D. Masuda et al., Enhanced external counterpulsation improved myocardial perfusion and coronary flow reserve in patients with chronic stable angina - Evaluation by N-13-ammonia positron emission tomography, EUR HEART J, 22(16), 2001, pp. 1451-1458
Aims The mechanism by which enhanced external counterpulsation therapy exer
ts its beneficial effects on chronic and symptomatic stable angina is large
ly unknown. To clarify the mechanism of action of enhanced external counter
pulsation, we used N-13-ammonia positron emission tomography to evaluate my
ocardial perfusion.
Methods and Results This was not a randomized controlled study. Eleven pati
ents (eight male, age: 61.6 +/-9.7) with angina pectoris underwent enhanced
external counterpulsation therapy for 35 1 h sessions. They underwent a tr
eadmill exercise test and N-13-ammonia positron emission tomography, both a
t rest and with dipyridamole; before and after enhanced external counterpul
sation therapy. Neurohumoral factors and nitric oxide were also evaluated.
Myocardial perfusion increased at rest after therapy (0.69 +/-0.27 to 0.85
+/-0.47 ml.min(-1).g(-1), P<0.05). In ischaemic regions, particularly the a
nterior region, myocardial perfusion at rest and with dipyridamole and coro
nary flow reserve improved significantly after therapy (at rest: 0.71<plus/
minus>0.26 to 0.86 +/-0.31; P<0.05, with dipyridamole: 1.26<plus/minus>0.65
to 1.84 +/-0.94; P<0.02, coronary flow reserve: 1.75<plus/minus>0.24 to 2.
08 +/-0.28; P<0.04). Exercise time was prolonged and the time to 1-mm ST de
pression improved markedly (P<0.01). After therapy, nitric oxide levels inc
reased (P<0.02) and neurohumoral factors decreased.
Conclusions Enhanced external counterpulsation therapy improved myocardial
perfusion at rest and with dipyridamole and was associated with an increase
d exercise tolerance with N-13-ammonia positron emission tomography and inc
reased nitric oxide levels. These results suggest that one of the enhanced
external counterpulsation mechanisms is development and recruitment of coll
ateral vessels. (Eur Heart J 2001; 22: 1451-1458, doi:10.1053/euhj.2000.254
5) (C) 2001 The European Society of Cardiology.