Successfully reported this slideshow.
We use your LinkedIn profile and activity data to personalize ads and to show you more relevant ads. You can change your ad preferences anytime.

Dr.Syed Imran


Published on

Published in: Education
  • Be the first to comment

Dr.Syed Imran

  1. 1. Lahore: Jan 2011 Principles of Coronary Disease Evaluation & Management Dr Syed Imran Ahmad MB, MRCP, FRCP (London) Consultant Cardiologist (Clinical & Invasive) Head, Cardiology Section, Clifton Campus, Faculty Member Ziauddin University, Karachi: & Medilink Clinic, Clifton Karachi
  2. 2. Global Disease Mortality Mortality (millions) World Health Organization. The World Health Report 2003: Shaping the Future. 2003. Cardiovascular disease Malignant neoplasms Injuries Respiratory infections COPD and asthma HIV/AIDS Perinatal conditions Digestive diseases Diarrhoeal diseases Tuberculosis Childhood diseases Malaria Diabetes
  3. 3. Atherosclerosis Is a Chronic Inflammatory Disease With LDL-C at the Core Libby P. J Intern Med. 2000;247:349-358. PHASE I: Initiation PHASE II: Progression PHASE III: Complication
  4. 4. CAD in relation to risk factors Probability of CAD occurring within next 10 years HBP (150-160) + + + + + + HDL (33-35) - + + + + + Chol (240-262) - - + + + + Cigarettes - - - + + + Diabetes - - - - + + LVH - - - - - + Kannel WB, Europ.Heart J. 1992; 13:34-42
  5. 5. Integrated Cellular Mechanisms of Cardiovascular Disease Endothelial Dysfunction Dyslipidaemia Hypertension Liao. Clin Chem . 1998:44:1799-1808; adapted from Mason. Cerebrovasc Dis. 2003;16(suppl 3):11-17. Diabetes Smoking  NO Synthesis Vasoconstriction Thrombosis Superoxide  COX Activity Thromboxane A 2 Prostaglandin H 2 Prostacyclin Inflammation Leukocyte adhesion Endothelial permeability Angiotensin II T-cell activation  Endothelin Vasoconstriction Calcium mobilization
  6. 6. Coronary Arteries
  7. 9. Coronary Artery Disease Angiogram of the left coronary artery and its branches
  8. 11. Manifestations of CAD <ul><li>Chronic stable angina </li></ul><ul><li>Unstable angina </li></ul><ul><li>Vasospastic angina (Variant Angina) </li></ul><ul><li>Silent ischaemia </li></ul><ul><li>Myocardial infarction </li></ul><ul><li>Congestive heart failure </li></ul><ul><li>Sudden death (SCD) </li></ul>
  9. 12. Classification of stable angina Severity I Conduct of daily work and activities without complaints (angina occurs only when load is extreme or over a very extended period of time) Severity II Slight restriction of daily work and activities (angina occurs when individual walks fast, climbs stairs or feels stressed) Severity III Marked restriction of daily work and activities(angina occurs after walking a short distance, or climbing a flight of stairs) Severity IV Daily work and activities not possible (angina constantly present)
  10. 13. Angina Pectoris <ul><ul><li>Angina is common </li></ul></ul><ul><ul><li>- affects over 10% of men and women > 60 </li></ul></ul><ul><ul><li>Angina is disabling </li></ul></ul><ul><ul><li>- quality of life can be poor </li></ul></ul><ul><ul><li>Angina affects outcome variably </li></ul></ul><ul><ul><li>- 3% to 20% annual rate of cardiac events </li></ul></ul>
  11. 14. Angina Pectoris <ul><ul><li>The Holy Trinity of treatment </li></ul></ul><ul><ul><ul><li>Oral Nitrates </li></ul></ul></ul><ul><ul><ul><li>Beta Blockers </li></ul></ul></ul><ul><ul><ul><li>Calcium Antagonists </li></ul></ul></ul><ul><ul><ul><li>Statins and Anti platelets </li></ul></ul></ul>
