ACS Management: Initial Diagnosis, Treatment Strategies, and Risk Factors
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Brief overview of acute coronary syndromes presented during Nizamabad CME
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ACS Management: Initial Diagnosis, Treatment Strategies, and Risk Factors
- 1. ACS – INITIAL DIAGNOSIS & MANAGEMENT Dr Uday Prashant M.D D.M
- 2. Very Alarming Scene • India is the Diabetic capital of the world:- Highest no of diabetics in world at present • Indians have one of highest rates of CAD • Obesity in India is in rapid rise
- 3. Coronary Artery Disease in Indians = CADI • How is it different from western world • CADI strikes early ! • CADI strikes almost any one !!! • CADI strikes unexpectedly !!!! • Conventional RF can’t explain it away • CADI is malignant in its onslaught.
- 4. The CADI Volcano • We are in the middle of the wave of CAD epidemic • This CADI epidemic will peak by 2015 • 50% deaths in India are CVD deaths. • CADI will overtake Infectious diseases in morbidity too • By 2015 CADI will be six times more than the West • CADI will be 20 times more than the Chinese,
- 5. ACS • Spectrum of presentation – – – – Myocardial infarction ( 25% – 30%) Non Q wave MI ( 30% - 35% ) unstable angina (30% - 35%) Sudden Cardiac Death (5% - 10%) Non Q wave MI / USA compromises 2/3 rd of ACS cases 15% - 20% of USA are high risk cases.
- 8. New Terminology in ACS Plaque Rupture Old term Stable Angina Unstable Angina New term Atherothrombosis Non– Q-wave MI STEMI UA/NSTEMI Daysweeks Antithrombotic Therapy Q-wave MI Minuteshours Thrombolysis Primary PCI ACS, acute coronary syndrome; MI, myocardial infarction; UA, unstable angina; NSTEMI, non–ST-segment elevation myocardial infarction; STEMI, ST-segment elevation myocardial infarction; PCI, percutaneous coronary intervention. Cannon CP. J Thromb Thrombolysis. 1995;2:205-218.
- 9. Acute Coronary Syndrome Ischemic Discomfort Unstable Symptoms No ST-segment elevation Unstable angina History Physical Exam ST-segment elevation Non-Q AMI Q-Wave AMI ECG Acute Reperfusion
- 10. Pathogenesis of ACS Vulnerable Non-Vulnerable Atherosclerotic Atherosclerotic Plaque Plaque
- 11. The Matrix Skeleton of Unstable Coronary Artery Plaque Fissures in the fibrous cap Davies MJ. Circulation. 1996;94:2013-2020.
- 12. Vulnerable plaques • Vulnerable plaques cause ACS • Depends upon inner free lipid content, thin fibrous cap, active inflammation, hemodynamic stresses. • More than one vulnerable plaques can be present which are not Rx by PCI. • Vulnerable plaques cannot be detected by routine CAG. • Can be inferred indirectly by hsCRP – Rx high dose statins
- 13. Chest pain with ACS • 15 -25 % of chest pain cases in ED have ACS • 2 % of ACS are missed • These are current US data • In India the percentages are far higher • For Pt mortality / for us medicolegal implications
- 14. Clinical Classification of Chest Pain Diamond . J Am Coll Cardiol 1983
- 15. Typical Angna • Cardiac symptoms: Presence of acute chest, epigastric, neck, jaw, or arm pain or discomfort or pressure without apparent noncardiac source. • Levine`s sign may be +ve. • More general, atypical symptoms, such as fatigue, nausea, vomiting, diaphoresis, faintness, and back pain, should not be used as a diagnosis of Angina
- 16. CHD Risk Equivalents 1. Diabetes Mellitus 2. Peripheral Vascular Disease (PVD) 3. Framingham risk score of > 20% 4. Carotid artery disease – • • Stroke, TIA > 50% Narrowing, Carotid Bruit 5. Abdominal Aortic Aneurysm (AAA) Adult Treatment Panel III. NIH publication 01-3095.
- 17. Epidemiological definition of MI • Typical chest pain lasting for > 30 min not relieved by nitrates • ECG showing characteristic changes of MI • Positive cardiac biomarkers of injury WHO states any of two from above three should be present.
