Adenosine-induced chest pain in patients with silent and painful myocardiai ischaemia: another clue to the importance of generalized defective perception of painful stimuli as a cause of silent ischaemia

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Abstract
Adenosine is formed from adenosine triphosphate within the ischaemic cells from where it is released into the coronary circulation. Adenosine exhibits several cardiovascular effects which tend to protect the ischaemic myocardium. Based on the observation that in healthy volunteers the intravenous infusion of adenosine produces angina-like chest pain, it has been recently proposed that another cardioprotective action of this substance could be provocation of angina. If this is the case adenosine should not produce chest pain in patients with silent ischaemia. To test this hypothesis we infused this substance intravenously at increasing doses of 50, 100, 150, 200, 250 and 300 μg kg−1 min−1 in eight patients with silent ischaemia (group A). All of them developed ST depression (1.8 ± 0.2 mm) during exercise testing and seven also during adenosine infusion (1.1 ± 0.8 mm). However, none of the patients had chest pain during exercise while seven had chest pain during adenosine. We then infused adenosine in eight other patients (Group B) who had painful ischaemia and an exercise tolerance similar to that of Group A patients (time to 1 mm ST depression 8.6 ± 2.7 min and 8.4 ± 3 min, respectively, P = NS). Adenosine induced chest pain in all Group B patients. The time to pain onset during adenosine was similar in the two groups (9.3 ± 2.3 min in Group B and 12.4 ± 4.9 min in Group A). However, the severity of chest pain during adenosine both at its onset and at peak, assessed using a visual analogue scale, was greater in Group B than in Group A (26 ± 12 mm vs. 11 ± 10 mm, respectively, P < 0.06 and 67 ± 20 mm vs. 31 ± 30 mm, respectively, P < 0.05). Thus, the presence of chest pain during adenosine infusion in patients with silent ischaemia appears to suggest that adenosine-induced chest pain is unlikely to be entirely cardiac in origin. Furthermore, the dose of adenosine which induced chest pain was similar in patients with silent and with painful myocardial ischaemia confirming that adenosine-induced chest pain and the anginal pain during spontaneous myocardial ischaemia are probably mediated by different mechanisms. The greater severity of adenosine-induced chest pain in patients with painful myocardiai ischaemia compared with that in patients with silent ischaemia probably reflects the presence in the latters of a generalized defective perception of painful stimuli.

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