  12. 15. New mechanistic approaches to stable angina Sinus node inhibition (ivabradine) Late I Na inhibition (ranolazine) Rho kinase inhibition (fasudil) Metabolic modulation (trimetazidine) Preconditioning (nicorandil) O H 3 C O H 3 C O N CH 3 O CH 3 O CH 3 O O NO 2 H N N N N O N CH 3 H CH 3 CH 3 O O H N SO 2 NH N O OH CH 3 CH 3 OCH 3 H N N N O
  13. 16. Acute Coronary Syndrome
  14. 17. Pathophysiology of ACS: Disrupted Plaque Unstable angina or NSTEMI Temporary resolution of instability Future high-risk lesion Acute STEMI Adapted from Yeghiazarians et al. N Engl J Med . 2000;342:101-114. Plaque rupture Thin cap High macrophage content Large lipid core Incomplete coronary occlusion Complete coronary occlusion Spontaneous lysis, repair, and wall remodeling
  15. 18. Pathogenesis of ACS White HD. Am J Cardiol. 1997; 80(4A):2B-10B.
  16. 19. Cumulative 6-month mortality from CAD 0 1 2 3 4 5 6 5 10 0 15 20 25 Months after hospital admission Deaths / 100 pts / month Acute MI Unstable angina Stable angina Duke Cardiovascular Database N = 21,761; 1985-1992 Diagnosis on adm to hosp
  17. 20. EARLY RISK STRATIFICATION <ul><li>In all patients with CP the likelihood of Acute coronary Ischaemia should be determined ( High, Intermediate and Low ) </li></ul><ul><li>The process of early RS focuses on: Anginal Symptoms Clinical Examination ECG findings Biomarkers of Cardiac Injury </li></ul>
  18. 21. Why Early Risk Stratification? <ul><li>Assessment of prognosis, based upon the likelihood of death/MI should set the pace of Initial Evaluation & Management of ACS. </li></ul><ul><li>The process of RS is needed for </li></ul><ul><ul><li>Selection of the site of care (CCU, Monitored unit, OPD) </li></ul></ul><ul><ul><li>Selection of Therapy specially newer agents like GP IIb/IIIa inhibitors </li></ul></ul><ul><ul><li>Determination for the need of an early invasive course. </li></ul></ul>
  19. 22. Tools for Risk Assessment (12-lead ECG) <ul><li>It remains the sheet-anchor of the decision making for evaluation and management in CP </li></ul><ul><li>A tracing during CP is of particular importance. </li></ul><ul><li>High Risk: </li></ul><ul><li>ST-segment deviation > 0.05 mV </li></ul><ul><li>New or presumed new LBBB </li></ul><ul><li>Sustained VT </li></ul><ul><li>Intermediate Risk: </li></ul><ul><li>T wave inversion or presence of Q waves </li></ul><ul><li>Low Risk: </li></ul><ul><li>No ECG changes during CP </li></ul>
  20. 24. Anginal Symptoms <ul><li>High Risk: </li></ul><ul><li>Accelerating Tempo of CP in preceding 48 hrs or prolonged CP for >20 min </li></ul><ul><li>Intermediate Risk: </li></ul><ul><li>Recent prolonged angina at rest for >20 min now resolved; Rest angina of <20 min. </li></ul><ul><li>Low Risk: </li></ul><ul><li>New onset Angina with no other High/Intermediate risk features on symptoms or ECG. </li></ul>
  21. 25. BIOMARKERS <ul><li>Biomarkers of Cardiac Injury should be measured in all patients with suspected ACS </li></ul><ul><li>Cardiac Specific Troponin (cTnT or cTnI) is the preferred marker, if available. </li></ul><ul><li>CK-MB is also acceptable </li></ul><ul><li>Total CK (without MB), AST, LDH are considered useless now in this setting. </li></ul>
