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Penyakit Jantung Koroner

Dr. Triadhy Nugraha, SpJP (K), FIHA

Kardiologi dan Kedokteran Vaskular
FK UNS- RSUD dr. Moewardi Surakarta
LOGO
 Epidemiology of ACS in the United States

Single largest cause of death

515,204 US deaths in 2000
1 in every 5 US deaths
Incidence
1,100,000 Americans will have a new or recurrent coronary
attack each year and about 45% will die*
550,000 new cases of angina per year
Prevalence
12,900,000 with a history of MI, angina, or both

* Based on data from the ARIC study of the National Heart, Lung, and Blood Institute, 1987-1994. Includes
Americans hospitalized with definite or probable MI or fatal CHD, not including silent MIs. ACS indicates acute
coronary syndrome; MI, myocardial infarction; ARIC, Atherosclerotic Risk in Communities; and CHD, coronary
heart disease. From American Heart Association. Heart Disease and Stroke Statistics2003 Update.

Slide reproduced with permission from Cannon CP. Atherothrombosis slide compendium. Available at:
www.theheart.org.
 Atherothrombosis* is the
Leading Cause of Death Worldwide1

Pulmonary Disease 6.
3
Injuries 9

AIDS 9.7

Cancer 12.6

Infectious Disease 19.3

Atherothrombosis* 22.3
0 5 10 15 20 25 30
Causes of Mortality (%)

*Atherothrombosis defined as ischemic heart disease and cerebrovascular disease.

1The World Health Report 2001. Geneva: WHO; 2001.

Reprod.with permission from Cannon CP. Atherothrombosis slide compendium. Available at: www.theheart.org.
LOGO
LOGO
THE EVOLUTION OF THE ATHEROSCLEROTIC PLAQUE
 The Longitudinal Section Of An Artery Depicts The
Timeline Of Atherogenesis

(1) A normal artery , to (2) lesion initiation & accumulation of

extracellular lipid in the intima, to (3) the evolution to the fibrofatty
stage, to (4) lesion progression with procoagulant expression &
weakening of the fibrous cap. An ACS develops when the vulnerable
or high risk plaque undergoes disruption of the fibrous cap (5);
disruption of the plaque is the stimulus for thrombogenesis.
Thrombus resorption may be followed by collagen accumulation &
smooth muscle cell growth (6)
 Atherothrombosis: Thrombus
Superimposed on Atherosclerotic Plaque

Adapted with permission from Falk E, et al. Circulation. 1998;92:657-671. Slide reproduced with
permission from Cannon CP. Atherothrombosis slide compendium. Available at: www.theheart.org.
 Characteristics of Unstable and
Stable Plaque

Unstable Stable
Lack of
Inflammatory inflammatory
Thin cells Thick cells
Few fibrous cap More fibrous cap
SMCs SMCs

Intact
Eroded endothelium
endothelium
Activated
macrophages Foam cells
Adapted with permission from Libby P. Circulation. 1995;91:2844-2850. Slide reproduced with
permission from Cannon CP. Atherothrombosis slide compendium. Available at: www.theheart.org.
 Timeline Acute Coronary Syndrome

Vulnerable Plaque

Modification Yeghiazarians Y, Braunstein

JB, Askari A, et al. Unstable angina
pectoris. N Engl J Med. 2000;342:101-114.
 Thrombus Formation and ACS
Plaque Disruption/Fissure/Erosion

Thrombus Formation

Old
Terminology: UA NQMI STE-MI

New Non-ST-Segment Elevation Acute ST-Segment

Terminology: Coronary Syndrome (ACS) Elevation
Acute
Coronary
Syndrome
(ACS)
 Spectrum of IHD

Guidelines relevant to the spectrum of IHD are in parentheses

Clinical Classification of Chest Pain
Penyebab Nyeri Dada Non Angina
Figure 2. Management of atherosclerosis: matching therapy with pathophysiology.

Peter Libby, and Pierre Theroux Circulation. 2005;111:3481-

3488

Copyright American Heart Association, Inc. All rights reserved.

