No abstract

BACKGROUND Myocardial perfusion imaging during adenosine-induced hyperemia with dipyridamole or adenosine is an accepted method to diagnose coronary artery disease (CAD) and risk assessment. The mechanism of perfusion abnormality may be caused by disparate flow responses or coronary steal. This study examined the relation between 201Tl perfusion pattern and hemodynamic/angiographic changes during intravenous adenosine infusion. METHODS AND RESULTS Patients with suspected CAD underwent sequential hemodynamic, coronary arteriographic, and left ventriculographic studies simultaneously with 201Tl imaging during adenosine infusion (140 micrograms.kg-1.min-1 for 6 minutes). There were 33 patients with CAD and 12 patients without CAD. The 201Tl images (using single-photon emission computed tomography) were abnormal in 31 patients with CAD (sensitivity, 94%) and normal in the patients without CAD (specificity, 100%). In patients with and without CAD, there were significant increases in heart rate and cardiac output (p less than 0.0001) and decreases in systemic vascular resistance and blood pressure (p less than 0.0001). There was a 77 +/- 38% increase in pulmonary capillary wedge pressure in normal subjects and a 125 +/- 83% increase in patients with CAD (p = 0.02). ST segment depression was observed in 11 patients with CAD (33%). In CAD patients, there was no change in percent diameter or area stenosis measured quantitatively during adenosine infusion. In 15 patients, contrast left ventriculography was repeated during adenosine infusion. In these patients, 201Tl perfusion defects were seen in 31 of 75 segments (41%) whereas only six of 75 segments (8%) developed regional wall motion abnormality (p less than 0.001); the remaining segments showed either no change or improved function. The left ventricular ejection fraction did not change significantly (73% versus 75%). CONCLUSIONS There is a disparity between the effects of adenosine on left ventricular perfusion and function; most patients with CAD have perfusion defects whereas the global and regional systolic function remains unchanged or improves. Diastolic left ventricular dysfunction is a probable mechanism of the increase in pulmonary capillary wedge pressure.