The mechanism by which enhanced external counterpulsation therapy exerts its beneficial effects on chronic and symptomatic stable angina is largely unknown. To clarify the mechanism of action of enhanced external counterpulsation, we used(13)N-ammonia positron emission tomography to evaluate myocardial perfusion. This was not a randomized controlled study. Eleven patients (eight male, age: 61.6+/-9.7) with angina pectoris underwent enhanced external counterpulsation therapy for 35 1 h sessions. They underwent a treadmill exercise test and(13)N-ammonia positron emission tomography, both at rest and with dipyridamole, before and after enhanced external counterpulsation 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 x min(-1) x g(-1), P<0.05). In ischaemic regions, particularly the anterior region, myocardial perfusion at rest and with dipyridamole and coronary flow reserve improved significantly after therapy (at rest: 0.71+/-0.26 to 0.86+/-0.31;P<0.05, with dipyridamole: 1.26+/-0.65 to 1.84+/-0.94;P<0.02, coronary flow reserve: 1.75+/-0.24 to 2.08+/-0.28;P<0.04). Exercise time was prolonged and the time to 1-mm ST depression improved markedly (P<0.01). After therapy, nitric oxide levels increased (P<0.02) and neurohumoral factors decreased. Enhanced external counterpulsation therapy improved myocardial perfusion at rest and with dipyridamole and was associated with an increased exercise tolerance with(13)N-ammonia positron emission tomography and increased nitric oxide levels. These results suggest that one of the enhanced external counterpulsation mechanisms is development and recruitment of collateral vessels. Copyright 2001 The European Society of Cardiology.
