Acute Coronary Syndromes

1. Acute Coronary Syndromes By: Dr azimian

2. The motion of the heart is best understood by God alone. - Harvey

3. Time lost life lost

8. Definitions • Acute coronary syndrome is defined as myocardial ischemia due to myocardial infarction (NSTEMI or STEMI) or unstable angina or Sudden cardiac death

9. 23.8% of admissions to resus. unit for chest pain/acs related (stats 1Jan 2009 – 28 Feb 2009) 150/628 entries. • In US – 1.56 million admissions for ACS – 669 000 for unstable angina, 896 000 for MI • Higher prevelance for NSTEMI.

10. CAD is a continuum of disease…. • Angina -> unstable angina -> AMI -> sudden cardiac death • Acute coronary syndrome encompasses unstable angina, NSTEMI, STEMI • Stable angina – transient episodic chest pain d/t myocardial ischaemia, reproducible, frequency constant over time.usually relieved with rest/NTG. • Classification of angina – Canadian Cardiovascular Society classification.

11. Canadian Cardiovascular Association Classification of Angina

12. WHY IS IT IMPORTANT TO RECOGNISE PATIENTS WITH UNSTABLE ANGINA?? • 5 -17% suffer an MI within a week after admission. • 3 -15% die within a year.

13. UNSTABLE ANGINA – • Pain occurring at rest – duration > 20min, within one week of first visit • New onset angina – ~ Class 2 severity, onset with last 2 months • Worsening of chest pain – increase by at least 1 class, increases in frequency, duration • Angina becoming resistance to drugs that previously gave good control. • NB! ECG – normal, ST depression(>0.5mm), T wave changes

15. Pathophysiology of ACS • Plaque rupture and subsequent formation of thrombus – this can be either occlusive or non-occlusive (STEMI, NSTEMI, USA) • Vasospasm such as that seen in Prinzmetal’s angina, cocaine use (STEMI, NSTEMI, USA) • Progression of obstructive coronary atherosclerotic disease (USA) • In-stent thrombosis (early post PCI) • In-stent restenosis (late post PCI • Poor surgical technique (post CABG)

17. ATHEROSCLEROSIS START END

18. Pathophysiology of ACS • Acute coronary syndromes can also be due to secondary causes • Thyrotoxicosis • Anemia • Tachycardia • Hypotension • Hypoxemia • Aterial inflammation (infection, arteritis)

19. تاکی کاردی هیپرتانسیون سیگار عفونت تب استرس فعالیت یبوست پرخوری درد هیپوولمیا تنگ کننده های عروق گشادی عروق Demand Supply O2

20. Assesment 1. Hx 2. Physical Exam 3. EKG 4. Exercise EKG 5. Thallium Scan 6. Coronary Angiography 7. Cardiac Enzymes

21. Diagnosis • Dx of acute coronary syndrome is based on history, physical exam, ECG, cardiac enzymes • Patients can then be divided into several groups • Non-cardiac chest pain (i.e., Gastrointestinal, musculoskeletal, pulmonary embolus) • Stable angina • Unstable angina • Myocardial infarction (STEMI or NSTEMI) • Other cardiac causes of chest pain (i.e., aortic dissection, pericarditis)

24. ECG for acute chest pain • Not a perfect diagnostic tool (specificity-sensitivity) • 10% of new ST-elevations are not caused by MI • Up to 50% of MI patients present with normal or inconclusive ECG (e.g. previous MI, LV hypertrophy) • 2% of patients with normal ECG will develop MI • 15-lead ECG for right ventricular or posterior MI • Request previous ECG for comparison • Serial ECGs (and continuous ST-monitoring?) improve sensitivity

25. Ischemia ,Acute Injury, Infarction

26. Ischemia • T wave inversion, ST segment depression • Acute injury: ST segment elevation • Dead tissue: Q wave

32. Gender Differences in MI Females, when compared to males: -present with MI later in life -have poorer prognosis and high morbidity -are 2x as likely to die in the first weeks -are more likely to die from the first MI -have higher rates of unrecognized MI -NSTEMI MI vs STEMI

33. The perfect marker • Marker for myocardial necrosis, and also for cardiac ischemia • Linear relationship between blood levels and extent of myocardial injury (and prognosis) • 100% sensitive • 100% specific • Immediate increase (+ constant blood level for hours to days) • Test kits : reliable, rapid, universally available and inexpensive

