Læknablaðið : fylgirit - 01.06.1982, Qupperneq 14

3
PLENARY LECTURE
MYOCARDIAL METABOLISM IN PATIENTS WITH ANGINA PECTORIS INDUCED
BY ATRIAL PACING. T. Tofteqaard Nielsen, J.P. Bagger, P.Henning
sen, A.R. Thomassen, Department of Cardiology, Arhus Kommunehos
pital, Denmark.
Compared with normal heart, substrate utilization by the i-
schaemic myocardium is characterized by an increased glucose
and decreased fatty acid oxidation. Widely, a change in myocar-
dial lactate exchange from uptake to output is accepted as mar-
ker of the augmented glucose utilization in hypoxic states. A
myocardial lactate release can, however, be demonstrated in far
from all patients during pacing-induced angina pectoris. Metabo-
lic responses to hypoxia and ischaemia differ. While hypoxia
leads to a sustained increase in the glycolysis, ischaemia in-
creases myocardial lactate production only initially,thereafter
the glycolytic pathway is profoundly inhibited. Because citrate
is a potent inhibitor of muscular glycolysis (inhibition of
phosphofructokinase) the hypothesis was put forward, that myo-
cardial plasma citrate exchange might be a useful marker of the
inhibition of glycolysis during ischaemia. Further, citrate for
inhibition of myocardial glucose utilization was proposed to be
synthesized in part from glutamate by transamination with pyru-
vate to form alanine.
Arterio-coronary sinus concentration differences of lactate,
glucose, citrate, free fatty acids (FFA), glutamate and alanine
together with coronary sinus blood flow were measured in con-
trols (n=14) and patients with angiographic documented coronary
artery disease (CAD) (n=74) at rest and during pacing-induced
tachycardia and angina pectoris.
In accordance with the idea of citrate as a regulator sub-
stance for the inverse interrelation between myocardial FFA and
glucose oxidation, citrate release across the non-stressed heart
correlated positively to arterial FFA concentration and inverse-
ly to glucose extraction. At rest myocardial citrate release
was significantly lower in CAD patients than in controls.
When comparing responses in CAD patients with those of con-
trols, a metabolic profile for pacing-induced ischaemia could be
set up. Features of myocardial ischaemia included: 1) a myocar-