Cardiology Cme04

7/25/2019 Cardiology Cme04

1/69

Management ofHypertriglyceridemia

Sponsored byACCESS Medical Group

Department of Continuing Medical Education

Funded by an unrestricted educational grant from Abbott Laboratories.

2001 ACCESS Medical Group


2/69

Atherosclerosis

re!ention "rials


3/69

"he yramid of #ecent "rials

4S

CARE

WOSCOP

Relative Size of the Various Segmets of the !opulatio

AFCAPS/TexCAPS

LIPID

Very high cholesterol with

CHD or I

o!er"tely high cholesterol i#

high ris$ CHD or I

%or&"l cholesterol with

CHD or I

High cholesterol

witho't CHD or I

%o history o( CHD or I


4/69

$S% E!aluating Lo&ering

Cholesterol on Coronary E!ents

" 'aseline total cholesterol le!els% ()*+,)* mg-dL

" High+ris group /high LDL0 prior M1 or angina2

" #eduction of LDL le!els% ,34

" #eduction of ma5or coronary e!ents% ,$4

" #eduction of total mortality% ,*4

!atiets #ith C$% ad $&percholesterolemia

End of the cholesterol controversy

'S Group(Lancet.1))'*+'',1+-+.1+-)(


5/69

Coronary E!ents Defined

by 'aseline LDL+C

CARE suggests a lower boundary for a clinicallyimportant influence of the LDL level on CHD.

Sac/s M et al(N Engl J Med.1))*++3,1001.100)(

Change in #is6ariable 7 atients 7 /42 atients &ith e!ent

LDL+C lacebo ra!astatin ra!astatinlacebo 834 /C12

)(3+)3*

mg-dL

)3*+)93

mg-dL

)(3

mg-dL$$)

))9(

$:3

$)*

));,

$;;

8, /()2

,)) /(92

)$3 /,)2

;8 /((2

(,8 /(*2

)*( /()2


6/69

#eduction in LDL Cholesterol

and Coronary E!ents)0(0,

1( 'S Group(Lancet( 1))'*+'',1+-+.1+-)( 2( 78SC8!S Group( Circulation( 1))-*)9,1''0.1''3(

+( ric/ M$ et al(N Engl J Med( 1)-9*+19,12+9.12'3(

.30

.'0

.+0

.20

.10

0

'S 78SC8!S $elsi/i

5%5

Coroar&Evets

!ercetR

eductio


7/69

Lowering cholesterol is effective and

safe in hypercholesterolemic patients

with evidence of CHD and leads to areduction in coronary events.

'S Group(Lancet.1))'*+'',1+-+.1+-


8/69

"LDL reduction in primary and secondary pre!ention can

significantly reduce clinical cardiac e!ents

"1t can also significantly reduce the rate ofarteriographically defined disease progression

LDL #eduction and CHD #is:he latest studies have cofirmed the positive correlatio

