The CT revolution: the role of PIOPED II in establishing CT pulmonary angiography as the reference standard for pulmonary embolism diagnosis.

The PIOPED II study provided a robust estimate of the diagnostic accuracy of multidetector CTPA in suspected pulmonary embolism and played a pivotal role in establishing CTPA as the current diagnostic gold standard https://bit.ly/3HEyVxy.

Determinants and prognostic implication of diagnostic delay in patients with a first episode of pulmonary embolism.

Signs and symptoms of pulmonary embolism (PE) are not specific and this can lead to a diagnostic delay. Little is known about the determinants of this delay and its prognostic implication. We conducted a retrospective analysis of a prospective cohort involving 514 patients with a first episode of PE. The diagnostic delay was defined as a time from first symptom onset to diagnosis of >3 days, corresponding of the median time in the population. Multivariable logistic regression analysis was performed to identify determinants of diagnostic delay. Prognostic implication was measured as the occurrence of 30-day all-cause mortality, haemodynamic collapse or recurrent PE. A total of 240 (47%) among 514 patients had a time from first symptom to diagnosis > 3 days. Previous deep vein thrombosis (OR 0.55, 95% Confidence Interval (CI), 0.32-0.93), immobilization (OR 0.52, 95% CI, 0.28-0.96), surgery (OR 0.31, 95% CI, 0.16-0.62), chest pain (OR 0.58, 95% CI, 0.39-0.86), syncope (OR 0.48, 95% CI, 0.23-1.01), dyspnea (OR 2.48, 95% CI, 1.57-3.91) and hemoptysis (OR 3.57, 95% CI, 1.40-9.07) were associated with diagnostic delay. Twenty-two patients (4.3%, 95%CI, 2.8-6.5) experienced an outcome event within 30 days. Among them, 15 patients (6.2% 95%CI, 3.7-10.3) had a diagnostic delay and 7 (2.6%, 95% CI 1.1-5.4) did not (p = 0.039). In this cohort, diagnostic delay is associated with the absence of major risk factors for PE or clinical features such as chest pain or syncope and the presence of dyspnea or hemoptysis. Diagnostic delay is associated with a worse 30-day prognosis.

Co-injection of mesenchymal stem cells with endothelial progenitor cells accelerates muscle recovery in hind limb ischemia through an endoglin-dependent mechanism.

Endothelial colony-forming cells (ECFCs) are progenitor cells committed to endothelial lineages and have robust vasculogenic properties. Mesenchymal stem cells (MSCs) have been described to support ECFC-mediated angiogenic processes in various matrices. However, MSC-ECFC interactions in hind limb ischemia (HLI) are largely unknown. Here we examined whether co-administration of ECFCs and MSCs bolsters vasculogenic activity in nude mice with HLI. In addition, as we have previously shown that endoglin is a key adhesion molecule, we evaluated its involvement in ECFC/MSC interaction. Foot perfusion increased on day 7 after ECFC injection and was even better at 14 days. Co-administration of MSCs significantly increased vessel density and foot perfusion on day 7 but the differences were no longer significant at day 14. Analysis of mouse and human CD31, and in situ hybridization of the human ALU sequence, showed enhanced capillary density in ECFC+MSC mice. When ECFCs were silenced for endoglin, coinjection with MSCs led to lower vessel density and foot perfusion at both 7 and 14 days (p<0.001). Endoglin silencing in ECFCs did not affect MSC differentiation into perivascular cells or other mesenchymal lineages. Endoglin silencing markedly inhibited ECFC adhesion to MSCs. Thus, MSCs, when combined with ECFCs, accelerate muscle recovery in a mouse model of hind limb ischemia, through an endoglin-dependent mechanism.