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PENYAKIT JANTUNG KORONER

Bahan kuliah mahasiswa FK Unsyiah

Tanggal 10 Mei 2008



Clases of Recommendations

Class I Evidence and/or general agreement that a

given treatment or procedure is beneficial,

useful and effective

Class IIConflicting evidence and/or a divergence of

opinion about the usefullness/efficacy of a

given treatment or procedure

Class II a Weight of evidence/opinion is in favour of

usefullness/efficacy

Class II b Usefulnes/efficacy is less well estabilished

by evidence/opinion

Class III Evidence or general agreement that the

treatment is not useful/evidence and in some



Levels of Evidence

Level of Evidence A

Data derived from multiple

randomized clinical trials or

meta-analyses

Level of Evidence B

Data derived from single

randomized clinical trial or

large non-randimized studies

Level of Evidence C

Consensus of the opinion ofthe experts and/or small

studies, restropective studies,

registries



Recommendations for diagnosis

and risk stratification

• Should be based on a combination of

clinical history symptoms ECG

biomakers and risk score results

I-B)

• The evaluation of the individual risk is thedynamic process that is to be updated

as the clinical situation evolves



continued

• A 12 leads ECG should beobtains in 10 minutes of firstmedical contact andimmediately read by anexperienced physician (I-C)

• Blood must be drawn promptlyfor t ropo nin(cTnT or cTnI) measurement. The shouldavailable within 60 minutes(I-C).

• The test should be repeated

after 6-12 hours if the initial testnegative (I-A)

• Estabilish r isk score ( such asGRACE) should be implement

• ed for initial and subsequentrisk assessment (I-B)

• An Echocardiogram is

recommended to rule in/outdifferential diagnosis (I-C)

• In patients with recurrence ofpain, normal ECG findings, andnegative troponins tests, a non-invasive stress test forinducible ischaemia isrecommended before disgharge(I-A)



Predictors of long-term “Death or MI” should

be consider in risk stratification (I-B):

Clinical ind icators : age, heart rate, BP, Killip class,

diabetes, previous MI/CAD

•ECG markers : ST segment depression

• A b lood markers : troponin, GFR/CrCl/Csystatin C,

BNP/NT-proBNP, hsCRP

• Imaging f inding : low ejection fraction, main stem

lesion, 3 VD

• Risk sc ore result.



INTRODUCTION

• ANGINA

• NON ST ELEVATION AMI

• ST ELEVATION AMI



ANGINA

• Clinical syndrome characteristic by

discom fort in the chest, jaw , shou lder,

back or arms .

• typically elicited by exertion or

emot ional stress and rel ieved by rest o r

ni t roglycer in

• Less typ ical ly ep igastr ic area



DIAGNOSIS AND

ASSESSMENT

1. Clinical assessment

2. Laboratory test

3. Specific cardiac investigation



Purpose of investigation

1) Confirmation of the presence of

ischaemia in patients w/ suspected

stable angina

2) Identification or exclusion of associated

cond i tions or p recip i tat ing factors

3) Risk s trat if icat ion

4) To plan treatmen t options

5) Evaluation of the eff icacy o f treatmen t



Symptoms and Signs

1. History very important

2. Characteristic of discomfort :

a) Location

b) Character

c) Duration

d) Relation to exertion

e) Exacerbating or relieving factors



Unstable Angina

1) Rest angina

2) Rapidly increasing or crescendo angina

Previously stable w/ rapid prograssive increase

in severity

3) New onset anginarcent onset of severe angina w/ marked

limitation of ordinary activity witjin 2 mo



Grading system

I. Canadian cardiovascular Society

II. Duke Specific Activity Index

III. Seattle angina questionaire



Classification of angina severity

according to the Canadian

cardiovascular SocietyClass Level of symptoms

I Ordinary act iv i ty does not cause angina. Angina

w/ strenuous or rapid or prolonged exert ion only

II “Slight limitation of ordinary activity” Angina on walking or climbing stairs rapidly, walking uphill or

exertion after meals in cold weather, whwn under emotional

stress, or only during the first few hours after awakening

III “ Marked limitation of ordinary activity “

Angina on walking one or two blocks on the level or one flight of

stairs at a normal pace under normal conditions

IV “Inability to carry out any physical activity w/o

discomfort “or “angina at rest”