;et#ee CA% ris/ ad lo#erig cholesterol

However, elevated LDL is only one of several factors

contributing to CAD ris


9/69

'eyond

LDL


10/69

'eyond LDL #eduction:here is somethig more tha 5%5

" Such a large um;er of poor respoders implicates factors other

tha trigl&cerides>

" Aggressivel& treatig other importat ris/ factors such as lo#

$%5 ma& further ;eefit patiets

Super/o $R( Circulation.1))*)',2+31.2+3'(

StudyControl Group

Clinical E!ents

"reatment Group

Clinical E!ents

4 #eduction

Clinical E!ents

:(( /(;.*42

($; /9.342

$,) /)8.$42

)9$ /3.,42 ,).*4

,*.:4$S

=>SC>S


11/69

CHD #is Factors 'eyond LDL

" "riglycerides" HDL

" Small0 dense LDL

" Apo C111

" Lp/a2

" Homocysteine

" Fibrinogen


12/69

:he Role of

"riglycerides

as a C$% Ris/ actor


13/69

ossible Atherogenic Changes

Accompanying Hypertriglyceridemia

$&pertrigl&ceridemia

?creased

ch&lomicroremats

Smalldese 5%5

Coagulatio

chages

?creased V5%5cholesterol.rich

remats

5o# $%5

Miller M(Eur Heart J.1))-*1)=Suppl $>,$1-.$22(


14/69

De!elopment of Hypertriglyceridemia

5iver

V5%5 Ch&lomicro

?testie

%efective5ipol&sis

Remats

Miller M( @iversit& of Mar&lad upu;lished data 1))


15/69

#is of CHD by "riglyceride Le!el=:he ramigham $eart Stud&>

43129

Castelli 7!(Am J Cardiol.1))2*90, +$.)$(

0

0(3

1

1(3

2

2(3

+

30 100 130 200 230 +00 +30 '00

Me 7ome

Relati

veRis/

:rigl&ceride 5evel =mg6d5>


16/69

"he Copenhagen Male Study

" 2)0 #hite me

" Age rage, 3+.9' &ears

" ?itiall& free of overt cardiovascular disease

" -.&ear follo#.up period

" 22) me had first ?$% evet" :rigl&ceride tertile cut poits, )( mg6d5 ad 1'1(- mg6d5

" Crude cumulative icidece rates of ?$%, '(B for lo#est

9(9B for middle 11(3B for highest third =for the tred

P0(001>

Deppese D et al( Circulation.1))-*)9,102).10+


17/69

"he Copenhagen Male StudyAd


18/69

'altimore Coronary >bser!ational Long+"erm Study

:rigl&cerides Compared 7ith Survival Rates

Evetree

Survival=B>

:ime =mo> ollo#ig 1)99.9- Coroar& Arteriogram

:G 100 mg6d5 =11'>

:G 100 mg6d5 =2+>

P0(00-

Miller M et al(J Am Coll Cardiol( 1))-*+1,1232.1239(


19/69

Cumulative

!ercet

reHuec&

:rigl&ceride =mg6d5>

!heot&pe A

!heot&pe

Austi M et al( Circulation. 1))0*-2,')3.30(

Distribution of Ad5usted lasma "riglycerides5%5 !heot&pe A ad

i C i


20/69

1ncrease in C6D #is

Due to High "riglycerides=@ivariate Aal&sis>

0B

20B

'0B

0B

-0B

100B

Me 7ome

''1+ 10-'

,*4

934

$o/aso DE et al(J Cardiovasc Risk.1))*+=2>,21+.21)(

Relative riss and !"# C$ calculated and standardi%ed with respect to a

& mmol'L increase in triglyceride.


21/69

:he Role of

HDL+Cholesterol

as a C$% Ris/ actor


22/69

HDL% A Ma5or #is Factor for CHD

" A lo& plasma HDL is an important ris factor forCHD in the general population

" A high le!el of HDL may confer cardioprotection

" #e!erse cholesterol transport by HDL may be theprinciple cardioprotecti!e mechanism

(n average, a &)# decrease in CHD ris occurs for

each increase of * mg'dL in the HDL level.

The ILI Li!id Hand"ook #or Clinical Practice( 1))3,2(

HDL M 5 F t


23/69

HDL% Ma5or Factor

in redicting #educed CAD

0

20

'0

0

-0

100

120

+3 +3 . 33 33

$%5.cholesterol =mg6d5>

?cideceofC$%=per

1000i2

&ears>

Assma G et al(Atherosclerosis( 1))*12'=suppl>,S11.S20

4''09

i i


24/69

HDL redicti!e 6alue=:he ramigham $eart Stud&>

0

3

10

13

'0 '0.') 30.3) 3)

