Update in Coronary a.

Disease
(CAD)
OVERVIEW

Skema TAUFIQ
jantung : Collection
pembuluh koroner & bilik jant
Dr. TAUFIQ
RSPAD AW SpBTKV
1.CHEST PAIN
2.ANGINA PECTORIS
3.CAD (Coronary Artery Disease)
4.Stable Angina
5.Acut Coroner Syndrome (ACS)
6.UAP (Unstable Angina Pectoris)
7.AMI (Acut Myocard Infarc)
8.NSTEMI (Non ST Elevasi Myocard Infarc)
9.STEMI (ST Elevasi Myocard Infarc)
10.Cardiac Arrest , Suddent Death
Skema jantung : pembuluh koroner & bilik jantung

Pembuntuan /
penyumbatan
 Locus
minoris
Resistance,:
Junction:
cap endotel

Viscosity and Poiseuille’s Law

P1-P2 = V . 8 L n = Q . 8 L n
r2 phi r4
P = potensial energi (dyne/cm2)
V = mean flow velocity (cm/detik) = Q/phi r2
L = jarak (cm)
n = koefisien viskositas (poise =dyne.detik/cm2)
Q = flow (cm3/detik)
r = jari jari
(energy loss P turun 4x tiap r turun)
Culprit lesion= stenosis>70%,proximal,near branch,
atherom: rich macrofag&lipid
stenosis=50%:angina effort
stenosis=90% angina at rest
 USA INDONESIA
population 330.000.000 237.600.000
1,000 CILEGON
392.341
CAD (30 persentil) 9.900.000 7.128.000
11.770
IMA (6 persentil) PERSENTILE
1.980.000 CAD
1.425.600
2.354
mortality (30%) 594.000 427.680 785
pre hospital (15/30%) 3 118.800
1 85.536 392
2
readmission 1 y (35/70%) 633.600 456.192 CAD 589
6
Cath/PCI 1.210.110 871.279 INFARK 1.177
30
CABG 356.730 256.846 MORTAL 392
Cath/PCI
CABG

JAMA.2011;305(17):1769-1776. doi:10.1001/jama.2011.55
 392,341 CILEGON
PENDUDUK: 392.341
CAD: 11.770
INSIDENSI CAD
INFARK: 2.354
Per Hari
MORTAL: 785

1 Pre RS: 392

3
2 Re admission: 589
CAD
6 PCI: 1.177
32 INFARK
MORTAL CABG: 392

Cath/PCI
CABG
 SPEKTRUM: ChestPain-Stable Angina-Unstable Angina (UAP)-Infark
A.Chronic Stable Angina (demand ischemi)
plaque aterosklerosis masih stabil.
lumen coroner menyempit (50% stenosis?), masih cukup suplay,
ttp saat demand J(exercise, stress, eat)transitory imbalance suplay demand
iskemisymptom (+).

saat demand Kimbalance suplay demand (-)symptom (-)

[tdk ada perub dlm frek dan beratnya serangan]/durasi 5-15mnt.(Umumnya 1-5)
menghentikan aktivitas dan atau NTG akan menghilangkan symtom.
B.Plaque membesar,tdk stabil/rapuh/dinding plaque robek,ruptur
thrombogenic surface agregasi platelet/trombi .
Coroner vasospasme dan atau agregasi platelet/trombi: akut
coroner flow turun atau sama sekali tak adaacut reduction O2 suplay
suplay ischemibiasanya bersamaan demandk 
acut coroner sindrome(ACS):
sumbatan total>6jam=irreversible necrose
 flow dynamic & endothelial shear stress
Vulnerable plaque:
-large lipid pool
-thin-fibrous cap Plaque disruption
-numerous inflamatory cell

-agregasi
Activated Dissolution -cascade coagulasi
Inflamatory cell Fibrous cap -vasokonstriksi

Release: metalloproteinase
(collagenase) THROMBOSIS

ACS
Resistensi coroner,ditentukan oleh:
1.Epicard coroner vessel=conductive vessel=5%
2.Small coroner/arteriol=resisten vessel=95% case

Plaque disruption

Sub endotel exposure:

Vessel wall collagen

Local agregates:
Thromboxan, ADP

Platelet agregation

thrombin Release substance:

Promote vasoconstriction
 Atherosclerosis

CAD

Angina pectoris

ACS

Unstable angina Myocardial infarction

NSTEMI STEMI
CORONARY ARTERY DISEASE (CAD):

