K. Ylitalo et al., NO EVIDENCE FOR ISCHEMIC PRECONDITIONING DURING REPEATED VESSEL OCCLUSION IN CORONARY ANGIOPLASTY, International journal of cardiology, 55(3), 1996, pp. 227-237
Coronary angioplasty has been the favoured model in studying ischemic
preconditioning in humans, but results have remained controversial, po
ssibly due to some artefacts related to coronary balloon angioplasty a
s an ischemia model. We examined this issue by monitoring the sequenti
al metabolic, functional and neurohumoral changes during repeated vess
el occlusion in coronary angioplasty performed in patients with chroni
c angina pectoris. Two groups of patients undergoing two successive ba
lloon inflations of approximately 2 min duration were studied. These b
alloon inflations were preceded by a short inflation performed immedia
tely after introduction of the balloon into the stenosis. The aim of t
his primary inflation was to establish adequate coronary blood flow wi
th the deflated balloon in the stenosis and to guarantee that the subs
equent two balloon inflations were truly comparable in time. Group I c
onsisted of 23 patients, in whom the changes in the degree of angina,
pulmonary capillary wedge pressure (PCWP), atrial natriuretic peptide
(ANP) and circulating catecholamines during the procedure were studied
. The sequential changes in myocardial metabolism were monitored in gr
oup II of nine patients by determining the lactate extraction ratios a
nd femoroarterial coronary sinus (Fa-CS) differences in pH and pCO(2)
before and after each balloon inflation. In group I, PCWP and total ca
techolamines increased similarly during both balloon inflations, but A
NP remained unchanged. In group II patients the lactate extraction rat
ios turned negative, the Fa-CS pH-differences increased and the pCO(2)
-differences decreased during vessel occlusions, the changes being som
ewhat more prominent during the second balloon inflation. To study ada
ptation to ischemia, the group I patients were divided into two subgro
ups with and without signs of ischemic dysfunction during balloon infl
ations (PCWP increase > 5 mmHg and < 5 mmHg, respectively), and the gr
oup II patients were divided into two subgroups with and without metab
olic ischemia (lactate-producers and non-producers). The ANP levels we
re constantly higher in the patients demonstrating ischemic dysfunctio
n during balloon inflations, but catecholamine levels increased only a
fter the second balloon inflation. The anginal pain experienced by the
patients and the signs of metabolic ischemia were identical during bo
th balloon inflations. We conclude that acute ischemic preconditioning
does not occur in patients with repeated vessel occlusions of approxi
mately 2 min duration. The patients without ischemia during the proced
ure had more critical stenoses and pre-existing collaterals. However,
other protective mechanisms, such as chronic adaptation at the cellula
r level or recruitment of new collaterals, cannot be excluded.