascular or noncardiovascular causes. Among the latter are the skin, the chest wall, intrathoracic structures, or subdiaphragmatic organs. The problem to attribute the chest discomfort to either the heart or extracardiac organs arises because the heart, pleura, aorta, and esophagus are all supplied by sensory fibers from the same spinal segments. ⋯ Diffuse esophageal spasm is the extracardiac condition that is confused most often with ischemic cardiac chest pain. This pain presents as a deep thoracic pain that may be present over most of the thorax. It may extend down the anterome
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Ebstein's anomaly is a complex malformation of the tricuspid valve where the hinges of the septal and/or posterior leaflets are displaced downward into the right ventricle. The leaflets show variable deformations. In general, the anterior leaflet is enlarged. ⋯ An analysis of the postoperative deaths revealed that all patients but one suffered from endstage cardiac disease and had a cardio-thoracic ratio greater than 0.65. This supports the importance of surgical intervention in time. In our opinion, operation is even indicated for those patients in functional Class II who reveal clinical deterioration.
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Radiofrequency catheter ablation is now considered as a curative approach in patients with typical atrial flutter. Typical atrial flutter is due to a macrore-entrant circuit within the right atrium and it can be eliminated by a linear lesion in the isthmus between the tricuspid annulus and the vena cava inferior. The electrophysiological criterion of a bidirectional isthmus block has been shown to reduce the recurrence rate of atrial flutter after catheter ablation, thus achieving long-term cure of typical atrial flutter. ⋯ While AV junction ablation and AV node modification can palliate some of the symptoms of atrial fibrillation by a control of ventricular rate, the arrhythmia persists with the loss of AV synchrony and continued risk of thromboembolism. The surgical MAZE procedure implies a compartimentation of the atria by surgical incisions resulting in areas to small to sustain the arrhythmia. Based on this procedure experimental and clinical studies are currently performed in order to develop catheter ablation cure of atrial fibrillation.
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The influence of Mg2+ and K+ on reoxygenation arrhythmias following 18 min of hypoxia (pO2 about 1 mm Hg, no glucose, 10 mmol/l2-desoxyglucose) has been investigated in isolated guinea-pig left atria (stimulation rate 1 Hz). Duration of reoxygenation arrhythmias was slightly reduced by increase in Mg2+ (0.6 to 4.8 mmol/l) and enhanced by decrease in Mg2+ (0.1 mmol/l), however, this effect was not significantly different from control (0.6 mmol/l). In contrast, low K+ (< 4 mmol/l) led to a significant (p < or = 0.05) prolongation and high K+ (> 5 mmol/l) to a significant abbreviation of reoxygenation arrhythmias. ⋯ Mg2+ (0.6 to 4.8 mmol/l) suppressed late afterdepolarizations and -contractions in K(+)-depolarized guinea-pig papillary muscles (27 mmol/l K+, 0.5 mmol/l Ba2+) induced by 2 x 10(-8) mol/l isoprenaline. The change in the triphasic contraction cycle by elevation of Mg2+ indicates that Mg2+ additionally increases stimulus-induced release of Ca2+ from the sarcoplasmic reticulum and reduces slow Ca2+ inward current. The described electrophysiological actions of the electrolytes represent mechanisms, which may explain their antiarrhythmic actions observed in clinical studies.