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238
References
1 Smith VE, Schulman P, Karimeddini M, White W,
Meeran M, Katz A. Rapid ventricular filling fraction
in left ventricular hypertrophy: II pathologic hypertrophy. JAm Coll Cardiol 1985;5:869-74.
2 Inouye I, Massie B, Loge D, et al. Abnormal left
ventricular filling: an early finding in mild to
moderate systemic hypertension. Am J Cardiol
1984;53:120-6.
Correspondence
3 Lahiri A, Al-Khawaja I, Rodrigues EA, Raftery EB.
Diastolic filling parameters of the left ventricle from
radionuclide ventriculography. In: Ripley KL, ed.
Computers in cardiology. Washington DC: Computer
Society Press of IEEE, 1988:275-8.
4 Protnick GD, Kahn B, Rogers WJ, Fisher ML, Becker
LC. Effect of postural changes, nitroglycerin and
verapamil on diastolic left ventricular function as
determined by radionuclide angiography in nornal
subjects. J Am Coll Cardiol 1988;12:121-9.
Plasma atrial natriuretic peptide in patients with
acute myocardial infarction: effects of streptokinase
Sir,
Phillips et al studied plasma concentrations of atrial
natriuretic peptide after acute myocardial infarction
(1989;61:139-43). They did not report a significant
correlation between plasma concentrations of atrial
natriuretic peptide and peak concentrations of
creatine kinase, which is an index of the severity of
infarction. In their study, blood was sampled for the
determination of atrial natriuretic peptide on the
morning after admission, which was, as we understand, at least 0-32 hours after the onset of symptoms.
The exact timing of blood sampling for atrial
natriuretic peptide is of great importance. We
measured atrial natriuretic peptide concentrations at
fixed times during 48 hours in 38 patients who were
admitted to the coronary care unit within 4 hours 25
minutes after the onset of symptoms.' Three hours
after admission, the mean atrial natriuretic peptide
concentration was significantly lower than it was on
admission. Thereafter, atrial natriuretic peptide concentrations rose till 15 hours after admission. Both
the atrial natriuretic peptide value on admission and
the individual mean atrial natriuretic peptide value
during the study period of 48 hours were significantly correlated with the maximum creatine kinase
value.
We agree with the hypothesis of Phillips et al that
acute myocardial dysfunction after myocardial infarction, by raising atrial pressures, causes a release of
atrial natriuretic peptide from atrial storage granules.
The ensuing decrease in atrial natriuretic peptide
concentrations found in our study may possibly be
attributed to depletion of these storage granules. At
this stage, circulating atrial natriuretic peptide concentrations will decrease despite increased intracardiac pressures. Subsequently atrial natriuretic peptide is synthesised at a greater rate causing its
concentrations in the blood to rise again. Our results
imply that the correct interpretation of atrial
natriuretic peptide values after acute myocardial
infarction depends on the timing of blood sampling.
*A C I T L Tan,
$T T van Loenhout,
$E J P Lamfers,
$P M J Corten,
tP W C Kloppenborg,
*Th J Benraad
*Department of Experimental and Chemical
Endocrinology, St Radboud Hospital, University of
Nijmegen,
tDivision of Clinical Endocrinology, Department of
Medicine St Radboud Hospital, University of Nijmegen,
$Departnent of Cardiology, Canisius Wilhelmina
Ziekenhuis, Nijmegen, The Netherlands.
Reference
1 Tan ACITL, Van Loenhout TT, Lamfers EJP,
Hooghoudt TEH, Kloppenborg PWC, Benraad TJ.
Atrial natriuretic peptide after myocardial infarction.
Am Heart J 1989 (in press).
This letter was shown to the authors, who reply as
follows:
Sir,
We found that plasma concentrations of atrial
natriuretic peptide were higher in patients with acute
myocardial infarction who were not treated with
thrombolysis than in similar patients admitted with
non-ischaemic chest pain and patients with myocardial infarction treated with streptokinase. Patients
with ischaemic chest pain had intermediate concentrations of atrial natriuretic peptide. The finding of
raised plasma atrial natriuretic peptide in the acute
stages of myocardial infarction was confirmed by
Tan et al and others.'