- 18. Definition of Acute/Evolving/Recent MI 1) Typical rise and fall of biochemical markers of MI with atleast 1 of them • Ischaemic symptoms • ECG changes indicative of ischaemia (ST elevation or depression or LBBB) • Development of pathological Q waves in ECG • New RWMA or imaging e/o loss of viable myocardium ACC/AHA/EU/WHO Task force for redefinition of MI 2007 guidelines
- 19. ST elevation • Occurs in the early stages R ST P Q • Occurs in the leads facing the infarction • Slight ST elevation may be normal in V1 or V2
- 20. Deep Q wave • Only diagnostic change of myocardial infarction R ST • At least 0.04 seconds in duration P T Q • Depth of more than 25% of ensuing R wave
- 21. T wave changes • Late change R • Occurs as ST elevation is returning to normal ST P • Apparent in many leads T Q
- 22. Bundle branch block Anterior wall MI I II III aVR aVL aVF V1 V2 V3 Left bundle branch block V4 V5 V6 I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
- 23. Sequence of changes in evolving AMI R R T R ST ST P P P QS T Q 1 minute after onset Q 1 hour or so after onset A few hours after onset R ST P P T Q A day or so after onset ST T P T Q Later changes Q A few months after AMI
- 24. Anterior infarction Anterior infarction I II III Left coronary artery aVR aVL aVF V1 V2 V3 V4 V5 V6
- 25. Inferior infarction Inferior infarction I II III Right coronary artery aVR aVL aVF V1 V2 V3 V4 V5 V6
- 26. Lateral infarction Lateral infarction I II III Left circumflex coronary artery aVR aVL aVF V1 V2 V3 V4 V5 V6
- 28. Right Ventricular Infarction V4R Modified from Wellens. N Engl J Med 1999;340:381. Clinical findings: Shock with clear lungs, elevated JVP Kussmaul sign Hemodynamics: Increased RA pressure (y descent) Square root sign in RV tracing ECG: ST elevation in R sided leads Echo: Depressed RV function Rx: Maintain RV preload Lower RV afterload (PA---PCW) Inotropic support Reperfusion
- 29. Diagnostic criteria for AMI • • • • • Q wave duration of more than 0.04 seconds Q wave depth of more than 25% of ensuing r wave ST elevation in leads facing infarct (or depression in opposite leads) Deep T wave inversion overlying and adjacent to infarct Cardiac arrhythmias
- 35. Cor pulmonale
- 37. MI presenting as Syncope • 60 yrs sudden onset chest pain f/b syncope • H/o associated sweating + • Afterwards no chest pain • No risk factors other than age • Dilemma whether it is arrythmogenic syncope.
- 39. Trop T -Ve
- 43. Non ischaemic causes of ST elevation • • • • • • • Early repolarization changes. Prinzmetal angina Ventricular aneurysm Pericarditis myocarditis Hyperkalemia, Hypercalcemia LVH, LBBB IC bleed mistaken as MI
- 47. Mistaken MI • Lingam diagnosed as AWMI • CAG revealed critical lesion LAD • Underwent successful stenting to LAD • But patient still symptomatic • Presented with Grade IV dyspneoa • ECHO showed COR PULMONALE
- 50. Non MI causes of pathalogical Q waves • Norma septal Q waves V1-V2, III & AVF (narrow) • Cardiomyopathies. • Severe LVH, LBBB • Dextrocardia/version. • COPD
- 58. Young MI • • • • • • Devender 27 yrs male Non smoker Non diabetic H/O travel to dubai, elctrician Middle class family Chest pain 3 hrs duration
- 64. Homocysti(e)ne • Normal value is up to 10 μ mols/L • Excess of homocystine generates oxidative stress on the cell membranes. • Folic acid 5 mg/ day + Vit. B6 and B12 are to be given on regular basis
- 65. Hyper-homocyst(e)inemia Blood Homocyst(e)ine Levels Classification Normal Moderate Intermediate Severe Values mmol/L 05 – 10 11 – 30 31 – 100 > 100
- 66. Lipid Profile in Young Indian Patients Angiographically Proven CHD Parameter with % Patients Total cholesterol >200 mg/dl 54.3 Triglyceride >200 mg/dl 56.1 HDL <35 mg/dl 59.6 Lp(a) >30 mg/dl 61.4 n=57; age <40 yrs Mishra et al (Cuttack) Indian Heart J 2001; 53: Abst 60
- 67. CHD Risk Factors - Makers • Modifiable – The New Six – hs-CRP – Lp(a) – sLDL – Endothelial Dysfunction – Apo B / Apo A1 ratio – Homocysteine
- 70. Risk Factors for Future Cardiovascular Events: WHS Lipoprotein(a) Homocysteine IL-6 TC LDL-C sICAM-1 SAA Apo B TC:HDL-C hs-CRP hs-CRP + TC:HDL-C 0 1.0 2.0 4.0 6.0 Relative Risk of Future Cardiovascular Events Ridker PM et al. N Engl J Med 2000;342:836-843.