Definition of myocardial infarction

Criteria for acute myocardial infarction

Evidence of myocardial necrosis in clinical

setting consistent w/ myocardial ischemia

Detection of rise and/or fall of cardiac biomarker

(troponin) at least one value abovethe 99th percentile URLtogether w/ myocardial ischaemia w/ at least one of

the following :

-Symptoms of ischaemia-ECG changes indicative of new ischaemia

-Development pathological Q waves in ECG

-Imaging evidence of new loss of viable

myocardium or new regional wall motionabnormalit



Sudden , unexpected cardiac death,

• involving cardiac arrest,often w/ symptoms

suggestive myocardial ischaemia, andaccompanied by presumably new ST-

elevation, or new LBBB, and/or evidence of

fresh thrombus by coronary angiographyand/or at autopsy, but death occuring before

blood sample could be obtained,or at

time before the appearance cardiac biomarkers

in the blood



Criteria for prior myocardial

infarction

• Any one of the following criteriameets the diagnosis for priormyocardial infarction :

Development the new pathological Q waves w/or w/ out symptoms

Imaging of evidence of a regionof loss of viablemyocardium that is thinned and fails to contract,

in the absence of a non-ischemic causePathological findings of healed or healing of

myocardial infarction



Classification of myocardial

infarction

Type 1 Spontaneous MI related to ischaemia due to primary coronary

event such as plaque eruption and/ or rupture, fissuring, or

dissection

Type 2 MI secon dary to ischaemia due to either increased O2 demand or

decreased supply e.g. coronary artery spasm, coronaryembolism, anemia, arrthythmia, hypertension, or hypotension

Type3 Sudden unexpected cardiac death , incuding cardiac arrest, often

w/ symptoms suggestive of myocardial ischaemia, accompanied

by presumably new ST-elevation in coronary artery by

angiography and/or pathology, but death occuring before blood

samples could be obtained, or at a time before the appearance of

cardiac biomarkers in the blood

Type 4a MI assoc iated w / PCI

Type 4b MI assoc iated w/ stent thromb osis as documented by

angiography or autopsy



ECG

ST-elevation

- New ST-elevation at J-point in two

contiguous leads w/ the cut-off points

: > 0,2 mV in men or

- 0,15 mV in women in leads V2-V3

and/or

- > 0,1 mV in other leads



ST-depression and T wave changes

New horizontal or down sloping ST depression >0,05 mV

in two contiguous Leads; and/or

T-inversion > 0,1 mV in two contiguous leads w/ prominent

R Wave or R/S ratio > 1

ECG changes associated w/ prior MI

1. Any Q wave in V2-V3 > 0.02 sec or QS comp in V2 – V3

2. Q wave > 0.03 sec and >0,1 mV deep or QS comp in I, II,

aVL, aVF, or V4-V6 in any two leads of contiguous lead

grouping ( I, aVL, V6,V4-6, II, III, aVF)

3. R wave > 0.04 sec in V2-3 and R/S >1 w/ concordant

positive T-wave in the absence of conduction effect



Common ECG pitfalls in

diagnosing MI

• False Positive :

Benign early

repolarization

LBBB

Pre-excitation

Brugada syndrome

Peri-/myocarditis

Pulmonary embolism

Subarachnoidl

haemorrhage

Metabolic disturbances

such as hyperkalemia

Failure to recognizenormal limits for J-point

displacement

Leads transposition or

use of modified Mason-

Likar configuration

Cholecystitis



Common ECG pitfalls in

diagnosing MI

• False Positive :

Benign early

repolarization

LBBB

Pre-excitation

Brugada syndrome

Peri-/myocarditis

Pulmonary embolism

Subarachnoidl

haemorrhage

Metabolic disturbances

such as hyperkalemia

Failure to recognize

normal limits for J-point

displacement

Leads transposition or

use of modified Mason-

Likar configuration

Cholecystitis



DEFINITIONS

• 1.Patient with typical acute chest pain and

persistent (>20 minutes) ST segment

elevation (STE ACS ):- reflects an acute total coronary occlusion

- theurapeutic is to achieve rapid,

complete and sustained reperfusion byprimary angioplasty or fibrinolytic therapy



• 2. Patients with acute chest pain but

• without persistent ST segmen elevation:

