e326 Journal of Hypertension Vol 35, e-Supplement 2, September 2017
disorders (CD), and obesity accelerates the development of CD on the base of
metabolic disorders.
Design and method: 274 patients with controlled hypertension were examined.
The average age was 53,8 ± 5,7 years. The average duration of hypertension was
10,5 ± 4,9 years. Body mass index (BMI) was increased in 62.8%. All patients
with higher and secondary education were employed.The average systolic blood
pressure was within 137,9 ± 1,82 mm Hg, average diastolic blood pressure -
80,3 ± 3,06. Overweight and obesity were recorded in 65 patients (20.4%). Stan-
dard examinations, BMI and additional diagnostic procedureswere performed:
ambulatory blood pressure monitoring, ultrasound of the main arteries of the head
and neck and neuropsychological profile of cognitive functions by MMSE scale,
Luria memory test - Remembering the 10 words, attention and speed of senso-
rimotor reactions - by Schulte and Rybakov.
Results: Only 12% of patients in the total group complained of storing informa-
tion problems. CD were revealed in 93 patients - 33.9%, and among those with
overweight and obesity, CD was registered in 58 - 89%. Thickening of intima-me-
dia was identified only in 48 patients, primarily in patients with obesity (58.3%).
Light CD were in 37.6%, moderate in - 55.5% and mild dementia only in 6.9%.
The most significant were violations of attention and speed of sensorimotor reac-
tions that affect a relevant role-scale functioning of life quality (SF-36 HSS).
Conclusions: Every third patient, even with controlled hypertension, and two
thirds of those with overweight and obesity present mild to moderate CD, that
indicates early brain damage as the target organ.
PP.29.16 NITROSONIFEDIPINE, A NOVEL ANTIOXIDANT,
AMELIORATES NEUROLOGICAL SYMPTOMS
AND PROLONGS THE SURVIVAL IN A
MALIGNANT STROKE-PRONE SPONTANEOUSLY
HYPERTENSIVE RATS
Y. Izawa-Ishizawa1, K. Ishizawa2,3, M. Tabuchi4, M. Imanishi3, M. Takata5,
E. Sairyo1, Y. Zamami2, Y. Horinouchi1, Y. Ikeda1, K. Tsuchiya5, T. Tamaki1.
1Department of Pharmacology, Institute of Biomedical Sciences, Tokushima
University Graduate School, Tokushima, Japan, 2Department of Clinical
Pharmacy, Institute of Biomedical Sciences, Tokushima University Graduate
School, Tokushima, Japan, 3Department of Pharmacy, Tokushima University
Hospital, Tokushima, Japan, 4Faculty of Human Health, Sonoda Women’s University,
Amagasaki, Japan, 5Department of Clinical Pharmacology, Institute of Biomedical
Sciences, Tokushima University Graduate School, Tokushima, Japan
Objective: Nitrosonifedipine (NO-NIF) is photolytic metabolite of nifedipine, an
anti-hypertensive drug. We have revealed that NO-NIF possesses potent radical
scavenging activity and protective effects against several pathological conditions
involving oxidative stress. A malignant stroke-prone spontaneously hypertensive
rat (M-SHRSP) is a model animal showing high rate of cerebral stroke. The onset
and progressions of stroke are known to be involved in oxidative stress. Therefore,
we investigated the effects of NO-NIF on the onset and progressions of stroke in
M-SHRSP.
Design and method: M-SHRSPs were treated with NO-NIF (30 mg/kg/day, i.p.)
or vehicle from the age of five weeks. Neurological symptoms were observed
every day and scored by severity of general status and disordered motility of ante-
rior/posterior limbs. The day of the stroke onset was determined by neurological
symptoms and the change in body weight. Brain was harvested after death and
histologically analyzed. For in vitro study, nerve growth factor (NGF)-induced
neurite elongation and intracellular signaling pathway were investigated using
PC12 cells.
Results: There was no significant difference in the incidence and the timing of
stroke onset between control and NO-NIF treated group. However, the periods
until 50% rats died from stroke were extended for 29 days in NO-NIF group com-
pared to control. Although the neurological score showed linear worsening after
stroke onset, NO-NIF significantly suppressed its exacerbation. Consistently, rats
showed less pathological lesion, such as hemorrhage, thrombus, and liquefaction
degeneration in brains. In PC12 cells, NGF-induced neurite elongation was en-
hanced by NO-NIF existence. Moreover, NO-NIF prolonged the co-localization
of NGF receptor and flotillin, a lipid raft marker, and the activations of Akt and
ERK1/2. In our previous study, we have already showed that NO-NIF affects the
fluidity of cellular membrane. Therefore, it was considered that NO-NIF enhanced
NGF signaling by changing the cellular membrane fluidity and localization of
NGF receptor.
Conclusions: In the present study, we demonstrated that NO-NIF could prolong
the lifespan after stroke induced by malignant hypertension. NO-NIF were sug-
gested to elongate neurite by enhancing NGF-stimulated intracellular signal-
ing activities and finally improved the stroke-related neurological symptoms in
M-SHRSP.
Copyright © 2017 Wolters Kluwer Health, Inc. All rights reserved.