LOGO
 Acute Coronary Syndrome

The spectrum of clinical conditions

ranging from:
unstable angina
non-Q wave MI
Q-wave MI
characterized by the common
pathophysiology of a disrupted
atheroslerotic plaque
 Spectrum of Acute Coronary Syndromes

Presentation Ischemic Discomfort

at Rest

Emergency No ST-Segment ST-Segment

Department Elevation Elevation

+
+ +
In-Hospital

Unstable Non-Q-wave MI Q-wave MI

Angina ( : positive cardiac biomarker)
ST elevation injury miocard
Q wave infarction
Nyeri dada pada angina pectoris tidak stabil
 General Guidelines to Differentiate Chest Pain of
Myocardial Infarction, Unstable and Chronic
Stable Angina

Chest Pain Myocardial infarction Unstable Angina Chronic Stable Angina

Severity Very severe Moderate severe Mild
Duration > 30 minutes 15 - 30 minutes < 15 minutes
Frequency Persistent pain Increasing frequency Stable, less frequent
Timing At rest At rest or with exertion With exertion
Relief With No Usually no yes
Nitroglycerine
Other anxiety, diaphoresis, Less than MI Less than MI
symptoms dyspnea, nausea
 Criteria for Diagnosis

Modified WHO Criteria : Two Out of 3 of the

Following Establishes the Diagnosis

1. Prolonged chest discomfort or chest pain

2. ECG evidence of myocardial infarction or
ischemia
3. At least a 2 fold rise in CK-MB, Troponin
 A. Normal B. Acute C. Recent D. Late E. Old
(<24 hours) (1-3 days) (3 days-6wks) (> 6 weeks)

II

III

aVR

aVL

aVF

V1-2

V3-4

V5-6

A B C D E
 Cardiac Marker - Release Kinetics
Cardiac Spesificity Increase Peak Returns
Duration to
of action
Marker Specificity Appears At Peaks At Normal
Myoglobin Non-specific 1- 3 hours 6 - 9 hours 24 hours
CK-MB Moderately 4 - 6 hours 12 - 24 hours 72 hours
Troponin I Specific 4 - 6 hours 12 - 24 hours 5- 10 days
6

Blood 5
Myoglobin
CK-MB
level of Troponin I
Marker 4

above

upper 3
limit of
normal
2

1

0 4 8 12 16 20 24 48 72 96 120

Time After
TimeOnset Post post
of onset AMI MCI
( Hours )
(hours)
( Peter ,2001 )
 Complications of MI :

Cardiac arrhythmias and sudden death (usually

within 24 hours of MI)
Congestive heart failure or ventricular dysfunction
Cardiogenic shock
Deep venous thrombosis and pulmonary embolism
Pericarditis (Dresslers syndrome)
Rupture of papillary muscle
Rupture of ventricular septum
Rupture of cardiac wall
Systemic arterial embolism
Ventricular aneurysm
 Langkah Awal tata laksana sindrom
koroner akut
1. Tirah baring (Kelas I-C)
2. Suplemen oksigen harus diberikan segera
bagi mereka dengan saturasi O2 arteri <95%
atau yang mengalami distres respirasi
(Kelas I-C)
3. Suplemen oksigen dapat diberikan pada
semua pasien SKA dalam 6 jam pertama,
tanpa mempertimbangkan saturasi O2 arteri
(Kelas IIa-C)
 Langkah Awal tata laksana sindrom
koroner akut
4. Aspirin 160-320 mg diberikan segera pada semua pasien yang
tidak diketahui intoleransinya terhadap aspirin (Kelas I-A). Aspirin
tidak bersalut lebih terpilih mengingat absorpsi sublingual (di
bawah lidah) yang lebih cepat (Kelas I-C)