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Correspondence
Both Tan et al and Svanegaard et al' found that
initially raised plasma atrial natriuretic peptide concentrations in patients with myocardial infarction fell
soon after admission. The extent of the fall found by
Tan et al is unclear. Despite this fall plasma atrial
natriuretic peptide concentrations remained raised in
the patients reported by Svanegaard et al especially
when cardiac failure was present.' This fall in plasma
atrial natriuretic peptide may reflect the beneficial
effect of treatment (for example, bed rest, diuretics,
glyceryl trinitrate, analgesia, thrombolysis) on left
ventricular function as well as the initial depletion of
atrial storage granules. Not enough detail is given by
these other workers for us to comment further on the
cause of the fall. Depletion of storage granules,
however, seems to be an unlikely mechanism,
because plasma atrial natriuretic peptide concentrations fell in all patients irrespective of the initial atrial
natriuretic peptide concentration.
We agree with Tan et al that both the timing ofthe
blood sample and the degree of infarction are important variables in interpreting plasma atrial natriuretic
peptide concentrations. Indeed we found that in an
experimental model of myocardial infarction the
concentration of plasma atrial natriuretic peptide
correlated well not only with the haemodynamic
changes but also with the degree of infarction
measured histologically.2 In this experimental model
it was also possible to show an inverse relation
between plasma atrial natriuretic peptide and atrial
atrial natriuretic peptide. That we did not find a
relation between peak concentrations of cardiac
enzymes and plasma atrial natriuretic peptide in our
human study was probably the result of the confounding effects of streptokinase treatment, which
increased peak enzyme concentrations but lowered
239
plasma atrial natriuretic peptide, and the inclusion of
patients with ischaemic chest pain who had normal
concentrations of cardiac enzyme but intermediate
concentrations of plasma atrial natriuretic peptide, as
well as the variable times of blood sampling (7-32
hours after admission). This underscores the difficulty ofstudying and interpreting the dynamics and
mechanism of atrial natriuretic peptide release in
patients with heart disease.
The finding of raised concentrations of plasma
atrial natriuretic peptide during the acute stage of
myocardial infarction before appreciable volume
expansion could occur suggests that acute myocardial dysfimction alone may raise plasma atrial
natriuretic peptide concentrations, probably by
reducing ventricular compliance and increasing
atrial pressures. This may be a beneficial homoeostatic response that acts to reduce cardiac preload and
limit salt and water retention during the acute stages
of myocardial ischaemia.
P A Phillips,
G P Hodsman,
C I Johnston,
Department of Medicine, University of Melbourne,
Austin Hospital, Heidelberg, Victoria 3084,
Australia.
References
1 Svanegaard J, Angelo-Nielsen K, Pindborg T. Atrial
natriuretic peptide and acute myocardial infarction.
Am Heart J 1989;117:194-5.
2 Tsunoda K, Hodsman GP, Sumithran E, et al. Atrial
natriuretic peptide in chronic heart failure in the rat: a
correlation with ventricular dysfunction. Circ Res
1986;59:256-61.
Pulmonary capillary haemangiomatosis
Sir,
A registry is being formed to document and study
cases of pulmonary capillary haemangiomatosis, an
exceptionally rare disease (only eight cases have been
described) that leads to proliferation of capillaries in
the lung and pulmonary hypertension. Anyone
knowing of patients with this disorder is asked to
contact either (1) CANADA and EUROPE: Dr
David Langleben, Jewish General Hospital, 3755
C6te St Catherine, Montreal, Quebec H3T 1E2,
Canada; or (2) USA, MIDDLE EAST, and
ORIENT: Dr Carl W White, Division of Pulmonary
Disease, The Children's Hospital, 1956 East 19th
Avenue, Denver, Colorado 80218-1088, USA. Strict
confidentiality will be maintained and a newsletter
will be circulated to all contributors.
David Langleben,
Jewish General Hospital,
3755 C6te St Catherine,
Montreal,
Quebec H3T 1E2,
Canada.
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The authors reply
P A Phillips, G P Hodsman and C I Johnston
Br Heart J 1989 62: 238-239
doi: 10.1136/hrt.62.3.238-b
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