BACKGROUND: Myocardial (123) I-metaiodobenzylguanidine (MIBG) kinetics reflect the integrity and function of cardiac presynaptic sympathetic nerve terminals. Heart rate variability (HRV) is an indicator of cardiac sympatho-vagal balance. However, the function of cardiac sympathetic nerve terminals as a modulator of HRV in asymptomatic subjects has remained elusive. In addition, the physiological background for different components of HRV is not fully established. METHODS: We evaluated the relationship between myocardial MIBG washout and HRV in 30 asymptomatic subjects with familial risk of coronary artery disease (CAD). Early and delayed myocardial MIBG uptakes as well as MIBG washout between these two scans were assessed. Myocardial perfusion at rest and during bicycle exercise was evaluated with (99m) Tc-sestamibi (MIBI). HRV was measured from 24-hour ambulatory ECG recordings. RESULTS: Myocardial MIBG washout averaged 40 ± 8%. The mean heart rate at rest was 76 ± 14 beats/min. Standard deviation of all normal RR intervals (SDNN) was 94 ± 22 ms and very low frequency (VLF) was 1625 ± 958 ms(2) on average. Myocardial MIBG washout correlated inversely with SDNN (r =-0.390; P < 0.05) and with VLF (r =-0.459; P < 0.01) component of HRV but not with heart rate at rest (r = 0.207, P = ns). All subjects had normal myocardial perfusion at rest and during exercise. CONCLUSIONS: Increased cardiac presynaptic sympathetic nervous activity was related to reduced HRV in subjects with the risk of CAD but without evidence of myocardial ischemia or previous myocardial infarction. In addition, we found that VLF component of HRV includes information about sympathetic neural modulation of the heart rate.
BACKGROUND: Myocardial (123) I-metaiodobenzylguanidine (MIBG) kinetics reflect the integrity and function of cardiac presynaptic sympathetic nerve terminals. Heart rate variability (HRV) is an indicator of cardiac sympatho-vagal balance. However, the function of cardiac sympathetic nerve terminals as a modulator of HRV in asymptomatic subjects has remained elusive. In addition, the physiological background for different components of HRV is not fully established. METHODS: We evaluated the relationship between myocardial MIBG washout and HRV in 30 asymptomatic subjects with familial risk of coronary artery disease (CAD). Early and delayed myocardial MIBG uptakes as well as MIBG washout between these two scans were assessed. Myocardial perfusion at rest and during bicycle exercise was evaluated with (99m) Tc-sestamibi (MIBI). HRV was measured from 24-hour ambulatory ECG recordings. RESULTS: Myocardial MIBG washout averaged 40 ± 8%. The mean heart rate at rest was 76 ± 14 beats/min. Standard deviation of all normal RR intervals (SDNN) was 94 ± 22 ms and very low frequency (VLF) was 1625 ± 958 ms(2) on average. Myocardial MIBG washout correlated inversely with SDNN (r =-0.390; P < 0.05) and with VLF (r =-0.459; P < 0.01) component of HRV but not with heart rate at rest (r = 0.207, P = ns). All subjects had normal myocardial perfusion at rest and during exercise. CONCLUSIONS: Increased cardiac presynaptic sympathetic nervous activity was related to reduced HRV in subjects with the risk of CAD but without evidence of myocardial ischemia or previous myocardial infarction. In addition, we found that VLF component of HRV includes information about sympathetic neural modulation of the heart rate.
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