Pathophysiology & Clinical Presentations

1. Pathophysiology & Clinical Presentations Acute Coronary Syndromes 1

2. Ischemic Heart Disease - Overview Parameters Anatomy: Atheroma / Atherothrombosis Subjective: Angina Objective: EKG T wave ST seg changes Chemistry: Cardiac serum biomarkers: CPK, CK-MB, Troponins Pathophysiology Atherosclerosis Epicardial & Microvascular Spam Atherothrombosis Silent ischemia Acute Coronary Syndromes Stable angina Prevalence & severity of stenosis 2 Clinical Presentations

3. Events During Atherogenesis 3

4. P x r 2h Wall Stress = 4

5. Nuclear Echo TIME FROM ONSET OF ISCHEMIA ISCHEMIC CASCADE • Flow Maldistribution • Biochemical metabolic actions Predictable sequence of pathophysiologic events post myocardial supply/demand imbalance • Hypoperfusion • Compliance • (S4) • LVEDP • (Rales) • Contractility • EF EKG ±45 sec. Angina / SI 5

6. Effect of Fixed Stenosis on Myocardial Blood Flow 6

7. Angina pectoris Progression of coronary plaque over time Clinical Findings Acute Coronary Syndromes Sudden Cardiac Death Acute silent occlusive process Endothelial dysfunction Atherogenic risk factors Thrombogenic risk factors Age 7 60 years 20 years

8. IHD – Clinical Spectrum Chronic • Stable Angina • Silent Ischemia • Mixed Angina • Microvascular Angina (Syndrome X) • Stunned & Hibernating Acute • Unstable Angina • Acute Myocardial Infarction (NSTEMI, STEMI) • Sudden Cardiac Death Prinzmetal Angina 8

9. Clinical Classification of Chest Pain Canadian Cardiovascular Society Classification ( CCSC) Typical angina (define) • Substernal chest discomfort with a characteristic quality and duration that is • Provoked by exertion or emotional stress and • Relieved by rest or nitroglycerin Atypical angina ( probable) Meets 2 of the above characteristics Noncardiac chest pain Meets one or none of the typical angina characteristics DIFFERENTIAL DIAGNOSIS OF CHEST PAIN • Cardiovascular: Pericarditis, Aortic Valve Disease, Aortic Dissection, Pulmonary Embolism, Mitral Valve Prolapse • Gastrointestinal: Esophageal, Biliary, Peptic ulcer, Pancreatitis • Pulmonary: Pneumothorax, Pneumonia, Pleuritis • Chest Wall: Costochondritis, Rib fracture, Herpes zoster • Psychological: Anxiety disorders *CHRONIC STABLE ANGINA – 2 TO 10 Min & CCSC I – II ACUTE CORONARY SYNDROMES > 15 Min. – Hours & CCSC III - IV 9

10. CAD - Clinical Spectrum • Chronic ischemic heart disease Ischemia precipitated by increased myocardial oxygen demand in the setting of a fixed, not vulnerable atherosclerotic lesion. It is called Stable Angina when the clinical characteristics (Angina attacks) do not change in frequency, duration, precipitating causes, or easy with the angina is relieved, for at least 60 days. -Silent Ischemia, -Mixed Angina -Syndome X -Stunning & Hibernating. • Acute Coronary Syndromes (ACS) Ischemia or infarction are caused from a primary reduction in coronary flow, precipitated by plaque disruption and subsequent thrombus formation: Unstable Angina, NSTEMI, STEMI Prinzmetal Angina 10

11. Stable Plaque Vulnerable Plaque 11

12. Plaque Disruption UA NSTEMI STEMI + S. Markers 12

13. ST elevation ( and Q waves later) Cardiac Serum Biomarkers STEMI NSTEMI Positive (+) Positive (+) Negative (-) Unstable Angina ST depression and/pr T Wave inversion Dynamic, transiet < 24 hours T-wave inversion and/or ST seg depression EKC initial findings Prolonged ( > 30 min ) crushing, strangling chest pain more severe and wider radiation than usual angina • Rest angina - Rest or nocturnal Angina ≥ 20 minutes occurring within a week of presentation. • New onset angina - ( < 2 months ) exertional angina progressing to CCSA III • Crescendo angina - < 2 moths acceleration of previously stable angina to at least CCSA III. • Within 30 day post MI, PCI or CABG Anginal Presentations Myocardial Infarction Distinguishing Features of Acute Coronary Syndromes 13

14. Acute Coronary Syndromes Coronary Atherothrombosis 14

15. -RCA, 1yr. Before of the acute MI (B) 15

16. Acute MI • Typical rise and gradual fall (troponin) or more rapid rise and fall of CK-MB, markers of myocardial necrosis, with at least one of the following: • Ischemic symptoms • EKG changes indicative of ischemia (ST-seg elevation or depression) 16

17. Lateral T Wave – ST seg. changes T-wave ∆ ST-seg ∆ Zone of ischemia Path. Q waves Zone of injury Zone of necrosis >0.03 seconds >1/3 the total of QRS Anterior Septal 17 Inferior

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21. “ Time is muscle” Myocardial Infarction is a true emergency in cardiac care. 21

22. If the clinical picture is consistent with acute STEMI (including True Posterior MI) or new left bundle branch block (LBBB) is present in EKG, select and implement reperfusion therapy, Fibrinolysis or PCI as quickly as possible within 12 hours of symptoms onset to obtain and sustain optimal flow in the infarct-related artery (IRA). Do not wait for serum cardiac biomarkers result before implementing reperfusion strategy ! 22

23. ACS Treatment • Revascularization • Mechanical: PCI, CABG • Pharmacologic: Thrombolytics • Stabilization of Vulnerable Plaque Aspirin • Antithrombotics • Beta-Blockers • ACE-Inhibitors • Lipid-Lowering Agents (+stantins) • Antioxidants • Aggressive Risk Factors Modifications 23

24. Complications of Ml 24

25. COMPLICATIONS OF INFARCTION Papillary Muscle Rupture Left Ventricular Thrombus Ventricular Septal Rupture 25 Ventricular Free Wall Rupture