Adaptive radiotherapy for head and neck cancer reduces the requirement for rescans during treatment due to spinal cord dose.

BACKGROUND: Patients treated with radiotherapy for head and neck (H&N) cancer often experience anatomical changes. The potential compromises to Planning Target Volume (PTV) coverage or Organ at Risk (OAR) sparing has prompted the use of adaptive radiotherapy (ART) for these patients. However, implementation of ART is time and resource intensive. This study seeks to define a clinical trigger for H&N re-plans based on spinal cord safety using kV Cone-Beam Computed Tomography (CBCT) verification imaging, in order to best balance clinical benefit with additional workload. METHODS: Thirty-one H&N patients treated with Volumetric Modulated Arc Therapy (VMAT) who had a rescan CT (rCT) during treatment were included in this study. Contour volume changes between the planning CT (pCT) and rCT were determined. The original treatment plan was calculated on the pCT, CBCT prior to the rCT, pCT deformed to the anatomy of the CBCT (dCT), and rCT (considered the gold standard). The dose to 0.1 cc (D0.1cc) spinal cord was evaluated from the Dose Volume Histograms (DVHs). RESULTS: The median dose increase to D0.1cc between the pCT and rCT was 0.7 Gy (inter-quartile range 0.2-1.9 Gy, p < 0.05). No correlation was found between contour volume changes and the spinal cord dose increase. Three patients exhibited an increase of 7.0-7.2 Gy to D0.1cc, resulting in a re-plan; these patients were correctly identified using calculations on the CBCT/dCT. CONCLUSIONS: An adaptive re-plan can be triggered using spinal cord doses calculated on the CBCT/dCT. Implementing this trigger can reduce patient appointments and radiation dose by eliminating up to 90% of additional un-necessary CT scans, reducing the workload for radiographers, physicists, dosimetrists, and clinicians.

Impaired endothelium-dependent and -independent vasodilation in elderly patients with chronic heart failure.

BACKGROUND: Impaired endothelium-dependent and independent vasodilator responses in chronic heart failure (CHF) have been well described. Previous studies involved younger patients and omitted medications prior to study. AIMS: We explored if new therapeutic interventions would restore vasodilator responses in typical patients with chronic heart failure. METHODS AND RESULTS: 24 patients and 15 controls were recruited, patients were maintained on their usual medications. Forearm blood flow responses were measured by venous occlusion plethysmography in response to incremental doses of sodium nitroprusside (SNP) (6, 9 and 12 nmol/min), acetylcholine (ACH) (120, 180 and 240 nmol/min), angiotensin II (AII) (1, 10 and 100 nmol/min) and N(g)-Nitro-L-arginine methyl ester (L-NAME) (1, 2 and 4 nmol/min) infused into the non-dominant brachial artery. FBF responses to SNP were impaired in patients compared with controls (13.7(9.9,17.4) vs. 24.8(18.6,30.9)) arbitrary units, P<0.001). Similarly FBF responses to ACH were reduced in patients compared with controls (7.5(4.2,10.9) vs. 24.8(16.4,33.2)) arbitrary units, P<0.001. Decreased FBF was noted in response to AII and L-NAME but was significant only for AII and did not differ between groups. CONCLUSIONS: In elderly patients with CHF, endothelium-dependent and independent vasodilator responses were blunted compared with controls. Defects in nitric oxide bioavailability and smooth muscle responsiveness are not reversed by modern medical management of the heart failure syndrome.