5. Penghambat reseptor ADP (adenosine diphosphate)

a. Dosis awal ticagrelor yang dianjurkan adalah 180 mg
dilanjutkan dengan dosis pemeliharaan 2 x 90 mg/hari kecuali
pada pasien STEMI yang direncanakan untuk reperfusi
menggunakan agen fibrinolitik (Kelas I-B)
atau
b. Dosis awal clopidogrel adalah 300 mg dilanjutkan dengan dosis
pemeliharaan 75 mg/hari (pada pasien yang direncanakan untuk
terapi reperfusi menggunakan agen fibrinolitik, penghambat
reseptor ADP yang dianjurkan adalah clopidogrel) (Kelas I-C).
 Langkah Awal tata laksana sindrom
koroner akut
6. Nitrogliserin (NTG) spray/tablet sublingual bagi pasien dengan
nyeri dada yang masih berlangsung saat tiba di ruang gawat
darurat (Kelas I-C). jika nyeri dada tidak hilang dengan satu kali
pemberian, dapat diulang setiap lima menit sampai maksimal tiga
kali. Nitrogliserin intravena diberikan pada pasien yang tidak
responsif dengan terapi tiga dosis NTG sublingual (kelas I-C).
dalam keadaan tidak tersedia NTG, isosorbid dinitrat (ISDN) dapat
dipakai sebagai pengganti

7. Morfin sulfat 1-5 mg intravena, dapat diulang setiap 10-30 menit,

bagi pasien yang tidak responsif dengan terapi tiga dosis NTG
sublingual (kelas IIa-B).
Percutaneous Coronary Intervention (PCI)
Percutaneous Transcutaneous Coronary Angioplasty (PTCA)
Stenting
Coronary Bypass Surgery
ARITMIA
Batasan :

- ARITMIA :
Gangguan pembentukan dan atau
penghantaran impuls
- IRAMA SINUS normal : 60 100x/menit
- PEMBAGIAN :
- Gangguan pembentukan impuls : sinus ,
atrium penghubung AV ,ventrikel
- Gangguan penghantaran impuls :
blok SA, AV, intra ventrikel
- PEMBAGIAN SECARA KLINIS :
- Taki, bradi, bradi-taki-aritmia
The Cardiac Conduction System
 Normal sinus rhythm
Sinoatrial node is cardiac
pacemaker
Normal sinus rhythm 60-100
beats/min
Depolarisation triggers
depolarisation of atrial
myocardium (forest fire)
Conducts more slowly
through AV node
Conducts rapidly through
His bundles and Purkinje
fibres
Clinical classification of
arrhythmias
Heart rate (increased/decreased)
Heart rhythm (regular/irregular)
Site of origin
(supraventricular/ventricular)
QRS complexes on ECG
(narrow/broad)
 Mechanisms Responsible
for Arrhythmias
Abnormalities of impulse generation
A. Alterations of normal automaticity
B. Abnormal automaticity
C. Triggered activity
Early/Delayed afterdepolarization
Abnormalities of impulse conduction
A. Reentry: 1. Unidirectional block; 2. Anatomic or
functional reentrant circuit ; 3. wavelength
B. Conduction block
Combined abnormalities of impulse generation and
conduction
 Transmembrane Potentials of
Myocardial Cells

A: Contractile cell
B: Autorhythmic cell:
spontaneous depolarization at phase 4
Alterations of normal
automaticity

Autonomic neurotransmitters
Triggered activity:
Early/Delayed
afterdepolarization
 Re-Entry Mechanism

Branch 2 has a unidirectional block

Impulses can travel retrograde (3 to 2) but not
orthograde.
An AP will travel down the branch 1, into the
common distal path (br 3), then travel
retrograde through the unidirectional block in
branch 2.
When the AP exits the block, if it finds the
tissue excitable, it will continue by traveling
down (reenter) the branch 1.
If it finds the tissue unexcitable (ERP) the AP
will die.
Timing is critical AP exiting the block must
find excitable tissue to propagate.
If it can re-excite the tissue, a circular
pathway of high frequency impulses
(tachyarrhythmia) will become the source of
APs that spread throughout a region of the
heart (ventricle) or the entire heart.
 Reentrant Arrhythmias
Necessitating 3 requirements
Anatomic or
functional
reentrant circuit
Unidirectional
block on one path;
Slow conduction on
the other path
 Diagnostic Approaches to
Arrhythmias
History and physical examination
ECG
Ambulatory ECG recording: Holter
recording
Exercise ECG: treadmill test
Trans-esophageal electrophysiological
study
Invasive electrophysiological study
(EPS)
Management of Arrhythmias
Antiarrhythmic drugs
Cardiac pacemakers
DC cardioversion/defibrillation
Implantable cardioverter/defibrillater (ICD)
Radiofrequency catheter ablation
Surgical operation
Non-pharmacological
Pharmacological (All antiarrhythmic
agents may also be proarrhythmic)
 ALGORITMA ARITMIA
Keluhan :
Nyeri dada , sesak nafas , berdebar ,sinkop
Kesadaran menurun , hipotensi / shock
Curiga aritmia

