Guidelines Applied to Practice (GAP)

1. Guidelines Applied to Practice (GAP) American College of Cardiology, Puerto Rico Chapter

2. Guidelines Applied in Practice (GAP) INTRODUCTION Chronic Coronary Syndromes(Chronic Stable Angina) San Juan : Hotel Intercontinental, Feb. 6, 2007 - Jorge Ortega Gil, MD Mayagüez : Casa del Médico, Feb. 7, 2007 – Marcos Velázquez, MD Ponce : Casa del Médico, Feb. 8, 2007 – José Gómez Rivera, MD

5. Ischemic Heart Disease in the United StatesThe Magnitude of the Health Problem • Despite the well documented recent decline in cardiovascular mortality, IHD remains the leading cause of death • The initial clinical presentation is about the same for both chronic and acute coronary syndromes (50% each) • About 1.5 million myocardial infarctions occur each year, one third to one half are fatal • 200,000 have silent infarctions • 16 million people have symptomatic CAD • Approximately 2.5 % of totally asymptomatic middle-aged men have silent myocardial ischemia • One million each PCI and CABG are performed each year • Annual cost in 2004 was about $368 billion

6. The ACC/AHA Guideline Classifications Class I: Evidence and / or agreement that treatment is effective Class IIa: Weight of evidence favors use Class IIb: Usefulness less well established Class III:Evidence and/ or agreement that treatment is not effective Level of evidence: A (high rank) – Based on large randomized trials B (Intermediate rank) Based on smaller trials or careful analyses C (low rank) – Based on expert consensus

7. Chronic Coronary Syndromes(Chronic Stable Angina) GAP Pathophysiology & Clinical Presentations San Juan : Hotel Intercontinental, Feb. 6, 2007 - Jorge Ortega Gil, MD Mayagüez : Casa del Médico, Feb. 7, 2007 – Marcos Velázquez, MD Ponce : Casa del Médico, Feb. 8, 2007 – José Gómez Rivera, MD

8. 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 Clinical Presentations

9. Events During Atherogenesis

10. P x r 2h Wall Stress =

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

12. Effect of Fixed Stenosis on Myocardial Blood Flow

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

14. 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

15. ANGINA PECTORIS Canadian Cardiovascular Society Classification ( CCSC) • Location: Usually Substernal, Jaw & Epigastrium • Quality: Sensation of Pain / Discomfort, Oppression, Pressure, Burning, Tightness, Crushing or Squeezing. Can Resemble Ïndigestion” • Radiation: Radiates To Left Or Right Arm Or Shoulder, Jaw or Epigastrium. • Assocatie Symptoms:. Dyspnea, Diaphoresis, Weakness, Nausea, Vomiting, and/or Feeling of Anxiety Or Impending Doom • Duration: 2 Min. – 30 Min. - To Several Hours • - Relieved By TNG In 1-10 Min or Rest • Related To: Exercise, Cold, Meals, Emotion, Coitus. Rest. 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 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

16. 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

17. Silent Ischemia Is the objective evidence-ST segment shifts- of myocardial ischemia which is not associated with angina or angina equivalents. ST seg. depression Iceberg’s sign Angina

18. Mixed Angina • Exertional Angina Plus Angina at Rest or Cold-induced Angina or Emotion-Induced Angina. • Angina at Variable Thresholds of Exercise. Classic Angina Prinzmetal Angina Transient ST seg elevation Transient ST seg depression

19. (positive stress testing) Pathophysiology: Dynamic small vessel constriction (vasospasm)

20. PRINZMETAL OR VARIANT ANGINA • Prolonged bouts of chest pain at rest with EKG ST seg. elevation. Pathophysiology: profound spasm of one of the three major epicardial coronary arteries. A = Marked transitory ST Elevation during a bout of severe chest pain B = Thirty min. after A (Normal EKG)

21. Post-ischemic LV Dysfunction Impaired LV contractility despite the presence of viable myocytes Acute phenomenon – The LV dysfunction is due to short periods of coronary occlusion, and persists for minutes, hours or even days after blood flow has been restored. This process is reversible spontaneously. Chronic phenomenon – The LV dysfunction is the result of months or years of chronic ischemia. This process requires revascularization ( PCI, CABG) in order to restore contractility.

22. Chronic Coronary Syndromes Treatment • Pharmacologic • Antithrombotics • Beta-Blockers • ACE-Inhibitors • Lipid-Lowering Agents (+stantins) • Aggressive Risk Factors Modifications • Influenza Vaccine • Revascularization • Mechanical: PCI, CABG

23. Treatment of Chronic Ischemic Heart Disease I. Medical A) Antianginal and Anti-ischemic therapy b - Blockers; Calcium antagonists;Nitroglycerin and Nitrates B) Pharmacotherapy to prevent Myocardial Infarction and Death Antiplatelet / Antithrombotic agents Lipid – Lowering agents Angiotensin – converting enzymes inhibition (ACE-I) b – Blockers C) Risk Factor Modification Smoking cessation; Blood pressure control D) Influenza Vaccine II. Mechanical Revascularization A) Percutaneous coronary intervenntion (PCI): Conventional Angioplasty (PTCA) Stents implantation: Bare metal & drug - eluting stents B) Surgical - Coronary artery bypass graft (CABG)

25. Guidelines Applied to Practice (GAP) American College of Cardiology, Puerto Rico Chapter

27. Holter * EBCT *MRI / LVG