1. The diagnosis and treatment of acute coronary syndromes
Radka Adlová

2. 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)

3. Cardiovascular Mortality

4. Definiton The clinical presentations of CAD include: silent ischaemia
stable angina pectoris
heart failure
unstable angina
myocardial infarction (MI)
sudden death

5. 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

6. Acute coronary syndromes

7. 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).

8. ST elevation on the ECG

9. 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.

10. ST depresion on the ECG

12. 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

13. 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

14. Vulnerable plaque

15. Vulnerable plaque
Hamm, Cardiovascular Medicine 2006

16. 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

17. 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

18. 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 %
- pre-reperfusion era of the mid-1980s - 16%
- at present ~ 10%

19. 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

21. 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

22. 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

23. 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

27. 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

28. Diagnosis of ACS Clinical presentation History of patient
Physical examination
Electrocardiogram
Biochemical markers - troponin
Non-invasive imaging - Echo
Imaging of coronary arteries - coronary angiography

29. 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.

30. Clinical presentation
1) Typical chest pain
2) Nauzea
3) Sweating

31. 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.

32. 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)

33. 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)

34. Physical examination Heart failure Hypotension ↓ 100/60 mmhg
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

35. 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.

36. Location of MI

37. 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

38. Location of MI

39. Location of MI

40. Location of MI

41. Biochemical markers cardiac troponins (I and T)
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

42. Biochemical markers in ACS

43. 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 …

44. 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.

45. 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)

46. 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

48. Decesion-making algorithm in ACS

49. 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 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

50. 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

51. Reperfusion strategies in ACS-STE

52. Therapy Meta-analysis of 23 trials (n=7739 pts.)
Keeley EC. Lancet 2003

53. Reperfusion Strategy Reperfusion therapy 37-93%
PPCI rate varies between 5 and 92%; Thrombolysis 0-55%
EUROPE IS VERY HETEROGENOUS!!!

54. Annual Incidence of Primary PCIs
≥600 p-PCI / million / year
p-PCI / million / year
p-PCI / million / year
<200 p-PCI / million / year
Data not known

55. Process of the percutaneous coronary intervention

56. Process of the implantation of stent

57. Aspiration trombectomy
elimination of trombus to prevent embolisation

58. Pre-hospital management
Antiplatelet therapy
Acetylosalicid acid mg (i.v. or p.o.),
Clopidogrel 600mg or ticagrelor 180mg or prasugrel 60mg
Antithrombin therapy
Heparin IU i.v. or enoxaparine
Resolve pain and fear
analgesic drugs
benzodiazepine

59. 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

60. 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 mg i.v.
Anti-arrhythmic drugs -no prophylaxis
Mesocain 1% 10 mL i.v.
Amiodarone 150 mg i.v. bolus

61. 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 mg, rosuvastatin mg
ACE inhibitors - benefit for all patient with IM, more expressed in left ventricular dysfunction
perindopril - dose 5-10 mg oral
Betablockers years after MI, longer for pts. With left ventricular dysfunction, tachyarrhythmia

62. Case report - 1
57-old female smoker, family history of CAD, pain 6 hours, nausea

63. Coronary angiography

64. Trombus aspiration

65. Stent implantation

66. Case report - 2
61-year old male with hypertension, pain 4 hours, vomiting, sweating

67. Coronary angiography of LCA

68. Trombus aspiration

69. Stent implantation and final result

70. Complications of MI Early complications Late 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

71. Tamponade

72. VSD

73. VSD

74. Aneurysm

75. Treatment of NSTEMI Risc score and bleeding risk assesment
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
Risc score and bleeding risk assesment

76. 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

77. 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

78. 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

79. Case report - 3

80. Stenosis of LMCA

81. CABG - LIMA ad RIA,SVG ad RMS

82. Thank you for your attention