Impairment of central retinal artery hemodynamics in affected and fellow eyes in giant cell arteritis patients with unilateral vision loss.

OBJECTIVES: Permanent visual impairment is a major complication of giant cell arteritis (GCA). We investigated the added value of color Doppler imaging (CDI) of the central retinal artery (CRA) in patients with suspected GCA for early risk evaluation before temporal artery biopsy (TAB) results become available. METHODS: We conducted a non-interventional observational study of 30 consecutive patients hospitalized for suspected GCA, including a comprehensive analysis of clinical, laboratory, imaging, CDI and pathology data. GCA was diagnosed or excluded (GCA+, GCA-, respectively) according to American College of Rheumatology (ACR) criteria and TAB findings. Three patients not meeting ACR criteria were excluded secondarily. The GCA- group contained ten patients, and the GCA+ group contained 17 patients, including eight with unilateral, transient or permanent clinical visual impairment (CVI). RESULTS: Mean blood flow velocity (mBFV) in the CRA was impaired in the affected eyes of GCA + CVI+ patients (1.9 ± 0.9 cm.s-1, p < 0.001) relative to controls (4.1 ± 1.0 cm.s-1), GCA- patients (3.6 ± 0.7 cm.s-1) and GCA + CVI- patients (3.8 ± 0.8 cm.s-1). The mBFVs of the CRA was similar for affected and fellow eyes (right or left). CRA mBFV measurements effectively differentiated between patients with and without CVI (ROC-curve analysis, AUC = 0.925 [95%CI: 0.700 to 0.996], p < 0.0001, 88% sensitivity, 89% specificity, and cutoff of ≤2.7 cm.s-1 for affected eyes; 75% sensitivity, 100% specificity and cutoff of ≤2.2 cm.s-1 for fellow eyes). CONCLUSION: CDI facilities the early detection of visual ischemia risk in GCA+ patients, justifying urgent high-dose corticosteroid administration to save at least the fellow eye before pathology results become available.

Blood Flow and Shear Stress Allow Monitoring of Progression and Prognosis of Tumor Diseases.

In the presence of tumor angiogenesis, blood flow must increase, leading to an elevation of blood flow velocities (BFVels) and wall shear stress (WSS) in upstream native arteries. An adaptive arterial remodeling is stimulated, whose purpose lies in the enlargement of the arterial inner diameter, aiming for normalization of BFVels and WSS. Remodeling engages delayed processes that are efficient only several weeks/months after initiation, independent from those governing expansion of the neovascular network. Therefore, during tumor expansion, there is a time interval during which elevation of BFVels and WSS could reflect disease progression. Conversely, during the period of stability, BFVels and WSS drop back to normal values due to the achievement of remodeling processes. Ovarian peritoneal carcinomatosis (OPC), pseudomyxoma peritonei (PMP), and superficial arteriovenous malformations (AVMs) are diseases characterized by the development of abnormal vascular networks developed on native ones. In OPC and PMP, preoperative blood flow in the superior mesenteric artery (SMA) correlated with the per-operative peritoneal carcinomatosis index (OPC: n = 21, R = 0.79, p < 0.0001, PMP: n = 66, R = 0.63, p < 0.0001). Moreover, 1 year after surgery, WSS in the SMA helped in distinguishing patients with PMP from those without disease progression [ROC-curve analysis, AUC = 0.978 (0.902-0.999), p < 0.0001, sensitivity: 100.0%, specificity: 93.5%, cutoff: 12.1 dynes/cm2]. Similarly, WSS in the ipsilateral afferent arteries close to the lesion distinguished stable from progressive AVM [ROC-curve analysis, AUC: 0.988, (0.919-1.000), p < 0.0001, sensitivity: 93.5%, specificity: 95.7%; cutoff: 26.5 dynes/cm2]. Blood flow volume is indicative of the tumor burden in OPC and PMP, and WSS represents an early sensitive and specific vascular marker of disease progression in PMP and AVM.

Risk of venous thromboembolism in rheumatoid arthritis.

Rheumatoid arthritis (RA) is a chronic autoimmune joint disease with persistent systemic inflammation. Patients with RA suffer from joint pain and physical disability, but have their prognosis mostly driven by cardiovascular events, including venous thromboembolism (VTE). The risk of VTE is more than double in patients with RA compared with the general population. The incidence rate in patients with RA is estimated around 4 cases per 1000 person-years. The etiology of thrombotic tendency in RA is linked to various mechanisms and causal factors (antiphsolpholid antibodies, hyperhomocyteinemia, inflammation…): vascular injury, hypercoagulation, and venous stasis, the three components of the Virchow's triad, are activated in patients with RA. In clinical practice, situations that put patients for VTE should be identified (e.g., surgery, first year after RA diagnosis, hospitalization for acute illness…). Patients with RA are exposed to reversible risk factors, such as major surgery (knee or hip surgery) or hospitalization with immobilization. Similarly, uncontrolled RA, which is defined by the necessity to switch a biological disease-modifying anti-rheumatic drugs (DMARD), increases the incidence of VTE in observational studies. Moreover, DMARDs may impact the risk of VTE, especially in the time window after first prescription. Several biological DMARDs like tofacitinib have been associated with an increased risk of VTE. Therefore, patients with RA may require specific measures in terms of VTE diagnosis and management. In this review, we provide current insights into the pathophysiology, epidemiology, clinical considerations, and treatment strategies of VTE highlighting gaps in evidence and perspectives in patients with RA.

Pathophysiological Processes Underlying the High Prevalence of Deep Vein Thrombosis in Critically Ill COVID-19 Patients.

Coronavirus disease 2019 (COVID-19) predisposes to deep vein thrombosis (DVT) and pulmonary embolism (PE) particularly in mechanically ventilated adults with severe pneumonia. The extremely high prevalence of DVT in the COVID-19 patients hospitalized in the intensive care unit (ICU) has been established between 25 and 84% based on studies including systematic duplex ultrasound of the lower limbs when prophylactic anticoagulation was systematically administrated. DVT prevalence has been shown to be markedly higher than in mechanically ventilated influenza patients (6-8%). Unusually high inflammatory and prothrombotic phenotype represents a striking feature of COVID-19 patients, as reflected by markedly elevated reactive protein C, fibrinogen, interleukin 6, von Willebrand factor, and factor VIII. Moreover, in critically ill patients, venous stasis has been associated with the prothrombotic phenotype attributed to COVID-19, which increases the risk of thrombosis. Venous stasis results among others from immobilization under muscular paralysis, mechanical ventilation with high positive end-expiratory pressure, and pulmonary microvascular network injuries or occlusions. Venous return to the heart is subsequently decreased with increase in central and peripheral venous pressures, marked proximal and distal veins dilation, and drops in venous blood flow velocities, leading to a spontaneous contrast "sludge pattern" in veins considered as prothrombotic. Together with endothelial lesions and hypercoagulability status, venous stasis completes the Virchow triad and considerably increases the prevalence of DVT and PE in critically ill COVID-19 patients, therefore raising questions regarding the optimal doses for thromboprophylaxis during ICU stay.