EKG ,hemodinamika

Aritmia jantung gawat

Takiaritmia Bradiaritmia
Cardiac arrest
Sinus bradikardi Asistol
Henti kardiopulmoner
Blok AV/Frekw.ventr lambat
Fibrilasi ventrikel (VF)
QRSsempit
QRS lebar
Reguler Irreguler Reguler Irreguler
1. VT 1. AF + WPW 1. Sinus takikardi 1. AF
2. SVT+RBBB 2. Torsade depointes
2. A. fluter 2. A. fluter
3. LBBB 3. TSVP (PAT)
 Vaughan Williams classification
of antiarrhythmic drugs
Class I: block sodium channels
Ia (quinidine, procainamide,
disopyramide) AP
Phase 1
Ib (lignocaine) AP IV
Ic (flecainide) AP Phase 2
0 mV
Class II: -adrenoceptor
antagonists (propranolol, sotalol)
Phase 0 I III
Class III: prolong action potential Phase 3
and prolong refractory period
(suppress re-entrant rhythms)
(amiodarone, sotalol) -80mV Phase 4
Class IV: Calcium channel II
antagonists. Impair impulse
propagation in nodal and damaged
areas (verapamil, diltiazem)
 Atrial fibrillation:
Common Causes
Coronary artery disease
Hypertensive heart disease
Valvular heart disease, mitral stenosis
Cardiomyopathy
Thyrotoxicosis
Occasionally, no structural heart
disease, especially paroxysmal atrial
fibrillation
 Atrial Fibrillation:
ECG Characteristics

Absence of P waves
Very irregular baseline, f waves, with a rate of
350-600 bpm, best seen in V1,
Irregular QRS complex rate, usually normal
shape
Atrial Fibrillation
 Atrial Fibrillation:
Auscultation Features
Variation in the intensity of S1
Extremely irregular heart rate
Pulse deficit (because each contraction
is not sufficiently strong to open the
aortic valve or transmit an arterial
pressure wave through the peripheral
arteries)
 Atrial fibrillation:
Clinical Considerations
Decreased hemodynamic functions
rapid ventricular rates
the loss of atrial contraction
Risk of systemic embolism
5 to 7 times greater than that in
controls
Atrial fibrillation: Classification
and Management Strategies

Paroxysmal (<24-48hr): preventing

further attacks
Persistent: attempting restoration of
sinus rhythm
Permanent: offering good control of
ventricular rate
 Atrial Fibrillation:
Treatment
Etiological therapy
Restoration of sinus rhythm
paroxysmal: beta-blocker, propafenone,
cedilanid, amiodarone
persistent: drugs, DC cardiovertion
Control on the ventricular rate
digoxin, betablocker
Prevention of thromboembolism
aspirin or clopidogrel, warfarin
 Atrial flutter:
Characteristics
Regular sawtooth like wave with a rate
of 250-350 bpm
Ventricular response may be 1:1 (300),
2:1 (150), 3:1 (100) or 4:1 (75), etc
Severity of the symptoms depends on
the ventricular rate
Causes are similar to atrial fibrillation
Atrial flutter:
ECG
Atrial flutter:
ECG
 Paroxysmal SVT
AVNRT & AVRT: ECG Features
Sudden initiation and termination
Fixed relationship between p wave and
QRS complex, with p often
superimposed in ORS-T
Regular rate of 150-250 bpm
Narrow QRS complexes unless there is
an aberrant ventricular conduction or
pre-existing bundle branch block
Paroxysmal SVT
AVNRT & AVRT: ECG
Features
Mechanism Responsible for
AVNRT
Pre-excitation syndrome