200

200.2+0

2+1.20

20

Men and &omen &ithout CHD history

$%5.cholesterol =mg6d5> :ota

l.cholest

erol=mg

6d5>

?cidece

=Bi'&ears>

Castelli 7!(JAMA. 1)-*23=20>,2-+3.2-+-


25/69

LDL and HDL 1mpact on CHD #isA Compouded Rather :ha Additive ?mpact

0

100

200

+00

'00

+3 +3.33 33

1+3

1+3.13'

133.1)3

1)3

$%5.cholesterol =mg6d5> 5%

5.ch

olesterol

=mg6d

5>

?cidece

per

1000

=i

2

&ear

s>

Assma G et al(Atherosclerosis( 1))*12'=suppl>,S11.S2


26/69

HDL in Clinical ractice

" #outinely measured in all adult patients" HDL+C ?,3 mg-dL is a ma5or ris factor

" 7onpharmacologic therapy /e@ercise0 &eight

loss0 smoing cessation2" harmacologic therapy

Consider drug therapy that lowers LDL+C and

also increases HDL+C levels.

EFpert !ael(JAMA( 1))+*2),+013.+02+


27/69

:he Role of

Small0 Dense LDLas a C$% Ris/ actor


28/69

Small0 Dense LDL

Dangerous%Small0 dense LDL trait increasesheart disease ris up to three fold

Common%$*4 to 3*4 of men &ith heart disease

ha!e small0 dense LDL

Measurable%"ests are no& a!ailable to physicians

"reatable%Approaches can in!ol!e lifestyle

changes and-or drugs

The ILI Li!id Hand"ook #or Clinical Practice( 1))3,2

Austi MA et al(JAMA( 1)--*20=1+>,1)19.1)21(


29/69

Atherogenicity of Small0 Dense LDL

Evidence from in vitro studies suggests that large, buoyant LDL particles are more

resistant to oidative stress and small, dense LDL particles more susceptible to oidation

Endothelial

Chemoattractants

Foam Cell

Highly o@idiBed

Smooth Muscle

Cell

Mildly o@idiBedMacrophage

5%5

5%5

Endothelium Mooc&te

Macrophage


30/69

Small0 Dense LDL and Drug "herapy

" $n a trial measuring the effects of simvastatin on Apo-metabolism and LDL subfraction distribution, it was found

that small, dense LDL were not significantly affected.

Ga# A et al(Arterioscler Throm".1))+*1+,190.1-)(

" $n a study investigating the ability of pravastatin to affect

small, dense LDL, it was found that although this agent

favorably altered total cholesterol and LDL levels, the

abnormal LDL particle distribution and composition were not

affected.raceschii G et al(Arterioscler Throm".1))'*1',13).1393(


31/69

:he Role of

Fibrinogen

as a C$% Ris/ actor

El d l Fib i


32/69

Ele!ated lasma FibrinogenA Ma


33/69

Fibrinogen and Atherosclerosis432 me

0B

20B

'0B

0B

-0B

100B

5o#er Middle @pper

Present

Absent

!r e

s e c e

o rA; s e c e

o f!la H u e

5eveso D et al(Arterioscler Throm" (asc iol.1))3*13,12+.12-

Effects of Lipid Lo&ering Agents


34/69

Effects of Lipid+Lo&ering Agents

on Fibrinogen

1

.1

.10

20

'0

.+0

.20

.10

0

10

20

+0

%ietI eoII ezaII GemII SimvaI !ravaI

Chageii;rioge=B>

rachi A et al( Throm" Haemost. 1))+*90,2'1.2'+(

I4ot sigificat

IIP0(01


35/69

Fibrate Clinical >!er!ie&

Fibrates


36/69

Fenofibrate

Bezafibrate

Gemfibrozil

CH3

CH3

O CH2 CH2 CH2 CH2

CH3

COOH

CH3

C

C O

O

C

CH3

COO CH

CH3

CH3

Cl

CH3

Fibrates

OO

O

OH

CH3H3C

Cl

NH

Metabolic Action of Fibrates


37/69


Lipoprotein

lipase

6LDL1DL

Apo C+11

Apo C+111

Chylomicrons

5iver

!ac/ard CD(Eur Heart J( 1))-*1)=suppl A>,A2.A3

Apo E

Apo C+111

FFA



38/69

Fibrate

A#

7ucleus

H7F+$

C111 GeneC,

lasma Apo C+111 :*4

Apo E-Apo C+111

!ac/ard CD(Eur Heart J( 1))-*1)=suppl A>,A2.A3(

Metabolic Action of Fibrates:he !eroFisome !roliferator Activator Receptor =!!AR>

