Introduction: Hypertension is considered resistant to treatment when optimal/best-tolerated doses of recom-mended therapeutic strategy fail to bring the blood pressure within the normal range. The inadequate con-trol should be confirmed by ambulatory blood pressure monitoring or home blood pressure monitoring and pseudo-resistant hypertension and secondary hyper-tension causes should be excluded. Studies applying this definition reported a prevalence of resistant hyper-tension (RH) <10% of treated patients.

Methods: A 67-year-old female, ex-smoker, has pre-sented to our clinic for the evaluation of 4 episodes of orthostatic syncope in the last year. The patient’s medi-cal history included: third grade hypertension, therape-utically neglected by 2017, and treated at presentation with the combination of furosemide, nebivolol, olme-sartan, amlodipine, spironolactone, moxonidine; dia-betes mellitus known since 1994 and treated only sin-ce 2008, initially with oral antidiabetics, subsequently with very high doses of slow insulin (56 IU / 24 hours) and nonstenotic bilateral carotid atheromatosis. On the occasion of one of the syncope, both the cerebral and abdominal tomography was examined and a left adrenal node, right adrenal gland hypertrophy, and renal artery stenosis were identified. Basal and stimu-lated hormonal dosages did not confirm the presence of hyperaldosteronism, but the level of basal plasma cortisol was repeatedly at the upper limit of normal. At the presentation in our clinic, the patient had a first-degree atrioventricular block (PR: 240 ms), anterosep-tal sequelae infarction, severe orthostatic hypotension (up to 60mmHg) and nocturnal hypertension (up to 220mmHg). Blood glucose monitoring has shown epi-sodes of symptomatic hypoglycemia associated with in-creases in blood pressure. Antihypertensive medication has been modified, with a triple combination with the lowest risk for orthostatic hypotension (Clonidine, Ol-mesartan and Amlodipine) being preferred, and anti-diabetic treatment and diet have been modulated. Ma-ximum antihypertensive doses did not reduce systolic BP below 170mmHg, despite the removal of any other potential causes of poor BP control, the highest valu-es being recorded in decubitus, especially at night; the association of diuretics furosemide and spironolacto-ne was added. The benefit of medication modification was the suppression of symptomatic orthostatic hypo-tension. Since, under 4 antihypertensive drugs, tension control was not optimal, renal artery angiography was performed, who did not show the presence of any re-nal artery stenosis, but has identified critical stenosis of the right popliteal artery, which was treated by balloon angioplasty. High blood glucose oscillations were re-duced over a two-month period, maintaining the com-bination of metformin and slow-acting insulin with gradual adjustments to better blood glucose control, as well as reducing high blood pressure oscillations. Af-ter 3 months of anti-hypertensive therapy with 5 drugs administered at the maximum tolerated dose, with no significant adverse effects, the mean diurnal tension equaled that of nocturnal voltages and was not below 150mmHg, assuming the patient had real RH. Conclusions: The case presented raised several problems: the diagnosis of resistant hypertension, which was laborious and required the elimination of multiple confounding factors (the discovery of adrenal inciden-taloma, refutation of the existence of a renal artery ste-nosis) and the management of hypertension under the condition of a complex syncope: the presence of symp-tomatic side effects of antihypertensive drugs making it difficult to apply the RH recommendations; high blood glucose fluctuations that potentiated high blood pressure oscillations and vice versa. Symptomatic relief was only obtained after correction of all these imbalan-ces, but the history of hypertension and diabetes melli-tus over many years has made it impossible to control blood pressure perfectly.