The COVID-19 disease is a multisystem disease due in part to the vascular endothelium injury. Lasting effects and long-term sequelae could persist after the infection and may be due to persistent endothelial dysfunction. Our study focused on the evaluation of endothelial quality index (EQI) by finger thermal monitoring with E4 diagnosis Polymath in a large cohort of long COVID-19 patients to determine whether long-covid 19 symptoms are associated with endothelial dysfunction. This is a cross-sectional multicenter observational study with prospective recruitment of patients. A total of 798 patients were included in this study. A total of 618 patients (77.4%) had long COVID-19 symptoms. The mean EQI was 2.02 ± 0.99 IC95% [1.95–2.08]. A total of 397 (49.7%) patients had impaired EQI. Fatigue, chest pain, and neuro-cognitive difficulties were significantly associated with endothelium dysfunction with an EQI <2 after adjustment for age, sex, diabetes, hypertension, dyslipidemia, coronary heart disease, and the severity of acute COVID-19 infection. In multivariate analysis, endothelial dysfunction (EQI <2), female gender, and severe clinical status at acute COVID-19 infection with a need for oxygen supplementation were independent risk factors of long COVID-19 syndrome. Long COVID-19 symptoms, specifically non-respiratory symptoms, are due to persistent endothelial dysfunction. These findings allow for better care of patients with long COVID-19 symptoms.

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Background Our purpose was to describe a patient who developed combined central retinal vein occlusion (CRVO), cilioretinal artery occlusion, branch retinal artery occlusion (BRAO), and anterior ischaemic optic neuropathy (AION) followed by CRVO in the second eye because of the heterozygous factor V Leiden (FVL) mutation. Case presentation A 39-year-old female with a history of recurrent pregnancy losses presented with acute blurred vision in the right eye (RE), with visual acuity limited to counting fingers. She was diagnosed with combined impending CRVO, cilioretinal artery occlusion, BRAO, and AION. The results of thrombophilia testing, not including the FVL mutation, were negative. Retinal atrophy with vascular attenuation and optic disc pallor developed after resolution of acute retinal findings. Nine months after initial presentation, the patient developed an impending CRVO in the left eye (LE), with a secondary progression to a complete CRVO causing a decrease in best corrected visual acuity (BCVA) to 20/40. The patient was determined to be heterozygous for the FVL mutation. She subsequently was treated with acenocoumarol. At the last follow-up visit, the BCVA was 20/400 in the RE and 20/20 in the LE, and there was a complete resolution of the acute CRVO findings in the LE. Conclusion Our case shows that the heterozygous FVL mutation may manifest with combined retinal vascular occlusion involving multiple sites in both eyes. Early recognition of such an inherited thrombophilic disorder is important because it implies the need for long-term anticoagulative therapy to reduce the patient’s risk of recurrent, sight-threatening and life-threatening thrombotic events.

Ventricular non-compaction (VNC) is a rare myocardium disorder, which can be both genetic and sporadic. A poor wall compaction process or an excessive trabeculae formation may be at the genesis of myocardial hypertrabeculation with multiple recesses. It is often complicated by ventricular dysfunction, arrhythmias and cardiac embolism. Herein we report a case of a 20-year-old male patient with no particular past medical history who was followed up at the cardiology department for dyspnea. Echocardiography showed reduced ejection fraction of the left ventricle with potential hypertrabeculation in the right ventricle, confirmed by cardiac MRI. The patient was not put under medication and was later lost to follow-up. He died few months later without a clear cause explaining death. A forensic autopsy was performed that attributed death to acute ventricle arrhythmia secondary to VNC, emphasizing the major role of an early and specific treatment to avoid such a fatal outcome.

Ventricular non-compaction (VNC) is a rare myocardium disorder, which can be both genetic and sporadic. A poor wall compaction process or an excessive trabeculae formation may be at the genesis of myocardial hypertrabeculation with multiple recesses. It is often complicated by ventricular dysfunction, arrhythmias and cardiac embolism. Herein we report a case of a 20-year-old male patient with no particular past medical history who was followed up at the cardiology department for dyspnea. Echocardiography showed reduced ejection fraction of the left ventricle with potential hypertrabeculation in the right ventricle, confirmed by cardiac MRI. The patient was not put under medication and was later lost to follow-up. He died few months later without a clear cause explaining death. A forensic autopsy was performed that attributed death to acute ventricle arrhythmia secondary to VNC, emphasizing the major role of an early and specific treatment to avoid such a fatal outcome.