Abnormal connection
between the atrium and
the ventricle
 Pre-excitation syndrome
ECG Features
Short PR interval
Slurred upstroke of
QRS complexes (the
delta wave)
broad QRS complexes
Secondary ST-T
abnormalities
(reflecting modified
ventricular
repolarization
secondary to
abnormal
depolariozation
Pre-excitation Syndrome (WPW)
 Paroxysmal SVT:
Treatment
Vagal maneuvers: Valsalva maneuver or
carotid sinus massage
First choice of drugs: adenosine 6-12 mg iv,
or verapamil 5 mg iv
Preferred choice of drugs: propafenone 70
mg iv; cedilanid 0.4-0.6 mg iv
Synchronized DC cardioversion (shock
delivery that is timed within the QRS complex
Radiofrequency catheter ablation
 Radiofrequency
Catheter Ablation
 Radiofrequency
Catheter Ablation
 Premature Beats

Atrial
AV junctional
Ventricular
Clinical considerations
ECG features
Management strategies
 Normal AP Conduction in
Ventricles

Initiation site

Normal conduction VPB conduction

Ventricular Premature Beats
Ventricular Premature Beats
Atrial Premature Beats
 Ventricular Tachycardia

ECG: 3 VPBs in succession at a rate of

100-250 bpm; suggesting VT: ventricular
captures, fusion complexes
Clinical: coronary heart disease, AMI;
dilated cardiomyopathy; signifying
myocardial damage
Treatment: drugs (lidocaine, amiodarone)
DC cardioversion (synchronized)
Ventricular Tachycardia
ECG: 3 VPBs in
succession at a rate
of 100-250 bpm;
Non-sustained VT
( 30 sec),
sustained VT
suggesting VT:
ventricular captures,
fusion complexes
 Ventricular Tachycardia
A wide QRS tachycardia is VT until proven otherwise.
Features suggesting VT include:
evidence of AV dissociation
independent P waves (shown by arrows here)
capture or fusion beats
beat to beat variability of the QRS morphology
very wide complexes (> 140 ms)
same morphology in tachycardia as in ventricular ectopics
history of ischaemic heart disease
absence of any rS, RS or Rs complexes in the chest leads
concordance (chest leads all positive or negative)
 Ventricular Tachycardia

A54 year-old woman collapsed 24 hours post MI

 Torsades de Pointes (TDP)

ECG: an irregular rapid ventricular

rhythm with a periodic twisting axis seen
on ECG; long QT interval
Etiology: congenital long QT syndrome;
acquired long QT syndrome, as
antiarrhythmic drugs (Classa,
Class); hypokalamia,
hypomagnesemia
Torsades de Pointes (TDP)
Torsades de Pointes (TDP)
 Torsades de Pointes
Management
Identifying and treating any precipitating
factors
MgSO4, IV; avoidance of drugs
lengthening APD
Atropine, isoprenaline infusion or
ventricular pacing to increase heart rate
Beat-blocker for congenital long QT
sydrome
 Ventricular Flutter / Fibrillation
Irregular rapid ventricular depolarization
No organized ventricular contractions, no
pulse, loss of consciousness
Most common cause: AMI, drug toxicity,
electrolyte disturbances, electric shock, end
stage of many disease processes
Management: non-synchronized DC
defibrillation, cardiopulmonary resuscitation
 Ventricular Fibrillation

Chaotic ventricular electrical activity

which causes the heart to lose the ability to function
as a pump.
Ventricular Fibrillation
 DC Defibrillation

Defibrillator:
used to "shock" the heart from an abnormal
rhythm pattern back into a normal rhythm
Ventricular Fibrillation
Ventricular Fibrillation
 Sick Sinus Syndrome (SSS)

Definition:characterized by intrinsic
inadequacy of sinus node pacemaking and
/or conduction failure between sinus node
and the rest of the atrium
Etiology: coronary heart disease,
degenerative process, cardiomyopathy
Clinical manifestations: insufficiency of
blood supply to important organs
 Sick Sinus Syndrome (SSS)
ECG Features
Marked sinus bradycardia
< 50 bpm measured as
SNRT, SACT and IHR
Sinus arrest / sinoatrial
block Holter
recording
Bradycardia-tachycardia
syndrome atrial
tachyarrhythmias
Probable coexistence with
atrioventricular block
Sick Sinus Syndrome (SSS)
Sick Sinus Syndrome (SSS)
Atrioventricular Block
Atrioventricular Block
 Pacemaker Implantation

Failure to generate enough impulses on time

Pauses may last for several seconds and cause syncope
Definitive therapy for symptomatic bradyarrhythmias requires
pacemaker implantation
TERIMA KASIH