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The diagnosis and treatment of
acute coronary syndromes
Radka Adlová
ACS - introduction
 an umbrella term for any condition where the blood supplied to
the heart muscle is reduced
 the most feared complications of coronary artery disease (CAD)
 are associated with high mortality and morbidity
 Cardiovascular diseases (CVD) - presently
the leading causes of death in industrialized countries
 Coronary artery disease is the cause of 13% of deaths worldwide,
every sixth man and every seventh woman in Europe die because
of acute myocardial
infarction (AMI)
Cardiovascular Mortality
Definiton
The clinical presentations of CAD include:
 silent ischaemia
 stable angina pectoris
 heart failure
 unstable angina
 myocardial infarction (MI)
 sudden death
Acute coronary syndromes
ACS are usually divided into:
 Unstable angina - only ischemia, lack of necrosis
 STEMI - ST - elevation MI
 NSTEMI - non-ST elevation MI
 Sudden death - due to cardiac arrhythmias
Acute coronary syndromes
Definition
 ST-elevation ACS
(STE-ACS):
 typical acute chest pain and
persistent (>20 min)
 ST-segment elevation
 generally reflects an acute total
coronary occlusion
 most will ultimately develop an STelevation MI (STEMI).
ST elevation on the ECG
Definition
 non-STE-ACS
(NSTE-ACS):
 acute chest pain
 without persistent
ST-segment elevation
 persistent or transient ST segment
depression or
T-wave inversion
 further qualified into non-ST
elevation MI (NSTEMI) or unstable
angina.
ST depresion on the ECG
Pathophysiology of ACS
Atherothrombosis
 Atherosclerosis - a fixed and barely reversible process of
gradual luminal narrowing
(slowly over decades)
 Thrombosis - a dynamic and potentially reversible process
causing rapid complete or partial occlusion of the coronary
artery
Vulnerable plaque
 a large lipid core
 a low density of smooth
muscle cells
 a high concentration of
inflammatory cells
 a thin fibrous cap covering
the lipid core
 acute thrombosis induced
by a plaque rupture
Vulnerable plaque
Vulnerable plaque
Hamm, Cardiovascular Medicine 2006
Vulnerable patient
 Multiple sites of plaque rupture with or without
intracoronary thrombosis
 Elevated levels of various systemic markers of inflammation,
thrombosis and coagulation system activation
 Hypercholesterolaemia
 Tobacco smoking
Epidemiology
 The annual incidence of NSTE-ACS is higher than STEMI
 The annual incidence of hospital admissions for NSTE-ACS is
in the range of 3 per 1000 inhabitants
 sex differences - men account for more than 90% of patients
with AMI at the age under 40y.
(a hormonal profile of woman has a protective effect)
 age differences - in patients aged under 40y. only one heart
artery is affected
History of STE-ACS
• overall case fatality:
- about half of the deaths caused by acute coronary syndromes
occur during the first two hours - no change at present
time
• in-hospital mortality:
- prior to the introduction of coronary care units
in the 1960s - 25 - 30%
- pre-reperfusion era of the mid-1980s - 16%
- at present ~ 10%
Prognosis of STE vs. NSTE-ACS
Hospital mortality
- higher in patients with STEMI than among those with NSTE-ACS
(7 vs. 5%)
6 months mortality
- the mortality rates are very similar in both conditions (12 vs. 13%)
Long-term follow-up
- death rates higher among those with NSTE-ACS than with STEACS
Prognosis of STE vs. NSTE-ACS
The causes of the higher death rates of NSTE-ACS
than of STE-ACS pts. during long-term follow-up
are:
 older pts.
 more co-morbidities (diabetes and renal failure).
 a greater extent of coronary artery and vascular diseases
 persistent triggering factors such as inflammation
Classification of MI
 Type 1 – spontaneous MI related to ischemia due to a primary
coronary event such as plaque erosion and/or rupture,
fissuring, or dissection
 Type 2 – MI secondary to ischemia due to either increased oxygen
demand or decreased supply, e.g. coronary artery spasm,
coronary embolism, anemia, arrhythmias, hypertension, or
hypotension
 Type 3 – sudden unexpected cardiac death, including cardiac arrest
but death occurring before blood samples could be
obtained
 Type 4 – associated with PCI:
 Type 4a – MI associated with the procedure of PCI
 Type 4b – MI associated with stent thrombosis
 Type 5 – MI associated with CABG
Myocardial infarction
1. Atherosclerotic aetiology (type 1)
2. Non-atherosclerotic aetiology: (type 2-5)
 arteritis
 trauma
 dissection
 congenital anomalies
 cocaine abuse
