S-35-3: HAMA, AN EUROPEAN REGISTRY OF MALIGNANT HYPERTENSION SUPPORTED BY THE EUROPEAN SOCIETY OF HYPERTENSION: PRELIMINARY RESULTS AND CURRENT PERSPECTIVES

Introduction: Malignant hypertension (MH) is one of the most severe acute forms of hypertension. It is very high blood pressure and an acute lesion of target organ damage. Incidence is currently increased in high-income countries and is higher in low-income countries due to difficulty with antihypertensive drug access. Causes of MH are very various, and probably prognosis of MH depends on the etiology. However, MH is not well known. We are conducting a multicentric prospective registry of MH patients started in 2019, primarily in France and is currently undergoing a European expansion with the support of the European Society of Hypertension (ESH) to describe the different forms and prognosis of MH and increase our knowledge of the disease (NCT03755726). Method: From 2019, in the 36 centres in France, Patients with a BP > 180/100 mmHg AND Severe Hypertensive Retinopathy - stade II or III of Kirkendall classification - OR with three criteria among the following: 1) Heart damage (Left ventricular Mass > 140 g/m2 for men of > 120 g/m2 for women); 2) Brain damage (PRES or acute stroke or severe white matter lesions (WML) with a Fazekas score > 2 before 60 years old); 3) Kidney damage (acute kidney injury defined by KDIGO criteria) 4) presence of Thrombotic Microangiopathy (TMA) with the presence of schizocytes and low haptoglobin or high LDH) were included. Results: To date, 278 patients were enrolled. The reason for hospital admission was symptomatic hypertension for 210/272 (77%) and asymptomatic hypertension for 62/272 (23%) BP was 218 ± 28 / 127 ± 23 mmHg. The mean age was 48 ± 15 years old. Males were 186/278 (67%). Non-Caucasians were 114/278 (41%), 101/278 (36%) smoked and 45/278 (16%) had diabetes. Before enrollment, 108/278 (39%) patients had chronic hypertension. Severe retinopathy was present in 251/278 (90%), Heart damage in 172/278 (62%), kidney damage in 176/278 (63%), and creatinine was 261 ± 326 μmol/l at admission. Brain damage was present in 105/278 (38%), 47/105 (45%) patients had severe WML. TMA was present in 40/278 (14%) patients. At discharge, BP was 148 ± 19 / 89 ± 15 mmHg; creatinine was 248 ± 274 μmol/l. The etiology of hypertension was assessed in 181/278 (65%), and a specific cause was found in 75/181 (41%). Conclusion: This multicentric prospective cohort is the opportunity to considerably increase our knowledge of MH, a non-uncommon severe disease. A biobank is currently being started to identify patients clustering to differentiate the etiology, prognosis and pathogenesis of each form of MH.