Background:T2-weighted MRI is well established for detection of clinically significant prostate cancer (csPCa), but prior studies have primarily focused onT2within MRI-visible lesions.Purpose:To determine whether patients with csPCa have systematically abnormalT2-weighted signal in non-lesion, background prostate tissue (BP).Materials and Methods:This retrospective study included two patient cohorts who underwent 3T MRI examination for suspected csPCa between August 2016 and February 2020. Median (urine-normalized)T2-weighted signal was computed for BP. BP signal was compared between patients with and without csPCa, using two-samplet-tests (α=0.05). csPCa discrimination performance ofT2-weighted BP signal was evaluated using area under receiver operating characteristic curves (AUC).T2andS0(a proxy for proton density) were computed and compared between patients with and without csPCa using two-samplet-tests (α=0.05).T2was also recomputed with larger buffers around csPCa lesions. Finally, csPCa discrimination performance was compared between two predictors: maximum Restriction Spectrum Imaging (RSI)C1and maximum RSIC1normalized by global prostate medianT2-weighted signal.Results:Cohort 1: 46 patients (mean age: 64 years ±10 [standard deviation]). Cohort 2: 151 patients (age: 65±8 years). Urine-normalizedT2-weighted signal was systematically lower in BP of subjects with csPCa compared to those without (p≤0.034). BPT2-weighted signal indicated the presence of cancer (cohort 1: AUC=0.80; cohort 2: AUC=0.68). BPT2was significantly lower in csPCa patients compared to those without (p≤0.011), whileS0was not (p≥0.30). BPT2measurements were stable to within 5% using a buffer of 0 to 30 mm around visible csPCa lesions. csPCa discrimination improved with incorporation of global prostate medianT2-weighted signal (cohort 1: AUC=0.72 for maximum RSIC1alone versus 0.81 when normalized by medianT2-weighted signal; cohort 2: AUC=0.63 versus 0.76).Conclusion:LowerT2-weighted signal in BP suggests the presence of csPCa.
Pulmonary arterial hypertension (PAH) is a rare disorder characterized by elevated blood pressure and pulmonary vascular resistance, often followed by right ventricular hypertrophy and heart failure. The effect of PAH and its treatments on the mechanics, function, and remodelling of the right ventricle (RV) is currently not well understood. To study cardiac biomechanics and functionality as PAH progresses, we implemented a computational model of the heart simulating right ventricular maladaptive remodelling. Our Windkessel-based model, which accounts for direct ventricular interaction and the presence of the pericardium, is utilized to simulate various disease stages of PAH. We find that the pericardium has a larger effect on heart performance than ventricular interaction through the septum.We also examined the effectiveness of two treatments, ventricular assist device (RVAD) and atrial septostomy, on diseased hearts. We show that while both pulsatile and continuous RVADs restore cardiac function, pulsatile RVAD improves cardiac output 29.4% more than continuous RVAD. We also demonstrate that atrial septostomy improves cardiac output by 19.5%. Our model can be further extended by simulating the heart’s response to other treatments such as extracorporeal membrane oxygenation (ECMO), and by incorporating ventricular remodelling growth simulations and finite-element ventricular modelling.
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