Læknablaðið : fylgirit - 01.06.1982, Síða 15

dial lactate release indicating tissue anaerobiosis, 2) an aug-
mented myocardial citrate release within the first min of re-
covery from angina pectoris, suggesting a citrate inhibition of
glycolysis at end of ischaemia, and 3) increased myocardial a-
lanine release and glutamate uptake at rest and during recovery.
The importance of frequent blood sampling for evaluating meta-
bolic responses correctly is emphasized. Despite of this, a myo
cardial lactate release was found in only about 60% of the pa-
tients who experienced angina pectoris. However, whether or not
a myocardial lactate production was found, abnormal myocardial
exchanges of citrate, glutamate and/or alanine suggested ischae
mia in all patients complaining from chest pain during pace.
Our interpretation of abnormal citrate, glutamate and alani-
ne exchanges as events of ischaemia was further justified from
normalization of these responses after treatment of CAD pati-
ents with verapamil (n=V2), propranolol (n=12) as after clini-
cal improvement by coronary bypass surgery (n=5).
Measurements of myocardial exchanges of citrate, glutamate
and alanine in addition to that of lactate are suggested as a
sensitive metabolic test in assessing myocardial ischaemia in
man. Metabolic evaluation of ischaemia may be a useful diagno-
stic tool in patients in whom coronaHy angiography is inconclu-
sive or normal.