-

-

Mechanisms of Action of Fibrates


39/69

Mechanisms of Action of Fibrates

" ?hi;it trigl&ceride s&thesis* reduces V5%5 release ito circulatio

" ?crease lipoprotei lipase activit& #hich cata;olizes ch&lomicrosad V5%5

" ?crease cata;olism of trigl&ceride.rich V5%5 there;& lo#erigserum V5%5 levels

" ?crease $%5 through improved Apo A.? ad Apo A.?? s&thesis

Serum 6LDL/"riglyceride+rich2

Fibrate

......... ..

.. . .....

Lo&ered Serum 6LDL/#educed triglycerides2

Fenofibrate for the "reatment of


40/69

Before After Percent

(mean SE) ( mean SE) Changes* P

"ype 16 and 6 HyperlipoproteinemiasA %ou;le.lid !lace;o.Cotrolled Multiceter @S Stud&

Gold;erg AC et al( Clin Ther( 1)-)*11,).-+

Fenof!rate

2"#.$ ".3

%2.# &.$

#2$.' .#

33. #.#

'32. #%.#

3'%.$ 3'.3

22.' &.

'".$ '."

#3&. ".3

'.3 #.%

223.' #3.%

#.$ 2'.&

-%.#

-''.

NS

#%.&

-'&.2

-''.#

*These are mean percentage changes, not percentage changes in means.

NS=Not statistically significant when compared with placebo (1! increase".

+otal cholesterol

,-cholesterol

-cholesterol

H-cholesterol

+otal trgl/cer0e

,-trgl/cer0e

1.#

1.#

.$"

.#'

1.#

1.#

ro4 A(3"-'%% mg50)



41/69


Gold;erg AC et al( Clin Ther( 1)-)*11,).-+(

Fenof!rate

2. &.

#2&.2 .

#3.# &.$

2%.& #.3

2".& 3.'

"'3.3 ".$

223.3 &.&

"3. 3.'

#3#. &.

3&. #.$

3$. #%.%

2'. 23.

-#3.$

-'%.'

'".

22.%

-"'."

-".&

*These are mean percentage changes, not percentage changes in means.

+otal cholesterol

,-cholesterol

-cholesterol

H-cholesterol

+otal trgl/cer0e

,-trgl/cer0e

Before After Percent(mean SE) ( mean SE) Changes* P

.#

.#

.2

.2%

.#

.#

ro4 B("-#" mg50)



42/69


" Ma& patiets #ith mar/edl& elevated trigl&cerides havereduced 5%5 levels ;ecause of a deragemet i the ormal

