Dynamic T1-weighted magnetic resonance imaging and positron emission tomography in patients with lung cancer: correlating vascular physiology with glucose metabolism.

The management of primary lung cancer relies on sophisticated imaging methods to assist in the diagnosis, staging, and evaluation of tumor regression during treatment. The information provided is generally anatomical in nature, except for that provided by positron emission tomography with [18F]fluorodeoxyglucose, a modality that yields physiological data that have been shown to be useful in identifying neoplasia, based on an elevated glucose metabolic rate. Because the metabolism of malignant tissue depends intimately on neovascularization to provide oxygen and glucose in sufficient quantities to allow tumor growth, the characterization of tumor vascular physiology could be an important tool for assessing and predicting the likely effectiveness of treatment. Our goal was to show the feasibility and practical value of parameters of tumor vascular physiology obtained using dynamic T1-weighted magnetic resonance imaging (MRI), to correlate them with glucose metabolism and to demonstrate changes in these parameters during and after treatment in patients with lung cancer. Parameters of vascular physiology [permeability-surface area (PS) product and extracellular contrast agent distribution volume] and glucose metabolism were assessed in 14 patients with lung cancer. Glucose metabolism was measured by using [18F]fluorodeoxyglucose-positron emission tomography. Vascular physiology was assessed by dynamic T1-weighted, contrast-enhanced MRI. The mean PS product in tumor was 0.0015 +/- 0.0002 s(-1) (n = 13) before, 0.0023 +/- 0.0003 s(-1) (n = 3, P = 0.053) midway through, and 0.00075 +/- 0.0002 s(-1) (n = 5, P < 0.03) 2 weeks after treatment. Values for the extracellular contrast distribution space were 0.321 +/- 0.03 before, 0.289 +/- 0.02 midway through, and 0.195 +/- 0.02 (P < 0.01) 2 weeks after therapy. The glucose metabolic rate was significantly correlated with the PS product (P < 0.01) but not with the extracellular contrast distribution space. Our results demonstrate that tumor PS product correlates with glucose metabolism, that chemo- and radiotherapy induce observable and quantifiable changes in these parameters, and that such changes can be measured by in vivo dynamic MRI. Quantitative dynamic T1-weighted MRI of tumor vascular physiology may have a useful role in the clinical management of lung cancer.