1481
monitoring aminoglycoside toxicity. We think that most evidence points to duration of exposure and therefore that trough concentration is more important.1,2 We agree that individualised dosage regimens are always better, as we repeatedly emphasise in our
report.
We agree with Rensma et al that our unqualified statement about the simplified equation described by Cockroft and Gault (CC-D) can be easily misinterpreted because many patients needing aminoglycosides may have weights of under 60 or over 90 kg. Khare comments on the limitations of estimated CLcr, which we also noted in our discussion. He implies that our statement "aminoglycosides and vancomycin are almost totally eliminated by the kidney" is a presumption; we believe this to be a fact. Nor did we imply that non-renal clearance is never affected by renal insufficiency. If non-renal clearance is abnormal, that too should be considered in the equation. We agree with Khare’s points about severe renal dysfunction and about children. Calculation of CLcr in children needs correction for weight and height, and we do not recommend the use of DREM in children.
development or trial. There is little reason to think that they would meningococcal meningitis, in which they would be unlikely to cross the blood-brain barrier in substantial amounts. Confusion between meningitis and septicaemia has arisen firstly since both were thought historically to be the same illnesscerebrospinal fever-and secondly, since septicaemia and meningitis may commonly co-exist in the same patient. It is thus clear that meningococcal septicaemia and meningococcal meningitis are very different diseases; with the rapid advances in understanding of the pathophysiology of severe infections, and consequent development of new therapeutic approaches, real dilemmas in clinical management have arisen; these can only be addressed if the two conditions are clearly be of value in
-
1. Gilbert DN. Once-daily aminoglycoside therapy. Antimicrob Agents Chemother 1991; 35: 399-405. 2. Levison ME. New dosing regimens for aminoglycoside antibiotics. Ann Intern Med 1992; 117: 693-94. 3. Brook I, Craig WA, Drusano GL, et al. Continuous vs. intermittent infusion of beta-lactam antibiotics: a potential advance (Proceedings from a roundtable. Moellering RC, moderator). Infect Med 1992; 9B: 6-32.
differentiated and defined. A check of the 1991 Index Medicus under the heading meningococcal meningitis shows that about 70 % of articles actually deal with meningococcal septicaemia. Current terms used for epidemiology and data collection may thus be insufficiently precise for our changing ideas about pathophysiology and management; we need to differentiate clearly between those patients with meningitis alone, with a fairly good outlook, and those with septicaemia, with or without meningitis, in whom the outlook is poorer and management needs to be very different. Only meningococcal meningitis is a notifiable disease in the UK. This leads to a falsely high case-fatality ratio being cited because almost all deaths attributed to meningococcal meningitis are in fact due to meningococcal septicaemia. The presence of a purpuric rash could be regarded as evidence of systemic meningococcal illness and might be used as the primary feature differentiating septicaemia from meningitis. When both conditions co-exist this should be noted but the illness should be classified as "septicaemia"-as the more serious of the two ilnesses. Only when the two illnesses are perceived as different will we be able to understand each as a separate entity and to advance our understanding of them further.
