A 74-year-old woman weighing 48 kg was admitted for a simple mastectomy 14 months after advanced carcinoma of the breast had been treated by radiotherapy. She was in good general health, her only complaint being dyspnoea on exertion. Examination showed a pansystolic murmur, which was attributed to mild mitral incompetence. Arterial pressure was 180/ 65 mm Hg. There was no evidence of cardiac failure, but an electrocardiogram contained some evidence of myocardial ischaemia. Haemoglobin was
1 Thirty patients on maintenance digoxin therapy and admitted for cardioversion of atrial fibrillation were closely monitored with regard to plasma levels of digoxin and quinidine. 2 Seventeen of these patients were kept on maintenance digoxin therapy. After an initial lag period of 6 to 18 h after the addition of quinidine their digoxin levels started to increase and had increased by between 20 and 330% after 3 days on quinidine. Side-effects attributed to the raised digoxin concentration occurred in 6 of these patients. 3 As studied in 5 of these 17 patients the renal clearance of digoxin decreased markedly when quinidine was added to the therapy. There was also a slight but significant reduction in creatinine clearance (n = 4). 4 In 13 patients digoxin was discontinued 36 h prior to the first quinidine dose. Also in these patients digoxin plasma levels increased significantly. 5 It is concluded that quinidine causes an unpredictably large increase in plasma digoxin and that this effect is probably at least initially to a large part due to a redistribution of digoxin in the body. The relative contributions of re-distribution and impaired renal clearance of digoxin to the increase in digoxin steady-state levels are presently unknown. 6 It is recommended that close monitoring of digoxin concentration and appropriate reduction of the maintenance dose is undertaken when quinidine is to be given to patients on digitalis therapy.
In a prospective study of quinidine syncope, 71 patients with atrial fibrillation/flutter were ECG monitored for four days after the start of quinidine therapy. Six patients developed ventricular tachycardia (VT) or ventricular fibrillation (VF) during the first 48 hours in sinus rhythm. Q-T prolongation was seen in most patients with and without VT/ VF and was non-predictive in this respect. However, a diastolic wave (DW) of larger amplitude than the preceding T wave and usually followed by a ventricular premature beat (VPB) appeared in five of the six VT/VF patients (13-185 min before the first event) and in none of the remaining 63 patients reaching sinus rhythm. For comparison, two of our own cases and nine from the literature with idiopathic long Q -T or alternating T wave syndromes were studied for these DW-VPBs. They were found in all ten cases with a VPB recording, but among 19 patients with acute myocardial infarction and VT/VF no such case was seen. As VT/VF was more common after large and VPB after small amplitude DWs, it is discussed whether the DW not only precedes but also initiates the ventricular tachyarrhythmias.
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