STUDY OBJECTIVE: The aim was to study the tentative role of adenosine as a messenger between myocardial ischaemia and angina pectoris. DESIGN: Adenosine was administered in serial doses of 0.1-20 mg either as an intravenous bolus, or intra-arterially over 10 s into the left coronary artery, the aorta and the iliac artery. Coronary sinus flow was determined by thermodilution. ECG was monitored continuously. The patient was not aware of which site or dose was used. After each injection, the start of, maximum, end, magnitude, and location of pain were noted. PATIENTS: Six patients with angina pectoris referred for coronary angiography entered the study. MEASUREMENTS AND RESULTS: After intracoronary adenosine injection in the absence of ischaemic ECG changes, a dose dependent degree of chest pain was experienced not different in quality or location from the patients' habitual angina pectoris. Adenosine into the aorta provoked pain in lower chest and upper abdomen, whereas injection into the iliac artery provoked pain in the ipsilateral leg. On intravenous injection equipotent doses of adenosine caused chest pain of the same degree and quality as after intracoronary injection. Immediately after intracoronary injection the coronary sinus blood flow started to increase, but the onset of chest pain was delayed. Onset of pain was earlier the higher the dose, the maximum dose resulting in onset after 18(SEM 2) s. Coronary sinus blood flow increased dose dependently after left coronary artery injection but following intravenous injection no further increase was seen beyond that induced by the lowest dose. CONCLUSIONS: We suggest that adenosine is an important messenger for the sensation of angina pectoris and the effect is not due to coronary steal leading to myocardial ischaemia.
STUDY OBJECTIVE: The aim was to study the tentative role of adenosine as a messenger between myocardial ischaemia and angina pectoris. DESIGN:Adenosine was administered in serial doses of 0.1-20 mg either as an intravenous bolus, or intra-arterially over 10 s into the left coronary artery, the aorta and the iliac artery. Coronary sinus flow was determined by thermodilution. ECG was monitored continuously. The patient was not aware of which site or dose was used. After each injection, the start of, maximum, end, magnitude, and location of pain were noted. PATIENTS: Six patients with angina pectoris referred for coronary angiography entered the study. MEASUREMENTS AND RESULTS: After intracoronary adenosine injection in the absence of ischaemic ECG changes, a dose dependent degree of chest pain was experienced not different in quality or location from the patients' habitual angina pectoris. Adenosine into the aorta provoked pain in lower chest and upper abdomen, whereas injection into the iliac artery provoked pain in the ipsilateral leg. On intravenous injection equipotent doses of adenosine caused chest pain of the same degree and quality as after intracoronary injection. Immediately after intracoronary injection the coronary sinus blood flow started to increase, but the onset of chest pain was delayed. Onset of pain was earlier the higher the dose, the maximum dose resulting in onset after 18(SEM 2) s. Coronary sinus blood flow increased dose dependently after left coronary artery injection but following intravenous injection no further increase was seen beyond that induced by the lowest dose. CONCLUSIONS: We suggest that adenosine is an important messenger for the sensation of angina pectoris and the effect is not due to coronary steal leading to myocardial ischaemia.