Key word: 1. chest pain

2. angina, angina pectoris, ankhone pectus =strangling chest

A. Stable Angina .

B. Acute Coronar syndrome (ACS):

a spectrum continuum representing
on going myocardial ischemia or injury

1. Unstable Angina Pectoris (UAP)

2. Miokard Infark: -a. Non ST Elevasi Miokard Infark (NSTEMI)
-b. ST Elevasi Miokard Infark (STEMI)

Imbalance suplay demand  myocard ischemia  an aerob tjd gangguan:

ggn metabolik,
ggn electrical,
ggn mekanik
chest pain: P-QRST=Pain-Quality-Radiation-Severity-Timing
(tightness-squeezing-pressure)
 Klinis CAD: broad spectrum:
-Asymptomatic state (subclinical phase)
-Stable angina pectoris
-Unstable angina (ie/yaitu: ACS)
-Acute MI
-Chronic ischemic cardiomyopathy
-Congestive heart failure
-Sudden cardiac arrest

Symptom & Sign:(25% silent)(intense &unremitting for30-60’)

-chest pain: P-QRST=Pain-Quality-Radiation-Severity-Timing
(tightness-squeezing-pressure)
radiate: jaw,arm (trtm kiri),neck,back,epigastrium
(EXCLUDE: Nyeri up mandible,belowepigast,<1mnt (bbrp dt)
-dispneu(buktikhas adanya poor ventricular compliance),whezing
-palpitasi, takikardi, sinkope -cough
-dizziness, weakness, diaphoresis,anxiety -asimptomatik
-nausea,abdomen pain-vomitus (trtm infark inferior & posterior)
-simptom yg berhub FR hiccup: iritasi frenic, diafragma

Onset sering pd pagi krn: naiknya katekolamin induce-platelet

dan naiknya plasminogen activator inhibitor-1 (PAI-1)
(katekolamin juga naik pd: anxiety, pain),
angina decubitus:tidur malamvenous return naik
demand meningkatangina
 Canadian Cardiovascular Society Grading System
for effort –related angina, Functional Class Canadian Society (FCCS I-IV)

Grade I - Angina with strenuous, rapid, or prolonged exertion

(Ordinary physical activity such as climbing stairs
does not provoke angina.)
Grade II -Slight limitation of ordinary activity (Angina
occurs with postprandial, uphill, or rapid walking;
when walking more than 2 blocks of level ground
or climbing more than 1 flight of stairs; during
emotional stress; or in the early hours after
awakening.) (1 block = 100-250 m)
Grade III -Marked limitation of ordinary activity (Angina
occurs with walking 1-2 blocks or climbing a flight
of stairs at a normal pace.)
Grade IV-Inability to carry on any physical activity without
discomfort (Rest pain occurs.)
 KILLIP CLASSIFICATION:
Class Description
1 Absence of rales over the lung fields and absence of S3.
2 Rales over 50% or less of the lung fields or the presence of an S3.
3 Rales over more than 50% of the lung fields.
Cardiogenic shock. Hypotension (a systolic blood pressure of less than 90 mmHg for at least 30 minutes or the need for supportive
measures to maintain a systolic blood pressure of greater than or equal to 90 mmHg), end-organ hypoperfusion (cool extremities or a
urine output of less than 30 ml/h, and a heart rate of greater than or equal to
4
60 beats per minute). The hemodynamic criteria are a cardiac index of no more than 2.2 l/min per
square meter of body-surface area and a pulmonary-capillary wedge pressure of at least 15 mmHg.

Class Description

1 No heart failure. No clinical signs of cardiac decompensation

2 Heart failure. Diagnostic criteria include rales, S3 gallop and venous hypertension.

3 Severe heart failure. Frank pulmonary edema.

Cardiogenic shock. Signs include hypotension (systolic pressure < 90 mm Hg) and evidence of peripheral vasoconstriction such as
4 oliguria, cyanosis and diaphoresis. Heart failure, often with pulmonary edema, has also been present in the majority of these
patients.

KILLIP > 2 = POOR PROGNOSIS

From ACC Key Data Elements and Definitions for Measuring the Clinical Management and Outcomes of Patients With Acute Coronary Syndromes. JACC Vol. 38, No. 7, 2001.
From T. Killip III and J.T. Kimball, Treatment of myocardial infarction in a coronary care unit: A two year experience with 250 patients, Am J Cardiol 20 (4) (1967), pp. 457–464.
 Definisi infark miokard:
Irreversible necrosis of
heart muscle
secondary to prolong ischemia
Cut of point: serial per 6-8j
Trop-I : >4 (0,4 ngr/ml)
or >10%: CV, or percentile99
T: >1 (0,1 ng/ml)
CV= coeficient of variation=
= % variation in assay result
CKMB:>52 , atau
CKMB >10% CK