 complications of cardiac catheterization, CABG
Diagnosis of acute MI
2 from 3 criteraia must be fulfilled :
• Clinical symtoms
– Chest pain
• ECG changes
– ST elevation or depression
– negative T wave
• Elevated cardiac biomarkers
– Troponin I or T
– CK-MB
– myoglobin
Diagnosis of ACS
 Clinical presentation
 History of patient
 Physical examination
 Electrocardiogram
 Biochemical markers - troponin
 Non-invasive imaging - Echo
 Imaging of coronary arteries - coronary angiography
Clinical presentation
STE/NSTE-ACS:
 Intense prolonged (20 min) pain at rest - retrosternal pressure or
heaviness (‘angina’) radiating up to the neck, shoulder and jaw and down
to the ulnar aspekt of the left arm
 May be accompanied by other symptoms such as
diaphoresis, nausea, abdominal pain, dyspnoea,…
Unstable angina:
 New onset severe angina (class III of CCS)
 Recent destabilization of previously stable angina with
at least CCS III angina characteristics (crescendo
angina)
 Post-MI angina.
Clinical presentation
1) Typical chest pain
2) Nauzea
3) Sweating
Clinical presentation
Atypical presentations are not uncommon
 epigastric pain
 recent-onset indigestion
 stabbing chest pain
 chest pain with some pleuritic features
 increasing dyspnoea
- often can be observed in younger (25-40y.), older (75y.),
in women, in pts. with diabetes, chronic renal failure, or
dementia.
Clinical presentation
 The presence of tachycardia, hypotension,
or heart failure needs rapid diagnosis and management,
often indicating a poor prognosis of this patient with ACS
 It is important to identify the clinical circumstances such
as anaemia, infection, inflammation, fever, and metabolic
or endocrine (in particular thyroid) disorders (may
exacerbate or precipitate ACS)
Physical examination
 Frequently normal
 Signs of heart failure or haemodynamic instability
 Dif. dg.:
- nonischaemic cardiac disorders: pulmonary
embolism, aortic dissection, pericarditis,
valvular heart disease)
- extra-cardiac causes: pulmonary
diseases - pneumothorax, pneumonia,
pleural effusion)
Physical examination
 Heart failure
 Tachycardia, tachypnoe
 Pulmonary rales (pulmonary congestion)
 RV failure - ↑ jugular congestion, hepatomegaly
 Hypotension ↓ 100/60 mmhg
 cardiac shock (tachycardia)
 ↑ vagal nerve activity (bradycardia - inferior IM)
 Bradycardia
 AV block
 Inferior IM - non-serious, frequent
 Anterior IM - serious, rare
Electrocardiogram
 The resting 12-lead ECG is the first-line diagnostic tool in
the assessment of patients with suspected ACS.
 STE-ACS… ST-elevation
 NSTE-ACS…ST-segment shifts and T-wave changes
 A completely normal ECG does not exclude the possibility of
ACS.
Location of MI
Location of MI
ST elevation only:
 Anteroseptal -V1-V3
 Anterolateral - V1-V6
 Inferior wall - II, III, aVF
 Lateral wall - I, aVL, V4-V6
 Right ventricular - RV4, RV5
 Posterior- R/S ratio >1 in V1 and T
wave inversion
Location of MI
Location of MI
Location of MI
Biochemical markers
Markers of myocardial injury:
 cardiac troponins (I and T)
 creatinine kinase (CK)
 CK isoenzyme MB (CK-MB)
 Myoglobin
 repeated blood sampling and measurements are required 6–
12 h after admission and after any further episodes of severe
chest pain
Biochemical markers in ACS
Biochemical markers
Non-coronary condition with Troponin elevation
• Severe congestive heart failure
• Aortic dissection, valve disease
• Myocarditis
• Hypertrophic CMP, Stress CMP
• Hypertesive crisis
• Acute and chronic renal failure
• Acute neurological disease
• …
Other biomarkers
 C-reactive protein - inflamation
 long-term prognosis
 Natriuretic peptides - heart failure
 shor-term prognosis
 Serum creatinine - renal function
 Short and long-term prognosis
No role for the diagnosis of ACS, but effect on short- or longterm prognosis and dif. Dg.
Non-invasive myocardial imaging
 Echocardiography
- to evaluate LV systolic function, aortic
stenosis, aortic dissection, pulmonary
embolism, or hypertrophic cardiomyopathy
- should be routinely used in emergency units
for the risc stratification
 Stress echocardiography, stress scintigraphy evidence of ischaemia or myocardial viability (in
stabilized patients)
Imaging of the coronary anatomy
 The imaging of the coronary anatomy is the most
importat diagnostics method in evaluation of acute
coronary syndrome
 The gold standard of patients with ACS is conventional
invasive coronary angiography
Decesion-making algorithm in ACS
Treatment of MI
 while STEMI is an urgent situation with turbulent




