An interventional study of fludeoxyglucose(18f) and blood sample in Aging and Inflammation, sponsored by Central Hospital, Nancy, France. Completed at 1 site in France. Open to participants aged 65 Years and older, including healthy volunteers. Per ClinicalTrials.gov, last updated 2013-10-16.
Sponsored by Central Hospital, Nancy, France · Not applicable, Interventional, and Diagnostic
The purpose of this study is to determine the relationship between thoracic aortic inflammation and arterial stiffness in elderly patients.
Vascular-aging is accompanied by a gradual remodeling affecting both cardiac and arterial walls. Arterial hypertension, an established cardiovascular risk factor, has been suggested to exert pro-inflammatory actions threw several biological mediators enhancing arterial stiffness. Both effects of aging and hypertension are associated with higher levels of arterial stiffness, but their respective role is not well established in the pathophysiology of arterial stiffening.
Few data are available neither on the real anatomic aortic impact of aging and hypertension on aortic compliance and ventricular function and its relationship to arterial stiffness assessed by carotid-femoral pulse wave velocity, nor on the reliability of cine phase contrast magnetic resonance imaging arterial stiffness measurements.
Recent studies using positron emission tomography imaging (PET) with 18 F fluorodeoxyglucose (FDG) has been advocated as a means of measuring arterial wall inflammation in various population referred for oncology staging. FDG uptake is correlated with the number of cardiovascular risk factors and even the risk of future cardiovascular events. This method, combined with X-ray computed tomography (CT), has also demonstrated that aortic calcifications quantified by CT and local signs of inflammation detected by FDG uptake contribute to arterial stiffness. A strong relationship between large vessels stiffening assessed by carotid-femoral pulse wave velocity measurement, aortic calcifications quantified by CT and inflammation evaluated by FDG uptake has been demonstrated.
Therefore, in the current study, we use FDG PET associated to CT to characterize aortic inflammation and aortic calcifications coupled to pulse wave velocity measurement and cardiac function in elderly individuals.
In fact, if vascular aging promoting a local inflammatory process is a risk factor for cardiovascular disease, then vascular changes assessed by non-invasive vascular imaging (MRI,FDG PET) could represent a potential target for treatment and prevention Thirty individuals ≥ 65 years of age were examined, 15 hypertensive subjects and 15 controls. Pulse wave velocity, a surrogate for aortic stiffness, was measured both by cine phase contrast magnetic resonance imaging and applanation tonometry. Brachial pulse pressure, carotid calculated pulse pressure and pulse pressure amplification (brachial to carotid ratio), predictors of cardiovascular mortality were also quantified. Thoracic aorta local inflammation and calcification were measured by 18 F-fluorodeoxyglucose positron emission tomography/computed tomography imaging. Moreover, biomarkers of low grade inflammation (high-sensitivity C-reactive protein, interleukin 6 were also determined).
3,439 studies on the registry are indexed under Inflammation; 629 are open to participants now.
This study's enrollment of 30 is below the median of 50 across 2,437 interventional studies indexed under Inflammation.
Browse Inflammation studies →Central Hospital, Nancy, France is the lead sponsor of 778 studies on the registry; 183 are open to participants now.
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Exclusion Criteria:
Radiation: fludeoxyglucose(18f) · Other: blood sample · Other: cardiac and aortic magnetic resonance imaging · Other: carotid femoral pulse wave velocity · Radiation: positron emission tomography · Radiation: computed tomography
Also known as: GLUSCAN, solution for injection, 600 MBq/ml : 564 461-8, ADVANCED ACCELERATOR APPLICATIONS (AAA) Laboratory
Aortic inflammation assessed by 18 F FDG maximal standard uptake value measurement
Combined FDG PET/CT imaging was performed using a hybrid scanner hybrid system. For analysis, the thoracic aorta was divided into three segments: the ascending aorta, the aortic arch and the descending aorta. The standard uptake value (SUV) was calculated by dividing the activity measured in each voxel by the total injected activity, which was expressed per g of body weight and corrected for radioactive decay. Aortic activity was quantified using a conventional method on consecutive slices, which were orientated perpendicular to the aorta like described in previous publication. Region of interest (ROI) were drawn around the aorta on each trans-axial slice, allowing mean (SUVmean) and maximal aortic SUV (SUVmax) to be determined on every slice. These values were averaged to determine SUVmean and SUVmax for the ascending aorta, the aortic arch and the descending aorta. All PET scans were analyzed independently by two trained observers (VR, PM).
Time frame: one year
parietal thoracic aorta volume of calcification measured by computed tomography
Volumes of aortic calcifications (VCa) were also determined for the three predetermined segments of thoracic aorta using a dedicated software and a threshold of 130 Hounsfield Unity. All scans were analyzed independently by two trained observers (VR, PM).
Time frame: one year
carotid femoral pulse wave velocity
For carotid femoral pulse wave velocities determinations, measurements were done with a well-validated device. Aortic pulse wave velocity was measured at a central level, between carotid and femoral sites. The carotid femoral pulse wave velocity value was obtained by dividing the corresponding arterial length between two arterial sites by the time separating the onset of the pulse waves. Time intervals were determined by subtracting the delays, which were measured at each site between the R waves of ECG and the onset of the pulse waves and while averaging results from ten consecutive beats. Arterial length was defined as the distance from the suprasternal notch to the femoral radial minus the distance from the carotid artery to the suprasternal notch. Central systolic, diastolic and mean arterial pressures were estimated by recording the carotid pulse wave velocity.
Time frame: at the time of the measurement
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Central Hospital, Nancy, France