Association of baseline subject characteristics with changes in coronary calcification assessed by 18F-sodium fluoride PET/CT.

OBJECTIVE: The goal of this study was to test if changes in coronary microcalcification over a two year period assessed by fluorine-18-sodium fluoride (18F-NaF) positron emission tomography/computed tomography (PET/CT) are associated with baseline subject characteristics. SUBJECTS AND METHODS: This prospective study included healthy female (N=8, age 52±10 years, body mass index(BMI) 24±1.7kg/m2) and male (N=15, age 50±10 years, BMI 27±2.9kg/m2) participants who had 18F-NaF PET/CT scans taken two years apart. Imaging was performed 90 minutes after intravenous injection of 2.2MBq of 18F-NaF per kilogram of body weight. The analysis regions were selected on CT images by drawing volumes of interest around the entire heart using a semi-automatic segmentation method.Mean standardize uptake value (SUVmean) and maximum SUV (SUVmax) were calculated in the same regions of the registered PET images. Percent change in SUV between the two time points were correlated against baseline age, BMI, cardiovascular risk factors, and blood chemistry. RESULTS: In males, percent change in SUVmean over the two year period was positively correlated with baseline BMI (r=0.85, P<0.0001) and systolic blood pressure (r=0.65, P=0.0082). These baseline values were not significantly correlated with SUVmax in either gender. CONCLUSION: High BMI is a known risk factor for atherosclerosis. Our data showed that rate of increase in coronary microcalcification over time measured by 18F-NaF PET/CT is associated with baseline BMI and some clinical risk factors in males. Lack of such associations in females could be due to low sample size (N=8). Further prospective studies are needed to determine if baseline BMI and clinical factors could be used to predict rate of increase in coronary microcalcification which could provide the basis for managing the progression of atherosclerosis in patient-specific manner.

High resolution mapping of the pulmonary vein and the vein of Marshall during induced atrial fibrillation and atrial tachycardia in a canine model of pacing-induced congestive heart failure.

OBJECTIVES: The study examined the activations in the pulmonary veins (PVs) and the vein of Marshall (VOM) during atrial fibrillation (AF) in dogs with congestive heart failure (CHF). BACKGROUND: The patterns of activation within the PVs and the VOM during AF in CHF are unclear. METHODS: We induced CHF in nine dogs by rapid ventricular pacing. The patterns of activation during induced AF were studied one week after ceasing ventricular pacing. RESULTS: The duration of induced AF averaged 80.7 +/- 177.3 s. The termination of low-amplitude fractionated activity in the PVs preceded the termination of AF in 25 of 29 episodes. High-density mapping (1-mm resolution) showed that the PV was activated by a focal wave front independent of left atrial (LA) activation in 22 AF episodes. Frequent intra-PV conduction blocks and multiple wave fronts in the PVs were recorded during 10 AF episodes. Focal activations were observed within the VOM in 4 of 12 episodes of AF. Three atrial tachycardia (AT) episodes originated from a focus within a PV. Histological studies showed extensive fibrosis in the PVs and in the atria. The PVs in five normal dogs did not have focal or fractionated activity during induced AF. CONCLUSIONS: Atrial fibrillation in canine CHF is associated with independent focal activations in the PVs and the VOM, and with complex wave fronts within the PVs. The PVs may also serve as the origin of AT. These findings suggest that electrical and anatomical remodeling of the PVs and the VOM are important in the maintenance of AF and AT in dogs with CHF.

Nonreentrant focal activations in pulmonary veins in canine model of sustained atrial fibrillation.

Repetitive rapid activities are present in the pulmonary veins (PVs) in dogs with pacing-induced sustained atrial fibrillation (AF). The mechanisms are unclear. We induced sustained (>48 h) AF by rapidly pacing the left atrium (LA) in six dogs. High-density computerized mapping was done in the PVs and atria. Results show repetitive focal activations in all dogs and in 12 of 18 mapped PVs. Activation originated from the middle of the PV and then propagated to the LA and distal PV with conduction blocks. The right atrium (RA) was usually activated by a single large wavefront. Mean AF cycle length in the PVs (left superior, 82 +/- 6 ms; left inferior, 83 +/- 6 ms; right inferior, 83 +/- 4 ms) and LA posterior wall (87 +/- 5 ms) were significantly (P < 0.05) shorter than those in the LA anterior wall (92 +/- 4 ms) and RA (107 +/- 5 ms). PVs in normal dogs did not have focal activations during induced AF. No reentrant wavefronts were demonstrated in the PVs. We conclude that nonreentrant focal activations are present in the PVs in a canine model of pacing-induced sustained AF.