34. What about troponin T and I ? • Very high sensitivity for myocardial necrosis • Related to prognosis • Not 100% specific for atherosclerotic coronary artery disease • (myocarditis, cardiomyopathy, myocardial contusion, renal failure, auto-immune diseases, ...) • Up to 6 hours before raised blood levels no early MI diagnosis possible • Raised blood levels for many days troublesome diagnosis of re-infarction BUT

35. TROPONINS T/I • Troponin T vs I – • both equivalent in diagnostic and prognostic abilities ( except in renal failure – Trop T less sensitive) • Elevation ~ 2hrs to 12hrs • ~30 – 40% of ACS patients without ST elevation – had normal CKMB but elevated troponins on presentation • Meta-analysis (Heindereich et al) – odds of death increased 3 to 8 fold with positive troponin

36. Role for myoglobin ? • Initial elevation : 1 to 4h after onset better early marker than troponins BUT : early myoglobin is less sensitive and less specific (due to skeletal muscle trauma) than late troponin decisions mainly based on clinical skills, ECG and late troponin (except rarely for reperfusion therapy) • Duration of elevation : 24 – 48h useful for re-infarction diagnosis

37. Role for CK-MB ? • Initial elevation comparable with troponins • Less sensitive than troponins • High specificity (comparable with troponins) • Rapid rise and fall (instead of gradual fall for troponins) allowing more accurate estimation of MI extent

38. MYOGLOBIN • Rapid release within 2 hours • Not cardiac specific • Rule out for NSTEMI rather than rule in. CKMB Used in conjunction with troponins Useful in diagnosing re-infarction

39. Pre-test Probability • In the absence of abnormal findings on physical exam, ECG, or enzymes, the pre-test probability of acute coronary syndrome must be determined by the clinician • A good history is crucial (is the chest pain typical or atypical; what are the associated symptoms) • Determination of risk factors is also crucial (male, age >55, smoking, DM, HTN, FamHx, hyperlipidemia, known CAD)

40. Angiogram pre/post PTCA

41. در اكوكارديوگرافي تجمع مايع در حفره پريكارد مشاهده مي شود .

42. imaging

43. Treatment of ACS; Aspirin • Aspirin is an antiplatelet agent that initiates the irreversible inhibition of cyclooxygenase, thereby preventing platelet production of thromboxane A2 and decreasing platelet aggregation • Administration of ASA in ACS reduces cardiac endpoints

44. ACC/AHA Guidelines for Aspirin Therapy • Aspirin should be given in a dose of 75-325 mg/day to all patients with ACS unless there is a contraindication (in which case, clopidogrel should be given) • Newest guidline: clopidogrel+ asprin

45. Treatment of ACS; Nitrates • Nitroglycerin is considered a cornerstone of anti-anginal therapy, despite little objective evidence for its benefit • Benefit is thought to occur via reduction in myocardial O2 demand secondary to venodilation induced reduction in preload as well as coronary vasodilation and afterload reduction • Titrate to relief of chest pain; chest pain = death of myocardial cells • No documented mortality benefit

46. Side/Adverse Effects Vascular HA (may be severe) Hypotension (may be marked) Tachycardia Palpitations

47. Treatment of ACS; Beta Blockers • Beta Blockers reduce myocardial oxygen demand by reducing heart rate, contractility, and ventricular wall tension • Administration of beta blockers in ACS reduces cardiac endpoints

48. Beta Blocker Trials • HINT (metoprolol) • Beta Blocker Heart Attack Trial (propranolol) • Esmolol vs. placebo • Carvedilol vs. placebo • Propranolol vs. placebo • Overall, treatment with beta blockers reduces primary endpoints when compared to placebo

49. AHA/ACC Guidelines for Beta Blocker Therapy • Intravenous beta blockers should be used initially in all patients (without contraindication) followed by oral beta blockers with the goal being decrease in heart rate to 60 beats per minute • A combination of beta blockers and nitrates can be viewed as first line therapy in all patients with ACS

50. Treatment of ACS; Heparin • Heparin (unfractionated heparin or UFH) has traditionally been the mainstay of therapy in acute coronary syndromes as its efficacy has been documented in several large, randomized trials