Spectral coronary multidetector computed tomography angiography: dual benefit by facilitating plaque characterization and enhancing lumen depiction.

OBJECTIVE: To assess ex vivo specimens of atherosclerotic coronary arteries by dual energy (DE) multidetector computed tomography (MDCT) imaging, and to correlate depicted vessel lumen morphology and detected tissue characteristics with histopathologic analysis. METHODS: Coronary arteries were imaged on a 16-slice MDCT using a DE protocol consisting of a 90- and 140-kV scan. Coronary arteries were perfused with iodine- and gadolinium-based contrast agents. The DE K-edge subtractions were performed. Regions-of-interest were placed on histopathologically/radiographically-matched vascular lumen and wall, fibromuscular and calcified plaque, and fat tissues. Vascular/tissue contrast-to-noise ratios (CNR) were calculated, and their dependence on tissue type and contrast agent type was statistically evaluated. RESULTS: Tissue CNR analysis confirmed that all tissue types were successfully distinguished. Vascular wall and fibromuscular plaque achieved a significant increase in CNR ratios when DE techniques were used compared with 140 kV protocols. CONCLUSIONS: Spectral DE MDCT imaging of ex vivo atherosclerotic coronary arteries allows successful tissue characterization and enhances depiction of coronary lumen.

Synergy of MDCT and cine MRI for the evaluation of cardiac motility.

OBJECTIVE: The objective of our study was to validate the feasibility of the synergistic use of cardiac MR and CT data sets for ventricular motility analysis and to correlate measurement variability with underlying heart rate. SUBJECTS AND METHODS: Twenty patients underwent concurrent ECG-gated MDCT and MRI for evaluation of ventricular motility, expressed as ventricular wall thickening and motion. Initially, individual measurement repetition series were analyzed by determining intraobserver variability and detecting intraobserver bias related to heart rates. Subsequently, absolute measurement differences of CT or MR data were statistically evaluated. Finally, absolute measurement differences were correlated with underlying heart rates by curve estimation regression. RESULTS: Analysis of measurement reproducibility proved that data variability was dependent on only the anatomic localization of the analyzed ventricular segment, not on the imaging technique used or underlying heart rate, in normofrequent patients. Comparing MR and CT image data sets, no statistically significant differences were identified when ventricular motility was evaluated based on data sets of either imaging technique in normofrequent patients. Tachycardic frequencies, above 100 beats per minute, led to exponential error propagation due to insufficient temporal resolution of the current CT technology. CONCLUSION: This study proved that cardiac motility assessment based on ECG-gated CT and MR data sets resulted in comparable ventricular function results for normofrequent patients; however, the high spatial resolution of cardiac MDCT cannot compensate for the lack of temporal resolution in patients with tachycardia, thus emphasizing the necessity of reporting ventricular motility analysis results in combination with heart rate to allow consideration of this possible cause for measurement variation.

Upregulation of functionally active vascular endothelial growth factor by human cytomegalovirus.

Human cytomegalovirus (HCMV) infection is known to modulate host gene expression and has been linked to the pathogenesis of vasculopathies; however, relevant pathomechanisms are still unclear. It was shown that HCMV infection leads to upregulation of vascular endothelial growth factor (VEGF) expression in human foreskin fibroblasts and coronary artery smooth muscle cells (SMC). Activation of VEGF transcription by HCMV infection was confirmed by transient-expression experiments, which revealed that a short promoter fragment, pLuc135 (-85 to +50), is sufficient for activation. Site-directed mutagenesis of Sp1-recognition sites within this fragment abolished the upregulation of transcription. Functional VEGF protein is released into the culture supernatant of infected SMC. Incubation of endothelial cells with supernatants from HCMV-infected SMC cultures induced upregulation of VEGF receptor-2 expression on endothelial cells, as well as a significant upregulation of DNA synthesis, implicating cell proliferation. The mean incline of DNA synthesis at 48 and 72 h post-infection was 148 and 197 %, respectively. Addition of neutralizing antibodies against VEGF completely abolished this effect. Supernatants from SMC cultures incubated with UV-inactivated virus induced a comparable effect. This virus-induced paracrine effect may represent a molecular mechanism for HCMV-induced pathogenesis, such as inflammatory vasculopathies, by inducing a proatherogenic phenotype in SMC.