• - persistent or transient ST Segmen

• depression or T waves inversion, Flat T• waves,pseudo-normalisation of T waves, or no

• ECG changes at presentation

• - working diagnosis based on measurement of

• TROPONINs

• - qualified as NSTEMI



Admission Chest pain

WorkingDiagnosis Suspicion of Acute Corornary Syndrome

ECGPersistent

ST- elevation

ST/T

Abnormalities

Normal or

Undetermined

ECG

Bio

chemistryTroponin

positive

Troponin

Twice negative

Risk

stratification

Diagnosis

Treatment

High Risk Low Risk

STEMINSTEMI Unstable

Angina

Reperfusion Invasive Non-invasive



Epidemioloy & Natural History

NSTE ACS is more frequent then STEMI

In Hospital mortality STEMI > NSTE-ACS

(7%vs5%)

In contrast to STEMI, where most events occurbefore or shortly after presentation, in NSTE-

ACS these events continue overdays and weeks

Mortality of STEMI and NSTE ACS after 6 moths

are comparable(12% vs 13%)Long term followup showed the death rate

higher in NSTEMI ACS



PATHOPHYSIOLOGY

A LIFE THREATING MANIFESTATION OF ATHEROSCLEROSIS

Precipated by acute thrombosis

Induced by ruptured or eroded athreroscleroticplaque, w/ or w/o concomittant vasoconstrictionsudden and critical reduction in blood flow

Inflammation key pathophisiologic el_nt

Rare cases : arteritis, trauma, dissection,thromb-embolism, congenital anomalies,cocaine abuse



DIAGNOSIS AND RISK

ASSESSMENT

Prolonged(> 20 minutes)anginal pain at

rest ( 80% )

New onset( de novo) severe angina class

III CCS ( 20% )

Recent destabilisation of previously stable

angina w/ at least CCS III angina

characteristics(crescendo angin )

Post MI angina



Clinical symptoms

failure or dementia Retrosternal pressure orheaviness radiating to left arm,neck or jaw.

Accompanied by diaphoresis, nausea,abdominal pain, dyspnoea, and syncope.

Atypical presentation : epigastric pain, recentonset indigestion, stabbing chest pain, chestpain w/pleuritic features, or increasing

dyspnoea. often observed in younger(25-4 yo) andolder(> 75 yo), women, diabetes, chronic renal



Diagnostic tools

1) Physical examination & clinical history

2) Electrocardiogram

3) Biochemicals markers4) Echocardiography

5) Imaging of coronary anatomy



Physical examination

Frequently normal.

Sign of heart failure

Haemodynamic instability

An important goal exclude non-cardiac

causes



Biomarkers

TROPONINS : initial rise after 3 to 4 hours. Persistelevated for up 2 weeks after MI

In NSTE-ACS over 48 to 72 hours

Troponin elevation can be encountered in many

conditions that do not constitute ACS

D-dimer(pulmonary embolism)

BNP/NT(dyspnoea, heart failure)

Haemoglobin( anaemia), Leucocyte( inflammatory disease )

Markers of renal function



Non-coronary conditions w/

troponin elevations

1. Severe congestive heart failure acute &chronic

2. Aortic dissection, aortic valve disease orhyperthropic cardiomyophaty

3. Cardiac contusion, ablatio, pacing,cardioversion, or myocardial biopsy

4. Inflammatory diseases, eg myocarditis, or

myocardial extension of endo-/pericarditis5. Hypertensive crisis

6. Tachy or bradyarrhythmias



7.Pulmonary embolism, severe pulmonary hypertension

8. Hypothyroidism

9. Apical balooning syndrome10 Chronic or acute renal dysfunction

11.Acute neurological disease including stroke, or

subarachnoidal haemorrhage

12. Infiltrative disease eg amyloidosis,haemochromatosis, sarcoidosis, scleroderma

13. Drug toxicity, eg adriamycin, 5 FU, herceptin, snake

venom

14. Burns, if affecting > 30 % of BSA

15.Rhadomyolisis16.Criticall ill patients, especially w/ respiratory failure,

or sepsis



Echocardiography

Recommended to detect wall motion

abnormalities

To rule out differential diagnosis

Can identify ischaemia and myocardial

viability

Can diagnose healing or healed infarction



Differential diagnoses

Cardiac Pulmonary Haematolog icalMyocarditis

Pericarditis

Myopericarditis

Cardiomyopathy

Valvular disease

Apical balooning

(Tako-Tsubo syndr)

