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Current

Management Strategy
In Acute Coronary Syndrome :
Intervention or Conservative?

Dr. Faris Basalamah, SpJP, FIHA FAPSIC FAsCC


Interven'onal Cardiologist-Electrophysiologist

RSUI. Harapan Anda
Tegal Februari 22, 2018
CURICULUM VITAE
Nama : FARIS BASALAMAH
Tempat/Tanggal Lahir : Tegal, 1 April 1973
Alamat : Jl. H. Mandor 47B
Cilandak – Jakarta Selatan
Mobile : 08176661473
E-mail : fbslmh@yahoo.com

Riwayat Pendidikan
1991 – 1997: S1 Kedokteran Umum FK UNDIP
2002 – 2006: S2 Spesialisasi Jantung & Pembuluh
darah FK Universitas Indonesia
2008 – 2009: Intervention Cardiology & EP fellow,
Pusat Jantung Nasional Harapan Kita.
2017- : S3 sedang berlangsung, FK UI
Riwayat Pekerjaan :
# Juni 2007 – 2008 Cardiologist @ Klinik Kardiovaskular Hospital Cinere
# Agustus 2009 – 2011 : Interventional and Electrophysiologist Cardiologist @
Klinik Utama Cinere Depok
# Juli 2010 – sekarang : Interventional Cardiologist and Electrophysiologist @
RS Mitra Keluarga BekasiTimur
# 2011 – sekarang : Dosen Pengajar FK Universitas Muhamadiyah Jakarta

overview
•  Atherosclerosis and Acute Coronary Syndrome
•  ClassificaHon and risks of ACS
•  STEMI cardiac care
•  IntervenHon in STEMI-ACS
•  Primary PCI vs FibrinolyHc
•  UA/NSTEMI cardiac care
•  InterveHon in NSTEMI-ACS
•  AnHplatelet therapy
•  PCI in animaHon
Scope of Problem
Coronary Heart Disease – a global burden disease
•  CVDs are the no. 1 cause of death globally

•  In 2005
An esHmate 17.5 million people died from CVDs,
represenHng 30% of all global deaths. Of these deaths, an
esHmated 7.6 million were due to coronary heart disease
and 5.7 million were rue to stroke.

•  CHD single leading cause of death in United States
•  452,327 deaths in the U.S. in 2004

•  1,200,000 new & recurrent coronary a[acks per year



•  38% of those who with coronary a[ack die within a year
of having it

•  Annual cost > $300 billion

•  Over 80% of CVD deaths take place in low- and middle-
income countries

•  By 2015
Almost 20 million people will die from CVDs, mainly from
heart disease and stroke. These are projected to remain
the single leading cause of death.
Source :
WHO Cardiovascular Fact Sheer. February 2007
Hospitalizations in the U.S. Due to ACS

Acute Coronary
Syndromes*

1.57 Million Hospital Admissions - ACS

UA/NSTEMI† STEMI

1.24 million 0.33 million


Admissions per year Admissions per year
5
*Primary and secondary diagnoses. †About 0.57 million NSTEMI and 0.67 million UA.
Heart Disease and Stroke Statistics – 2007 Update. Circulation 2007; 115:69–171.
Atherosclerosis Timeline
Foam Fa4y Intermediate Atheroma Fibrous Complicated
cells streaks lesion plaque lesion rupture

Endothelial DysfuncFon
From First Decade From 3rd decade From 4th decade

Growth mainly by lipid accumulaFon Smooth Thrombosis


muscle and hematoma
collagen
Ischemic Discomfort

Acute Coronary Syndrome


Presentation

Working Dx

ECG No ST Elevation ST Elevation


Non-ST ACS
Cardiac
Biomarker UA NSTEMI

Unstable Myocardial Infarction


Final Dx
Angina NQMI Qw MI 7
Libby P. Circulation 2001;104:365, Hamm CW, Bertrand M, Braunwald E, Lancet 2001; 358:1533-1538; Davies MJ. Heart 2000; 83:361-366.
Anderson JL, et al. J Am Coll Cardiol. 2007;50:e1-e157, Figure 1. Reprinted with permission.
Causes of UA/NSTEMI*

•  Thrombus or thromboembolism, usually arising on disrupted or


eroded plaque
•  Occlusive thrombus, usually with collateral vessels†
•  Subtotally occlusive thrombus on pre-existing plaque
•  Distal microvascular thromboembolism from plaque-associated
thrombus
•  Thromboembolism from plaque erosion
•  Non–plaque-associated coronary thromboembolism
•  Dynamic obstruction (coronary spasm‡ or vascoconstriction) of
epicardial and/or microvascular vessels
•  Progressive mechanical obstruction to coronary flow
•  Coronary arterial inflammation
•  Secondary UA
•  Coronary artery dissection§
8
*These causes are not mutually exclusive; some patients have 2 or more causes. †DeWood MA, et al. N Engl J Med 1986;315:417–23. ‡May occur
on top of an atherosclerotic plaque, producing missed-etiology angina or UA/NSTEMI. §Rare. Modified with permission from Braunwald E. Circulation
1998;98:2219–22. Anderson JL, et al. J Am Coll Cardiol. 2007;50:e1-e157, Table 3.
Acute Coronary Syndromes