Meningococcal meningitis septicaemia: plea for diagnostic clarity
Department of Paediatric Infectious Disease, University of Birmingham, East Birmingham Hospital, Birmingham B9 5ST, UK
Medical Research Laboratory, Antibiotic Management Program and Infectious Diseases Division, Department of Medicine and Drug Information Center,
Department of Pharmacy Services, Hospital, Hartford, Connecticut 06115, USA, Hartford
E. G. MADERAZO H. SUN G. T. JAY
and University of Connecticut Schools of Medicine and Pharmacy, Farmington and Storrs, Connecticut
or
a
SiR,—The term meningococcal meningitis is widely used both by lay individuals and by some health professionals to include both meningococcal meningitis and meningococcal septicaemia. This imprecision may not have mattered unduly in the past, but is causing increasing confusion as advances in pathophysiology and clinical management clearly separate them into different diseases. Meningococcal meningitis is a central nervous system infection with characteristic changes in the cerebrospinal fluid. In true meningococcal meningitis pathological changes are localised to the central nervous system and the mortality is 5% or less.1 Management is that of a bacterial infection of the central nervous system. Antibiotics are the mainstay of treatment. Fits can arise and associated cerebral oedema may lead to brain damage or death. Sensorineural deafness associated with cochlear inflammation is
a
major sequel. Adjunct therapy with steroids may be of value in shortening the course of the illness and improving prognosis.2 Meningococcal septicaemia, on the other hand, is a severe systemic illness in which the organism is disseminated throughout the body. Mortality is 15% or more, rising to over 80% in patients with severe shock.3 It is associated with the release into the circulation of endotoxin from the cell wall of Neisseria meningitidis; this initiates the release of large amounts of host cytokines, and leads to the clinical picture of gram-negative septic shock. Cytokine concentrations in the circulation in meningococcal septicaemia are many times higher than in most other types of gram-negative septic shock and the disease may progress very rapidly. Meningococcal septicaemia is not especially linked with the development of deafness, but unlike meningococcal meningitis, survivors often have severe vasculitic complications that may lead to the need for skin grafts or even the amputation of limbs. There is little evidence that steroids have a part to play in meningococcal septicaemia; indeed data for other forms of septic shock suggest that they may even worsen the prognosis. Systemic anti-endotoxin antibody is under trial in meningococcal septicaemia; other types of systemic immunotherapy are under
MICHAEL J. TARLOW ALASDAIR M. GEDDES
1. Anonymous. Defences against meningococcal infections. Lancet 1985; ii: 929-30. 2. Lebel MH, Freij BJ, Syrogiannopoulos GA, et al. Dexamethasone therapy for bacterial meningitis. N Engl J Med 1989; 319: 964-71. 3. Gedde-Dahl TW, Bjark P, Hølby A, Host JH, Bruun JN. Severity of meningococcal disease: assessment by factors and scores and implications for patient management. Rev Infect Dis 1990; 12: 973-92.
How accurate is death certification of
multiple system atrophy? SiR,—1 in 4 patients with, at death, a diagnosis of idiopathic Parkinson’s disease do not have that condition,1,2 and the misdiagnosis rate earlier in the clinical course may approach 1 in 3. The commonest cause of erroneous diagnosis in life is probably multiple system atrophy (MSA).2,3 The proportion of MSA cases in parkinsonian brain banks varies from 5 to 22% (mean 8%). This frequency indicates a prevalence of 13 per 100 000, which would make MSA more common than, for example, Huntington’s disease. However, such "necroepidemiology" is subject to bias. Thus, the shorter life expectancy of MSA relative to that of Parkinson’s disease patients and the tendency for cases of atypical parkinsonism to be preferentially "recruited" into brain banks could inflate the frequency of MSA. The population prevalence of MSA has not been studied, but might a survey of death certification indicate its
frequency? We therefore examined the accuracy of death certification in MSA in two ways. First, we traced the death certificates of 36 patients diagnosed in life as MSA. 6 (17%) had a diagnosis of Parkinson’s disease alone on their death certificate; 4 of them had MSA confirmed by necropsy. In the other 30, MSA was mentioned in 15, Shy-Drager syndrome (SDS) in 5, both in 1, and striatonigral degeneration in 1 (table). Second, we looked at the death certificates of 30 cases of pathologically proven MSA (including 19 of the above cases). 4 of these 19 diagnosed as MSA in life nevertheless had only Parkinson’s disease on their death certificate. The remaining 11 had all continued to carry an erroneous clinical diagnosis of Parkinson’s
1482
DEATH CERTIFICATE DIAGNOSES IN PATIENTS DIAGNOSED IN LIFE OR PATHOLOGICALLY DIAGNOSED AS MSA
three-vessel coronary artery disease, with a Y-shaped "trouser" graft to left anterior descending and left circumflex arteries, and a single-vein graft to the right coronary artery. She remained symptom free for 3 years after surgery, but presented to us with recurrent angina. Fasting lipids were normal, and anti-neutrophil antibodies, a marker of disease activity in Kawasaki disease, were not present. Coronary angiography showed diffusely diseased native coronary arteries, with multiple severe strictures, and a tight stenosis at the origin of the trouser graft. The right coronary artery graft was normal. The left internal mammary artery was also diffusely diseased, and was completely occluded about 5 cm from its origin. Left ventricular function was normal (ejection fraction 75%). Balloon angioplasty and insertion of a Medinvent self-
G.K.W. is supported by a grant from the UK Parkinson’s Disease Society. We thank the Office of Population Censuses & Surveys for providing death certificates.
