Multiple coronary risk factors increase rate of restenosis after PTCA

Multiple coronary risk factors increase rate of restenosis after PTCA

,J Mol Cell Cardiol22 (Supplement IV) (1990) 13 BRADYKININ MODIFIES THE PRESSOR EFFECT OF PHENYLEPHRINE. A. Benetos, M. Safar, Diagnosis Center...

83KB Sizes 0 Downloads 72 Views

,J Mol

Cell

Cardiol22

(Supplement

IV)

(1990)

13 BRADYKININ

MODIFIES THE PRESSOR EFFECT OF PHENYLEPHRINE. A. Benetos, M. Safar, Diagnosis Center, Broussais Hospital, Paris, France. The action of the bradykinin (BK) on the pressor effect of different vasoactive In a first set of experiments bolus drugs was studied in normotensive Wistar rats. intra-arterial injetions of Phenylephrine (PhE 5 vg) were administrated before, during and after a continuous infusion of 450 ng/min of Bradykinin (group I). In was followed replacing PhE by Arginingroups II and III, the same procedure Vasopressin (AVP 200 ng) or Angiotensin II (AI1 400 ng) respectively. Without BK With BK Inhibition (n=7) PhE 30+3mmHg 11+4mmHg 64% Gr I 5 I@ 32tSmmHg -19% Gr II (n=6) AVP 200 ng 26+2mmHg 8% Gr III (n=6) AI1 400 ng 28+6mmHg 26t6nunHg table shows that BK, decreases the pressor effect of the PhE by 64% (p
14

A

PEDIGREE

DNA

UITH

A

HAPLDTlPE C.

101,

FRANCE.

Toulouse,

Junien“'.

Femiliel

12,

This

the

is

twrmal

of

suppressor

MIJLTIPLE Benlian Clinique

1)

INSERT

URA

U

217,

CETP,

LDLR

ApoE,

gene

the

normal.

is

e

defect

family.

Strikingly,

Haplotypes that

that

YBS

bindiog

mgldl), nvxt

for might

LDL

the es

LDLR well

danain

and

the

subjects

gene interact,

the (19

LDL

studied

heterozygws

cholesterol of

ParC,

to

have

23 nest

of

defective

polymrphic were

"IT" J.C.

Swlogne,

SPECIFIC

Fruchart',

FRANCE.

receptor

CLDLR)

P.

3)

INSERH

19-meet-~

kb

deletion

fron

intros

ceding

region

for

the the

mg/dl)

and

u

A@

patients

(n=S) (123

had

confirm

the had

moderately

Lp(a) for

implication

introa

EGF-like

es

IOU and

the

femily. 1 to

mg,dl)

also

sites) to

usually

two-generation

deletion

restriction constructed

defects,

e

bearing (218

LDLR

ASSDClATlW

Sereriat4,

FRANCE.

related

en

G.

LILLE,

Ue

it

LEVELS:

Regeb3. Ardxoise

U 325,

disease

Surprisingly, (285

H6pital

INSERT

LIPID A.

heterozygofes.

LDL

described.

2)

daninent

in

the

5)

UNEXPECTED

Foweult3,

FRANCE.

showed for

AND

J.

FRANCE.

cholesterol

ApoAl)

GENE

Paris,

levels

deletion

in were

73,

Peris.

region

pLas",a

RECEPTOR BoiLes~'~~,

(FH)

largest total

LDL C.

cholesterol

coding

individuals levels

ApoS,

the

entire the

levels

Triglyceride (Lp(a).

THE

Lou',

CNRS

normal of

the

elevated to

the

mepping

removing

danain.

4)

IN N.

hypercholesterolemia

twice

Restrictica

DELETION

Benlien',

Do"*te-SleZy3,

increasing

15

LARGE

P.

other

capered levels. genes of

e

gene.

CORONARY RISK P., Wittenberg Cardiologique,

FACTORS INCREASE RATE OF RESTENOSIS 0.. Gallay P., Messner P., Puech P., HBpital Saint-Eloi, 34059 MONTPELLIEH

AFTER PTCA. Grollaau F(. cedex.

To evaluate the role of cororlary risk factors (CRF) in restenosis after PTCA. we reviewed all cases of PTCA performed in 1988 (n = ?i)Qj. Of 160 patients included, 40 had restsnosis during follow-up (25 SJ. Data collected were age, sex. family history, diabetes, hypertenslnr, cigarette smoking, lipid fractions, unstable angina at PTCA, number and type of vessels attempted. Hestenosis (R) and non-restenosis (NP) groups were comparable for all factors individually. The (R) g:ro)ip had a higher number of CRF (2 or more CRF : 88 % in tR) group versus -1 9; in (NR) group. p.co.ol), with a rate of restenosis increasing witn the number of CRF. Hypercholesterolemia and cigarette smoking represented the majnr part of these CRFs, being the mnst frequent asecciat:,:r ;c.';?: in (R) group versus 36 % in (NR) group, pCO.05). We concluded 10, restenosis shares conventional CRF with common atherosclerosis 20/ ~-ate Of restenosis is higher in the multirisk group 3O/ improvement should be expected when reducing CRFS, especially cigarette smoking and hypercholesterolemia. s.5