AKUTNI KORONARNI SINDROM, (AKS) DEFINICIJA, KLINIČKA …
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Transcript AKUTNI KORONARNI SINDROM, (AKS) DEFINICIJA, KLINIČKA …
Differential diagnosis and treatment
of acute coronary disease
Milev Ivan MD
Special Hospital for Surgical Diseases
“Filip II” - Skopje, Macedonia
June, 2009
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Acute coronary syndrome
defininiton
Chest pain is a major symptom of acute coronary
disease or syndrome (ACS). ACS includes non
stabile angina (NA), myocardial infarction (MI)
without ST elevation (NSTEMI) and MI with ST
elevation (STEMI).
Erosion or rupture of unstable atherosclerotic
plaque, and creation of thrombus formation
The limitation of flow, oxygenation of
myocardium and collateral circulation are major
determinants of clinical signs.
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Development of Atherosclerotic
Plaques
Fatty streak
Normal
Lipid-rich plaque
Foam cells
Fibrous cap
Lipid core
Thrombus
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Vulnerable vs Stable Atherosclerotic
Plaques
Vulnerable Plaque
Lumen
Fibrous Cap
Lipid
Core
• Thin fibrous cap
• Inflammatory cell infiltrates:
proteolytic activity
• Lipid-rich plaque
Stable Plaque
Lumen
Lipid
Core
Fibrous Cap
• Thick fibrous cap
• Smooth muscle cells:
more extracellular matrix
• Lipid-poor plaque
Libby P. Circulation. 1995;91:2844-2850.
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Thrombosis Influences the Severity
of a Cardiovascular Event
Nonocclusive thrombus
Occlusive thrombus
• Unstable angina
• Non—Q-wave MI
• Q-wave MI
• Sudden death
Factors limiting thromb.: Factors favoring thromb.
• Minor plaque
disruption
• High flow
• Low thrombotic
tendency
• Major plaque
disruption
• Low flow or vasospasm
• Thrombotic tendency
Kullo IJ, et al. Ann Intern Med. 1998;129:1050-1060.
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Other reasons for NA and
NSTEMI
Non-oclusive thrombus
Dynamic obstruction (coronary spasms)
Infection
-inflammation with increase markers (CRP)
-infection with Chlamidia pneumonie, Helicobacter
pylori, cytomegalovirusi, herpes simplex virus
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ECG changes vs risqué of death or MIepidemiology
death or IM
30-days 6- months 1-year
ST elevation 9,4%
12,3%
16,1%
ST depression 10,5%
15,45% 18,1%
ST elevacija
and depression 12,4%
15,7% 25,6%
T wave
inversion
5,5%
8,1%
13,6%
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Chest pain - origin
acute aortic dissection (AAD)
pulmonary embolism
pericarditis
mitral valve prolaps
chest pain in obstructive cardiomiopathy
primary pulmonary hypertension
*consider non-cardiac disesases of pleura,
mediastinum and abdomen
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Chest pain-origin
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Acute coronary syndrome
- the importance
Urgent presentation
Needs high level of health organization
Great morbidity and mortality rate
Increasing of percentage of pts with unstable
angina and NSTEMI in recent years
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ACSy - triggers
hypertension, tachycardia, hard work –the
intracoronary changes in hemodynamic state.
Peak - early in the morning (sympaticus)
Factors inside the plaque
Emotional stress
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Diagnostic of coronary disease
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ECG
Standard 12-lead ECG is the best test
Additional leads V4R-V6R (inferior IM) for RV
assessment. V7-V9 posterior leads
Continious recording every 20 sec.
New LBBB, ST depression 1 mm V1 - V3, ST
elevation > od 2 mm suggest IM
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Laboratory markers
Two folds increasing of CK after 6 h, peak 24 h.
CK-MB sensitivity 90%, increase 6 h.
Troponin I /T is more specific.
Activity rise after 6 h, peak 12-24 h, and high level in
serum up to 7-10 days.
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Echocardiography
Assessment of wall motion
Sensitivity of acute IM is 93%, specificity
53%
Can not distinguish acute from previous
IM
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Coronarography
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Action- time is short, move swiftly &
decide...