compositio of 5%5

" :his deragemet produces a trigl&ceride.rich ad

cholesterol.depleted 5%5

" 7he trigl&cerides are reduced #ith therap& the

compositio of 5%5 ormalizes* this chage ca elevate

5%5 levels

Gold;erg AC et al( Clin Ther( 1)-)*11,).-+

Fenofibrate for the "reatment of" 16 d 6 H li i i


43/69


7ee/ of :reatmet

.0

.30

.'0

.+0

.20

.10

0

10

20

0 2 ' -

!lace;o

eofi;rate

B

Cha g e f ro

m

Ea s e l i

e

Gold;erg AC et al( Clin Ther.1)-)*11,).-

:otal :rigl&ceride . Group

Fenofibrate for the "reatment of" 16 d 6 H li t i i


44/69


7ee/ of :reatmet

Gold;erg AC et al( Clin Ther.1)-)*11,).-

.10

.3

0

310

13

20

23

+0

0 2 ' -

!lace;o

eofi;rateB

Cha g e fro m

Ea s e lie

$%5.C . Group



45/69


/01enofibrate is both safe and effective in the

treatment of primary type $2 and 2

hyperlipoproteinemias in patients in whom

dietary modifications have proved ineffective

in reducing plasma triglycerides.3

Gold;erg AC et al( Clin Thera!eut( 1)-)*11,).-+(

Effects of Fenofibrate on lasma Lipids


46/69

%ou;le.lid Multiceter Stud& i !atiets

#ith :&pe ??a or ??; $&perlipidemia

ro# 7V et al(Arteriosclerosis( 1)-*,90.9-

4229

,ara!le Fenof!rate Place!oSam4le S6e (n) ##& ###

Age (/r 7 S)8eght (l!s 7 S)Se9 (n)

:aleFemale;ace (n)

CacasanBlac

7ee/s o Stud& Medicatio

Comparati!e Efficacy and Safety of MicroniBed

F fib t d Si t ti i ti t ith


50/69

Fenofibrate and Sim!astatin in atients &ith

rimary "ype 11a or 11b Hyperlipidemia

Study Design

arier M et al(Arch Int Med.1))'*13',''1.'')(

#Single+center0 Double+blind0 Crosso!er "rial

":* atients /,( type 11a and (; type 11b2

"#andomiBed to treatment for , months

"Single daily dose of fenofibrate (** mg or sim!astatin (* mg

"Changed to alternati!e treatment for a further , months


F fib t d Si t ti i ti t ith


51/69



/#andomiBed0 Crosso!er Study2


Fenof!rate2 mg50a/

Sm>astatn2 mg50a/

Sm>astatn2 mg50a/

Fenof!rate2 mg50a/

+/4e ==a? n@#&

+/4e ==!? n@#'

+/4e ==a? n@#&

+/4e ==!? n@#'

ro4 #

ro4 2

= = = = = = = 3 &

:onths




52/69



Characterstc Fenof!rate Sm>astatnSam4le S6e (n) 3 3

Age (/r 7 S)8eght (l!s 7 S)Se9 (n)

male

femaleH/4erl4o4rotenema (n)

+/4e ==a+/4e ==!

+otal Cholesterol (mg50)-C (mg50)

H-C (mg50)+rgl/cer0e (mmol5)

'#." 7 ##.' '&.# 7 #.2#'%.& 7 23." #"%.# 7 2.%

#&

#'

2#

%

#'

#'

3#" 7 " 323 7 '"23' 7 '$ 2'# 7 "" 7 #$ '$ 7 ##

#.$2 7 #.#% #.%# 7 #.#


Fenofibrate 6ersus Sim!astatin


53/69

.2- .2-

.+'

.+ .+9

.30

.'0

.+0

.20

.10

0

:otal.C 5%5.C $%5.C :rig

eofi;rate

Simvastati

Effect on >!erall Lipid rofile


=:&pe ??a>

B

C ha

ge

fro

m

Ea

seli

e

4C 4C 4C

4C4o chage

Fenofibrate 6ersus Sim!astatin


54/69

.2+ .21 .23 .+0

2)

19

.32

1-

.0

.'3

.+0

.13

0

13

+0

'3

:otal.C 5%5.C $%5.C :rig

eofi;rateSimvastati

Effect on >!erall Lipid rofile

arier M et al(Arch Int Med.1))'*13',''1.'')

