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 ST-
elevation 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 STE-
ACS
 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 long-

term 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% 7
14 12 13 10
1 17 15 15
90% 0
20
25 26 26
21
7 30
2 36 35 37
80% 12
5 15
40 39
44 42
48
3 31 52 50 50
70% 8 10
40
63

60% 15
15 35 55
50% 92 28 35
86 26 30
40% 81 81
75 75 72 25
44
33
70
66 64
30% 59 41 45
49
45 45 29
20% 35 33 30 30 28 24 23
10% 19 19
9 8 5
0%
CZ SLO DE CH NO DK PL HR SE HU BE IL IT FIN AT FR SK ES LAT UK BG PO SRB GR TR RO

P-PCI Thrombolysis No reperfusion

Reperfusion therapy 37-93%

PPCI rate varies between 5 and 92%; Thrombolysis 0-55%

EUROPE IS VERY HETEROGENOUS!!!

 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