1. 1 Pathophysiology & Clinical Presentations Acute Coronary Syndromes

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

3. 3 Events During Atherogenesis

4. 4 P x r 2h Wall Stress =

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

6. 6 Effect of Fixed Stenosis on Myocardial Blood Flow

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

8. 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

9. 9 Clinical Classification of Chest Pain Typical angina (define ) 1.Substernal chest discomfort with a characteristic quality and duration that is 2.Provoked by exertion or emotional stress and 3.Relieved by rest or nitroglycerin Atypical angina ( probable) Meets 2 of the above characteristics Meets 2 of the above characteristics Noncardiac chest pain Meets one or none of the typical angina characteristics 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 Class Activity evoking angina Limits to normal activityI Prolonge d exertion None II Walking > 2 blocks Slight III Walking < 2 blocks Marked IV Minimal or rest Severe Canadian Cardiovascular Society Classification ( CCSC) *CHRONIC STABLE ANGINA – 2 TO 10 Min & CCSC I – II ACUTE CORONARY SYNDROMES > 15 Min. – Hours & CCSC III - IV ACUTE CORONARY SYNDROMES > 15 Min. – Hours & CCSC III - IV

10. 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. 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. -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: Ischemia or infarction are caused from a primary reduction in coronary flow, precipitated by plaque disruption and subsequent thrombus formation: Unstable Angina, NSTEMI, STEMI Unstable Angina, NSTEMI, STEMI Prinzmetal Angina Prinzmetal Angina

11. 11 Stable PlaqueVulnerable Plaque

12. 12 UANSTEMI STEMI + S. Markers Plaque Disruption

13. 13 Distinguishing Features of Acute Coronary SyndromesSTEMINSTEMI Positive (+) Negative (-) Cardiac Serum Biomarkers ST elevation ( and Q waves later) 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. 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 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. Crescendo angina - < 2 moths acceleration of previously stable angina to at least CCSA III. Within 30 day post MI, PCI or CABG Within 30 day post MI, PCI or CABG Anginal Presentation s Myocardial Infarction Unstable Angina

14. 14 Acute Coronary Syndromes Coronary Atherothrombosis

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

16. 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)

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

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

22. 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 !

23. 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

24. 24 Complications of Ml

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