Kardiologiia · 2004
[Impairment of cardiac sympathetic function in patients with acute myocardial infarction and unstable angina].
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Kozlovskaia I Iu, Shitov V N, Samoĭlenko L E, Merkulova I N, Staroverov I I, Sergienko V B
Аннотация
AIM: To assess the state of sympathetic innervation of the heart in patients with acute coronary syndrome.
MATERIAL: Patients with Q-myocardial infarction (MI, n=36), non-Q-MI (n=13), and unstable angina (UA, n=9).
METHODS: Each subject underwent single-photon emission computed tomography (SPECT) and planar scintigraphy using iodine-123 metaiodobenzylguanidine ((123)I-MIBG) for assessment of cardiac sympathetic function. We analyzed early (15 minutes) and delayed (4 hours) images after (123)I-MIBG administration. Resting (99m)Tc-MIBI myocardial scintigraphy was performed for evaluation of myocardial perfusion. Location, extent (%) and severity (Un.) of defects were determined using <<CEqual 3.0>> program. (123)I-MIBG did not accumulate in myocardium of 3.5% patients. All other patients demonstrated (123)I-MIBG accumulation defects. These defects were colocolized with (99m)Tc-MIBI uptake abnormalities. However both extent and severity of sympathetic innervation defects exceeded those of perfusion defects in all patients. Mean extent and severity of sympathetic neuronal damage areas were the greatest in patients with Q-MI (41+/-8% and 1119+/-377 Un. respectively) and the least in patients with UA (22+/-12% and 602+/-353 Un., respectively). On the contrary the mean extent of areas with sympathetic endings dysfunction but normal perfusion was the largest in UA group and the least in Q-MI group (18+/-11 and 10+/-7%, respectively, p<0,05).
CONCLUSION: Impairment of cardiac sympathetic function in patients with acute coronary syndrome could be detected by SPECT with (123)I-MIBG. Locations of (123)I-MIBG and (99m)Tc-MIBI defects were similar but sympathetic dysfunction areas were larger than areas with reduced perfusion. This result suggests higher sensitivity of sympathetic endings to ischemia compared with cardiomyocytes. Myocardial areas with sympathetic endings dysfunction but normal perfusion can be defined as myocardium at risk.
MATERIAL: Patients with Q-myocardial infarction (MI, n=36), non-Q-MI (n=13), and unstable angina (UA, n=9).
METHODS: Each subject underwent single-photon emission computed tomography (SPECT) and planar scintigraphy using iodine-123 metaiodobenzylguanidine ((123)I-MIBG) for assessment of cardiac sympathetic function. We analyzed early (15 minutes) and delayed (4 hours) images after (123)I-MIBG administration. Resting (99m)Tc-MIBI myocardial scintigraphy was performed for evaluation of myocardial perfusion. Location, extent (%) and severity (Un.) of defects were determined using <<CEqual 3.0>> program. (123)I-MIBG did not accumulate in myocardium of 3.5% patients. All other patients demonstrated (123)I-MIBG accumulation defects. These defects were colocolized with (99m)Tc-MIBI uptake abnormalities. However both extent and severity of sympathetic innervation defects exceeded those of perfusion defects in all patients. Mean extent and severity of sympathetic neuronal damage areas were the greatest in patients with Q-MI (41+/-8% and 1119+/-377 Un. respectively) and the least in patients with UA (22+/-12% and 602+/-353 Un., respectively). On the contrary the mean extent of areas with sympathetic endings dysfunction but normal perfusion was the largest in UA group and the least in Q-MI group (18+/-11 and 10+/-7%, respectively, p<0,05).
CONCLUSION: Impairment of cardiac sympathetic function in patients with acute coronary syndrome could be detected by SPECT with (123)I-MIBG. Locations of (123)I-MIBG and (99m)Tc-MIBI defects were similar but sympathetic dysfunction areas were larger than areas with reduced perfusion. This result suggests higher sensitivity of sympathetic endings to ischemia compared with cardiomyocytes. Myocardial areas with sympathetic endings dysfunction but normal perfusion can be defined as myocardium at risk.