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Acute Coronary Syndromes GAP Pathophysiology & Clinical Presentations San Juan : Hotel Intercontinental, Dec. 12, 2006 - Jorge Ortega Gil, MD Mayagüez : Casa del Médico, Dec. 13, 2006 – Marcos Velázquez, MD Ponce : Casa del Médico, Dec. 14, 2006 – José Acevedo, MD 1 Ischemic Heart Disease - Overview Parameters Pathophysiology Anatomy: Atheroma / Atherothrombosis Atherosclerosis Epicardial & Microvascular Spam Atherothrombosis Subjective: Angina Objective: EKG T wave ST seg changes Chemistry: Cardiac serum biomarkers: CPK, CK-MB, Troponins Silent ischemia Stable angina Acute Coronary Syndromes Clinical Presentations Prevalence & severity of stenosis 2 Events During Atherogenesis 3 Wall Stress = Pxr 2h 4 ISCHEMIC CASCADE •Biochemical metabolic actions Nuclear •Hypoperfusion • Compliance • Echo Predictable sequence of pathophysiologic events post myocardial supply/demand imbalance •(S4) LVEDP •(Rales) • Contractility • EF EKG TIME FROM ONSET OF ISCHEMIA •Flow Maldistribution ± 45 sec. Angina / SI 5 Effect of Fixed Stenosis on Myocardial Blood Flow 6 Progression of coronary plaque over time Clinical Findings Acute Coronary Syndromes Sudden Cardiac Death Endothelial dysfunction Atherogenic risk factors Acute silent occlusive process Angina pectoris Thrombogenic risk factors Age 20 years 60 years 7 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 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 Canadian Cardiovascular Society Classification ( CCSC) Class Activity evoking angina I Prolong None ed exertion Atypical angina ( probable) Meets 2 of the above characteristics Noncardiac chest pain Limits to normal activity Meets one or none of the typical angina characteristics II Walking Slight DIFFERENTIAL DIAGNOSIS OF CHEST PAIN >2 Cardiovascular: Pericarditis, Aortic Valve blocks Disease, Aortic Dissection, Pulmonary III Walking Marked Embolism, Mitral Valve Prolapse <2 Gastrointestinal: Esophageal, Biliary, Peptic blocks ulcer, Pancreatitis Pulmonary: Pneumothorax, Pneumonia, IV Minimal Severe Pleuritis or rest 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 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 Stable Plaque Vulnerable Plaque 11 Plaque Disruption UA NSTEMI STEMI + S. Markers 12 Distinguishing Features of Acute Coronary Syndromes Unstable Angina Myocardial Infarction NSTEMI Anginal Presentatio ns •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 STEMI Prolonged ( > 30 min ) crushing, strangling chest pain more severe and wider radiation than usual angina 30 day post MI, PCI or CABG EKC initial findings Dynamic, transiet < 24 hours T-wave inversion and/or ST seg depression ST depression and/pr T Wave inversion ST elevation ( and Q waves later) Cardiac Serum Biomarkers Negative (-) Positive (+) Positive (+) 13 Acute Coronary Syndromes Coronary Atherothrombosis 14 -RCA, 1yr. Before of the acute MI (B) 15 Acute MI Typical rise and gradual fall (troponin) or more rapid rise and fall of CKMB, markers of myocardial necrosis, with at least one of the following: •Ischemic symptoms •EKG changes indicative of ischemia (ST-seg elevation or depression) 16 T Wave – ST seg. changes T-wave ∆ ST-seg ∆ Zone of ischemia Path. Q waves Zone of injury Zone of necrosis >0.03 seconds Lateral Inferior Septal Anterior >1/3 the total of QRS 17 18 19 20 “ Time is muscle” Myocardial Infarction is a true emergency in cardiac care. 21 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 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 Complications of Ml Deaths from MI 21% Prehospital 24 hours, in-hospital 8% 52% 48 hours, in-hospital 30 Days 19% 24 COMPLICATIONS OF INFARCTION Papillary Muscle Rupture Left Ventricular Thrombus Ventricular Septal Rupture Ventricular Free Wall Rupture 25