Copyright © 1989 by the European Society of Cardiology.
© 1989 The European Society of Cardiology
Angina pectoris-like pain provoked by i.v. bolus of adenosine: Relationship to coronary sinus blood flow, heart rate and blood pressure in healthy volunteers
*Departments of Medicine Huddinge Hospital Stockholm Sweden
Clinical Pharmacology Huddinge Hospital Stockholm Sweden
Clinical Physiology Huddinge Hospital Stockholm Sweden
Received 11 January 1988; revised 24 May 1988; .
Correspondence. Christer Sylvèn, MD PhD, Department of Medicine, Huddinge Hospital. S-141 86 Huddinge, Sweden.
Abstract
After finding the maximum tolerated i.v. bolus dose of adenosine, three fractions of this dose were given randomly to five volunteers in a double-blind manner. Pain, estimated by a 10-graded category-ratio scale, ECG and coronary sinus blood flow (CSBF), measured by thermodilution and intra-arterial blood pressure, were continuously recorded. At the highest tolerated dose (10.3 ± 2.3 mg), the ECG showed short lasting (<5 s) A V-block but no ischaemic signs. Following the maximum dose, pain started 15 ± 2s after injection, reached a maximum (median 6 of10 grades) after 25 ± 4 s and disappeared after 62 ± 7s. Basal CSBF was 84 + 14 ml min-1, and increased to 297 ± 48 ml/min. The rise in CSBF started 2.4 ± 0.8 s before pain appeared (P <0.005), but reached its peak 18 ± 2s after maximum pain (P <0.005). Although maximum coronary vasodilation was induced at the lowest dose of adenosine given—1/3 of the maximum dose—chest pain increased in a dose-dependent manner. When A V-block did not occur, diastolic pressure did not change from baseline, while systolic blood pressure increased by 5 ± 2% (ANO VA, P < 0.0001) and heart rate increased by 40 ± 7% (ANOVA, P <00001). Following AV-block, except for a decrease of short duration in heart rate and systolic and diastolic blood pressures, the responses were similar. In conclusion, the vasodilator adenosine given as am i. v. bolus to human volunteers who were awake increased heart rate and systolic blood pressure with unchanged diastolic pressure. Adenosine also provoked chest pain, which began shortly after the initial increase of CSBF but showed a more transient time profile. The results are compatible with myocardial origin for the pain by a mechanism different from vasodilation.
Key Words: Adenosine • chest pain • angina pectoris • coronary sinus • ECG • heart rate • volunteers
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