Relation between stimulation site of cardiac afferent nerves by adenosine and distribution of cardiac pain: results of a study in patients with stable angina

Cardiovascular Research Unit, Hammersmith Hospital, London, United Kingdom.

OBJECTIVES. The purpose of this study was to establish whether stimulation of cardiac sensory receptors in different myocardial regions results in different distributions of cardiac pain. BACKGROUND. Previous studies have shown that adenosine provokes cardiac pain through stimulation of sensory receptors in the absence of myocardial ischemia. In this study adenosine was used to obtain a regional stimulation of cardiac sensory receptors. METHODS. Increasing doses of adenosine (0.25, 0.5 and 1 mg/min) were selectively infused into the right and then into the left coronary artery in 26 patients with stable angina. RESULTS. No patient developed ischemic electrocardiographic changes during either adenosine infusion. Eighteen patients experienced cardiac pain during both infusions. Despite the stimulation of sensory receptors in different myocardial regions, 13 patients experienced cardiac pain in the same body area. Adenosine-induced pain was always similar to the anginal pain. By contrast, the remaining five patients experienced adenosine-induced cardiac pain in different body areas. In two of these patients, the distribution of anginal pain was similar to that experienced during one of the two adenosine infusions. In the remaining three patients, the distribution of anginal pain was similar to that experienced during adenosine infusion into the right coronary artery during some anginal episodes and to that experienced during adenosine infusion into the left coronary artery during other episodes. CONCLUSIONS. During stimulation by adenosine of sensory receptors in different myocardial regions, the majority of patients experience cardiac pain in the same body area; only a few experience pain in different areas. These differences might be caused by different organizations of the ascending neural pathways to the cortex. Our results suggest that in the same patient different distributions of pain during anginal attacks are probably due to ischemia in different myocardial regions.

This article has been cited by other articles:

				M. Magnoni, A. Esposito, S. Coli, L. Scuteri, F. De Cobelli, D. Cianflone, A. Del Maschio, and A. Maseri Two Different Mechanisms of Myocardial Ischemia Involving 2 Separate Myocardial Segments in a Patient With Normal Coronary Angiography Circulation, January 5, 2010; 121(1): e1 - e3. [Full Text] [PDF]

				F. Crea, P. G. Camici, R. De Caterina, and G. A. Lanza CHAPTER 17 Chronic Ischaemic Heart Disease ESC Textbook of Cardiovascular Medicine, January 1, 2009; 2(1): med-9780199566990-chapter - med-9780199566990-chapter. [Abstract] [Full Text] [PDF]

				P. A. Gwirtz, J. Dickey, D. Vick, M. A. Williams, and B. Foresman Viscerosomatic interaction induced by myocardial ischemia in conscious dogs J Appl Physiol, August 1, 2007; 103(2): 511 - 517. [Abstract] [Full Text] [PDF]

				R. J. Edwards, S. R. Redwood, P. D. Lambiase, and M. S. Marber The effect of an angiotensin-converting enzyme inhibitor and a K+ATP channel opener on warm up angina Eur. Heart J., March 2, 2005; 26(6): 598 - 606. [Abstract] [Full Text] [PDF]

				V. Pasceri, G. Patti, and A. Maseri Changing Features of Anginal Pain After PTCA Suggest a Stenosis on a Different Artery Rather Than Restenosis Circulation, November 18, 1997; 96(10): 3278 - 3280. [Abstract] [Full Text]

				F. Crea and A. Gaspardone New Look to an Old Symptom: Angina Pectoris Circulation, November 18, 1997; 96(10): 3766 - 3773. [Abstract] [Full Text]