Pulmonary embolism

Pulmonary infarction

Pneumonia

Pleuritis

Pneumothorax

Sickle cell anaemia

Vascu lar Gastro -intest inal Orthopaedic

Aortic dissection

Aortic aneurysm

Aortic coarctation

Cerebrovasc. Dis

Oesophageal spasm

Oesophagitis

Peptic ulcer

Pancreatitis

Cholecystitis

Cervical discophaty

Rir Fracture

Muscle

injury/inflammation

Costochondritis



Mortality in hospital and at 6 months in low, intermediate

and high risk categories in registry populations according

to the GRACE Risk Score

Risk Category

(tertiles)

GRACE Risk

Scorre

In-Hospital

deaths(%)

Low < 108 <1

Intermediate 109-140 1-3

High >140 >3

Risk category

(tertiles)

GRACE

Risk Score

Post-discharge

to 6 modeaths(%)

Low < 88 < 3

Intermediate 89-118 3-8

Hi h >118 >8



Treatment

The management of NSTE-ACS

includes five theuraphetic tools :

Anti-ichemic agents

Anticoagulants

Antiplatelet agents

Coronary revascularization

Long-term management



Recommendations

for anti-ischemic drugs:

Beta-blokers are recommended in the abcense of contraindication , particularly in patients w/ hypertension or tachycardia(I-B)

IV or oral nitrates are effective for symptom relief in the acutemanagement of anginal episodes (I-C)

CA – blokers provide symptoms relief in patients already receivingnitrates and beta-blokers, they are useful in patients w/contraindication to beta-blokade, and in the subgroup of patients w/vasospastic angina (I-B)

Nifedipine, or other dihydropyridines, should not be used unlesscombined w/ betablokers (III-B)



Recommendations of anticoagulan

Anticoagulan is recommended for all patients in addition toantiplatelet theraphy (I-A)

Anticoagulan should be selected according to the risk of ischaemic andbleedings events (I-B)

The choice depends in initial strategy urgent invasive, early invasive,or conservative strategies (I-B)

In an urgent invasive strategy UFH (I-C), or enoxaparin (IIa-B) orbivaluridin (I-B) should be immediately started

Anti coagulant can be stopped within 24 hours of the invasiveprosedure(IIa-C) . In a conservative strategy, fondaparinux,enoxaparin or other LMWH may be maintained up to hospitaldischarge (I-B)



Continued……….

• In non-urgent situation, when decision whether to follow earlyinvasive or conservative strategy is pending :

Fondaparinux is recommended on the basis of the most favorableefficacy/safety profile (I-A)

Enoxaparin with less favourable/safety profile than fondaparinuxshould b use only if the bleeding risk is low (IIa-B)

As efficacy/safety profile of LMWH (other than enoxaparin) or UFHrelative to fondaparinux is unknown, these anticoagulantsncannotbe recommended over fondaparinux (IIa-B)

At PCI procedures the the initial anticoagulan should be mainted

also during the procedure regarless whether this treatment is UFH(I-C), enoxaparin (IIa-B) or bivalurudin (I-B), while additional UFH instandart dose ( 50-100 IU/kg bolus) is necessary in case offondaparinux (IIa-C)

R d ti f l



Recommendations for oral

antiplatelet drugs

• Aspirin is recommended for all patients presenting

w/ NSTE-ACS w/ out contraindication at an initial

loading dose of 160-325 mg(non-enter ic ) (I-A) and at

a maintenance dose of 75 to 100 mg long-term (I-A)

• For all patients, immediate 300 mg loading dose of

clopidrogel is recommended, followed by 75 mg

clopidrogel daily (I-A). Clopidrogel should be

maintained for 12 months unless there is anexcessive risk of bleeding (I-A)

• For all patients w/ con traindicat ion to aspir in ,

clopidogrel should be given instead (I-B)



continued

• In patients considered for an invasive procedure/PCI, a loading dose of 600 mgof clopidrogel may be used to achieved

more rapid inhibition of platelet function(IIa-B)