=:&pe ??;>

B

C ha

ge

from

Ea

seli

e

Fenofibrate and laue #egression


55/69

g

" () atients &ith CHD had 8; narro&ings" Mean duration of follo&+up% () months /range

)( to ,: months2

" Comparison &ith a similar untreated group of

() patients &ith CHD presenting 8;

narro&ings

" uantitati!e coronary angiography /CA2

$ahma $7 et al(Am J Cardiol.1))1*9, )39.)1(

Fenofibrate and laue #egression


56/69

g

!erce

t!atiets

$ahma $7 et al(Am J Cardiol.1))1*9,)39.)1(

0

10

20

+0

'0

30

0

90

eofi;rate @treated

Regressio

Sta;ilizatio

!rogressio

MicroniBed FenofibrateA C i fi


57/69

A Comprehensi!e rofile

Joritzer M et al(Atherosclerosis. 1))'*110=suppl>,S').S'

.+0

.13

0

13

+0

'3

:C 5%5 $%5 i;rioge

4ormal$igh Ris/I

!er

ce

tC

ha

g

e

413'3 patiets

I$igh ris/, :C 230 mg6d5 5%5 1-3 mg6d5 $%5 +3 mg6d5 fi;rioge +00

mg6d5

LDL rofile of Fenofibrate


58/69

LDL rofile of Fenofibrate

.0B

.'0B

.20B

0B

20B

'0B

0B

Casla/e MD et al(Arterioscler Throm".1))+*1+,902.911

C

hage

:otalCholesterol

5%5.C 5%5 Receptor@pta/e

5argeuo&at 5%5

Small %ese5%5

"he Helsini Heart Study


59/69

y

"A 3.&ear trial that tested the efficac& of gemfi;rozil fordecreasig the ris/ of coroar& arter& disease i

h&percholesterolemic me #ithout coroar& arter& disease

" :he stud& ivolved '0-1 me ='0 to 33 &ears of age> #ith a

o.$%5 cholesterol level 200 mg6d5

" Gemfi;rozil use #as associated #ith a +'B reductio i

coroar& arter& evets

ric/ M$ et al(N Engl J Med( 1)-9,+19,12+9.12'3(

6eterans Affairs High+Density Lipoprotein

Cholesterol 1nter!ention "rial /6A H1"2


60/69

Cholesterol 1nter!ention "rial /6A H1"2

Study Design

Ru;is $ et al(N Engl J Med.1)))*+'1,'10.'1-(

" %ou;le.;lid trial that compared gemfi;rozil =1200 mg6da&>#ith place;o

" Stud& of 23+1 me #ith coroar& heart disease high.desit&

lipoprotei cholesterol levels '0 mg6d5 ad lo#.desit&

lipoprotei cholesterol levels 1'0 mg6d5

" :he primar& outcome #as ofatal m&ocardial ifarctio or

death from coroar& causes

"he 6eterans Affairs High+Density Lipoprotein Cholesterol

1nter!ention "rial /6A H1"2% 'aseline Characteristics


61/69


Age =&r> ' K 9 ' K 9

Age 0 &ears =B> 99 9

!rior M? =B> 1 1

:ime sice M? =&r> K K

%ia;etes =B> 23 2'