expanding coronary stent at the site of the ostial stenosis were undertaken. There were no complications after stent implantation, and the patient was discharged 2 days after the procedure. At the 6-week follow-up she could exercise for 12 min of the standard Bruce protocol without chest pain or electrocardiographic changes. She remains symptom free 2 years after stent implantation. It is now well recognised, in the treatment of atheromatous coronary disease, that the benefit of coronary revascularisation with saphenous vein bypass grafts is short-lived. The 18-year follow-up data from the Veterans Affairs Cooperative Study of Coronary Artery Bypass Surgery for Stable Angina’ showed convergence of the two groups (medical therapy versus bypass surgery) with respect to symptoms, rate of myocardial infarction, and survival after 5 years. After Iyears there was no longer any obvious benefit from surgery. These results seem to be related to accelerated graft closure after 5 years (cumulative graft patency rates of 71%, 64%, and 50% at 1,5, and 10 years, respectively). Evidence of improved graft survival and symptomatic outcome after the use of arterial bypass conduits is accumulating,2 and increasing numbers of coronary surgical procedures involve the use of at least one arterial bypass graft (usually the left internal mammary artery to the anterior descending coronary artery). In our patient, the left internal mammary artery seemed to have been affected by the same arteritic process as the coronary arteries, rendering it useless for coronary revascularisation. The decision to implant a stent in the ostium of her coronary vein graft was based on evidence that restenosis rates after balloon angioplasty of this site may be as high as 60%.3 There are, as yet, no long-term data on outcome after stent implantation in coronary vein grafts, but we have shown a restenosis rate of 11%, during a mean follow-up of II months, in 66 venous bypass grafts treated with self-expanding stents.4 This case illustrates the difficulties that the cardiologist may face in treating adult patients with the coronary artery sequelae of childhood Kawasaki disease.
University Department of Clinical Neurology, and Parkinson’s Disease Society Brain Bank, National Hospital,
Department of Cardiology, St Thomas’ Hospital, London SE1 7EH, UK
disease during life, which appeared on their death certificate (table). Thus in 17% of patients diagnosed as MSA in life, and in 50% of pathologically proven cases, the death certificate mentioned only Parkinson’s disease. These findings indicate that, in the UK, death certificates are an unreliable instrument for assessing the epidemiology of MSA, and that a clinical diagnosis of MSA is considerably more reliable than one of Parkinson’s disease. MSA3 encompasses many patients who are still otherwise classified under the 9th revision of the Application of the International Classification of Diseases to Neurology (ICD-NA)4 as
SDS (333.02), strionigral degeneration (333.03), olivopontocerebellar degeneration (333.04), or under other degenerative diseases of the basal ganglia (333.0), or "other" (333.08). Since MSA does not feature in ICD-NA, purists might suggest that the term should not be used on death certificates. However, official recognition of terms must inevitably follow common usage. After 23 years, we propose that the inclusion of MSA in ICD is long overdue.
London WC1 N 3BG, UK
GREGOR K. WENNING NIALL P. QUINN SUSAN E. DANIEL
J. T. STEWART
of Medicine and
Hughes AJ, Daniel SE, Kilford L, Lees AJ. Accuracy of clinical diagnosis of idiopathic Parkinson’s disease: a clinico-pathological study of 100 cases J Neurol Neurosurg Psychiatry 1992; 55: 181-84. 2. Rajput AH, Rozdilsky B, Rajput A. Accuracy of clinical diagnosis in parkinsonism: a prospective study. Can J Neurol Sci 1991; 18: 275-78. 3. Graham JG, Oppenheimer DR. Orthostatic hypotension and nicotine sensitivity in a case of multiple system atrophy. J Neurol Neurosurg Psychiatry 1969; 32: 28-34. 4. Application of the International Classification of Diseases to Neurology (ICD-NA, ninth revision). Geneva: WHO, 1987. 1.
