ABSTRACT
Background: Endothelial dysfunction is probably one of the mechanisms of long COVID-19 symptoms. Sulodexide has pleiotropic properties within the vascular endothelium that can prove beneficial in the long COVID-19 symptoms. Purpose: We aimed to evaluate the effect of sulodexide when used in patients with endothelial dysfunction and long COVID-19 symptoms. Methods: We conducted a prospective multicenter longitudinal case-control study. Endothelial function was evaluated with DTM “E4-Diagnose” Polymath based on the Endothelium Quality Index (EQI). A group of patients with endothelial dysfunction (EQI < 2.0) received sulodexide. All the patients were followed-up 21 days after inclusion. Primary outcomes were defined as endothelial function amelioration (delta EQI) and long COVID-19 symptoms evolution during the follow-up. Results: A total of 410 patients were included in this study. Patients were included at an average time of 1.89 ± 1.2 month after COVID-19 infection. At inclusion, 210 (51.2%) patients had an EQI < 2. The median age was 49 ± 13.8 (18–80) years. Among the patients with endothelial dysfunction, only 79 patients received sulodexide. Patients in sulodexide group had lower EQI than the non-medical intervention group (0.94 ± 0.6 vs. 1.52 ± 0.4;P < 10−3). They were more diabetic, hypertensive, had more coronary artery disease and received more long-term medications (aspirin, Bblockers and statins) than the others (P = 0.01, 0.002, 0.01, 0.009, 0.001 and 0.01, respectively). At the 21-days follow-up, patients in sulodexide group presented lower long COVID symptoms especially chest pain, palpitations, fatigue and neuro-cognitive difficulties associated to a significant amelioration of endothelial function (delta EQI 1.26 ± 1.07 vs. 0.22 ± 0.7;P < 10−3). Conclusion: Sulodexide in patients with long COVID-19 may be a good intervention to ameliorate chest pain, palpitations, fatigue and neuro-cognitive difficulties associated to endothelial dysfunction.
ABSTRACT
Background: The COVID-19 disease is a multisystem disease due to in part to the vascular endothelium injury. Lasting effects and long-term sequalae could persist after the infection and may be due to persistent endothelial dysfunction. Purpose: Our study focused on the study of endothelial function measurement by digital thermal monitoring (DTM) of endothelial quality index with E4 diagnosis Polymath in a large cohort of long COVID-19 patients to determine whether long COVID-19 symptoms are due to endothelial dysfunction. Methods: This is a prospective multicenter longitudinal observational cohort study. Endothelial function was evaluated with “E4-Diagnose” Polymath Tunisia based on the Endothelium Quality Index (EQI). A complete echocardiographic evaluation analysis was performed. Primary outcomes were defined as the occurrence of long COVID-19 symptoms in patients with endothelial dysfunction measured by EQI. Results: A total of 798 patients were included in this study. Patients were included at an average time of 68.93 ± 43.1 days. The mean EQI was 2.02 ± 0.99 [0–5]. A total of 397 (49.7%) patients had poor or very poor EQI and 211 (26.4%) patients had very poor EQI. The median age was 49.94 ± 14.2 (18–80) years. A total of 618 patients (77.4%) had long COVID-19 symptoms. Patients with long COVID-19 symptoms had a reduced EQI (1.99 ± 0.97 vs. 2.09 ± 1.05, P = 0.24). Among long COVID-19 symptoms, fatigue was the most common symptom reported in 42.2%. Fatigue and chest pain were significantly associated to the endothelial dysfunction (P = 0.04 and 0.001 respectively). Patients with chest pain had significantly lower EQI (1.74 ± 1.0 vs. 2.09 ± 0.9, P ≤ 10−3) and LVGLS (−16.35 ± 3.0 vs. −17.16 ± 2.5, P = 0.04). Conclusion: Long COVID-19 symptoms specifically chest pain and fatigue are due to persistent poor endothelial quality index. These findings allow a better care of patients with long COVID-19 symptoms.
ABSTRACT
Background: Since the emergence of the COVID-19 pandemic, there is an increasing evidence that affected patients have a higher incidence of thrombotic complications than the general population. This coagulopathy appears to be responsible for venous and less commonly arterial thromboembolic complications, in up to 50% of COVID-19 patients with severe manifestations. Abnormal coagulation parameters are considered a warning sign of such complications. The COVID-19 patients' laboratory findings include thrombocytopenia, elevated D-dimer levels, prolonged prothrombin time and disseminated intravascular coagulation. However, the exact underlying mechanism is not yet well understood. The evolution is rarely favorable on anticoagulant and anti-aggregating therapy, as in the case reported below. Case report: We report herein a case of aortic thrombosis in a 77-year-old patient with a history of hypertension and atrial fibrillation on Vitamin K antagonist (VKA), who presented to the emergency department with dyspnoea and abdominal pain. On examination, he was hemodynamically stable, but polypneic and hypoxic with 76% SpO2 in ambient air, his abdomen was painful on palpation. The ECG showed atrial fibrillation at 100 bpm without any repolarization disorder. He had lymphopenia, a prominent elevation of D-dimer rate at 26810ng/ml and fibrin/fibrinogen degradation products at 5.19 g/l, as well as over dosage in VKA with INR at 20, without abnormalities in platelet counts. COVID-19 pneumonia was confirmed by RT-PCR test and CT (Figure1) showed bilateral ground glass opacities (70% lung injury). Since the patient presented with abdominal pain, abdominal CT scan was performed, showing a non-obstructive abdominal aortic thrombosis: two pedunculated endoluminal thrombi based on parietal implantation at T9 and T11 stenosing the lumen by approximately 45-50% (Figure2), as well as large areas of splenic infarction (Figure3) and cortical lesions of the left kidney, suggesting renal infarction sites (Figure4). Patient was treated with therapeutic anticoagulation associated to aspirin, with a good initial result. One-month follow-up shows no complications. Conclusion: Our knowledge of this emerging human pathogen is rapidly progressing, and our understanding of management strategies to optimize outcomes in affected patients is evolving. This case supports the hypercoagulability state in COVID-19 and enhances the recommendation to use pharmacological prophylaxis of thrombosis.