1186
disopyramide or placebo in a randomised double-blind manner before therapy was started. During the trial, patients were excluded as treatment failures if they were noted by the nursing or medical staff to have heart block or arrhythmias requiring treatment. If the patients had any degree of cardiogenic shock they were also taken out of the study group-as possible complications of the therapy. of opinion whether the evidence presented in our report is "slender". Our experience with the use of disopyramide in the coronary-care unit’ suggested that this agent could prevent development of ventricular irritability after myocardial infarction and also seemed to affect the incidence of extension of myocardial infarction. When the drug was tested in clinical circumstances where cardiac monitoring was less than ideal, the difference between the active and placebo groups was even more apparent with regard to the development of myocardial irritability and extension of myocardial infarction. Indeed, the analysis of the 24 h tapes led us to suppose that, on the open ward, cardiac monitoring was far less than ideal and under no circumstances could be assumed even to approximate the monitoring within the coronary-care unit. It was also apparent to us that, under these circumstances, extension of myocardial infarction was associated with mortality. If there is any likelihood at all that development of myocardial irritability is in any way associated with extension of myocardial infarction, then it is important, we feel, to prevent arrhythmias. This is especially so when such a development is likely to be missed by the monitoring staff-for example, in the circumstances of the open ward. We therefore recommend the use of disopyramide in patients following infarction managed on the open ward. We are very well aware of the difficulties of assessing the efficacy of any intervention under these circumstances, and we wholeheartedly support the setting up of a multicentre trial looking specifically towards the prevention of extension of myocardial infarction and mortality by the prophylactic use of disopyramide. Such a trial is in preparation. We would like to acknowledge a regrettable oversight and apologise to the Guy’s poisons unit: without their help it would have been impossible to estimate the blood levels of disopyramide. D. J. S. CARMICHAEL It
must
be
a matter
Waller Cardio-pulmonary Unit, St Mary’s Hospital, London W2 1NY
E. M. M. BESTERMAN P. H. KIDNER
I have
a
further 4 patients in atrial fibrillation who do not take
digoxin. Does Dr Hull’s practice have a much larger proportion of fibrillators who do not receive digoxin? If so, perhaps many patients in atrial fibrillation could be taken off digoxin as well as those in sinus rhythm. Alton Health Alton, Hants
Centre,
H.
J. N. BETHELL
STROKES: A COMPLICATION OF MITRAL-LEAFLET PROLAPSE
SIR,—From the pathologist’s viewpoint the relationship
prolapse of the mitral valve and embolic disease is complex than either the paper by Dr Kostuk and his colleagues (Aug. 13, p. 313) or the subsequent correspondence (Oct. 27, p. 923) would suggest. Potentially embolic lesions are common with prolapsed mitral valves. Very careful naked-eye examination reveals thrombotic areas in about a third of cases. These appear as yellow, irregular, roughened areas on the atrial face of the abnormal part of the leaflet, as "jet" lesions on the opposite cusp or the base of atrial septum, and, as illustrated by Kostuk et al., as thrombi at the junction of abnormal cusp and related atrial wall.1,2 Histologically all these lesions show thrombus, usually superimposed on superficially damaged subendothelium, and abnormal valves with no naked-eye lesions will frequently show microscopic thrombi. In our experience of several hundred cases with prolapsing mitral valve, with and without atrial fibrillation, these thrombotic lesions are invariably small, unless infective endocarditis has developed. Although these thrombotic lesions might be responsible for retinal-artery occlusion or transient neurological symptoms it seems unlikely they could be a source of emboli large enough to cause serious strokes. Where the mitral-valve prolapse is between more
associated with atrial fibrillation the risk of cerebral embolism from this source is clear and, we suspect, no different from that in atrial fibrillation of ther causes. Harefield and Mount Vernon Pathology Laboratories, Mount Vernon Hospital, Northwood, Middlesex HA6 2RN
A. POMERANCE
Pathology Department, St. George’s Hospital Medical School, London
M. J. DAVIES
DISCONTINUATION OF MAINTENANCE DIGOXIN
SIR,—Ican confirm Dr Hull and Dr Mackintosh’s finding that, in general practice, maintenance digoxin therapy can be discontinued in most patients in sinus rhythm (Nov. 19, p.
