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ObjectivesWe investigated whether cardiac sympathetic nervous system (SNS) activity measured by iodine-123 meta-iodobenzylguanidine (123I-mIBG) imaging would be associated with both the occurrence of heart failure (HF) and the transit to permanent atrial fibrillation (AF) in patients with paroxysmal AF.BackgroundAtrial fibrillation occurs suddenly and transiently and can persist, and results in the occurrence of HF. An important feature of AF and HF is their propensity to coexist not only because they share antecedent risk factors, but also because the one may directly predispose the heart to the other. However, a useful modality for predicting the occurrences of both those has not been established in patients with paroxysmal AF.MethodsThe 123I-mIBG scintigraphy was performed to evaluate cardiac SNS activity presented as the heart/mediastinum ratio in 98 consecutive patients (age 66 ± 13 years, 63.3% male) with idiopathic paroxysmal AF and preserved left ventricular ejection fraction (≥50%).ResultsDuring 4 ± 3.6 years of follow-up, the transit to permanent AF was associated with the occurrence of HF (34.3% in 12 of 35 patients with permanent AF vs. 6.3% in 4 of 63 patients without, p < 0.0001). Lower heart/mediastinum ratio and lower left ventricular ejection fraction were the independent predictors of the transit to permanent AF with adjusted hazard ratios of 3.44 (95% confidence interval [CI]: 1.9 to 6.2, p < 0.0001) and 1.04 (95% CI: 1.01 to 1.08, p = 0.014). Further, these factors and higher plasma brain natriuretic peptide concentration were the independent predictors of the occurrence of HF with permanent AF, with adjusted hazard ratios of 5.08 (95% CI: 1.5 to 17.5, p = 0.011), 1.11 (95% CI: 1.03 to 1.19, p = 0.004), and 1.004 (95% CI: 1.001 to 1.008, p = 0.014).ConclusionsCardiac SNS abnormality was associated with the occurrence of both HF and permanent AF in paroxysmal AF patients, and 123I-mIBG imaging may be a useful modality for predicting the development of AF.

The aim of this study was to evaluate the relationship between exercise-induced QT dispersion and condition of infarct-related myocardium including myocardial scar after angioplasty assessed with exercise perfusion single photon emission computed tomography (SPECT).Exercise thallium-201 SPECT was performed 6 months after successful direct angioplasty in 67 male patients (60.6 +/- 11.5 years), who had Q wave infarction resulting from single vessel disease, and the number of perfusion defect areas (DS) was measured at rest and exercise together with QT (QTc) dispersion.In 52 patients with resting perfusion defects, the exercise-induced change in DS was correlated to the change in QT (or QTc) dispersion (r = -0.51 or r = -0.531, p0.0001). When the patients were grouped according to the patterns of transient perfusion defect, there were significant differences in DeltaQT dispersion and DeltaQTc dispersion among infarct-related three groups (reverse, fixed, and partial redistributions) and normal volunteers (DeltaQT dispersion; -5.7 +/- 12.7 ms in 13 patients with reverse redistribution, -16.3 +/- 13.1 ms in 30 patients with fixed redistribution, -28.9 +/- 29.5 ms in 9 patients with partial redistribution, and +3.4 +/- 20.9 ms in 12 normal volunteers, p = 0.0098; DeltaQTc dispersion; +18.2 +/- 20.8 ms, +1.4 +/- 16.7 ms, -15.4 +/- 30 ms, and +19 +/- 27.5 ms, p = 0.0017, respectively). DeltaQTc dispersion estimated the SPECT image patterns (p = 0.0002) with a sensitivity of 67.3%, a specificity of 83.7% and an accuracy of 78.2%.The change with exercise in QT dispersion may help detect the condition of infarct-related myocardium after angioplasty.

The aim of this study was to evaluate the significance of extension of exercise-induced ischemia toward apex of left ventricle.After injections of technetium-99m tetrofosmin at peak ergometer exercise and thallium-201 at 3 min post-exercise, dual-isotope single photon emission computed tomography (SPECT) images were obtained simultaneously with cross-talk compensation using triple-energy window in 70 patients (65.8+/-9.5 years) with angiographically proven ischemic heart disease. The left ventricle was divided into a total of 18 areas in 3 levels of apical, middle, basal, and the extent and localization of ischemia to long axis of left ventricle were measured at peak exercise and 3 min into the recovery.Of 57 patients with exercise-induced reversible ischemia, in 25 patients with the ischemia in 2 levels to long axis of left ventricle, the ischemia extended mainly to the middle and basal levels (p0.0001) and was localized during recovery mainly in the basal level (p0.0005). In 21 patients with the ischemia in all 3 levels, the ischemia was localized during recovery mainly to the middle and basal levels (p0.05). The persistence of ischemia in apex at post-exercise reflected the delay of recovery from ischemia on the whole of left ventricle and was related to the enlargement of resting end-diastolic volume of left ventricle as compared to the quick recovery of ischemia in apex (p0.0005 and p0.05, respectively).Although the ischemia recovers earliest in the peripheral apical level within exercise-induced ischemic territory, the delay of recovery from the ischemia in the apical level may be related to the development of heart failure, independent of intensity of occurred ischemia during exercise.