Adult coronary artery disease secondary to childhood Kawasaki disease SIR,-Professor Kato and colleagues (Nov 7, p 1127) make no mention of the longer term problems that may be faced by patients with Kawasaki disease, even after coronary artery surgery. We have treated a 27-year-old Japanese woman with an 18-month history of progressive angina on effort. Exercise testing showed diagnostic ST segment depression in leads V4-6 at stage 3, and was stopped because of angina pectoris. Kawasaki disease had been diagnosed at age 12 in Japan but she had received no specific therapy. Angina pectoris had developed at age 17, and at 22 she underwent saphenous vein coronary artery bypass surgery for
Western
Department Therapeutics, Infirmary, Glasgow
A.
Department of Invasive Cardiology, Royal Brompton National Heart and Lung Hosptal,
L. DENNE U. SIGWART A. F. RICKARDS
London SW3
JAMIESON
1. The Veterans Affairs Coronary Bypass Surgery Cooperative Study Group. Eighteenyear-follow-up in the Veterans Affairs cooperative study of coronary artery bypass surgery for stable angina. Circulation 1992; 86: 121-30. 2. Loop FD, Lytle BW, Cosgrove DM, Stewart RW. Influence of the internalmammary-graft on 10-year survival and other cardiac events. N Engl J Med 1986; 314: 1-6. 3. Webb JG, Myler RK, Shaw RE, et al. Coronary angioplasty after coronary bypass surgery: initial results and late outcome in 422 patients. J Am Coil Cardiol 1990; 16: 812-20. 4. Stewart JT, Williams MG, Goy J-J, et al. Self-expanding stents for diseased saphenous vein coronary artery bypass grafts. Br Heart J 1992; 68: 153.
CORRECTION Effects of dual-chamber pacing with short atrioventricular delay in dilated cardiomyopathy. -An error appeared in table u of this article by Dr S. J. D. Brecker and colleagues (Nov 28, p 1308): under Longest AV interval, the RVFT for patient 12 should have been 160 ms.
monitoring aminoglycoside toxicity. We think that most evidence points to duration of exposure and therefore that trough concentration is more important.1,2 We agree that individualised dosage regimens are always better, as we repeatedly emphasise in our
report.
We agree with Rensma et al that our unqualified statement about the simplified equation described by Cockroft and Gault (CC-D) can be easily misinterpreted because many patients needing aminoglycosides may have weights of under 60 or over 90 kg. Khare comments on the limitations of estimated CLcr, which we also noted in our discussion. He implies that our statement "aminoglycosides and vancomycin are almost totally eliminated by the kidney" is a presumption; we believe this to be a fact. Nor did we imply that non-renal clearance is never affected by renal insufficiency. If non-renal clearance is abnormal, that too should be considered in the equation. We agree with Khare’s points about severe renal dysfunction and about children. Calculation of CLcr in children needs correction for weight and height, and we do not recommend the use of DREM in children.
development or trial. There is little reason to think that they would meningococcal meningitis, in which they would be unlikely to cross the blood-brain barrier in substantial amounts. Confusion between meningitis and septicaemia has arisen firstly since both were thought historically to be the same illnesscerebrospinal fever-and secondly, since septicaemia and meningitis may commonly co-exist in the same patient. It is thus clear that meningococcal septicaemia and meningococcal meningitis are very different diseases; with the rapid advances in understanding of the pathophysiology of severe infections, and consequent development of new therapeutic approaches, real dilemmas in clinical management have arisen; these can only be addressed if the two conditions are clearly be of value in
-
1. Gilbert DN. Once-daily aminoglycoside therapy. Antimicrob Agents Chemother 1991; 35: 399-405. 2. Levison ME. New dosing regimens for aminoglycoside antibiotics. Ann Intern Med 1992; 117: 693-94. 3. Brook I, Craig WA, Drusano GL, et al. Continuous vs. intermittent infusion of beta-lactam antibiotics: a potential advance (Proceedings from a roundtable. Moellering RC, moderator). Infect Med 1992; 9B: 6-32.