1054). Over the past
18 months I have reviewed all the
patients in my practice who have taken long-term digoxin. In a practice of 3000 there were 44 patients on maintenance digoxin. 25 were in atrial fibrillation, 3 had paroxysmal atrial fibrillation, 1 had recurrent supraventricular tachycardia, and 15 were in sinus rhythm. Of the patients in sinus rhythm, 11 have been taken off digoxin with no ill-effects. 2 patients with intractable heart-failure were left on digoxin as was 1 old lady who was reluctant to stop her "heart tablets". 1 patient went into pulmonary oedema when the dose of digoxin was reduced. There were 2 deaths in the sinus-rhythm group, both in patients who continued with digoxin. It would seem prudent to tail off the dose of digoxin gradually rather than stop it suddenly. I was interested by the discrepancy in the number of patients in atrial fibrillation on digoxin therapy in the two practices. In Dr Hull’s practice, there were 7 ouf of 4630 (0.15%) and in my practice there were 25 out of 3000 (0.83%). 1.
Jennings, G., and others. Lancet, 1976, i, 51.
CARBAMAZEPINE IN RAYNAUD’S DISEASE SIR,—Raynaud’s disease is characterised by digital blanching which may be triggered by exposure to cold, by smoking, or by anxiety, or it may have no obvious cause. It must be distinguished from a variety of other peripheral vascular diseases. We have been treating with carbamazepine a 31-year-old woman with nocturnal complex partial seizures who also has migraine headaches and Raynaud’s disease. On carbamazepine, 300 mg a day (blood level 6-8 ug/ml) her symptoms of Raynaud’s disease have disappeared. She is not taking propranolol or ergot compounds and does not smoke. If this finding can be reproduced it may have interesting implications for the pathogenesis of this disorder. Many clinicians have noted an association between "nervous instability" and Raynaud’s disease. Psychiatric Institute and Clinic, University of Pittsburgh, Pittsburgh, Pennsylvania 15261, U.S.A. Western
JAMES R. MERIKANGAS RALPH AUCHENBACH
1. Pomerance, A. Br. Heart. J. 1969, 31, 343. 2. Pomerance, A., Davies, M. J. Pathology of the Heart.
Oxford, 1975.
disopyramide or placebo in a randomised double-blind manner before therapy was started. During the trial, patients were excluded as treatment failures if they were noted by the nursing or medical staff to have heart block or arrhythmias requiring treatment. If the patients had any degree of cardiogenic shock they were also taken out of the study group-as possible complications of the therapy. of opinion whether the evidence presented in our report is "slender". Our experience with the use of disopyramide in the coronary-care unit’ suggested that this agent could prevent development of ventricular irritability after myocardial infarction and also seemed to affect the incidence of extension of myocardial infarction. When the drug was tested in clinical circumstances where cardiac monitoring was less than ideal, the difference between the active and placebo groups was even more apparent with regard to the development of myocardial irritability and extension of myocardial infarction. Indeed, the analysis of the 24 h tapes led us to suppose that, on the open ward, cardiac monitoring was far less than ideal and under no circumstances could be assumed even to approximate the monitoring within the coronary-care unit. It was also apparent to us that, under these circumstances, extension of myocardial infarction was associated with mortality. If there is any likelihood at all that development of myocardial irritability is in any way associated with extension of myocardial infarction, then it is important, we feel, to prevent arrhythmias. This is especially so when such a development is likely to be missed by the monitoring staff-for example, in the circumstances of the open ward. We therefore recommend the use of disopyramide in patients following infarction managed on the open ward. We are very well aware of the difficulties of assessing the efficacy of any intervention under these circumstances, and we wholeheartedly support the setting up of a multicentre trial looking specifically towards the prevention of extension of myocardial infarction and mortality by the prophylactic use of disopyramide. Such a trial is in preparation. We would like to acknowledge a regrettable oversight and apologise to the Guy’s poisons unit: without their help it would have been impossible to estimate the blood levels of disopyramide. D. J. S. CARMICHAEL It
must
be
a matter
Waller Cardio-pulmonary Unit, St Mary’s Hospital, London W2 1NY
E. M. M. BESTERMAN P. H. KIDNER
I have
a
further 4 patients in atrial fibrillation who do not take
digoxin. Does Dr Hull’s practice have a much larger proportion of fibrillators who do not receive digoxin? If so, perhaps many patients in atrial fibrillation could be taken off digoxin as well as those in sinus rhythm. Alton Health Alton, Hants
Centre,
H.
