Angina pectoris is chest pain due to reduced blood flow to the heart muscle. It usually occurs when the heart's arteries are narrowed or blocked. There are different types of angina including stable angina, unstable angina, and variant angina. Tests used to diagnose angina include EKGs, blood tests, chest x-rays, cardiac catheterization, and CT scans. Treatment includes lifestyle changes, medications like nitrates, calcium channel blockers, and antihypertensive drugs, as well as cardiac procedures and rehabilitation.

1. What is Angina Pe,
croris....:l
c:.~ ~ .....
► It is chest pain or discr1m1·11rl due l.o co.ronary heart
disease
► It occurs ·w.b1
en the heart .muscl.
e 1
d.
oes1
n't gl
et as ·mucb
.
BLOOD & O.
XYGEN as It n.eeds
► This, usually happens because one or more of the
heart's arte·
ries are .narrowed or blocked, also called
. .
b ,
.,
ISC: ·em1a
q/21/70 l~ P,. die il-Of Be lcdJe111

2. Types ,
ofAngina Pectoris
► Sta:
ble·Anlina I Anli,
na Pec;
toris
► Unstable.
An1ioa1
► Varl1
an.
t (Prlnzmeta'I) Angina
► Microv·ascularAngina
9/B/]fJ19

3. Tests,:
► EK1
G (Electrocardiogra:
m)
~ 1
s··· trnc,s ..,esu
··no
r _.·'-...a ,_· It ·- -
111
► Blood,Tests
► 1
Cbesl,X-Rays
► 1
C1
0.
ronary AnlJi,
ograpby,and Cardiac Catllete:
rization
► Computed Tomo&raplly Angio~aphy
Treatment i1
n1
cl
ludes:
► Lifestyle chan1esl
► Medicines
► 1
C1
ardiac p~edures
► 1
Ca.
nliac Rehab1
~/l'l/2{] 19

4. Anti..anginal Agents
As pe.
r PC1
l 1
SJ·llahus
, VasodilBt1
ors :
Nilrates & Nitrites: Amyl nilrite, Nitn11Jycerio, Penta1
erylbrilol
tetranitrate, 'lsosorb1
i.
d1
e dinitrlte, Dipyridamole
, Calcium channel bl1
ockers:
, ,. ·1,
- a
-- ·m1 h ~1
--.-1.1 ·d oo
·ti
.. h d. cbl1 - ·d
.erapam1~ ...epr1 1
Juruua_
on· e, . . azem , .. ro· o·n·1 e.
Nifedipine, Aml.
odip·ine, Felodipine, Nlcardip·
ine, Nimodlp.lne
, Anti-hyperrensi-we Agents:
Timolol, Capto·
prll, Llsinop.rll, Enal,
a·pril,, Bena1'eprl1
hyd.rochloride, 1
01
11iDBpril bydrm:'blaride, Me~yldop,ate
hydmcbloride, Clonldlne hydrochloride, Guanelhldlne
mo,nosolpb,■te, Guanabenz acetate, Sod'lum nitroprusside•
.D,
iazoxid.
e, .Minoxidil, :
Reserpine,]Hydralazioe h.
y1
drochloride
~ 113/201~
Ii

5. ~ Diure1ics:
• Carbonic anhydrase inhibitors: .Acetazolamide, Metbazolam·
ide,
Dichlorphena,mld:
e
• 'Thiazid1
es: Chlo1
.rt'hiazid1
e, Hydrocblerotlriazide,
HydroD11111ethiazide, Cyclotldadd,
e
L di t.. Fu ··11e B et •d
' Etha ., ·
•d
• ot)p ure 1cs: ..1 n1Jem1 , .. ··11m _ an1 e, .. · ·11crymc ac1 _.
• Polass.
ium sparing Diuretic..~: Splronolactone, 'Trlamterene,
AmiJorid.
e
•
1
0sm1
otic Diuretics: Mannito1
l
~nJ/Z019 rr-atcuor Bl.'.! UEtvu

6. 1
Vasodilators
Nitrates & Nitrites:
1
• Organic nlen,RC1
00R' are nten 01
'f 1
0rgj
a11lc ■cld1 RC001
,
H wllh a,aanlc:
111£ol101
l1R1
-o·n
• 0rga'nlc nllr■tes(R11
0NOJ1 &,1
0 1
rpnl1 nllrilt1(R
1
'0N-O) ■N esten 0.1
f nl1
t111u1
add (HNOJ) 1
ar nJlrlc acid (HNOJ) with 1n1organic alcohol R' O,
H where
altacbmenl ,
r6 NO1 ls on,Osy1m I.e.
RO.H
Alcohol
'RO-H ·+·
,
Alcollol
9/B/1019
HO-N=O
N. A "d
llrolll · ,Cl··
0
0
e/
I
MO N
~ . -
~
N1mc act 1
0
Pra:,re1S.Or &1ut1e-t1l
.. RO-N=O +
I ~ ' l1
tnte
Alkyl N~ ,
.
0
1
0
.._
@
/ +·
AO N
~
Alkyl N"tr tc
~.,_ 1 ,a ·o
1

