[LB.03.03] FOLLOW-UP RESULTS OF ROENTGENOENDOVASULAR DESTRUCTION OF ADRENAL GLAND IN PATIENTS WITH ESSENTIAL HYPERTENSION
Annotatsiya
Objective: Purpose: To examine followup results of roentgenoendovascular destruction of adrenal glands in patients with essential hypertension. Design and method: Reviewed results of roentgenoendovascular treatment on 1362 patients (763 males and 599 females, average 36,2 years, duration of arterial hypertension accounted at an average 8,3 years), with essential hypertension. All patients were underwent a complex examinations from routine blood and urine analysis to abdominal aortography therefore it is excluded renal parenhimatous and renovascular hypertension, hormonal active tumors of the adrenal glands. In these patients arterial hypertension assessed as essential hypertension and found hyperplasia and hyperfunction of adrenal glands. A lesion has an asymmetrical character as follows: hyperplasia in left adrenal only was found in 1264(92.8%) patients, one in right only - in 16(1.2%) patients, and one in both adrenals revealed to be in 82(6%) patients. Hormonal investigations corroborated a presence of hyperfunction in adrenal cortex, specifically an increase in concentration of plasma aldosterone and aldosteron renin ration was more than 20 ml.dl fixed in 84% patients. For all patients done transluminal transvenous destruction of left adrenal glands. Results: The mean blood sistolic and diastiolic pressure levels at the time of before treatment were 183 mmHg and 127 mmHg respectively. All patients had unsuccessful hypotensive drug treatment history. The primary technical success of transluminal adrenal destruction was 96% and complications observed in 7(0.6%) patients, two of them fatal (retroperitoneal bleeding from perforated adrenal veins). Kaplan-Meier analysis indicated 5- year free hypertension rate of 80.4% in patients after transluminal destruction of adrenal glands. Causes of inefficacy of roentgenoendovascular destruction of adrenal gland or relapse arterial hypertension in follow-up period were satellite renal parenchymal disease, insufficient devitalization of adrenal glands and development of renal artery stenosis and renovascular hypertenson. Conclusions: In cases of excepted renal parenchymal disease and renovascular hypertension, main cause of increasing arterial pressure (patients with essential hypertension) is diffuse or diffusenodulous hyperplasia of adrenals, mainly of the left adrenal gland with development of hyperaldosteronism. To oppress adrenal hyperfunction and thereby to reduce arterial pressure it is possible by roentgenovascular destruction of left adrenal gland.
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