Door (events prior to arrival)
Data – actual (obtain ECG, Lab)
Decision (AMI & decide Th)
Drug (Fibrinolytic or passing Angioplasty Cath)
Triage ID AMI, Immediate Cardio consult
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EKG fibrinolytic Therapy eligibility
ST elevation 1mm+ in 2 or more limb leads & 2mm+ in 2 or
more contiguous precordial leads, 2-6 hours before
OR new or presumed new LBBB
No benefit in ischemic pt who lack above EKG findings
LBBB + AMI = poorer outcome due to likely proximal LAD
occlusion, putting signif. portion LV in ischemic jeopardy
DO NOT USE in ST-depression... signif. poorer outcomes!!!
Remember age is NO longer excluder, but age > 75 ICH
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When TO & When NOT TO
Active Diabetic Retinopathy... strong relative C/I risk blindness
DM pts + AMI 2X more likely to DIE
CPR > 10 minutes long or extensive chest trauma from CPR
Hemithorax/cardiac tamponade
IM > 12 hours before
Prior Stroke/TIA, major risk for ICH, relative C/I, prior
Hemorrhagic stroke ABSOLUTE C/I
Prior MI in setting AMI; 26% mortality even if prior
fibrinolytics th
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When TO & When NOT TO
Recent Surgery/Trauma/GI Bleed w/in 10 days is absolute C/I
Women menses w/ AMI consider use; excessVag bleeding after
Fibrinolytics CTRL w/ Vag packing compressible site of
bleeding
GI bleed in 10 days Absolute C/I
HTA; SystBP > 180 or Diast.BP 110
Significant liver dysfunction
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Our results (2005-2009,n=115)
Other;
50
CAD
Other
diseases
; 55
CAD; 65
Other
AAD
Differential diagnosis was confirmed with
clinical signs, repeated ECG, serum level of
cardiac markers (troponin I,T),
echocardiography and finaly with
coronarography.
Other diseases
STEMI;
15
NA; 40
STEMI
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AAD; 35
NSTEMI;
10
NSTEMI
NA
Results (2005-2009)
female;
20
previous
MI; 25
Major
risks; 60
male; 45
male
female
Major risks
previous MI
Fibrinolytic
therapy; 2
coronarography; 63
Fibrinolytic therapy
coronaro-graphy
IABP in PCI
CABG; 4
IABP; 6
reperfusion;
65
PCI; 59
PCI; 59
CABG
PCI
IABP
PCI
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reperfusion
Results (2005-2009)
Mortality in PCI
In hospital stay, days
mort; 2
PCI; 5
CABG;
11
All; 59
PCI
CABG
mort
Recoronarography in PCI
All
CABG in PCI group
Only rePCI; 3
PCI; 9
New
CABG; 7
All pts; 56
PCI
All pts
Only re-PCI
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New CABG
Case report (2005-2009)
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Case report(2005-2009)
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Case report (2005-2009)
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Catheterisation laboratory – Filip II
2000-2009
May 2005 - May 2009:
-802 intervention
800
700
690
600
-Coronary intervention: 690 pat.
500
-Intervent. of congenital
anomalies: 104 pat.
-Carotid stenting:
5 pat
400
300
200
104
100
-Peripheral stenting:
3 pat.
0
coronary
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congenital
anom.
5
3
carotid
peripheral
Coronary intervention
May 2005-May 2009
690 PCI -treatment:
39
-Out patients treatment:
651(94.3%)patients
-Hospital treatment (more than 24h):
39(5.9%) patients
651
Out patients Hospital
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Coronary intervention
May 2005-May 2009
690 PCI- approach:
TBA; 2
TUA; 11
TFA; 3
-TRA: 673 (97.5%) pat.
-TUA: 11 (1.5%) pat.
TRA; 673
-TFA: 3 (0.6%) pat.
TRA
-TBA: 2 (0.4 %) pat.
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TUA
TBA
TFA
Conclusion
Time from begining of chest pain to
reperfusion / D2B is a major factor in
treatment of pts with ACS.
Early diagnosis, urgent transport to PCI
centar, early begining of fybrinolitic
therapy and early differential diagnosis is
essential in treatment of ACS pts and
decreasing of mortality.
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