Troponin I & T: marker lain:- myoglobin, CRP, IL-6,serum Amiloid-A

naik dlm 3–12 j dr onset pain, peak 24-48 j, N 5-14 hari. - LDH (onset dlm 24 jam, peak 3-6 hr, durasi 8-12 hr)
(tjd perub kadar naik > 0,2 ng/ml setelah 2 jam). Trop.T>0,03 - NT-pro BNP (naik pd kenaikan LVEDP/wall stress)
CK-MB(creatine kinase-miocardband)):sensitif hh,spesifiki (N-Terminal pro Brain Natriuretic Peptide).
- kadar enzim naik dlm 3 s/d 12 j onset pain (umumnya 6-9 j) Low level bila < 80 pgr/mL
- peak dlm 24 j, baseline 48 – 72 j kmd.
- (tjd perub kadar  naik >1,5 ng/ml)
- Normal: CKMB = 3 – 6 % dari total CK
-Non ST Elevation Miocard Infarc (NSTEMI):
ST depress, T change (+/-)
-ST Elevasi Miocard Infarc (STEMI):- Q wave dan Non Q wave
hati-hati: NSTEMI pun (meski kecil insidensi):dpt tjd Q wave
 ECG: Normal-Ischemia-Injury-Infarct
Recognition
Well Perfused Myocardium Epicardial Coronary Artery

Lateral Wall of LV
Septum

Inferior Wall of LV
Positive Electrode
VAT

QRS
interval
INJURY
INJURY:

Prolonged ischemia
Sel miokard (++)
(+)

Represented by ST elevation
K+

Na-K-
ATP
Na+
 referred to as an “injury pattern”
 Transmural injury ST elevasi
Injury
Usually results in infarct
 may or may not develop Q wave Thrombus

ISCHEMIA Subendocard transmural

INJURY Ischemia
 ECG has important rule in ACS

Transmural infarction Subendocardial infarction

 VAT Kecepatan rekaman : 25 mm/dt 1 mm=1/25 dt = 0.04 dt
Kekuatan voltase : 10 mm = 1 mV
5 mm
0,2 dt - 90
0,1 mV - 30
PR
segment ST
segment
0
J
point

ST
+ 120
PR
interval QRS interval
interval
QT
interval

N ST depress ST elevasi

Sequence of changes seen during evolution of myocardial infarction

TREATMENT: Sudah Suspect kuat: AMI
chest pain: P-QRST
10 menit Pertama Pain-Quality-Radiation-Severity-Timing
(tightness-squeezing-pressure)

Nilai segera (dlm < 10 mnt I): Terapi Umum segera (MONA):
-vital sign, sat., iv line, EKG 12 lead -Oksigen kanul 4 ltr/mnt (sat>90%)
-perdalam anamnesis & pem.fisik -Aspirin 160 – 325 mg PO
fokus ke indikasi-KI trombolitik: -NTG SL/spray(dptdiulang/5 mnt,3x
-lab:troponin, CK-CKMB, elek,CBC -Morfin iv10mg, (4-8mg/5-15 mnt)
koag (door to lab result < 30 mnt) (bila nyeri tak membaik dg NTG3x)
-Ro thorax (<30 mnt, sdh dapat) maintenance: 20 ugr/kg/jam
KI thrombolitik:Mutlak: KI relatif thrombolitik:
-post stroke hemoragi atau -usia > 80 th
unknown,onset kapanpun -hipertensi tak terkontrol:
-poststroke infark dlm6bln EKG LVH, T>180/110 meski sdh di
-post ops:berat;intracranial th/ nitrat SL; sudah aspirin kunyah &
serius head trauma<3mgg morfin 5 mg iv(1/2 Amp)utk nyerinya.
-tumor intra cranial -sedang th/ antikoagulan dg INR > 1,5
-dissecsi aorta -syock kardiogenik
-kelainan hemostasi -pericarditis -kehamilan
-GI bleeding dlm 1 bln -th/ laser retina

Hasil EKG 12 lead, sadapan Pertama

TREATMENT: Hasil EKG 12 lead, sadapan Pertama 10 menit II
Keputusan: primerPCI
10 menit Kedua thrombolitik,
atau lainnya
Target: door to needle/drug = 30 mnt
door to balon= 90 mnt. >120mnt: + =4:0

Elevasi ST dan atau LBBB baru -ST depress(0.5mm), -EKG tak khas
T inverted suspect iskemi -resiko sedang/rendah:
-Resiko tinggi UAP/NSTEMI UAP/STEMI

Mulai th/:
-NTG iv(KI:S<90,bradi/taki,RV AMI) -aspirin 160-325 mg qd (clopidogrel bila SE)
-Heparin iv -bradiatropin -glikoprot. IIb/IIIa reseptor inhibitor Memenuhi kriteria
-ACE inhibitor,ARB -heparin (utk UAP,NSTEMI: pakai LMWH) UAP baru
b blocker iv -NTG iv
YA
atau
-HMG CoA reductase inhibitor -b blocker(bila nyeri berlanjut & Troponin positif
(terapi statin) Tx Ca chanel blok, bila KI bblocker)