- 71. Post stent MI • Mr Rathod 60 yrs male. • 1999 had ACS, uderwent stenting and not on reqular follow up • Asymptomatic since then • Presented with typical h/o of MI
- 75. Clinical indicators of successful reperfusion • Resolution of chest pain by > 50% • Resolution of ST elevations by > 50% • AIVR • Rapid rise and fall of cardiac enzymes • Clinically stable course
- 76. For Managment • ST elevation MI :- Rapid thrombolysis vs immediate revascularization (Complete occlusion of lumen by red thrombus) • Non ST elevation MI:- Antithrombotics and plaque stabilization or cooling off. Early invasive strategy is controversial (Partial occlusion of lumen by white thrombus)
- 78. Management of MI • All management strategies focus on faster reperfusion of culprit artery. • Spontaneous recanalization rates after MI is 40 % • But it is after 12 – 24 hrs • Permanent damage has already set in
- 79. Management of MI • Within 30 minutes if reperfused no damage to myocardium. • Within 2- 4 hrs of reperfusion the damages are minimal. • After 6 hrs what we save is much less than what myocardium we loose
- 80. Management of MI • After 12 hrs no use of repurfusion • permanent damage sets in though surrounding hibernating myocardium can be saved. • To assess for hibernating myocardium we have Presence of chest pain TMT Nuclear Scans Dobutamine Stress Echo MRI etc
- 82. • ITS NOT GIVING RIGHT TREATMENT THAT IS IMPORTANT IN MI MANAGEMENT BUT HOW FAST WE ADMINISTER THAT IS IMPORTANT • For every 30 min delay in reperfusion the one year risk of relative mortality increases by 8%
- 85. y
- 86. ? MI • Laksmi presented with 2 hrs duration of severe chest pain • She 35 years female • ECG not fulfilling criteria of MI • Enzymes useless • Later ECHO except mild apical hypokinesia normal • CAG Prox LAD 90% stenosis.
- 87. Reperfusion Options for STEMI Patients Step 2: Select Reperfusion Treatment. If presentation is < 3 hours and there is no delay to an invasive strategy, there is no preference for either strategy. Fibrinolysis generally preferred  Early presentation ( ≤ 3 hours from symptom onset and delay to invasive strategy)  Invasive strategy not an option  Cath lab occupied or not available  Vascular access difficulties  No access to skilled PCI lab  Delay to invasive strategy  Prolonged transport  Door-to-balloon more than 90 minutes  > 1 hour vs fibrinolysis (fibrin-specific agent) now
- 88. Reperfusion Options for STEMI Patients Step 2: Select Reperfusion Treatment. If presentation is < 3 hours and there is no delay to an invasive strategy, there is no preference for either strategy. Invasive strategy generally preferred  Skilled PCI lab available with surgical backup  Door-to-balloon < 90 minutes • High Risk from STEMI  Cardiogenic shock, Killip class ≥ 3  Contraindications to fibrinolysis, including increased risk of bleeding and ICH  Late presentation  > 3 hours from symptom onset  Diagnosis of STEMI is in doubt
- 89. Fibrinolysis I IIa IIb III Fibrinolytic therapy should not be administered to asymptomatic patients whose initial symptoms of STEMI began more than 24 hours earlier. I IIa IIb III Fibrinolytic therapy should not be administered to patients whose 12-lead ECG shows only STsegment depression, except if a true posterior MI is suspected.
- 90. Contraindications and Cautions for Fibrinolysis in STEMI • Any prior intracranial hemorrhage Absolute Contraindications • Known structural cerebral vascular lesion (e.g., arteriovenous malformation) • Known malignant intracranial neoplasm (primary or metastatic) • Ischemic stroke within 3 months EXCEPT acute ischemic stroke within 3 hours NOTE: Age restriction for fibrinolysis has been removed compared with prior guidelines.