J. N. BETHELL
STROKES: A COMPLICATION OF MITRAL-LEAFLET PROLAPSE
SIR,—From the pathologist’s viewpoint the relationship
prolapse of the mitral valve and embolic disease is complex than either the paper by Dr Kostuk and his colleagues (Aug. 13, p. 313) or the subsequent correspondence (Oct. 27, p. 923) would suggest. Potentially embolic lesions are common with prolapsed mitral valves. Very careful naked-eye examination reveals thrombotic areas in about a third of cases. These appear as yellow, irregular, roughened areas on the atrial face of the abnormal part of the leaflet, as "jet" lesions on the opposite cusp or the base of atrial septum, and, as illustrated by Kostuk et al., as thrombi at the junction of abnormal cusp and related atrial wall.1,2 Histologically all these lesions show thrombus, usually superimposed on superficially damaged subendothelium, and abnormal valves with no naked-eye lesions will frequently show microscopic thrombi. In our experience of several hundred cases with prolapsing mitral valve, with and without atrial fibrillation, these thrombotic lesions are invariably small, unless infective endocarditis has developed. Although these thrombotic lesions might be responsible for retinal-artery occlusion or transient neurological symptoms it seems unlikely they could be a source of emboli large enough to cause serious strokes. Where the mitral-valve prolapse is between more
associated with atrial fibrillation the risk of cerebral embolism from this source is clear and, we suspect, no different from that in atrial fibrillation of ther causes. Harefield and Mount Vernon Pathology Laboratories, Mount Vernon Hospital, Northwood, Middlesex HA6 2RN
A. POMERANCE
Pathology Department, St. George’s Hospital Medical School, London
M. J. DAVIES
DISCONTINUATION OF MAINTENANCE DIGOXIN
SIR,—Ican confirm Dr Hull and Dr Mackintosh’s finding that, in general practice, maintenance digoxin therapy can be discontinued in most patients in sinus rhythm (Nov. 19, p.
1054). Over the past
18 months I have reviewed all the
patients in my practice who have taken long-term digoxin. In a practice of 3000 there were 44 patients on maintenance digoxin. 25 were in atrial fibrillation, 3 had paroxysmal atrial fibrillation, 1 had recurrent supraventricular tachycardia, and 15 were in sinus rhythm. Of the patients in sinus rhythm, 11 have been taken off digoxin with no ill-effects. 2 patients with intractable heart-failure were left on digoxin as was 1 old lady who was reluctant to stop her "heart tablets". 1 patient went into pulmonary oedema when the dose of digoxin was reduced. There were 2 deaths in the sinus-rhythm group, both in patients who continued with digoxin. It would seem prudent to tail off the dose of digoxin gradually rather than stop it suddenly. I was interested by the discrepancy in the number of patients in atrial fibrillation on digoxin therapy in the two practices. In Dr Hull’s practice, there were 7 ouf of 4630 (0.15%) and in my practice there were 25 out of 3000 (0.83%). 1.
Jennings, G., and others. Lancet, 1976, i, 51.
CARBAMAZEPINE IN RAYNAUD’S DISEASE SIR,—Raynaud’s disease is characterised by digital blanching which may be triggered by exposure to cold, by smoking, or by anxiety, or it may have no obvious cause. It must be distinguished from a variety of other peripheral vascular diseases. We have been treating with carbamazepine a 31-year-old woman with nocturnal complex partial seizures who also has migraine headaches and Raynaud’s disease. On carbamazepine, 300 mg a day (blood level 6-8 ug/ml) her symptoms of Raynaud’s disease have disappeared. She is not taking propranolol or ergot compounds and does not smoke. If this finding can be reproduced it may have interesting implications for the pathogenesis of this disorder. Many clinicians have noted an association between "nervous instability" and Raynaud’s disease. Psychiatric Institute and Clinic, University of Pittsburgh, Pittsburgh, Pennsylvania 15261, U.S.A. Western
JAMES R. MERIKANGAS RALPH AUCHENBACH
1. Pomerance, A. Br. Heart. J. 1969, 31, 343. 2. Pomerance, A., Davies, M. J. Pathology of the Heart.
Oxford, 1975.