> 12 jam ?? Tidak

Onset serangan Tentukan status klinis
sd sekarang
Klinis tdk stabil stabil
< 12 jam
-Observasi di EMG+monitor
-enzim serial (8-12 jam kmd)
-monitor EKG/ST
-2DE/radionuklid

> 12 jam
Onset serangan
sd sekarang
< 12 jam
REPERFUSI: ideal<6jam
-angiografi angioplasty
-PCI (angioplasty + stent)
primer atau rescue PCI
Memenuhi kriteria UAP baru
atau Troponin positif
??
Tentukan status klinis
Tidak
Klinis tdk stabil stabil
-Observasi di EMG+monitor
Hipotensi, syock kardiogenik: -enzim serial (8-12 jam kmd)
echo: disfunction: -monitor EKG/ST
-2DE/radionuklid
1. miokard sd ruptur
2. valvular
Pasien resiko tinggi:
-angina menetap
Rawat CICU -iskemia berulang
Stabilisasi Hemodinamik: -fungsi LV turun
-perub. EKG: luas
Fluid, inotrop, IABP
-riwayat IMA,PCI,CABG

Coroner-angiografi Ada bukti:

Sesuai utk revaskularisasi? YA -iskemi / infark?
TDK
Rawat CICU:
CABG Revaskularisasi: -enzim serial
BLPL
(BoLehPuLang)
-EKG serial
PCI atau CABG -2DE/nuklir
Follow up

Treatmil, Etc
Revaskularisasi:
PCI atau CABG…???
 Operasi “CABG” :
“BYPASS”
koroner Coronary Artery
Bypass Graft

Sambungan / bypass
pemb.darah dari kaki

Bedah Pintas Koroner

 “PCI” :
Percutaneous
Coronary
Intervention

Instalasi
Diagnostik
Invasif
Kardiologik
(Kateterisasi/cat
hlab)
 PTCA
Percutaneus
Transluminal
Coronary
D.E.S : Drug Eluted Stent
Angioplasty
PTCA versus CABG pada pasien
dengan Multivessel Disease
 Menghilangkan PENDERITAAN
 Meningkatkan KUALITAS HIDUP

SELANJUTNYA……..
 Memperpanjang USIA, serahkan pd-NYA
TAUFIQ Collection
RSPAD
TAUFIQ Collection
Analisa hasil rekaman perfusi:TC99M STUNNING MIOKARD:
Prolong depression contractile function
-Fix defec - partial -mild after a reversible episode of ischemia
-Area necrosis,scar, reversible rvsble (miocyte remain viable, but depressed contractile)
-EF < 30% defect defect
-hipokinetik,dll HIBERNATION:
Chronic ischemia with contractile dysfunction
Vertical long axis: Horizontal long axis: Short axis:
Apex Anterior wall Infark coagulation necrosismyocardial fibrosis,
Anterior wall
(LAD, contraction-band necrosis, myocytolysis
(LAD)
RCA) (no evidence of damage respon to: apoptosis or inflamation)
Apex Septum
(LAD) SUPLAY:
(LAD,
Septum Lateral LAD:anterior LV, apex, 2/3 septal anterior
RCA) Lateral Cx :lateral & posterior LV
(LAD) Wall wall
Inferior wall RCA: RV, 1/3 septal posterior, inferior(diafragma surface) LV
(Cx)
(RCA) Inferior wall (Cx) (infero-posterior surface)
(RCA)
PDA: posterior wall LV
bila PDA (yg suplay 1/3 post septal) mendapat suplay
Kelainan tampak Perubahan Lokasi Tempat dari Cx  =left dominan
di lead dari RCA  right dominan  AV node
resiprocal infark sumbatan (90% pasien, 10% AV node dari Cx)
left coronerbundle hisLBLAF+LPF blok
I, aVL, V1-6 inferior Ekstensif anterior LAD 2/3 pasien: cab ke-1 RCA ke conus arteri 
conus arteriosus(RVOT)
V1-4 Inferior anteroseptal a. septalis 60% pasien: SA node dari RCA (40% dari Cx)
cab anterior RCA : suplay free wall RV
V4-6, I, aVL Inferior anterolateral Cx cab acut marginal : suplay RV
blok RCA=sinus bradi;AV blok;AMI:RV,inferopostr
I, aVL, V5-6 II, III, aVF Lateral wall Cx
SA node: 60%RCA,40%Cx
II, III, aVF I, aVL, V1-6 Inferior wall RCA AV node: 90%RCA,10%Cx

V8, V9, V4R,V3R V1, V2-3 Posterior wall -RCA tikungan s/d Septal branch,LPF,LAF:
(depresi ST, a. Desc posterior 100% dari left coroner
R tinggi) R/S>1 -ujung Cx