differentiated and defined. A check of the 1991 Index Medicus under the heading meningococcal meningitis shows that about 70 % of articles actually deal with meningococcal septicaemia. Current terms used for epidemiology and data collection may thus be insufficiently precise for our changing ideas about pathophysiology and management; we need to differentiate clearly between those patients with meningitis alone, with a fairly good outlook, and those with septicaemia, with or without meningitis, in whom the outlook is poorer and management needs to be very different. Only meningococcal meningitis is a notifiable disease in the UK. This leads to a falsely high case-fatality ratio being cited because almost all deaths attributed to meningococcal meningitis are in fact due to meningococcal septicaemia. The presence of a purpuric rash could be regarded as evidence of systemic meningococcal illness and might be used as the primary feature differentiating septicaemia from meningitis. When both conditions co-exist this should be noted but the illness should be classified as "septicaemia"-as the more serious of the two ilnesses. Only when the two illnesses are perceived as different will we be able to understand each as a separate entity and to advance our understanding of them further.
Meningococcal meningitis septicaemia: plea for diagnostic clarity
Department of Paediatric Infectious Disease, University of Birmingham, East Birmingham Hospital, Birmingham B9 5ST, UK
Medical Research Laboratory, Antibiotic Management Program and Infectious Diseases Division, Department of Medicine and Drug Information Center,
Department of Pharmacy Services, Hospital, Hartford, Connecticut 06115, USA, Hartford
E. G. MADERAZO H. SUN G. T. JAY
and University of Connecticut Schools of Medicine and Pharmacy, Farmington and Storrs, Connecticut
or
a
SiR,—The term meningococcal meningitis is widely used both by lay individuals and by some health professionals to include both meningococcal meningitis and meningococcal septicaemia. This imprecision may not have mattered unduly in the past, but is causing increasing confusion as advances in pathophysiology and clinical management clearly separate them into different diseases. Meningococcal meningitis is a central nervous system infection with characteristic changes in the cerebrospinal fluid. In true meningococcal meningitis pathological changes are localised to the central nervous system and the mortality is 5% or less.1 Management is that of a bacterial infection of the central nervous system. Antibiotics are the mainstay of treatment. Fits can arise and associated cerebral oedema may lead to brain damage or death. Sensorineural deafness associated with cochlear inflammation is
a
major sequel. Adjunct therapy with steroids may be of value in shortening the course of the illness and improving prognosis.2 Meningococcal septicaemia, on the other hand, is a severe systemic illness in which the organism is disseminated throughout the body. Mortality is 15% or more, rising to over 80% in patients with severe shock.3 It is associated with the release into the circulation of endotoxin from the cell wall of Neisseria meningitidis; this initiates the release of large amounts of host cytokines, and leads to the clinical picture of gram-negative septic shock. Cytokine concentrations in the circulation in meningococcal septicaemia are many times higher than in most other types of gram-negative septic shock and the disease may progress very rapidly. Meningococcal septicaemia is not especially linked with the development of deafness, but unlike meningococcal meningitis, survivors often have severe vasculitic complications that may lead to the need for skin grafts or even the amputation of limbs. There is little evidence that steroids have a part to play in meningococcal septicaemia; indeed data for other forms of septic shock suggest that they may even worsen the prognosis. Systemic anti-endotoxin antibody is under trial in meningococcal septicaemia; other types of systemic immunotherapy are under
MICHAEL J. TARLOW ALASDAIR M. GEDDES
1. Anonymous. Defences against meningococcal infections. Lancet 1985; ii: 929-30. 2. Lebel MH, Freij BJ, Syrogiannopoulos GA, et al. Dexamethasone therapy for bacterial meningitis. N Engl J Med 1989; 319: 964-71. 3. Gedde-Dahl TW, Bjark P, Hølby A, Host JH, Bruun JN. Severity of meningococcal disease: assessment by factors and scores and implications for patient management. Rev Infect Dis 1990; 12: 973-92.