- 91. Contraindications and Cautions for Fibrinolysis in STEMI • Suspected aortic dissection Absolute Contraindications • Active bleeding or bleeding diathesis (excluding menses) • Significant closed-head or facial trauma within 3 months
- 92. Contraindications and Cautions for Fibrinolysis in STEMI Relative • History of chronic, severe, poorly controlled Contraindications hypertension • Severe uncontrolled hypertension on presentation (SBP > 180 mm Hg or DBP > 110 mm Hg) • History of prior ischemic stroke greater than 3 months, dementia, or known intracranial pathology not covered in contraindications • Traumatic or prolonged (> 10 minutes) CPR or major surgery (< 3 weeks)
- 93. Contraindications and Cautions for Fibrinolysis in STEMI Relative • Recent (< 2 to 4 weeks) internal bleeding Contraindications • Noncompressible vascular punctures • For streptokinase/anistreplase: prior exposure (> 5 days ago) or prior allergic reaction to these agents • Pregnancy • Active peptic ulcer • Current use of anticoagulants: the higher the INR, the higher the risk of bleeding
- 94. Choice of Thrombolytic • Underuse:- 50 – 70% of cases only given thrombolytics. • tPA: • • Less allergic reactions • • Less fibrinogen depletion (“clot selective”) • • Faster thrombolysis • • Slightly lower overall mortality • • • • 2) Streptokinase (SK): • Less expensive ($300 vs $2500) • Lower stroke rate (0.3% vs 0.8%) • Can’t use again secondary to antibody formation
- 95. Thrombolysis • 90 minute patency better with rt-PA than SK (70% vs 55% in Euro CoopStudy and 70% vs 43% in TIMI-1) • Patency at 24 hours roughly equal between tPA and SK • ISIS-3 – mortality identical in head to head comparison of tPA and SK • Many studies favor tPA over SK
- 96. Primary PTCA • Gangasagar 52 yrs male • H/O Diabetes • Chest pain for 4 hrs
- 102. Classification of USA Class I:- New onset angina or 7.1% accelerated angina. Class II:- Angina at rest but not within 48 hrs. 10.3% Class III:- Angina at rest within 48 hrs. 10.9% A:- Secondary angina(14%), B:- Primary angina ( 8.5%), C:- Post infarct angina (18.5%) Adapted from Braunwald E. Circulation 1989;80:410-4
- 104. Medical Management of Unstable Angina • • • • • • • Nitrates:- ISIS 4 Beta Blockers:- HINT Aspirin:- Cohen, RISC, Theroux et al Clopidogrel:- CURE, CREDO, CAPRIE Heparin Or LMWH:- ESSENCE, TIMI 11B, FRIC, GP2b3a inhibitors:- PRISM, EPIC PURSUIT, CAPTURE, PARAGON • Statin:- LIPID, PROVE IT TIMI 18, TNT, A to Z • ACE:- SAVE, SOLVD
- 105. Death, myocardial infarction, and major bleeds at 30 days in randomized trials of glycoprotein IIb/IIIa inhibitors (filled bars) vs. control (open bars) in a conservative strategy Authors/Task Force Members, et al. Eur Heart J 2007 28:1598-1660; doi:10.1093/eurheartj/ehm161
- 106. SHOCK Trial • Early invasive strategy was first proved beneficial in high risk MI patients by SHOCK trail than No role for Wait & Watch & Intervene Primary PCI is better than thrombolysis PAMI, DINAMI, etc – 24 RCT`s
- 107. Does same apply for USA management? Answer is:- NO 1) Plaque volume (constant) & vulnerability. 2) Type of Thrombus differs (white vs red) 3) Patent lumen
- 108. New Terminology in ACS Plaque Rupture Old term Stable Angina Unstable Angina New term Atherothrombosis Non– Q-wave MI STEMI UA/NSTEMI Daysweeks Antithrombotic Therapy Q-wave MI Minuteshours Thrombolysis Primary PCI ACS, acute coronary syndrome; MI, myocardial infarction; UA, unstable angina; NSTEMI, non–ST-segment elevation myocardial infarction; STEMI, ST-segment elevation myocardial infarction; PCI, percutaneous coronary intervention. Cannon CP. J Thromb Thrombolysis. 1995;2:205-218.