• Unstable Angina
Similar pathophysiology

• Non-ST-Segment Similar presenta'on and
ElevaHon MI early management rules
(NSTEMI)
STEMI requires
• ST-Segment evalua'on for acute
reperfusion interven'on
ElevaHon MI
(STEMI)
Unstable
NSTEMI STEMI
Angina
Occluding thrombus Complete thrombus
Non occlusive sufficient to cause occlusion
thrombus Hssue damage & mild
myocardial necrosis ST elevaHons on
Non specific ECG or new LBBB
ECG ST depression +/-
T wave inversion on Elevated cardiac
Normal cardiac ECG enzymes
enzymes
Elevated cardiac More severe
enzymes symptoms

Timing of Release of Various Biomarkers
After Acute Myocardial Infarction

Shapiro BP, Jaffe AS. Cardiac biomarkers. In: Murphy JG, Lloyd MA, editors. Mayo Clinic Cardiology: Concise Textbook. 3rd ed. Rochester, MN:
Mayo Clinic Scientific Press and New York: Informa Healthcare USA, 2007:773–80. 11
Anderson JL, et al. J Am Coll Cardiol 2007;50:e1–e157, Figure 5.
Prognosis with Troponin

8 7,5 %
7
6,0 %
Mortality at 42 Days

6
5
4 3,4 % 3,7 %
3
2
1,7 %
1,0 %
1
831 174 148 134 50 67
0
0 to <0.4 0.4 to <1.0 1.0 to <2.0 2.0 to <5.0 5.0 to <9.0 ≥ 9,0

Cardiac troponin I (ng/ml)


Risk Stratification
Based on initial
Evaluation, ECG, and
Cardiac markers
STEMI
Patient?
YES NO

- Assess for UA or NSTEMI


reperfusion
- Evaluate for Invasive
- Select & implement vs. conservative
reperfusion therapy treatment
- Directed medical - Directed medical
therapy therapy
Cardiac Care Goals

• Decrease amount of myocardial


necrosis
• Preserve LV function
• Prevent major adverse cardiac events
• Treat life threatening complications
STEMI cardiac care
•  STEP 1: Assessment
–  Time since onset of symptoms
– 90 min for PCI / 12 hours for fibrinolysis

–  Is this high risk STEMI?


– KILLIP classification
– If higher risk may manage with more invasive rx

–  Determine if fibrinolysis candidate


– Meets criteria with no contraindications

–  Determine if PCI candidate


– Based on availability and time to balloon rx
Fibrinolysis/Primary PCI indications

•  ST segment elevation >1mm in two


contiguous leads
•  New LBBB
•  Symptoms consistent with ischemia
•  Symptom onset less than 12 hrs prior to
presentation
•  Symptom onset more than 12hrs with
prolonged pain (primary PCI only)
Absolute Contraindications for fibrinolysis
therapy in patients with acute STEMI

•  Any prior Intra Cranial Hemoragic


•  Known structural cerebral vascular lesion (e.g., AVM)
•  Known malignant intracranial neoplasm (primary or
metastatic)
•  Ischemic stroke within 3 months EXCEPT acute ischemic
stroke within 3 hours
•  Suspected aortic dissection
•  Active bleeding or bleeding diathesis (excluding menses)
•  Significant closed-head or facial trauma within 3 months
Relative Contraindications for fibrinolysis
therapy in patients with acute STEMI
•  History of chronic, severe, poorly controlled hypertension
•  Severe uncontrolled hypertension on presentation (SBP greater
than 180 mm Hg or DBP greater than 110 mmHg)
•  History of prior ischemic stroke greater than 3 months,
dementia, or known intracranial pathology not covered in
contraindications
•  Traumatic or prolonged (greater than 10 minutes) CPR or major
surgery (less than 3 weeks)
•  Recent (within 2-4 weeks) internal bleeding
•  Noncompressible vascular punctures
•  For streptokinase/anistreplase: prior exposure (more than 5
days ago) or prior allergic reaction to these agents
•  Pregnancy
•  Active peptic ulcer
•  Current use of anticoagulants: the higher the INR, the higher the
risk of bleeding
STEMI cardiac care
•  STEP 2: Determine preferred reperfusion
strategy
Fibrinolysis preferred if: PCI preferred if:
n  <3 hours from onset n  PCI available
n  PCI not available/delayed n  Door to balloon < 90min
n  door to balloon > n  Door to balloon minus
90min door to needle < 1hr
n  door to balloon minus n  Fibrinolysis
door to needle > 1hr contraindications
n  Door to needle goal n  Late Presentation > 3 hr
<30min n  High risk STEMI
n  No contraindications n  Killup 3 or higher
n  STEMI dx in doubt
Fibrinolysis Therapy

