Fibromuscular dysplasia (FMD) commonly affects the renal and cervical arteries but has been described to affect other vascular beds as well. The prevalence of and clinical characteristics associated with multisite FMD (string-of-beds or focal stenoses affecting at least 2 vascular beds) are not known. In the prospective ARCADIA registry (Assessment of Renal and Cervical Artery Dysplasia), symptomatic patients with renal artery (RA) FMD underwent tomographic- or magnetic resonance-angiography from the aortic arch to the intracranial arteries and those with cervical FMD from the diaphragm to the pelvis. Of 469 patients (84.0% women), 225 (48.0%) had multisite FMD. In addition, 86 of 244 patients with single-site disease had dissections or aneurisms affecting other vascular beds, totaling 311 patients (66.3%) with lesions in >1 vascular bed. Among patients with a cerebrovascular presentation, the prevalence of RA lesions was higher in patients with than in those without hypertension (odds ratio, 3.4; 95% confidence interval, 1.99–6.15). Among patients with a renal presentation, the prevalence of cervical lesions was higher in patients with bilateral than in those with unilateral RA lesions (odds ratio, 1.9; 95% confidence interval, 0.99–3.57). In conclusion, FMD is a systemic arterial disease. At least 2 vascular beds were affected by dysplastic stenoses in 48.0% of cases and by dysplastic stenoses, aneurysms, and dissections in 66.1% of cases. RA imaging should be proposed to hypertensive patients with a cerebrovascular presentation. Cervical artery imaging should be considered in patients with a renal presentation and bilateral RA lesions. Clinical Trial Registration— URL: www.Clinicaltrials.gov . Unique identifier: NCT02884141.

Severe acute respiratory syndrome coronavirus 2 is the cause of the ongoing coronavirus disease-19 (COVID-19) pandemic. Mortality is mainly due to acute respiratory distress syndrome (ARDS) [1]. High blood pressure appeared to be an independent factor for severity in patients with COVID-19 [2, 3]. The renin-angiotensin system (RAS) is a hemodynamic and biological system that regulates blood pressure, plasma potassium, and the stability of pulmonary epithelial membranes (Fig. 1) [4]. In this system, two antagonistic pathways are balanced. The first is the angiotensinogen pathway that transforms angiotensinogen into angiotensin I (by renin), and then converts it into angiotensin II by angiotensin converting enzyme (ACE). Angiotensin II attaches to angiotensin II type 1 receptor (AT1R) and activates the system to induce vasoconstriction, aldosterone secretion stimulation, hypokalemia, and pulmonary epithelium degradation [5]. The second way in which the angiotensin system is balanced involves a second angiotensin converting enzyme (ACE2) [6, 7]. This pathway transforms a part of angiotensin I [1-10] and angiotensin II [1-8] before it attaches to its AT1R receptor. The angiotensin I and II phosphorylation products are angiotensin 1-9 and angiotensin 1-7. They attach to the angiotensin II type 2 receptor receiver, inducing antagonist effects compared with AT1R [8]. In the infection phase (Fig. 2), COVID-19 virus uses the enzymatic receptor of ACE2 to penetrate the host cell [9, 10]. Coronavirus binding with ACE2 has been shown to lead to a downregulation of ACE2 [11], contributing to an increase in

Long-term mortality in patients with acute severe hypertension is unclear. The authors aimed to compare short-term (hospital) and long-term (12 months) mortality in these patients. A total of 670 adults presenting for acute severe hypertension between January 1, 2015, and December 31, 2015, were included. A total of 57.5% were hypertensive emergencies and 66.1% were hospitalized: 98% and 23.2% of those with hypertensive emergencies and urgencies, respectively (P = .001). Hospital mortality was 7.9% and was significantly higher for hypertensive emergencies (12.5% vs 1.8%, P = .001). At 12 months, 106 patients died (29.4%), mainly from hypertensive emergencies (38.9% vs 8.9%, P = .001). Median survival was 14 days for neurovascular emergencies and 50 days for cardiovascular emergencies. Patients with hypertensive emergencies or urgencies had bad long-term prognosis. Short-term mortality is mainly caused by neurovascular emergencies, but cardiovascular emergencies are severe, with high mortality at 12 months. These results justify better follow-up and treatment for these patients.