- 109. Risk Stratification Tools • Clinical Assessment • Standard ECG and Non-standard ECG leads • Markers – Other: IMA, BNP, CRP • Non-Invasive Studies – Echocardiogram – Exercise testing – Technetium-99m-sestamibi – MR angio, CT angio
- 110. Multimarker Strategy in ACS Myocyte Necrosis Troponin Inflammation hs-CRP, CD40L HbA1c Blood glucose Accelerated Atherosclerosis Morrow DA, et al. Circulation. 2003;108:250-252. Hemodynamic Stress BNP, NT-proBNP Ischaemia IMA
- 111. Short-Term Risk of Death or Nonfatal Myocardial Infarction in Patients With Unstable Angina Braunwald E et al.: Unstable angina: diagnosis and management. AHCPR Publication No 94-0602
- 112. Risk of Death or Myocardial Infarction According to Treatment Strategy and cTnI: TACTICS TIMI 18 Morrow DA et al. JAMA 2001;286:2405-12
- 113. TIMI Risk Score for UA/NSTEMI: 7 Independent Predictors – ≥3 CAD risk factors – Aged ≥65 years – Prior CAD (stenosis >50%) – Aspirin in last 7 days – >2 anginal events in ≤24 hours – ST deviation – Elevated cardiac markers (CK-MB or troponin) TIMI, thrombosis in myocardial infarction; UA, unstable angina; NSTEMI, non–ST-segment elevation myocardial infarction; CAD, coronary artery disease. Antman EM, et al. JAMA. 2000;284:835-842.
- 114. Global Registry of Acute Coronary Events (GRACE) risk score • The GRACE risk score (on a scale of 1 to 372, with higher scores indicating greater risk) is derived from readily available hospital admission variables, - including age, - heart rate, - systolic blood pressure, - creatinine level, - Killip class, - cardiac arrest at admission, - presence of ST-segment deviation, and - elevated cardiac biomarkers. Values for these variables can be entered into the GRACE risk calculator
- 115. GRACE Prediction Score Card and Nomogram for All-Cause Mortality From Discharge to 6 Months Anderson, J. L. et al. J Am Coll Cardiol 2007;50:e1-e157
- 116. Indications for early invasive strategy • Recurrent rest angina • Elevated troponin • New ST changes • LVF • Positive stress test • EF<40% • Haemodynamic instability • Malignant arrhythmias • PCI<6 months • CABG
- 118. Timing of Invasive strategy in Non ST Elevation MI
- 120. What is early and late • Early intervention is < 24 - 48 hours of presentation. • Late intervention is >36 - 48 hours of presentation
- 121. ISAR COOL • Early treatment reduces long term MI, mortality. • However procedure complications increase. • To offset it “cool off” or plaque pacifying strategy using prolonged antithrombotic & GP2b3a inhibitors.
- 122. ISAR COOL
- 124. Conclusions SYNERGY Trial • High-risk patients with NSTE ACS who received earlier coronary angiography had a decreased risk of death/MI through 30 days.
- 125. Decision-making algorithm for the management of patients with non-ST-elevation acute coronary syndrome Authors/Task Force Members, et al. Eur Heart J 2007 28:1598-1660; doi:10.1093/eurheartj/ehm161
- 126. Case of USA • • • • Mr Sheik Ahhmed 45 yrs male Chronic smoker Labourer For past 2 months not able to work due to chest pain • Somebody has to hit him in back for relief of pain • Increasing frequency & duration of pain
- 131. y
- 134. Wallen`s Warning
- 136. Care of IHD patients • Primary prevention • Secondary prevention
- 137. The Progressive Development of Cardiovascular Disease Intervene here } Risk Factors Endothelial Dysfunction Atherosclerosis CAD Myocardial Ischemia Coronary Thrombosis Myocardial Infarction Arrhythmia & Muscle Loss Remodeling Ventricular Dilation Congestive Heart Failure End stage Heart Disease
- 138. Public Awareness A survey of people with Diabetes • Findings – 68% do not consider cardiovascular disease to be complication of diabetes – 50%+ don’t feel risk for heart condition or stroke – 60% don’t feel at risk for high blood pressure or cholesterol – Awareness lowest among elderly, minorities 2
- 139. Why is CAD becoming so rampant • Is it people are living longer? • Is it increasing habits like smoking cocaine? • Is it raise in Diabetes? • Is it food we eat? • Or is it all in the genes?
- 140. With in no time !!
- 141. Where are we heading ? ? 20000 B.C. 2004 Paleolithic sup. age Neolithic age Hunting-gathering subsistence High level of physical activity Thrifty genotype 19th century 21st century Processed foods  Animal fats and glucides ¯ Dietary fibre Sedentary life Susceptibility genotype Journal of internal medicine 2003:254(2):114-25
- 142. This is how we take our dog to walk!