21
Importance of Rapid Time to
Treatment With Fibrinolysis in STEMI
4.0

3.5% ↓
in mortality at 35 days
Absolute % difference

3.0

2.5% ↓
2.0
1.8% ↓
1.6% ↓
1.0

0.5% ↓
0.0
0–1 2–3 4–6 7 – 12 12 – 24
Time from onset of symptoms to treatment (hours)
The Fibrinolytics Therapy Trialists’ collaborative group. Lancet. 1994; 343:311.
Comparing outcomes
Difference Mortality in Difference Era

24
Reperfusion Strategy
www.escardio.org/guidelines
www.escardio.org/guidelines
www.escardio.org/guidelines
www.escardio.org/guidelines
Unstable angina/NSTEMI
cardiac care
•  Evaluate for conservative vs. invasive
therapy based upon:
•  Risk of actual ACS
•  TIMI risk score
•  ACS risk categories per AHA guidelines

Low High
Intermediate
Risk Stratification to Determine the Likelihood of
Acute Coronary Syndrome
Assessment Findings indicating Findings indicating Findings indicating
HIGH likelihood of ACS INTERMEDIATE LOW likelihood of ACS
likelihood of ACS in in absence of high- or
absence of high- intermediate-likelihood
likelihood findings findings
History Chest or left arm pain or Chest or left arm pain or Probable ischemic
discomfort as chief discomfort as chief symptoms
symptom symptom Recent cocaine use
Reproduction of previous Age > 50 years
documented angina
Known history of coronary
artery disease, including
myocardial infarction

Physical New transient mitral Extracardiac vascular Chest discomfort


regurgitation, hypotension, disease reproduced by palpation
examination diaphoresis, pulmonary
edema or rales

ECG New or presumably new Fixed Q waves T-wave flattening or


transient ST-segment Abnormal ST segments or inversion of T waves in
deviation (> 0.05 mV) or T- T waves not documented leads with dominant R
wave inversion (> 0.2 mV) to be new waves
with symptoms Normal ECG

Serum cardiac Elevated cardiac troponin Normal Normal


T or I, or elevated CK-MB
markers
TIMI Risk Score
Predicts risk of death, new/recurrent MI, need for urgent
revascularization within 14 days
ACS risk criteria
Low Risk ACS
Intermediate Risk ACS
No intermediate or high
Moderate to high likelihood
risk factors
of CAD
<10 minutes rest pain
>10 minutes rest pain,
now resolved
Non-diagnositic ECG
T-wave inversion > 2mm
Non-elevated cardiac
markers
Slightly elevated cardiac
markers
Age < 70 years
High Risk ACS
Elevated cardiac markers
New or presumed new ST depression
Recurrent ischemia despite therapy
Recurrent ischemia with heart failure
High risk findings on non-invasive stress test
Depressed systolic left ventricular function
Hemodynamic instability
Sustained Ventricular tachycardia
PCI with 6 months
Prior Bypass surgery
Low Intermediate High
risk risk risk

Chest Pain
center
Conservative Invasive
therapy therapy
Invasive therapy option
UA/NSTEMI
•  Coronary angiography and revascularization within 12 to
48 hours after presentation to Emergency Room
•  For high risk ACS (class I, level A)

•  MONA + BAH (UFH)


•  Clopidogrel
–  20% reduction death/MI/Stroke – CURE trial
–  1 month minimum duration and possibly up to 9
months
•  Glycoprotein IIb/IIIa inhibitors
www.escardio.org/guidelines
www.escardio.org/guidelines
Spectrum of severity
of Acute Coronary Syndrome
Antiplatelet Therapy
Anti Platelet Therapy
Revaskularisasi

FibrinoliHk VS. Intervensi koroner


Perkutan

Aspirin Aspirin
AnH-Platelets

ADP antagonist ADP antagonist


(Loading) (Loading)
Clopidogrel •  Ticagrelor 180 mg rumatan
< 75 thn à 300 mg 90 mg bid
> 75 thn à (-) •  Clopidogrel 600 mg rumatan
75 mg bid
Aspirin Dosing in PaFents Treated With DAPT

COR LOE RecommendaFon


In paHents treated with DAPT, a daily aspirin dose of 81
I B-NR mg (range, 75 mg to 100 mg) is recommended.
Master Treatment Algorithm for Duration of P2Y12 Inhibitor
Therapy in Patients With CAD Treated With DAPT
Coronary Angiography
Coronary Angiography/
Kateterisasi
Coronary Angiography/
Kateterisasi

Penyakit Jantung
Koroner
Angioplasty / PCI
•  Most PCI are
performed with the
use of stents
•  Wire mesh coil pushed
against vessel wall to
prevent closure of the
vessel post procedure
•  Balloon is inflated
pushing plaque against
the vessel wall
Angioplasty with Drug Eluting
Stent

49
Sequence of Events in Ischemic
Heart Disease
•  Arrythmias
•  Lost of muscle
•  Angina MI
•  Silent Ischemia
Remodeling

CAD
Progresif dilatation

Endothelial dysfunction
Heart Failure
Death
Risk Factor
Thanks

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