penyakit jantung koroner(kuliah)
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PENYAKIT JANTUNG KORONER
Bahan kuliah mahasiswa FK Unsyiah
Tanggal 10 Mei 2008
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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
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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
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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
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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)
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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.
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INTRODUCTION
• ANGINA
• NON ST ELEVATION AMI
• ST ELEVATION AMI
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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
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DIAGNOSIS AND
ASSESSMENT
1. Clinical assessment
2. Laboratory test
3. Specific cardiac investigation
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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
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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
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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
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Grading system
I. Canadian cardiovascular Society
II. Duke Specific Activity Index
III. Seattle angina questionaire
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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”
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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
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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
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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
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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
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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
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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
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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
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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
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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
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• 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
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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
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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
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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
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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
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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
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Diagnostic tools
1) Physical examination & clinical history
2) Electrocardiogram
3) Biochemicals markers4) Echocardiography
5) Imaging of coronary anatomy
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Physical examination
Frequently normal.
Sign of heart failure
Haemodynamic instability
An important goal exclude non-cardiac
causes
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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
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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
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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
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Echocardiography
Recommended to detect wall motion
abnormalities
To rule out differential diagnosis
Can identify ischaemia and myocardial
viability
Can diagnose healing or healed infarction
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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
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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
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Treatment
The management of NSTE-ACS
includes five theuraphetic tools :
Anti-ichemic agents
Anticoagulants
Antiplatelet agents
Coronary revascularization
Long-term management
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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)
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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)
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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
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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)
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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
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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)
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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)
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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
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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
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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
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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
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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
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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
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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
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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
• ____________________________________________
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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
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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
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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
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Management of the later in-hospital course
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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
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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