How accurate is death certification of
multiple system atrophy? SiR,—1 in 4 patients with, at death, a diagnosis of idiopathic Parkinson’s disease do not have that condition,1,2 and the misdiagnosis rate earlier in the clinical course may approach 1 in 3. The commonest cause of erroneous diagnosis in life is probably multiple system atrophy (MSA).2,3 The proportion of MSA cases in parkinsonian brain banks varies from 5 to 22% (mean 8%). This frequency indicates a prevalence of 13 per 100 000, which would make MSA more common than, for example, Huntington’s disease. However, such "necroepidemiology" is subject to bias. Thus, the shorter life expectancy of MSA relative to that of Parkinson’s disease patients and the tendency for cases of atypical parkinsonism to be preferentially "recruited" into brain banks could inflate the frequency of MSA. The population prevalence of MSA has not been studied, but might a survey of death certification indicate its
frequency? We therefore examined the accuracy of death certification in MSA in two ways. First, we traced the death certificates of 36 patients diagnosed in life as MSA. 6 (17%) had a diagnosis of Parkinson’s disease alone on their death certificate; 4 of them had MSA confirmed by necropsy. In the other 30, MSA was mentioned in 15, Shy-Drager syndrome (SDS) in 5, both in 1, and striatonigral degeneration in 1 (table). Second, we looked at the death certificates of 30 cases of pathologically proven MSA (including 19 of the above cases). 4 of these 19 diagnosed as MSA in life nevertheless had only Parkinson’s disease on their death certificate. The remaining 11 had all continued to carry an erroneous clinical diagnosis of Parkinson’s
1482
DEATH CERTIFICATE DIAGNOSES IN PATIENTS DIAGNOSED IN LIFE OR PATHOLOGICALLY DIAGNOSED AS MSA
three-vessel coronary artery disease, with a Y-shaped "trouser" graft to left anterior descending and left circumflex arteries, and a single-vein graft to the right coronary artery. She remained symptom free for 3 years after surgery, but presented to us with recurrent angina. Fasting lipids were normal, and anti-neutrophil antibodies, a marker of disease activity in Kawasaki disease, were not present. Coronary angiography showed diffusely diseased native coronary arteries, with multiple severe strictures, and a tight stenosis at the origin of the trouser graft. The right coronary artery graft was normal. The left internal mammary artery was also diffusely diseased, and was completely occluded about 5 cm from its origin. Left ventricular function was normal (ejection fraction 75%). Balloon angioplasty and insertion of a Medinvent self-
G.K.W. is supported by a grant from the UK Parkinson’s Disease Society. We thank the Office of Population Censuses & Surveys for providing death certificates.
expanding coronary stent at the site of the ostial stenosis were undertaken. There were no complications after stent implantation, and the patient was discharged 2 days after the procedure. At the 6-week follow-up she could exercise for 12 min of the standard Bruce protocol without chest pain or electrocardiographic changes. She remains symptom free 2 years after stent implantation. It is now well recognised, in the treatment of atheromatous coronary disease, that the benefit of coronary revascularisation with saphenous vein bypass grafts is short-lived. The 18-year follow-up data from the Veterans Affairs Cooperative Study of Coronary Artery Bypass Surgery for Stable Angina’ showed convergence of the two groups (medical therapy versus bypass surgery) with respect to symptoms, rate of myocardial infarction, and survival after 5 years. After Iyears there was no longer any obvious benefit from surgery. These results seem to be related to accelerated graft closure after 5 years (cumulative graft patency rates of 71%, 64%, and 50% at 1,5, and 10 years, respectively). Evidence of improved graft survival and symptomatic outcome after the use of arterial bypass conduits is accumulating,2 and increasing numbers of coronary surgical procedures involve the use of at least one arterial bypass graft (usually the left internal mammary artery to the anterior descending coronary artery). In our patient, the left internal mammary artery seemed to have been affected by the same arteritic process as the coronary arteries, rendering it useless for coronary revascularisation. The decision to implant a stent in the ostium of her coronary vein graft was based on evidence that restenosis rates after balloon angioplasty of this site may be as high as 60%.3 There are, as yet, no long-term data on outcome after stent implantation in coronary vein grafts, but we have shown a restenosis rate of 11%, during a mean follow-up of II months, in 66 venous bypass grafts treated with self-expanding stents.4 This case illustrates the difficulties that the cardiologist may face in treating adult patients with the coronary artery sequelae of childhood Kawasaki disease.