• In patients pre-treated w/ clopidrogel whoneed to undergo CABG, surgery shouldbe postponed for 5 days for clopidrogelwithdrawl if clically feasible (IIa-C)

R d ti f GP



Recommendation for GP

IIb/IIIa inhibitors• In patients at intermediate to high risk , particularly patients w/

elevated troponin, ST-depression, or diabetes, either eptifibatide, or tiroffiban for initial early treatment are recommended in additionto oral anti platelet agents (IIa-A)

• The choice of combination of antiplatelet agents and anticoagulans

should be made in relation to risk of ischaemic and bleedingevents (I-B)

• Patients who reeived initial treatment w/ eptifibatide or tirofiban priorto angiograpfy, should be maintained on the same drugduring and after PCI (IIa-B)

• In high risk patients not pre-treated w/ GP IIb/IIIa inhibitors andproceeding to PCI, abciximab is recommended immediatelyfollowing angiography (I-A). The use of eptifibatide or tirofiban inthis setting is less well establiished (IIa-B)



continued

• GP IIb/IIIa inhibitors must be combined w/ an anticoagulan (I-A)

• Bivalirudin may be used as an alternative to GP

IIb/IIIa inhibitors plus IFH/LMWH (IIa-B)

• When the anatomy is known and PCI is planned tobe performed within 24 hours and using GP IIb/IIIa inhibitors, most secure evidence is for abciximab

• (IIa-B)



Emergency Care

• Inial diagnosis of AMI :

History of chest pain/discomfort

St segmen elevation or (presumed) new LBBB on

admission ECG.Repeated ECG recordings often needed Elevated markers of myocardial necrosis ( CK-MB,

troponins)

Do not wait for the results to initiate reperfusion

treatment 2D echo and perfusion scintigraphy helpful to rule out

AMI

R li f f i b thl d



Relief of pain, breathlessness and

anxiety

IV opoids ( e.g. 4 to 8 mg morphine )

w/ additional doses of 2 mg at 5 min

intervals

O2(2-4 l,min) if breathlessness or heart

failure

Consider IV B blockers or nitrate if opoids

fail to relieve pain

Tranquilizers may be helpful



Recommendations for reperfusion theraphy

Level of

evidence

I IIa IIb III

Reperfusion is indicated in all patients w/ historyof chest pain/discomfort of < 12 hours and

associated w/ ST_segment elevation or(presumed)

new LBBB on the ECG

X A

Primary PCI

Preferred treatment if performed by experienced

team < 90 min after first medical contact

X A

Indicated for patients in shock and those w/

contraindication to fibrinolytic theraphyX C

GP IIb/IIIa antagonist and primary PCI

no stenting

w/ stenting

X

X

A

A

Class

Level ofClass



Fibrinolytic treatment I IIa IIb III

In the abcense of contraindication and if PCI can

be performed in 90 minutes of first medcalcontact by an experienced team,

pharmacological reperfusion should be initited

as soon as possible

X A

•Choice of fibrinolytic agentsdepends on

individual assessment of benefit and risk,

avaiilability and cost•In patients presenting late(> 4-8 hours after

symptoms onset) a more fibrin spesific agent

such astenecteplase or ateplase is preferred

X B

• prehospital initiation of fibrinolytic theraphy if

appropriate facillities existX B

•Readministration of a non-immunogenic lyticagent if evidence of reocclusion and mechanical

reperfusion not available

X B

If not already on aspirin 150 – 325 mg chewable

aspirin ( no enteric coated tablets)X A

w/ ateplase and reteplase a weight a djusted

dose of heparin should be given w/early and X B

EvidenceClass

C t i di ti



Contraindications

to fibrinolytic therapy• Absolute :

- Haemorrhagic stroke or

unknown origin at any time

- ischemic stroke in preceding 6

months

- CNS damage or neoplasma- Recent major

trauma/surgery/head injury

(w/ preceding 3 weeks )

- GE bleedings within the last

month- Known bleeding disorder

- Aortic dissection

• Relative

• TIA in preceding 6 month

• Oral anticoagulant theraphy

• Pregnancy or within 1weekspost partum

• Non-compressiblepunctures

• Traumatic resuscitation

• Refractory hypertension(systolic BP > 180 mmHg)

• Advanced liver disease• Infective endocarditis

• Active peptic ulcer

Initial treatment Antithrombin Spec contr



co-theraphy

p

indications

Streptokinase

1,5 millions units in 100

ml of 5% dextrose or 0,9%

saline over 30-60 min

None or iv heparin

for 24 to 48 h

Prior SKS or

anistreplase

Alteplase

15 mg iv bolus

0,75 mg/ kg over 30 min

Then 0,5 mg/ kg

Over 60 min iv.

