Letter: Prevention of "January blues".
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Biomedical subjects
Publications and source records attributed to D Hunt.
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The correlation of clinical features with the operative findings in 14 patients with a floppy mitral valve is discussed. The clinical course is typified by rapidly progressive disability. An abrupt deterioration was present in five of our subjects and this may be due to rupture of chordae tendinea or stretching of the valve apparatus. The redundancy of the anterior cusp in 13 of our series may explain the absence of mid systolic clicks in all except one patient. The diagnosis of prolapse can be difficult to make prior to surgery because the prolapsed cusp may be masked by the regurgitant contrast medium. Hypokinesis and prominent inflow sacculation of the left ventricular inflow tract suggest an associated myocardial abnormality. Calcium was present in one valve and thus mitral valve calcification does not exclude the possibility of a floppy valve in patients with mitral regurgitation.
Seventy-two patients with acute myocardial infarction complicated by atrioventricular or bundle-branch block or a combination of both had His bundle electrogram studies performed during their stay in the coronary care unit. In 19 of the 72 patients a repeat His bundle electrogram was performed before discharge from hospital. These studies demonstrated that 30 of the 32 patients with atrioventricular block and narrow QRS complexes had a block above the origin othe His spike (proximal block). Eleven patients in this group had repeat His bundle electrograms performed before discharge and in 3 patients there was evidence of residual atrioventricular nodal dysfunction. Both the hospital and follow-up mortality in this group was low and there was no evidence to suggest that permanent pacing would benefit these patients. Of the 18 patients with bundle-branch block and a normal PR interval, 9 had prolongation of the HV interval, but there was no difference in mortality in patients with normal or prolonged HV intervals. Twenty-two patients with bundle-branch block also developed atrioventricular block. In 5 of these patients the site of the AV block was proximal and in 14 it was distal, while 3 patients had both proximal and distal block. The hospital mortality in those patients who progressed to second- or third-degree atrioventricular block was considerably higher than in those patients who remained in first-degree atrioventricular block.
A case of Prinzmetal variant angina with transient complete atrioventricular block and syncopal episodes following an anteroseptal myocardial infarction is described. The syncopal attacks were not prevented by demand cardiac pacing and were presumably caused by transient severe ischaemia of the left ventricle, with a consequent reduction in cardiac output. The left ventriculogram showed a large anterior dyskinetic area corresponding to the high grade proximal obstruction in the left anterior descending artery demonstrated by coronary angiography. All other coronary vessels appeared free of disease and it is suggested that the anginal episodes were caused by transient proximal segmental spasm of the right coronary artery. The anginal episodes were successfully prevented by a regimen of two-hourly coronary arterial vasodilator therapy.
A case of complete absence of the pulmonary valve in association with a ventricular septal defect and a pulmonary artery coarctation is described. Despite these defects the patient had minimal symptoms, probably because the pulmonary artery coarctation acted as a natural banding and limited the pulmonary regurgitant flow and reduced the left-to-right shunt across the ventricular septal defect. The patient was operated on at the age of 40 and the ventricular septal defect was closed but the pulmonary artery coarctation was left alone. In view of the long-term survival in this case, it is suggested that pulmonary artery banding would reduce the symptoms and increase the life expectancy of patients with congenital absence of the pulmonary valve and a ventricular septal defect.
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Atrioventricular and intraventricular conduction were assessed in 4 patients with tricyclic antidepressant overdosage. The proximal or A-V nodal conduction (A-H) was normal, but 3 patients showed a drug-related increase in the QRS duration and His-Purkinje (H-V) conduction time. One patient with a normal H-V interval had a normal width QRS. The findings were independent of the heart rate and suggested a "quinidine-like effect" of the tricyclic drugs when ingested in suicidal doses. All 4 patients had normal intracardic conduction when restudied 8 days later. Procainamide and quinidine have similar effects on the intracardiac conduction and would appear undesirable in the treatment of cardiac arrhythmias in patients with tricyclic overdosage. Practolol in a dose of 20 mg by intravenous injection reduced the heart rate and caused a relative increase in the A-H interval but did not affect either the distal atrioventricular or intraventricular conduction. Although there was a slight drop in blood pressure, it may be a safer drug to use.
Intracardiac conduction studies using His bundle electrography (HBE) were performed in 14 patients admitted to hospital following an overdosage of one of the tricyclic antidepressant drugs and in another 12 patients before and during administration of therapeutic doses of nortriptylline. Amongst the former group, 7 of 8 patients showed impaired distal intracardiac conduction (H-V interval) following overdosages of nortriptyline, imipramine or amitriptyline but none of the 6 patients with doxepin overdosage. The prolonged H-V interval had returned to normal at a repeat study 7 days later. In the therapeutic dose study, 5 of 12 patients showed an increase in the H-V interval by more than 10 msec during treatment with nortriptyline. Four of these 5 patients had plasma nortriptyline levels of over 200 ng/ml. Tricyclic antidepressant drugs show a quinidine-like effect in toxic, and in some patients, in therapeutic doses. This finding may having a bearing on the treatment of cardiac arrhythmias in patients following overdosage with these drugs and may provide a clue to the reported increase in the incidence of sudden deaths in 'cardiac patients' following therapeutic doses of such agents.
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