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 CLASS 1 NO PAIN WITH ORDINARY PHYSICAL ACTIVITY CLASS 2 SLIGHT LIMITATION OF PHYSICAL ACTIVITY – PAIN OCCURS WITH WALKING, CLIMBING STAIRS,STRESS CLASS 3 SEVERE LIMITATION OF DAILY ACTIVITY – PAIN OCCURS ON MINIMAL EXERTION CLASS 4 UNABLE TO CONDUCT ANY ACTIVITY WITHOUT PAIN, PAIN AT REST

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)

16. 16

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. O2 SupplyDemand تاکی کاردی هیپرتانسیونسیگارعفونتتباسترسفعالیتیبوستپرخوریدردهیپوولمیا تنگ کننده های عروق گشادی عروق

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. 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

51. Heparin Trials Heparin/Atenolol Trial The Canadian Heparin/Aspirin Trial The RISC Trial Overall, UFH therapy generally results in an important clinical benefit when compared to placebo. It is more effective when given in continuous infusion rather than intermittent boluses

52. Treatment of ACS; LMWH More recent studies indicate that low molecular weight heparin is also effective in the reduction of end points such as myocardial infarction or death Some studies report that LMWH, when used in combination with ASA, may be superior to continuous infusion of Heparin

53. ACC/AHA Guidelines for Heparin Therapy All patients with acute coronary syndromes should be treated with a combination of ASA (325 mg/day) and heparin (bolus followed by continuous infusion with goal of PTT 1-2.5X control) or ASA and low molecular weight heparin unless one of the drugs is contraindicated

54. Treatment of ACS; ACE-I The best documented mechanism by which these agents act is to reduce ventricular remodeling over days to weeks after myocardial damage. However, there is data that a mortality benefit exists when these agents are used early in the course of ACS Administration of ACE-I in ACS reduces cardiac endpoints

55. AHA/ACC Guidelines for ACE-I Therapy ACE-I should be administered to all patients in the first 24 hours of ACS provided hypotension and other clear cut contraindications are absent

56. Treatment of ACS; Statins Statins may be of benefit in ACS Possible mechanisms include plaque stabilization, reversal of endothelial dysfunction, decreased thrombogenicity, and reduction of inflammation

57. TIMI Risk Score Thrombolysis In Myocardial Infarction ', ThrombolysisMyocardial Infarction Age >65 yrs Daily ASA Therapy (>7 days prior to event) Symptoms of Unstable Angina Documented CAD (stenosis > 50%) 3 or more traditional cardiac risk factors Elevated cardiac enzymes ECG changes

58. TIMI Risk Score Score of 3 or less = low risk Score of 4-5 = intermediate risk Score of 6-7 = high risk

59. Treatment of ACS; Clopidogrel Clopidogrel is a potent antiplatelet agent It should be administered to all patients who cannot take ASA The CURE trial suggests a benefit to adding Clopidogrel to ASA/Heparin in patients going for PCI Give 300 mg loading dose followed by 75 mg/day

60. AHA/ACC Guidelines for Clopidogrel Clopidogrel should be administered to patients who cannot take ASA because of hypersensitivity or gastrointestinal intolerance In hospitalized patients in whom an early, noninterventional approach is planned, clopidogrel should be added to ASA as soon as possible on admission and administered for at least 1 month and up to 9 months. Do not use clopidogrel if there is any possibility patient may be candidate for CABG

61. Treatment of ACS; Emergent Revascularization In the setting of STEMI primary PCI is associated with better outcomes than thrombolysis Emergent PCI is also indicated in the setting of a new LBBB

62. AHA/ACC Guidelines for Primary PCI Primary PCI is indicated as an alternative to thrombolysis when the following criteria are met: –STEMI or new LBBB –Can undergo PCI within 12 hours of the onset of symptoms –The MD doing the intervention does more than 75 PCI’s/yr –The procedure is done in a center that does more than 200 PCI’s/yr and has surgical backup

63. Conclusions; Approach to Chest Discomfort Good History and Physical (note time and duration of symptoms) Careful evaluation of ECG (compare to previous when possible) Check Cardiac Enzymes Monitor on Telemetry Oxygen

64. Acute Angina Treatment Goal: Enhance 02 supply to myocardium: M- Morphine for pain O- Oxygen 4-6L as ordered N- NTG sublingual, repeat q5 minutes x3 A- Aspirin to prevent platelet aggregation

65. Patient education Lifestyle modifications for controllable risk factors. Support groups are helpful, Example: Weight watchers, Smoke-enders, stress workshops, cardiac rehabilitation. Supply patients with information, name of contact person and phone numbers Identify precipitating factors for Anginal pain Medication compliance

66. Nursing Interventions Obtain EKGs Monitor mentation Assess heart sounds Assess lungs Assess peripheral circulation/skin Assess urinary output Assess GI function Assess pain

67. Nursing Interventions Activity Safety Reduce anxiety Patient Education Nutrition

70. زندگی چون گل سرخیست پرازخارو پراز برگ وپراز عطر لطیف یادمان باشد اگر گل چیدیم عطروبرگ وگل وخار همه همسایه دیوار به دیوار همند دکترعلی شریعتی