Total dose dosage not to

exceed 100 mg

Iv heparin

For 24 to 48 h

Reteplase 10 U + 10 U iv bolus given

30 min apart

Iv heparin for 24 to

48 h

Tenecteplase

(TNK-tPA)

Single iv bolus

30 mg if < 60 kg35 mg if 60 to <70 kg

40 mg if 70 to <80 kg

45 mg if 80 to <90 kg

50 mg if >90 kg

Iv heparin for 24 to

48 h



Heparin co-theraphy

• Heparin : iv bolus 60 U/kg w/ a max of 4000 U

•

• ______________________________

Iv infusion 12 U ./kg for 24 to 48 h w/ a max of

1000 U/h. Target a PTT : 50-70 ms

____________________________________

aPTT to be moitored at 3, 6, 12, 24 h after starting

treatment

Treatment of pump failure and



Treatment of pump failure and

shock

• Diagnosis :• CXR, echocardiography, RH catheter isat ion

• ___________________________________________

• Treatment of mild and moderately severe heart

failure• O2

• Furosemide

• 20-40 mg iv repeated at 1-4 h interval if necessary

•Nitrates : if no hypotension• ACE inh ib i tors : in absenceof hypotension,hypovolemia or renal failure

• ____________________________________________



Treatment of severe heart failure

• O2

• Furosemide:

• 20-40 mg iv repeated at 1-4 hourly interval if

necessary• Nitrates : if no hypotension

• Ino trop ic agents : dopamine and/or

dobutamine• Haemodynamic assessment w/ balloon

floating catheter

• Vent i latory suppo rt : if inadequate oxygen

tension consider early revascularisation



Treatment of Shock

• O2

• Haemodynamic assessment w/ ballon floating

catheter

• Ino trop ic agents : dopamine and dobutamine• Vent i latory support if adequate oxygen tension

• Int raaort ic balloon pump

• Consider lef t ventr icu lar assist devices andearly revascularisat ion

Recomm. for routine prophylactic therapies in acute phase



Level of

evidence

I IIa IIb III

Aspirin : 150-325 mg( no enteric

coated formulation)X A

IV B Bloker : for all patients forwhom it is not contraindicated Oral

B-blokersX A

ACE Inh itor : oral formulation on

first day:

-To all patients for whom it is not

- contraindicated

- To high-risk patientsX

X A

A

- Nitrates X A- Ca antagonist & Lidoc aine

X B-

Class



Management of the later in-hospital course



Management of the later in hospital course

Myocardial infarction

Clinical risk assessment

High Risk Medium or low risk

Coronary angiogram Assess LV function

Suitable anatomy +Viable myocardium

High risk Medium risk Low risk

Significant

anginaMedical Rx

Revascularise

Yes

Yes No

No

Recommendations forClass

Levelof evi



secondary prevention

I IIa IIb III

• Stop smoking X C

• Optimal glycemic control in diabetic patients X B

• Blood pressure control in hypertensive patients x C

• Mediteranean-type diet x B

• Supplementation w/ 1g fish oil n-3 polyunsaturated

fatty acids

x B

• Aspirin: 75 to 160 mg daily. If aspirin is not tolerated

•Clopidrogel (75 mg daily)

• Oral anticoagulant

x

x

X

A

C

B

• Oral Beta bloker : to all patients if no contraindication X A

• Continuation of ACE-inhibition started on the first day X A

• Statins : I in spite of dietary measures total choletsterol >

190 mg/dl (5,06 mmol/l) and/or LDL cholesterol > 115 mg/dl

(2,98 mmol/l)X A

• Ca antagonist ( diltiazem or verapamil). If

t i di ti t b t bl k d h t f il

X B

Class of evi

dence

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