  22. 26. Principles of Hospital Care in ACS <ul><li>Bed Rest </li></ul><ul><li>Continuous ECG monitoring in a CCU for Ischaemia/Arrhythmia </li></ul><ul><li>Nitrates S/L followed by an IV infusion </li></ul><ul><li>Pulse Oximetry with Oxygen if needed </li></ul><ul><li>Morphine Sulphate IV if pain persists and specially with LVF </li></ul><ul><li>Beta Blockade with first dose IV, if CP persists </li></ul>
  23. 27. Principles of Hospital Care in ACS <ul><li>ACE-I , early on ( a lot of evidence with drugs like Ramipril : also evidence with ARB e.g. Valsartan) </li></ul><ul><li>Antiplatelets (Aspirin and Clopidogrel) </li></ul><ul><li>Anticoagulants (UFH/LMWH or Fondaparinux) </li></ul><ul><li>Statins </li></ul><ul><li>Early Invasive vs. planned ischaemia driven </li></ul>
  24. 28. Lipid Management in Clinical Practice <ul><li>For patients with CHD or diabetes , a new, lower optimal goal for LDL-C is <70 mg/dl —NCEP Coordinating Committee Circulation 2004;110:227–239 </li></ul>What is an appropriate therapeutic target for LDL-C?
  25. 29. Changes to NCEP ATP III LDL-C Goals NCEP=National Cholesterol Education Program; ATP III=Adult Treatment Panel III Adapted from Grundy SM et al Circulation 2004;110:227–239; Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults JAMA 2001;285:2486–2497. Modification Modification 2+ risk factors (10-year risk  20%) CHD or CHD risk equivalents (10-year risk >20%) Risk Category Optional goal of <100 mg/dl (2.5 mmol/L) for 10%–20% risk group Optional goal of <70 mg/dl (1.8 mmol/L) <130 mg/dl (3.4 mmol/L) ATP III <100 mg/dl (2.5 mmol/L) ATP III LDL-C Goal Publication
  26. 30. Rationale for Lower LDL-C Goals <ul><li>Both HPS and PROVE IT suggest that additional benefit may be obtained by reducing LDL-C levels to substantially less than 100 mg/dl (2.5 mmol/L) </li></ul><ul><li>Recent trials indicate that there is no threshold below which lower LDL-C concentrations provide no further benefit </li></ul>Adapted from Grundy SM et al Circulation 2004;110:227–239; HPS Study Group Lancet 2002;360:7–22; Cannon CP et al N Engl J Med 2004;350:1494–1502; O’Keefe JH et al J Am Coll Cardiol 2004;43:2142–2146; Stamler J et al JAMA 2000;284:311–318; Chen Z et al BMJ 1991;303:276–282.
  27. 31. Investigations in CAD <ul><li>Non-invasive Testing: </li></ul><ul><ul><li>Echocardiography (Resting and Stress) </li></ul></ul><ul><ul><li>ETT </li></ul></ul><ul><ul><li>Myocardial Perfusion Studies (Thallium) </li></ul></ul><ul><ul><li>CT Angiogram </li></ul></ul><ul><ul><li>Cardiac MRI </li></ul></ul><ul><ul><li>PET </li></ul></ul>
  28. 32. Investigations in CAD <ul><li>Invasive Testing: </li></ul><ul><ul><li>Selective Coronary Angiography & Ventriculography </li></ul></ul><ul><ul><li>Invasive Electrophysiological (EP) Studies </li></ul></ul>
  29. 33. Further Management <ul><li>Medical Treatment </li></ul><ul><li>Interventional Treatment </li></ul><ul><ul><li>Percutaneous Coronary Intervention (PCI) </li></ul></ul><ul><ul><li>Surgical Intervention (CABG) </li></ul></ul>
  30. 35. Prognosis in CAD <ul><li>More closely related to </li></ul><ul><ul><li>Left Ventricular Function; & </li></ul></ul><ul><ul><li>Extent of Coronary Disease </li></ul></ul><ul><ul><li>than </li></ul></ul><ul><ul><li>The severity of Symptoms </li></ul></ul>
  31. 36. Thank You Dr Syed Imran Ahmad MB,FRCP(London)