symptomatology, NSTEMI may have symptoms
much milder and above its immediate prognosis is better
Pts. should stay on coronary care unit - 2-3 days, than standard
cardiology department
the total length of hospitalization is around 1 week
even after leaving the CCU patients are able to move around the
room and in the following days rehabilitate and before discharge they
are able to walk up the stairs
return to job possible approximately one month after the onset of
the symptoms
Treatment of STEMI
Open the occluded artery as soon as possible to restore
blood flow for the heart
‘‘Time is muscle“

 Check for complication of myocardial infarction and treat
them:
 arrhythmia
 heart failure
 bleeding
Reperfusion strategies in ACS-STE
Therapy
Meta-analysis of 23 trials (n=7739 pts.)
Keeley EC. Lancet 2003
Reperfusion Strategy
100%
90%
80%
70%
60%
50%
40%
30%
20%
10%
0%
7
1
14
0
12
7
17
2
13
12
20
10
15
25
26
15
26
36
15
5
3
21
30
39
40
31
8
35
44
37
42
48
52
50
50
10
63
40
15
35
15
92
55
35
28
86
81
81
30
26
75
75
72
70
66
64
44
33
25
59
41
49
45
35
33
30
30
28
24
23
19
19
9
CZ
SLO
DE
CH
NO
DK
PL
HR
SE
P-PCI
HU
BE
IL
IT
FIN
Thrombolysis
AT
FR
SK
ES
LAT
UK
BG
No reperfusion
Reperfusion therapy 37-93%
PPCI rate varies between 5 and 92%; Thrombolysis 0-55%
EUROPE IS VERY HETEROGENOUS!!!
45
29
45
PO
SRB GR
8
5
TR
RO
Annual Incidence of Primary PCIs
≥600 p-PCI / million / year
400-599 p-PCI / million / year
200-399 p-PCI / million / year
<200 p-PCI / million / year
Data not known
Process of the percutaneous
coronary intervention
Process of the implantation of
stent
Aspiration trombectomy
 elimination of trombus to prevent embolisation
Pre-hospital management
 Antiplatelet therapy
 Acetylosalicid acid 400-500 mg (i.v. or p.o.),
 Clopidogrel 600mg or ticagrelor 180mg or prasugrel 60mg
 Antithrombin therapy
 Heparin 5 000 - 10 000 IU i.v. or enoxaparine
 Resolve pain and fear
 analgesic drugs
 benzodiazepine
Pre-hospital management
 Nitrate - pain, hypertesion, heart failure
 Isosorbide dinitrate 1-5 mg i.v.
 Monitoring vital function and ECG
ventricular fibrilation
terminated by cardioversion
Pre-hospital management
 Betablockers - tachycardia, hypertension
 Metoprolol - dose 25-50mg oral or 2 mg i.v.
 ACE inhibitors - hypertension
 Perindopril - dose 5 mg oral
 Diuretic - heart failure
 Furosemide 20 - 40mg i.v.
 Anti-arrhythmic drugs -no prophylaxis
 Mesocain 1% 10 mL i.v.
 Amiodarone 150 mg i.v. bolus
Hospital and discharge therapy
 Antiplatelet therapy
 Acetylosalicid acid - dose 100 mg p.o.
 Clopidogrel 75mg or ticagrelor 90mg twice a day or prasugrel 10mg
 Statins - benefit for all patients with IM
 Atorvastatin 40 - 80mg, rosuvastatin 20 - 40mg
 ACE inhibitors - benefit for all patient with IM, more expressed in left ventricular
dysfunction
 perindopril - dose 5-10 mg oral
 Betablockers - 1 - 3 years after MI, longer for pts. With left ventricular dysfunction,
tachyarrhythmia
Case report - 1
57-old female smoker, family history of CAD, pain 6 hours, nausea
Coronary angiography
Trombus aspiration
Stent implantation
Case report - 2
61-year old male with hypertension, pain 4 hours, vomiting, sweating
Coronary angiography of LCA
Trombus aspiration
Stent implantation and final result
Complications of MI

Early complications
Heart failure, cardiogenic shock
 Mechanical complications :
- rupture of free wall of left ventricle
- ventricular septal defect
- acute mitral regurgitation
 Arrhythmia
- ventricular (up to 48 h)
- bradycardia (9-25% of pts)


Late complications
pericarditis
 Aneurysm of left or right ventricle

Tamponade
VSD
VSD
Aneurysm
Treatment of NSTEMI
Risk short-term factors:
- repeated ischemia
- ST depresion
- dynamic changes of ECG (ST and wave T)
- troponin positivity
- trombus during CAG
Risk factors for long-term prognosis:
- older age (≥75 years)
- previous MI
- diabetes
- CRP
- 3-vessels or left main disease
- left ventricular dysfunction
Treatment of NSTE-ACS
To immediate examination are indicated patients
with:
 history of CAD or previous revascularization
 severe recurrent angina
 left ventricular dysfunction, heart failure or ventricular
arrhythmias
Treatment of NSTE-ACSvs.STE
 thrombolysis is not at NSTEMI used
 the base of treatment is again antithrombotic therapy and
revascularization - mostly via PCI
 in patients with multiple coronary disease more frequently to
surgery revascularization
Revascularization strategy
Conservative treatment
 non-significant stenosis on CAG
Percuenous coronary intervention
 BMS - „bare metal stents“
 DES - „drug-eluting stent“
Surgical revascularization
 better long-term results
 diffuse coronary artery involvement
 diabetics
Case report - 3
Stenosis of LMCA
CABG - LIMA ad RIA,SVG ad RMS
Thank you for your attention