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Figure 1 Serum lactate dehydrogenase (LDH)
activity pattern and the arterial p02 of the presented
patient who developed a drug-induced pneumonitis
due to amiodarone. 0 =pa0 2; • =LDH; T =stop
amiodarone.
Departments of *Pulmonology,
tClinical Chemistry, and tCardiology,
University Hospital Maastricht,
The Netherlands
References
[1] Jesserun GAJJ, Crijns HJGM. Amiodarone pulmonary toxicity. Dose and
duration of treatment are not the only
determinants of toxicity. Br Med J
1997; 314: 619-20.
[2] Failing LJ, Mark EJ. A 65-year-old
woman with dry cough and pulmonary
nodules. New Engl J Med 1997; 13:
1449-58.
Eur Heart J, Vol. 19, June 1998
[3] Drent M, Cobben NAM, Henderson
RF, Jacobs JA, Wouters EFM, DieijenVisser van MP. Usefulness of lactate
dehydrogenase and its isoenzymes as
indicators of lung damage or inflammation. Eur Respir J 1996; 9: 1736-42.
[4] Matusiewicz SP, Williamson IJ, Sime
PJ et al. Plasma lactate dehydrogenase:
a marker of disease activity in cryptogenic fibrosing alveolitis and extrinsic
allergic alveolitis? Eur Respir J 1993; 6:
1282-6.
[5] Schultze AE, Gunaga KP, Wagner JG,
Hoorn CM, Moorehead WR, Roth
RA. Lactate dehydrogenase activity
and isoenzyme pattern in tissues and
bronchoalveolar lavage fluid from rats
treated with monocrotaline pyrrole.
Toxicol Appl Pharmacol 1994; 126:
301-10.
Arginine consumption in coronary
disease
We wish to make the following comments on the issue of the significance
of arginine consumption in preventing
coronary disease.
The importance of diet in the
secondary prevention of coronary
disease was recently reiterated by de
Lorgeril and coworkers[ll. In their
study, coronary patients of Lyon ate
the Mediterranean diet consumed by
the rural population of Crete as determined by the seven countries study[21.
The 76% reduction in clinical complications of coronary disease reported
by the authors exceeds the benefit
accrued by the most aggressive pharmaceutical lipid lowering intervention
and suggests additional contributing
factors.
By using tables on amino
acid content of food[31 we determined
the daily arginine intake of the
Haifa, [,rael
References
[I] de Lorgeril M, Salman P, Martin lL
et al. Effect of mediterranean type diet
on the rate of cardiovascular complications in patients with coronary artery
disease. lACC 1996; 28: 1103-8.
[2] Keys A. Coronary heart disease in
seven countries. Circulation 1970; 41
(Suppl. 1): 1-211.
[3] Paul AA, Southgate AT, Russel J. McCance and Widdowsons' The composition of foods aminoacid composition
mg/IOO gm food. Ministry of agriculture fisheries and food medical research
council. London: Her Majesty's
Stationery Office, 1987.
[4] Renound S, de Lorgeril M, Delay J
et al. Cretan Mediterranean diet for
prevention of coronary heart disease.
Am J Clin Nutrition 1995; 61: 1360S1367S.
[5] Kromhout D, Blomberg BP, Feskens
JM et al. Alcohol, fish, fibre and antioxidant vitamins in take do not explain
population differences in coronary
heart disease mortality. Int J Epidemiol
1996; 25: 753-9.
[6] Kromhout D, Menotti A, Bloemberg B
et al. Dietary saturated and trans fatty
acids and cholesterol and 25 year mortality from coronary heart disease: The
seven countries study. Prvent Med
1995; 24: 308-15.
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Remarkably, in this case, the
high LDH activity was accompanied
by shifts in the isoenzyme pattern in
similar directions for both serum and
BALF. The fact that this shift in
serum resembles that in BALF, suggests that the major source of the
serum LDH was the lung. The source
of the LDH activity in the lung may be
inflammatory cells, such as alveolar
macro phages rapidly recruited to rid
the lung of the phospholipid[51. This
case report highlights the promising
role of serum LDH activity -- a
simple potential marker of disease
activity -- in monitoring and followup of drug-induced pneumomtls
caused by amiodarone. Moreover, this
determinant seems to be a sensitive
marker to predict such reaction. An
isolated increase of serum LDH indicates the necessity to discontinue
amiodarone.
M. DRENT*
N. A. M. COBBEN*
M. P. VAN DIEIJEN-VISSERt
S. H. J. G. BRAATt
E. F. M. WOUTERS*
study group prior to the diet
administration and following its application and arrived at 3·5 g and 7 g
respectively.
We believe that by doubling
arginine consumption, nitric oxide
availability may have increased and
endothelial dysfunction may have
been corrected in these coronary
patients. This would facilitate vasodilatation and fibrinolysis and mitigate blood coagulation, adhesion of
leucocytes and platelets as well as
smooth muscle cell proliferation.
Further more the work of
Kromhout and coworkers enables us
to examine whether arginine has a role
to play in primary prevention of heart
disease. Kromhout in a number of
publications[5-71 correlated several
dietary factors consumed by the original 16 cohorts of the seven countries
study with their 25 years coronary
heart disease mortality. Extending this
correlation to arginine by using the
tables on amino acid content in food[31
would show whether consumption of
arginine by healthy middle-aged men
is related to their long-term coronary
heart disease mortality.
E. C. MEYER
A. PALANT
Letters to the Editor
[7] Hertog MG, Kromhout D, Aravanis C
et al. Flavonoid intake and long term
risk of coronary heart disease and
cancer in the seven countries study.