University Department of Clinical Neurology, and Parkinson’s Disease Society Brain Bank, National Hospital,
Department of Cardiology, St Thomas’ Hospital, London SE1 7EH, UK
disease during life, which appeared on their death certificate (table). Thus in 17% of patients diagnosed as MSA in life, and in 50% of pathologically proven cases, the death certificate mentioned only Parkinson’s disease. These findings indicate that, in the UK, death certificates are an unreliable instrument for assessing the epidemiology of MSA, and that a clinical diagnosis of MSA is considerably more reliable than one of Parkinson’s disease. MSA3 encompasses many patients who are still otherwise classified under the 9th revision of the Application of the International Classification of Diseases to Neurology (ICD-NA)4 as
SDS (333.02), strionigral degeneration (333.03), olivopontocerebellar degeneration (333.04), or under other degenerative diseases of the basal ganglia (333.0), or "other" (333.08). Since MSA does not feature in ICD-NA, purists might suggest that the term should not be used on death certificates. However, official recognition of terms must inevitably follow common usage. After 23 years, we propose that the inclusion of MSA in ICD is long overdue.
London WC1 N 3BG, UK
GREGOR K. WENNING NIALL P. QUINN SUSAN E. DANIEL
J. T. STEWART
of Medicine and
Hughes AJ, Daniel SE, Kilford L, Lees AJ. Accuracy of clinical diagnosis of idiopathic Parkinson’s disease: a clinico-pathological study of 100 cases J Neurol Neurosurg Psychiatry 1992; 55: 181-84. 2. Rajput AH, Rozdilsky B, Rajput A. Accuracy of clinical diagnosis in parkinsonism: a prospective study. Can J Neurol Sci 1991; 18: 275-78. 3. Graham JG, Oppenheimer DR. Orthostatic hypotension and nicotine sensitivity in a case of multiple system atrophy. J Neurol Neurosurg Psychiatry 1969; 32: 28-34. 4. Application of the International Classification of Diseases to Neurology (ICD-NA, ninth revision). Geneva: WHO, 1987. 1.
Adult coronary artery disease secondary to childhood Kawasaki disease SIR,-Professor Kato and colleagues (Nov 7, p 1127) make no mention of the longer term problems that may be faced by patients with Kawasaki disease, even after coronary artery surgery. We have treated a 27-year-old Japanese woman with an 18-month history of progressive angina on effort. Exercise testing showed diagnostic ST segment depression in leads V4-6 at stage 3, and was stopped because of angina pectoris. Kawasaki disease had been diagnosed at age 12 in Japan but she had received no specific therapy. Angina pectoris had developed at age 17, and at 22 she underwent saphenous vein coronary artery bypass surgery for
Western
Department Therapeutics, Infirmary, Glasgow
A.
Department of Invasive Cardiology, Royal Brompton National Heart and Lung Hosptal,
L. DENNE U. SIGWART A. F. RICKARDS
London SW3
JAMIESON
1. The Veterans Affairs Coronary Bypass Surgery Cooperative Study Group. Eighteenyear-follow-up in the Veterans Affairs cooperative study of coronary artery bypass surgery for stable angina. Circulation 1992; 86: 121-30. 2. Loop FD, Lytle BW, Cosgrove DM, Stewart RW. Influence of the internalmammary-graft on 10-year survival and other cardiac events. N Engl J Med 1986; 314: 1-6. 3. Webb JG, Myler RK, Shaw RE, et al. Coronary angioplasty after coronary bypass surgery: initial results and late outcome in 422 patients. J Am Coil Cardiol 1990; 16: 812-20. 4. Stewart JT, Williams MG, Goy J-J, et al. Self-expanding stents for diseased saphenous vein coronary artery bypass grafts. Br Heart J 1992; 68: 153.
CORRECTION Effects of dual-chamber pacing with short atrioventricular delay in dilated cardiomyopathy. -An error appeared in table u of this article by Dr S. J. D. Brecker and colleagues (Nov 28, p 1308): under Longest AV interval, the RVFT for patient 12 should have been 160 ms.