PP.29.17 HYPERTENSIVE ENCEPHALOPATHY IN A
TERIFLUNOMIDE TREATED PATIENT
C. Homentcovschi1, R. Siliste1, R. Ianula1, C. Cristescu1. 1Coltea Clinical
Hospital, Internal Medicine DPT, Bucharest, Romania, 2UMF Carol Davila,
Virusology DPT, Bucharest, Romania
Objective: One of the challenges of the last years is to take care of pa-
tients with complex treatments, including new drugs. Teriflunomide is
a pyrimidine synthesis inhibitor, for the tratament of multiple sclerosis.
Hypertension is, according to clinical trials, a rare adverse reaction- 4% for
the 14 mg/day.
Design and method: Case report: We present the case of a 56 years old women
with multiple sclerosis- who begun a treatment with teriflunomide (14 mg/day).
She was known as having a grade 2 HTA, obesity and hypercholesterolemia and
her treatment consisted in telmisartanum, indapamide and atorvastatine. With this
treatment the blood pressure was under 130/ 85 mmHg and she was considered
with controlled hypertension when the new drug was introduced. After the second
dose- the patient experienced, during nighttime, headache and in the third day
of treatment she developed a severe headache, with photophobia and vomitig,
and in the Emergency Room the blood pressure was 260/130 mmHg. The rest
of clinical examination showed: normal pulmonary auscultation and no signs of
systemic congestion, a regular cardiac rhytm and tachycardia (120 beats/min), no
focal neurological signs or meningeal irritation. She was admitted to the hospital
as hypertensive encefalopathy. The blood tests were normal, excepting a total cho-
lesterol above the recommended limits; the ECG- without changes and an echo-
cardiogram - no signs of left ventricular hypertrophy, a normal kinetic and valves,
with a mild dyastolic dysfunction.
Results: Under treatment with i.v. vasodilatators and supplementation of the oral
treatment with a calcium blocker, the patient become asymptomatic and the blood
pressure values return to the recommended limits. She was discharged with a new
treatment scheme (adding amlodipine 5 mg/day to the previous drugs), and the
ambulatory blood pressure measurement, performed 14 days after that, showed a
good control of hypertension.
Conclusions: New therapies come with new adverse reactions and in everyday
patients, which are rather complex, the close followup is mandatory. The useful
tratment for Multiple Sclerosis was, in this patient, followed by a rise of the anti-
hypertensive treatment.
PP.29.18 PULSE PRESSURE INDEX: AN INDICATOR OF
SEVERITY OF SILENT CEREBROVASCULAR
DAMAGE IN ESSENTIAL HYPERTENSIVE PATIENTS
O. Gulkevych, O. Kupchynska, T. Ovdienko, A. Logvinenko, M. Sheremet.
National Scientific Center M. D. Strazhesko Institute of Cardiology-Department
of Hypertension, Kiev, Ukraine
Objective: To evaluate the relationship between brachial pulse pressure index
(PPI) and target organs (such as brain, carotid arteries) damage in essential hy-
pertensive patients (EH)
Design and method: Clinic blood pressure (BP) was measured in 136 uncompli-
cated pts (49,2 ± 0,94 years; 85 males) with EH. Pulse pressure index (PPI) was
calculated as ((systolic BP - diastolic BP)/ systolic BP). Cerebrovascular dam-
age was evaluated by studying the presence or absence of cerebral white mat-
ter lesions (WML), assessed by magnetic resonance imaging and by determining
ultrasonographically carotid diameter (CD) and intima-media thickness (IMT),
blood flow velocities (BFV) in middle cerebral arteries (MCA) and calculated the
resistance index (RI) of MCA. All pts were divided into 2 groups depending on
the value of brachial PPI: group I (n = 66) - PPI < 0,38 (mean value of brachial
PPI), group II (n = 70) - PPI >/ = 0,38. WML, MCA RI, CD, IMT were related to
brachial PPI by bivariate correlation analysis.
Results: Patients with brachial PPI >/ = 0,38 had significantly greater carotid
structural changes: pts of gr.I had CD 7,18 ± 0,14 mm and IMT 0,81 ± 0,05 mm
vs pts of gr.II 7,72 ± 0,14 mm (p < 0,05) and 1,05 ± 0,05 mm (p < 0,05) ac-
cordingly. We observed significantly higher MCA RI in pts with brachial PPI
>/ = 0,38, than pts of gr.I: 0,57 ± 0,01 vs 0,53 ± 0,01 (p < 0,05) accordingly. Pa-
tients with cerebral WML (n = 79) had significantly (p < 0,05) higher brachial
PPI (0,42 ± 0,01), than pts without cerebral WML (n = 57) (0,32 ± 0,01). Bra-
chial PPI was significantly correlate with carotid structural changes (CD: r = 0,32;
p < 0,01, IMT: r = 0,31; p < 0,01), MCA RI (r = 0,41; p < 0,001) and cerebral
WML (r = 0,81; p < 0,001).
Conclusions: There is relationship between brachial PPI and target organs (such
as brain, carotid arteries) damage in patients with essential hypertension: higher
brachial PPI is associated with greater cerebrovascular alterations.