The aim of this study was to examine the prevalence, distribution, and topographic relationship of vascular 18 F-sodium fluoride uptake and arterial calcification in major arteries. Methods: Image data obtained from 75 patients undergoing whole-body 18 F-sodium fluoride PET/CT were evaluated retrospectively. Arterial radiotracer uptake and calcification were analyzed qualitatively and semiquantitatively. Results: 18 F-sodium fluoride uptake was observed at 254 sites in 57 (76%) of the 75 study patients, and calcification was observed at 1,930 sites in 63 (84%) of the patients. Colocalization of radiotracer accumulation and calcification could be observed in 223 areas of uptake (88%). However, only 12% of all arterial calcification sites showed increased radiotracer uptake. Conclusion: Our data indicate the feasibility of 18 F-sodium fluoride PET/CT for the imaging of mineral deposition in arterial wall alterations. 18 F-sodium fluoride PET/CT may provide relevant information about the morphologic and functional properties of calcified plaque.

Good correlation and agreement with (201)Tl SPECT indicate DE MR imaging may be used to estimate infarct size 6 days after reperfused acute myocardial infarction. DE MR imaging is more sensitive for detection of inferior infarction than is (201)Tl SPECT. Patients with microvascular obstruction on FPE MR images have larger infarcts.

Formation and progression of atherosclerotic plaque is a dynamic and complex process involving various pathophysiologic steps including inflammation and calcification. The purpose of this study was to compare macrophage activity as determined by 18 F-FDG PET and ongoing mineral deposition as measured by 18 F-sodium fluoride PET in atherosclerotic plaque and to correlate these findings with calcified plaque burden as assessed by CT. Methods: Forty-five patients were examined by whole-body 18 F-FDG PET, 18 F-sodium fluoride PET, and CT. Tracer uptake in various arterial segments was analyzed both qualitatively and semiquantitatively by measuring the blood-pool-corrected standardized uptake value (target-to-background ratio [TBR]). The pattern of tracer uptake in atherosclerotic lesions was compared after color-coded multistudy image fusion of PET and CT studies. The Fisher exact test and the Spearman correlation coefficient r s were used for statistical analysis of image-based results and cardiovascular risk factors. Intra-and interrater reproducibility were evaluated using the Cohen k. Results: 18 F-sodium fluoride uptake was observed at 105 sites in 27 (60%) of the 45 study patients, and mean TBR was 2.3 6 0.7. 18 F-FDG uptake was seen at 124 sites in 34 (75.6%) patients, and mean TBR was 1.5 6 0.3. Calcified atherosclerotic lesions were observed at 503 sites in 34 (75.6%) patients. Eighty-one (77.1%) of the 105 lesions with marked 18 F-sodium fluoride uptake and only 18 (14.5%) of the 124 lesions with 18 F-FDG accumulation were colocalized with arterial calcification. Coincident uptake of both 18 F-sodium fluoride and 18 F-FDG was observed in only 14 (6.5%) of the 215 arterial lesions with radiotracer accumulation. Conclusion: PET/ CT with 18 F-FDG and 18 F-sodium fluoride may allow evaluation of distinct pathophysiologic processes in atherosclerotic lesions and might provide information on the complex interactions involved in formation and progression of atherosclerotic plaque.

The purpose of this study was to correlate 18 F-sodium fluoride accumulation in the common carotid arteries of neurologically asymptomatic patients with cardiovascular risk factors and carotid calcified plaque burden. Methods: Two hundred sixtynine oncologic patients were examined by 18 F-sodium fluoride PET/CT. Tracer accumulation in the common carotid arteries was analyzed both qualitatively and semiquantitatively by measuring the blood-pool-corrected standardized uptake value (target-to-background ratio) and comparing it with cardiovascular risk factors and calcified plaque burden. Results: 18 Fsodium fluoride uptake was observed at 141 sites in 94 (34.9%) patients. Radiotracer accumulation was colocalized with calcification in all atherosclerotic lesions. 18 F-sodium fluoride uptake was significantly associated with age (P , 0.0001), male sex (P , 0.0001), hypertension (P , 0.002), and hypercholesterolemia (P , 0.05). The presence of calcified plaque correlated significantly with these risk factors but also with diabetes (P , 0.0001), history of smoking (P 5 0.03), and prior cardiovascular events (P , 0.01). There was a highly significant correlation between the presence of 18 F-sodium fluoride uptake and number of present cardiovascular risk factors (r 5 0.30, P , 0.0001). Conclusion: Carotid 18 F-sodium fluoride uptake is a surrogate measure of calcifying carotid plaque, correlates with cardiovascular risk factors, and is more frequent in patients with a high-risk profile for atherothrombotic events but demonstrates a weaker correlation with risk factors than does calcified plaque burden. This study provides a rationale to conduct further prospective studies to determine whether 18 F-sodium fluoride uptake can predict vascular events, or if it may be used to monitor pharmacologic therapy.

The parasympathetic nervous system plays an important role in the pathophysiology of atrial fibrillation. Catheter ablation, a minimally invasive procedure deactivating abnormal firing cardiac tissue, is increasingly becoming the therapy of choice for atrial fibrillation. This is inevitably associated with the obliteration of cardiac cholinergic neurons. However, the impact on ventricular electrophysiology is unclear. Here we show that cardiac cholinergic neurons modulate ventricular electrophysiology. Mechanical disruption or pharmacological blockade of parasympathetic innervation shortens ventricular refractory periods, increases the incidence of ventricular arrhythmia and decreases ventricular cAMP levels in murine hearts. Immunohistochemistry confirmed ventricular cholinergic innervation, revealing parasympathetic fibres running from the atria to the ventricles parallel to sympathetic fibres. In humans, catheter ablation of atrial fibrillation, which is accompanied by accidental parasympathetic and concomitant sympathetic denervation, raises the burden of premature ventricular complexes. In summary, our results demonstrate an influence of cardiac cholinergic neurons on the regulation of ventricular function and arrhythmogenesis.