The diagnosis and treatment of acute coronary syndromes

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

2. ACS - introduction • an umbrella term for anyconditionwhere the blood supplied to the heart muscle isreduced • themost fearedcomplications of coronaryarterydisease (CAD) • are associatedwithhigh mortality and morbidity • Cardiovasculardiseases (CVD) - presently theleadingcausesofdeath in industrializedcountries • Coronary arterydisease is the cause of 13% of deaths worldwide, every sixthman and every seventh woman in Europe die becauseof acute myocardialinfarction (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 hormonalprofile 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 - 25 - 30% - 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, ordissection • 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 theprocedureof 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 criteraiamustbefulfilled : • Clinicalsymtoms • Chestpain • ECG changes • ST elevationordepression • negative T wave • Elevatedcardiacbiomarkers • 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) painat rest - retrosternalpressureorheaviness (‘angina’) radiatingup to theneck, shoulderand jaw anddown to theulnar aspekt oftheleftarm • May beaccompanied by othersymptoms such as diaphoresis, nausea, abdominalpain, dyspnoea,… Unstableangina: • New onset severe angina (class III of CCS) • Recentdestabilizationofpreviouslystableanginawith atleast CCS III anginacharacteristics (crescendo angina) • Post-MI angina.

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

31. Clinical presentation Atypicalpresentationsarenot uncommon • epigastricpain • recent-onsetindigestion • stabbingchestpain • chestpainwithsomepleuriticfeatures • increasingdyspnoea - oftencanbeobserved in younger (25-40y.), older (75y.), in women, in pts. with diabetes, chronicrenalfailure, ordementia.

32. Clinical presentation • The presence oftachycardia, hypotension, orheartfailureneeds rapid diagnosisand management, oftenindicating a poorprognosisofthispatientwith ACS • Itisimportant to identifytheclinicalcircumstances such as anaemia, infection, inflammation, fever, andmetabolicorendocrine (in particularthyroid) disorders (mayexacerbateorprecipitate 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 • 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 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 STEMIis an urgent situation with turbulentsymptomatology,NSTEMI may have symptomsmuch milder and above its immediateprognosis is better • Pts. should stay on coronary care unit - 2-3 days, than standard cardiology department • the total length of hospitalization is around1 week • even after leaving the CCU patients are able to move around the room and in the following daysrehabilitate 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 theoccludedartery as soon as possibleto restorebloodflowfortheheart ‘‘Timeismuscle“ • Checkforcomplicationofmyocardialinfarctionandtreatthem: • arrhythmia • heartfailure • bleeding