$&pertesio =B> 39 39

5o#.desit& lipoprotei mg6d5 =mea> 112 K 2+ 111 K 22

$igh.desit& lipoprotei mg6d5 =mea> +2 K 3 +2 K 3

:rigl&cerides mg6d5 =mea> 10 K 9 11 K -

lacebo GemfibroBilCharacteristic /7)(:92 /7)(:$2

1nter!ention "rial /6A H1"2% 'aseline Characteristics

"he 6eterans Affairs High+Density Lipoprotein Cholesterol

1nter!ention "rial /6AH1"2 #esults


62/69


1nter!ention "rial /6A H1"2 #esults

0

5

10

15

20

25

30

Placebo Gemfibrozil

*

* Risk reduction =24 !P"0#001$

%it&

'eat&(

)*ocardia

l

+nfarction(or,troke

"he 6eterans Affairs High+Density Lipoprotein

Cholesterol 1nter!ention "rial /6AH1"2% Summary


63/69

Cholesterol 1nter!ention "rial /6A H1"2% Summary

" VA $?: compared treatmet #ith gemfi;rozil or place;o i

23+1 me #ith coroar& heart disease ad lo# levels of

high.desit& lipoprotei cholesterol

" :here #as a 2'B reductio i ris/ of ofatal m&ocardial

ifarctio stro/e or death due to C$% i the group #ho

received gemfi;rozil =P0(001>

" :he fidigs suggest that the rate of coroar& evets is

reduced ;& raisig $%5 ad lo#erig trigl&cerides #ithout

lo#erig 5%5


"he Diabetes Atherosclerosis 1nter!ention Study /DA1S2

rotocol


64/69

%ou;le.;lid radomized place;o.cotrolled agiographic stud& usig

200 mg6da& microized feofi;rate

!opulatio" +03 me 11+ #ome '0 to 3 &ears of age" Su;


65/69

'aseline Clinical Characteristics

lacebo Fenofibrate

/n())2 /n(*92Demographics

Age =&ears K S%> 3 K 39 K

7ome =B> 2 2-

Curret smo/ers =B> 1 1'

'lood pressure$istor& of $&pertesio =B> '- 33

S&stolic =mm $g K S%> 1'0 K 1- 1'0 K 1)

%iastolic =mm $g K S%> -1 K ) -2 K )

Coronary Disease

$istor& of CA% =B> '9 '-

!rior itervetio =B> +0 +2

%A?S ?vestigators(Lancet( 2001*+39,)03.)10

"he Diabetes Atherosclerosis 1nter!ention Study /DA1S2

Angiographic Changes from 'aseline


66/69

Angiographic Changes from 'aseline

Miimum 5ume

%iameter

0(000(00

.0(02.0(02

.0(0'.0(0'

.0(0.0(0

.0(0-.0(0-

.0(10.0(10

mmmm

.'0B.'0B

P ) 0(02)!rogre

ssioofCA%

BB

ChageChage

!ercet Steosis

'(00'(00

2(002(00

0(000(00

P 0(020

.'2B.'2B

Mea Segmet

%iameter

0(000(00

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mmmm

.23B.23B

P 0(191


!lace;oeofi;rate

"he Diabetes Atherosclerosis 1nter!ention Study /DA1S2Combined Clinical Endpoints


67/69

!lace;o eofi;rate0

3

13

EvetRate=B>

EvetRate=B>

23

20

10

.2+BI

I %A?S #as ot po#ered to eFamie cliical evets( Eve though theresults suggest a tred the& #ere ot statisticall& sigificat(

!articipats #ith at least

oe cliical oritervetioal edpoit

icludig death stro/e

M? CAG !:CA ad

hospitalizatio for

agia(


"he Diabetes Atherosclerosis 1nter!ention Study /DA1S2Clinical 1mplications


68/69

'+, assessed t&e effects on coronar at&erosclerosis of

correctin liorotein abnormalities in atients it& te 2 diabetes

6&e stud found t&at treatment it& fenofibrate reduced t&e

aniora&ic roression of coronar arter disease in men and

omen it& te 2 diabetes/ t&is effect as related( at least in art

to t&e correction of liorotein abnormalities

'+, findins suest t&at eole it& te 2 diabetes s&ould

&a7e lioroteins measured at dianosis and annuall t&ereafter

89istin e7idence suests t&at an liorotein abnormalit s&ould

be corrected( e7en if small( to reduce t&e risk of coronar disease

in atients it& te 2 diabetes


"he Diabetes Atherosclerosis 1nter!ention Study /DA1S2Comparison to Clinical "rials =ith Diabetic atients


69/69

p

Study Agent

E!ent

#eduction

DA1S eofi;rate 2+B

CA#E !ravastati 23B

L11D !ravastati 1)B6A H1" Gemfi;rozil 2'B

46alue

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4S 4ot statisticall& sigificat

0(03

4S

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