arthyperАртериальная гипертензия"Arterial’naya Gipertenziya" ("Arterial Hypertension")1607-419X2411-8524Antihypertensive League10.18705/1607-419X-2008-14-4-360-368arthyper-1256Research ArticleОРИГИНАЛЬНЫЕ СТАТЬИORIGINAL ARTICLESК вопросу о патогенезе и лечении асимметричной гипертрофии левого желудочка при эссенциальной гипертензииActual aspects of pathogenesis and treatment of asymmetric left ventricular hypertrophy in essential hypertensionБарсуковА. В.BarsukovA.avbarsukov@yandex.ru <mailto:avbarsukov@yandex.ru>ПронинаЕ. В.ProninaE. ..noemail@neicon.ruШустовС. Б.ShoustovS. ..noemail@neicon.ruВоенно-медицинская академия, Санкт-ПетербургРоссияKirov Military Medical Academy, the 1st department of advanced medical studies, 41 Kirochnaya st., 193015 St Petersburg, RussiaRussian Federation200828082008144360368Copyright &#x00A9; Барсуков А.В., Пронина Е.В., Шустов С.Б., 20082008Барсуков А.В., Пронина Е.В., Шустов С.Б.Barsukov A., Pronina E..., Shoustov S...Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://htn.almazovcentre.ru/jour/article/view/1256

Background: asymmetric left ventricular hypertrophy (ALVH) is the rarest type of hypertensive left ventricular (LV) remodeling, which is prevalent in approximately 1% of people with essential hypertension (EH). Aim: to estimate 24-h blood pressure (BP) parameters, ultrasound left ventricle features, sympathetic and rennin-angiotensin-aldosterone system (RAAS) activity, insulin secretion level, and to assess the efficacy of RAAS pharmacologic blockade in EH patients with ALVH. Material and methods: we examined 101 EH subjects with 1-3 degree of BP increase (ESC/ESH, 2007) and I-II stages of hypertension. 37 of them had ALVH, 32 ones had symmetric LVH (SLVH), 32 people had normal LV geometry. Results: Patients with ALVH in comparison with SLVH people demonstrated a significantly higher LV mass index (LVMI, p < 0,001), LVH concentricity degree (p < 0,001), 24-h epinephrine excretion levels (p < 0,05), aldosterone and insulin secretion levels (p < 0,001). 24-week therapy based on angiotensin-converting enzyme inhibitor (ACEi) Quinapril resulted in significant reduction of 24-h systolic and diastolic BP (p < 0,05), LVMI (p < 0,001), 24-h epinephrine (p < 0,01) and norepinephrine (p < 0,001) excretion levels, aldosterone secretion level (p < 0,001). Conclusions: asymmetric (i.e. non classic) type of LVH is a result of interaction of traditional proliferateive haemodynamic and neurohumoral patterns and also it can be a target for RAAS-blockade.

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The authors declare that there are no conflicts of interest present.