J. Hartikainen et al., EXTENT OF CARDIAC ANTONOMIC DENERVATION IN RELATION TO ANGINA ON EXERCISE TEST IN PATIENTS WITH RECENT ACUTE MYOCARDIAL-INFARCTION, The American journal of cardiology, 74(8), 1994, pp. 760-763
According to the current concept, anginal pain results from stimulatio
n of sympathetic nerves within the heart. In this study, we evaluated
the role of cardiac adreneric denervation in exercise-induced angina p
ectoris in 15 men with recent acute myocardial infarction. Before disc
harge from the hospital, the patients were subjected to a symptom-limi
ted exercise test. Three months after the infarction, cardiac scintigr
aphic studies using 1-123 metaiodobenzylguanidine no (MIBG), 1-123 par
aphenylpentadecanoic acid (pPPA), and Tc-99m sestamibi (MIBI) were per
formed in order to determine the extent of denervated myocardium, the
size of infarction, and myocardium with reduced perfusion, respective
ly. MIBG defect (17.2 +/- 7.6% of left ventricular mass) (defect defin
ed as an activity distribution less than or equal to 30% of the maxima
l myocardial activity) was larger than pPPA defect (8.3 +/- 8.8%, p <
0.001) in all patients, which indicates that the area of myocardial ne
crosis was surrounded by viable myocardium with sympathetic denervatio
n. The extent of viable but denervated myocardium was significantly gr
eater in patients who developed angina pectoris than in patients witho
ut angina pectoris during the early exercise test (13.3 +/- 4.4% vs 5.
0 +/- 2.4%, p < 0.001). In addition, patients with silent ischemia ten
ded to have smaller areas of viable but denervated myocardium than pat
ients with painful ischemia (5.7 +/- 3.8% vs 13.8 +/- 5.1%, p = 0.07).
Thus, contrary to expectations, the extent of viable but denervated m
yocardium seems to be associated with increased pain sensitivity in pa
tients with recent myocardial infarction.