The energy needed to maintain cardiac function is supplied mainly by t
he oxidation of fatty acids. Carnitine is an essential cofactor of the
oxidative energy pathway, carrying long chain fatty acids into the mi
tochondria for beta oxidation. it is also necessary far the biosynthes
is of high-energy phosphates (ATP). Therefore carnitine maintains card
iac function. In order to record the indirect effects of myocardial en
ergy metabolism disturbances and the associated heart disease, carniti
ne and carnitine ester values in the plasma of dogs with heart disease
were investigated. 53 dogs with heart disease were classified accordi
ng criteria published by the New York Heart Association into the four
different NYHA stages, and then devided into groups according to their
primary heart disease. The primary heart diseases included mild heart
disease (without anatomical/functional changes), dilative cardiomyopa
thics, valvular, endocardial valve abnormalities (mitral and/or tricus
pidal valvular disease), congenital heart resp. vascular anomalies, ar
rhythmia, hemopericardium, and other nonendocardial valvular diseases.
The carnitine plasma values of the various groups were then compared
statistically to each other and to a control group. Dogs with heart di
sease showed a significant, step-like increase of plasma carnitine val
ues in all NYHA stages after a slight decrease in NYHA stage I (monofa
ctorial variance analysis with tukey method, multiple average comparis
ons). The significant increase in plasma carnitine values relative to
NYHA stage I pertained to the fractions total carnitine (from NYHA I t
o NYHA II, III, IV), free carnitine (from NYHA I to III, IV), acyl car
nitine (from NYHA I to NYHA IV) and short chain acyl carnitine (from N
YHA I to III, IV). Significant variations from the control group were
found in total and free carnitine in NYHA stages III and IV as well as
acyl and short chain acyl carnitine in NYHA stage IV.As an expression
of the severity of disturbances in myocardial metabolism; the carniti
ne values in the patient groups with hemopericardium and dilative card
iomyopathy (mostly NYHA stage III and IV) differed significantly from
the control group in 4 resp. 2 fractions. The carnitine variations in
the groups with the other primary heart diseases and lower NYHA stages
were less pronounced. Results: In the dog, the severity of heart dise
ase and the associated disturbances in myocardial energy metabolism co
rrelate to an increase in plasma carnitine values (total, free, acyl a
nd short chain acyl carnitine) and NYHA stage. Carnitine Variations in
crease dramatically in the more severe NYHA stages. A significant incr
ease in total carnitine values relative to NYHA stage I was found in a
ll more severe stages. A quantitative measurement of total carnitine c
an therefore be seen as an indicator or a diagnostic marker for the ot
her fractions (free and esterified carnitine), giving an overview of t
otal plasma carnitine situation. The quantified plasma carnitine value
s also allow a useful clinical and prognostic evaluation of heart dise
ase and indicate the current situation of myocardial energy metabolism
(beta oxidation). Variations in carnitine plasma Values associated wi
th myocardial carnitine Variations seem to be due to an unspecific bio
chemical mechanism, independent of the etiology of the heart disease.
This mechanism correlates only with the severity of the heart disease
and not with the type of primary heart disease.