CORONARY VASODILATION WITHOUT MYOCARDIAL ERECTION - SIMULTANEOUS HEMODYNAMIC, ECHOCARDIOGRAPHIC AND ARTERIOGRAPHIC FINDINGS DURING ADENOSINE AND DIPYRIDAMOLE INFUSION

Aim The aim of this study was to evaluate simultaneously echocardiogra phic, haemodynamic and angiographic changes that occur during: adenosi ne and dipyridamole infusion, in patients with one-vessel coronary art ery stenosis. This would assess whether deterioration in left ventricu lar haemodynamics during vasodilator agent infusion is influenced by v asodilation per se, or the development of myocardial ischaemia. Method s and results We performed adenosine (140 mu g . kg(-1). min(-1) over 4 min) and dipyridamole (up to 0.84 mg . kg(-1) over 10 min) stress ec hocardiography tests, together with angiographic and haemodynamic asse ssment, in 26 patients undergoing elective coronary angioplasty. In 12 of 26 patients, adenosine and dipyridamole tests were repeated 24 h a fter angioplasty. The criterion for echocardiography test positivity w as the appearance of a new transient regional wall motion abnormality. Coronary angiograms were analysed with quantitative coronary arteriog raphy. Adenosine and dipyridamole induced regional dysfunction in 18/2 6 (69%) and 14/26 (54%) patients before: angioplasty, respectively (P= ns). In the echocardiography-positive patients, the percent diameter s tenosis was significantly (P<0.05) tighter stenosis than in the echoca rdiography-negative patients (adenosine, 66.6+/-8.3% vs 58.0+/-8.9%; d ipyridamole, 69.2+/-7.1% vs 57.7 +/- 7.6%). During both tests, left ve ntricular end-diastolic pressure significantly increased (P<0.05) in e chocardiography-positive patients (adenosine, 9.8 +/- 2.7 mmHg to 13.5 +/- 4.1 mmHg; dipyridamole, 10.1 +/- 2.8 mmHg to 14.1 +/- 4.3 mmHg), but not in echocardiography-negative patients. In the patients who had undergone successful angioplasty (reduction to <50% diameter stenosis ), both adenosine and dipyridamole confirmed the arteriographic succes s of the procedure (echocardiography negative in all patients). In thi s group of patients, no significant change was observed in left ventri cular end-diastolic pressure during adenosine or dipyridamole infusion . Conclusions Intravenous infusion of either adenosine or dipyridamole was accompanied by an obvious increase in left ventricular end-diasto lic pressure only in patients with induced wall motion abnormalities. Corollary vasodilation per se has no significant effect on left ventri cular end-diastolic pressure when no ischaemia is induced, disproving any clinically significant 'erectile' and adverse effects of coronary vasodilation per se.