Non-pharmacological therapy for recurrent tachycardia.
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Biomedical subjects
Publications and source records attributed to I W Obel.
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Seventeen patients with recurrent symptomatic arrhythmias were treated with oral disopyramide (DP). Fifteen of the 17 patients had received other currently conventional anti-arrhythmic therapy, to which only 1 patient responded, yet 13 of these 15 patients with resistant arrhythmias responded to DP. Electrophysiological studies were performed on 9 patients. The most impressive electrophysiological findings were the depressant effect of DP on ventricular automaticity and its action in slowing conduction through the His-Purkinje system (including the bundle branches) without depressing sino-atrial rate and atrioventricular (AV) nodal conduction time. Retrograde ventriculo-atrial (VA) conduction was markedly prolonged in 4 patients with reciprocating supraventricular tachycardia (SVT), including 2 patients with Wolff-Parkinson-White syndrome. All 4 patients with reciprocating SVT appear to be cured of their arrhythmia, probably by this mechanism.
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Circulation was supported by intra-aortic balloon counterpulsation for 30 and 38 days respectively in two patients with cardiogenic shock after acute myocardial infarction. One was flown 1400 km to Cape Town for heart transplantation but died after being weaned from the pump while awaiting a suitable donor. The other underwent successful surgical closure of a ruptured ventricular septum on the 30th day, allowing time for the edges of the ventricular septal defect to fibrose. Neither significant damage to circulating blood elements nor infection occurred, confirming the feasibility of prolonged circulatory support.
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In this article 2 cases of myocardial infarction with haemodynamically dominant right ventricular infarction are reported. The incidence and significance of the condition are discussed. The use of haemodynamic monitoring in diagnosis and management is stressed and the response to fluid therapy, either alone or together with inotropic drugs, is discussed.
The findings in four young patients with the billowing mitral leaflet syndrome who presented with evidence of acute myocardial infarction are reported. Because technically adequate coronary arteriograms demonstrated patent vessels and the electrocardiograms initially showed pronounced elevation of the ST segments as occurs in Prinzmetal's angina, it is postulated that spasm of normal coronary arteries was the operative factor. Scrutiny of those cases of clinically apparent ischemic heart disease with normal coronary angiograms is suggested to establish whether there is in fact a causal relationship with the billowing mitral leaflet syndrome.
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