7. Mr
echanism ofAclion:
• Nilric oxide (NO) sliimulates the for.matioo of cGMP~
• Nitmdilaton are 'lhe dru1s~ that mimic the actio1
DS1 1
Df endOGCD.
OUS N1
0 by
r-elcasiog N·
o or forming NO widun li&-sues~
1
• These drugs acl directly on the vscular smooth muscle 101
cause relaxalim an.d
th.
ereforc serve as endothel-i~eJ-indqMmdem vasodilatcn..
•
1
There an: two basic lypcs of oiDucHlalOrs: dtose tbal. n:lcasc NO spontaneously
1
(e~
,g.., sodi.um oilJ7oprusside) r
and organic'nitrates th.al require ,
am enzymatic process
1
·
01
form N01
..
•
1
0i:ganic·nitrates do ·not dimcdy mlea1
SC NO, h,
OYJCYCr, tt.:ir nitrate sroups i.oteracl
with enzyrnes and inttacel'lwlar ,
sulfhydryl grou.ps tlu1.reduce the nitrate groups lo
N011
Dr to S·-llitmscthiol, wbicb then is reduced to NO.
• Nitric 0 1
xide activates smooth muscle soluble ,guan,ylyl cyclase tOC1
) to Jam
cO~
• Increased inncdlular cGMP1
inbilliJ
II cakium entry inl.
o lb£ ,
a:·
11. lhcn:by
decreasing intrace1·
1uls mdcium CODCColndioos and
·. cm1,i!!in-c- . ~•1... . )
__·:. - -- -- __ .... I li ■ uu·ulU muse .
C
relaxation.
~/.B/101.9 PrO'h.~·:uo,r Be u11rn.i.

8. • .NO al,o a~livale.s ·
K• channc~ which h:ads. lu hyperpo]arization and.relaxatiDn.
• Finally.
" N·o aciing 1hmu.gh cGMP can s1hnula1e a cGMP-d-ependmt protein
kina'ie Lbat activates m;
yosin lighl chain pbosphalase·, the 1
cnzym.
e that
dephosp..horylatcs myos·in li,ght mains,. which leads to rreho:ntion~
rllechanism o,f .
Action of Nitr,
ovas.,
odilators
hef l.111 t {)f'I C
_
I.
Ml( fit.
•d ffl p-otcm lu.fl!l:IE

9. CHs
I
H:1C ·
,
Amy.
I Nitrile
•
o
-· o
."- ✓ .
~ ''N'
u
0
0
11
1
- -+
,,.N,
1
Q o-
01 O
'"
- I I
. ' . .
•N
I;'
Ill
0
N"dm&IYmrille
9/B/1019
0 a~~-
Dlpv . . L I
_ . • ~ I .
. I • ~ - Peataery111r1to1 telraallrate,
,..._
_.
.....
Sodium Nlr.apnalde
Qr
~ --o
lsosarlllde1
dlnllnle
10

10. Cal!
cium ch•nnel bla,kers
• Cuneolly approved ,calcimn-dlanoel hlackers (CCBs) bind to L..type
1
caleium f!b,annels located on die lfascu1
ear woatb muscle, cardiac myocytes,
a11d ranliar nodal tluue (llnoalrlal and ■lrlavenlriadar oodes),
.
• Th.
ae, tbanoels ,
are respomd1
ble lor .
Rpllatlng lbe Influx of raltium mlo
muscle cells,1 whicll la 'tum stimulates smooth :
m111tle conlraclion alld
,
canlM myoryte 1
"tllll:n1:·tlon1
• In e_
ardiac nactal tiaae, L-lype ralemm eunoe.11 play an loqt0rtanl 111le
in pacemaller C?urr-entl,anti in rh■w 1
81
oflhe artlon palenlials.
■ Therefom, by blodmlg cal.dam entry into1
the tell,. CCBs cause YBKDlm:
.sm,
eoth musde· rrluation 1
(~81odUa,tmn), dea-eased myocardial Force
generation (neptiwe iaatropy),,decnased heart rate tneptive dlronolrop,
y).
and decreased comlacdon 1111od1J wl1
t'bln Ille. 'heart (aepllte dmmotnJp,
y),
partirularly at 'tbe 1
atrioventrlcular node.,
9/2l/XH9

11. Structural Activity Relationship
1,4-dihydropyridines(l,4-DHP)
Alk,
yl group •• C2 & R
2
C6 lncttases ••e
antagonistic activity
9!11/XJl'J
o/m-sub posscssN
optimum acti,·ity
Sub phen,·I ring at
iacrea1n th~ acth in,
X ho"e,·er Ub "itb small no~
planer alkyl or c,·cloalkyl
aroup decrea.~l~
~the acti, it)
.,,...Rs

12. a..04.
Nil, adipine
0
H,C..;1'0 .
H
Fcludipinc
lsradipine
9/ll/201!>
Structures
~o
1
.mlodipine
Diltian:m
r
NICedipln'.C
u