J. Hartikainen et al., CARDIAC SYMPATHETIC DENERVATION IN PATIENTS WITH CORONARY-ARTERY DISEASE WITHOUT PREVIOUS MYOCARDIAL-INFARCTION, The American journal of cardiology, 80(3), 1997, pp. 273-277
Myocardial infarction damages sympathetic nerve fibers coursing throug
h the infarct zone. In this study we investigated whether coronary art
ery disease without myocardial infarction results in sympathetic dener
vation. We examined 12 patients without a history of previous myocardi
al infarction and 19 postinfarction patients. I-123 metaiodobenzylguan
idine (MIBG) and technetium-99m sestamibi (MIBI) single-photon emissio
n tomography were conducted at rest to determine the extent of denerva
ted myocardium and the extent of myocardium with reduced perfusion, re
spectively. In addition, myocardial perfusion during exercise was asse
ssed with MIBI. A MIBG or MIBI defect was determined as being regional
uptake of less than or equal to 30% of the maximal myocardial activit
y. All but 1 patient without previous infarction had MIBG defects. MIB
G defects (10.3 +/- 8.5% of left ventricular moss) were significantly
larger than MIBI defects at rest (2.4 +/- 3.2%, p <0.001) and during e
xercise (4.8 +/- 6.1%, p <0.05). In multiregression analysis, the size
of an MIBG defect was associated with severity of coronary stenoses (
greater than or equal to 90% of lumen diameter; p <0.05), but not with
age, number of significant stenoses (greater than or equal to 50% of
lumen diameter), left main disease, functional doss, left venticular e
jection fraction, angina pectoris, maximal ST depression, or mean work
load during exercise test. MIBG and MIBI defects were significantly la
rger in patients with severe coronary stenoses than in patients with m
oderate stenoses (50% to 89% of lumen diameter) (16.4 +/- 8.9% vs 6.0
+/- 5.2% [p <0.0-5] and 5.0 +/- 3.1% vs 0.6 +/- 7.3% [p <0.001], respe
ctively). The size of MIBG (16.1 +/- 8.9%) and MIBI defects (7.3 +/- 6
.5%) at rest in postinfarction patients did not differ from patients w
ith severe stenoses. Our study demonstrates that cardiac adrenergic ti
ssue is very sensitive to ischemia and that regional cardiac sympathet
ic denervation can occur in patients with stable coronary artery disea
se without previous myocardial infarction. (C) 1997 by Excerpta Medica
, Inc.