Arch Int Med 1995; 155: 381-6.
An association of an antibody against
Chlamydia pneumoniae and coronary
heart disease observed in Japan
N. MIYASHITA*
E. TOYOTAt
T. SAWAYA MAt
T. MATSUSHIMA*
* Division of Respiratory Diseases
and t Division of Cardiology,
Department of Medicine
Kawasaki Medical School,
Kurashiki City,
Okayama 701-0192, Japan
References
[I] Grayston JT, Campbell LA, Kuo C-C
et al. A new respiratory tract pathogen:
Chlamydia pneumoniae strain TWAR. J
Infect Dis 1990; 161: 618-25.
[2] Saikku P, Mattila K, Nieminen MS
et al. Serological evidence of an association of novel chlamydia, TW AR, with
chronic coronary heart disease and
acute myocardial infarction. Lancet
1988; 2: 983-6.
[3] Shor A, Kuo C-C, Patton DL. Detection of Chlamydia pneumoniae in the
coronary artery atheroma plaque. S
African Med J 1992; 82: 158-61.
[4] Kuo C-C, Shor A, Campbell LA,
Fukushi H, Patton DL, Grayston JT.
Demonstration of Chlamydia pneumoniae in atherosclerotic lesions of coronary arteries. J Infect Dis 1993; 167:
841-9.
[5] Thom DH, Wang S-P, Grayston JT
et at. Chlamydia pneumoniae strain
TWAR antibody and angiographically
demonstrated coronary artery disease.
Arterioscler Thromb 1991; II: 547-51.
[6] Thom DH, Grayston ]T, Siscovick DS,
Wang S-P, Weiss NS, Daling JR.
Association of prior infection with
Chlamydia pneumoniae and angiographically demonstrated coronary artery disease. JAMA 1992; 268: 68-72.
[7] Saikku P, Leinonen M, Tenkanen L
et al. Chronic Chlamydia pneumoniae
infection as a risk factor for coronary
heart disease in the Hershinki heart
study. Ann Inter Med 1992; 116: 273-8.
[8] Linnanmaki E, Leinonen M, Mattila K.
Chlamydia pneumoniae-specific circulating immune complexes in patients with
chronic coronary heart disease. Circulation 1993; 87: 1130-4.
[9] Patel P, Mendall MA, Carrington 0
et al. Association of Helicobacter pylori
and Chlamydia pneumoniae infection
with coronary heart disease and cardiovascular risk factors. BMJ 1995; 311:
711-4.
Eur Heart J, Vol. 19, June 1998
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Chlamydia pneumoniae is an important
cause of acute respiratory illness,
including pharyngitis, bronchitis and
pneumonia[l). However, there has
been accumulating evidence implicating C. pneumoniae in atherosclerosis[2-9 1. Saikku et at. [2] first
reported on an antibody against C.
pneumoniae and coronary heart disease (CHD) in 1988. Subsequently,
Shor et al.[3) and Kuo et at.r41 detected
C. pneumoniae in coronary artery
atherosclerotic plaques by immunocytochemistry, polymerase chain reaction and electron microscopy. Their
findings have been confirmed by other
investigators worldwide. We have also
investigated the association of C. pneumoniae antibody and angiographically
diagnosed CHD in Japan.
The study was conducted in
four separate hospitals in Okayama,
Osaka and Shizuoka, Japan between
April 1993 and December 1994. There
were 160 patients with CHD (34-81
years of age, mean 60·0 years; liS
males and 4S females). Cases were
defined as patients who had at least
one coronary artery lesion occupying
at least SO% of the luminal diameter
by angiography. One hundred and
fourteen patients had myocardial infarction as defined by ECG and angiography. Controls who were matched
for age and sex were enrolled from the
patients attending the same hospitals.
The criteria for inclusion were absence
of signs and symptoms of CHD, as
judged by a negative history and a
normal resting ECG. Informed consent was obtained from all subjects. C.
pneumoniae IgG and IgA antibodies
were measured by the microimmunofluorescence (MIF) test[l) using a
Japanese isolate KK-pnIS as antigen.
The serologic criteria for a positive test
was a titre of greater than or equal to
1:16 for IgG or 1:8 for IgA. Logistic
regression was used for statistical
analysis.
The odds ratios (ORs) were
2·1 (9S% confidence interval [CI], 1·2
to 3'9) for IgG and 2'S (9S% CI, 1·7 to
4· 3) for IgA. After adjustment for
other cardiovascular risk factors of
age, hypertension, diabetes, cigarette
smoking and serum cholesterol, the
ORs were essentially unchanged at 2·2
(9S% CI, 1·2 to 4·1) for IgG and 2·7
(9S% CI, 1·7 to 4-4) for IgA. The
adjusted ORs were greater for patients
with IgG titres of greater than or equal
to I :64 and IgA titres of greater than
or equal to 1:32, i.e., 4'S (9S% CI, 2·2
to 9'1) and 6·1 (9S% CI, 2·4 to IS'7),
respectively. The geometric mean titres
of IgG and IgA were significantly
higher in patients with CHD than controls (39'2 vs 20·9 for IgG, P=O'OOOI
and 12·6 vs 6·2 for IgA, P=O'OOOI) by
the Mann-Whitney U tests.
This study confirmed the
observations of an association
between antibody against C. pneumoniae and CHD in Western nations is
also present in Japan. Our results are
comparable to the previous seroepidemiological studies reporting ORs of
2·0 or greater[2.5 .9).
97J