Pulse wave velocity in buerger's disease

r

I

Letter

Pulse wave

velocity

in

buerger's

disease

Pulse

$a!e

!elocrry

rP\W)

is

di,cclly

rela'Fd ro

arleridl wall thickness and stiffness. hcn'

e

i'

g;ves infonnation about the arterial functions.'? Therefore, this study $as aimed to find_out

Pwv

In Buerger's disease affecLrng Ioser hmbs' (asepric in0ammrlron

and thrombosis ofarteries and veins).

In this study, PWV was recorded

in

15 males having Buerger's disease (mean age 12.1616.84 yea6) of

l-6

years duration, and was compared

with

15 age-matched control male subjects. Excluded ftom the

study were patients having either history, examination

or

investigations suggestive

of:

cardiac disease,

collagen disorders, diabetes, h)?ertension, athero-sclerosis, intake of beta blockers or vasodilaton, and bilateral absence

of

dorsalis pedis artery. History

of

smoking was present

in all

subjects. However, all

subjects were told not

to

smokc one day prior to

examination.

Pulse wave velocity was recorded by means ofpulse

transducers

with

built-in

photodetectors and light

sources. The subjecrs were made

lo

lie in

suprne

position and 2 tmnsducers were placed and strapped in position. One transducer was placed and strapped

over the femoral artery (FA) just below the inguinal ligament, and the other over the dorsalis pedis artery

(DPA). Simultaneous recordings ofarterial pulse fiom

Fi*te

L Recodi g oII.noral and dotsah ped^ pulse

Feh Dp = Tine dela!

T

betwee theit ahs.t

Med J I4i16nA

above mentioned sites were made on two chalnrol

polygraph (Polyriie, INCO), at a paper speed of 50 mn/sec. The length of arterial segment (L) between FA and DPA was also measurcd. The time delay (T)

between the onset

of

pulse wave between FA and

DPA was recorded, and expressed jn m;lliseconds. At

least fivc rccordings werc taken and avemged. Pulse

wavf

velocity

(nvsecl

was calculated

by

using

lormula

(l

/T),' and was noted from

boli

lower limbs

even

if

one limb

is

involved more than the other. Statisticaj analysis was donc by'unpaired t'test.

There was significant

(P<.001)

increase in heart rate

in Buerger's patients without any variation in blood pressure. The PWV in lower extremities in FA

-

DPA segment showed considerable increase (P

<

.001) in Buergei's compared

to

age matched control group

(Table

l,

Figure

1).

There was

no

relationship between the increase

in

P\yV

and the duration

of

Buerger's

disease-Table l. Pulse wave velocity in control dd Buergels d;sease 284

Conirol

Bu€rgeas

P value

disede

(tm ofHg) Sysrolic

78.71:tll.88 95.74+5_48 <0.001

n5.63!t2.t7

107_77!9.11 <0.05

'72.72!6.78

74.44!t\.30

NS

6.3!0.17

8.5a1.71

<0.001

P < .001 = signifi@nt, NS = non sig fic&t

[image:1.596.122.497.536.696.2]

\

t/o|9. Na 4, O.tabet- De.enbet 20A0

Functional status ofblood vessels can be evaluated by

PWV. lncreased PWV relects stiffening

of

arteries. Thc PWV is found increased with age, in coronary

artery

disease, diabetes

and

atherosclerosis.'? However,

there

is

controversy

on

PWV

in

aneriosclerotic peripheral vascular diseas€s.

I1

is

reponed that aderiosclerosis may hav€ no effect or an

effect similar to that of aging'? or decrease the PWy'

due

to

diversion

of

blood

to

smaller collateral vessels.s

PWV

in

lower

extremities

in

FA-DPA segment showed significant increase

in

Buerger's

\ersu.

controls

lachyca'dra. aq occuncd

rn

thi.

study. ha, no effccr on PU

V

H)"eilensron has been

reported to increase PWV,a but all Buerger's patients

in

this

study were normotensive- Therefore, the

increasc of PWV in Buerger's patients may be due to

intlammatron ol arteries' which ma) rdu5e changes in

arterial wall leading to increased PWV.

Kiran Singh

Department ofPhysiology, PCIMS, Rohtak

-

124001, Haryana, India

Nichok WW, Conti CR, walkcr WW, el al. Input

impedence oi systcmic cncDlation in nan. Cilc Res 197?:

40:451 8.

Eliakjm M, Sapohikov D, weinman J. Pulse wave

\.1o, Iy in hedlh' subJe.rc

'l

i-

p"ri.lrs Url" \lnod.

disease slates An Hean J 19? l; 82:448-57.

v.,leelcr

HB.

Thromboangitis obliteEns (Buergels

discasc). In: Sabiston DC k, Lysly HK, edito6. Sabiston

Texl Book of Surgery. The Biological basis oi nodem surgical p6ctice. l5$ cd. Pbiladelphia: Saundets; 1997. p.

1738 9.

Simpnson E, KoIf S, Keys A, Minckler J. Contour ofloe puhe, reactive hypereniaand pulse tmnsdission velocity. Group and repcat varlability, effect of agc, exercise and disease. Am Hen J 1955j 50:260 79.

winsor

T,

Raulslon BD. Pe.ipheral vascular disease. Sp.insfield: Cha.les C Thomasi 1954. p.220.

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