- 143. Secondary Prevention of CAD
- 144. Secondary prevention • The above drugs are minimum for post MI/USA patients • If diabetic then OHA`S 1 + 2 drugs • If severe LV dysfunction diuretics, digoxin • If PVD or BPH or OA or ED – extra drugs • Post stent tripple antiplatelets common • Antacids, vitamins, calcium etc
- 145. Hippocrates said …. Let your FOOD be your Medicine – Lest, Your Medicines will replace your Food !!
Editor's Notes
- Our current understanding of the unstable coronary syndromes is that they fall on a spectrum of disease and begin with a coronary plaque rupture. The degree of thrombus determines the severity of the clinical syndrome, with total occlusion in ST elevation myocardial infarction (MI) or severe (90%) stenosis in patients with non-ST elevation MI or unstable angina. In addition, it is worthwhile to note that 99% of all plaque ruptures are clinically silent. A small degree of rupture leads to a small thrombus, which heals over, but leads to progression of the plaque—like rings on a tree. This is the understanding of how atherosclerosis progresses. This emphasizes the key role that antithrombotic therapy plays in all, patients with unstable coronary syndromes, both acutely and chronically.
- ST elevation ST segment elevation usually occurs in the early stages of infarction, and may exhibit quite a dramatic change. ST elevation is often upward and concave, although it can appear convex or horizontal. These changes occur in leads facing the infarction. ST elevation is not unique to MIs and therefore is not confirming evidence. Basic requirements of ST changes for diagnosis are: elevation of at least 1 mm in two or more adjoining leads for inferior infarctions (II, III, and aVF), and at least 2 mm in two or more precordial leads for anterior infarction. You should be aware that ST elevation can be seen in leads V1 and V2 normally. However, if there is also elevation in V3 the cause is unlikely to be physiological.
- Deep Q wave The only diagnostic changes of acute myocardial infarction are changes in the QRS complexes and the development of abnormal Q waves. However, this may be a late change and so is not useful for the diagnosis of AMI in the pre-hospital situation. Remember that Q waves of more than 0.04 seconds , or 1 little square, are not generally seen in leads I, II or the precordial leads.
- T wave inversion The T wave is the most unstable feature of the ECG tracing and changes occur very frequently under normal circumstances, limiting their diagnostic value. Subtle changes in T waves are often the earliest signs of myocardial infarction. However, their value is limited for the reason above, but for approximately 20 to 30% of patients presenting with MI, a T wave abnormality is the only ECG sign. The T wave can be lengthened or heightened by coronary insufficiency. T wave inversion is a late change in the ECG and tends to appear as the ST elevation is returning to normal. As the ST segment returns towards the isoelectric line, the T wave also decreases in amplitude and eventually inverts.
- Bundle branch block Bundle branch block is the pattern produced when either the right bundle or the entire left bundle fails to conduct an impulse normally. The ventricle on the side of the failed bundle branch must be depolarised by the spread of a wave of depolarisation through ventricular muscle from the unaffected side. This is obviously a much slower process and usually the QRS duration is prolonged to at least 0.12 seconds (for right bundle branch block) and 0.14 seconds (for left bundle branch block). The ECG pattern of left bundle branch block (LBBB) resembles that of anterior infarction, but the distinction can readily be made in nearly all cases. Most importantly, in LBBB the QRS is widened to 140 ms or more. With rare exceptions there is a small narrow r wave (less than 0.04 seconds) in V1 to V3 which is not usually seen in anteroseptal infarction. There is also notching of the QRS best seen in the anterolateral leads, and the T wave goes in the opposite direction to the QRS in all the precordial leads. This combination of features is diagnostic. In the rare cases where there may be doubt assume the correct interpretation is LBBB. This will make up no difference to the administration of a thrombolytic on medical direction but for the present will be accepted as a contraindication for paramedics acting autonomously (see later slide). Right bundle branch block is characterised by QRS of 0.12 seconds or wider, an s wave in lead I, and a secondary R wave (R’) in V1. As abnormal Q waves do not occur with right bundle branch block, this remains a useful sign of infarction.
- Sequence of changes in evolving AMI The ECG changes that occur due to myocardial infarction do not all occur at the same time. There is a progression of changes correlating to the progression of infarction. Within minutes of the clinical onset of infarction, there are no changes in the QRS complexes and therefore no definitive evidence of infarction. However, there is ST elevation providing evidence of myocardial damage. The next stage is the development of a new pathological Q wave and loss of the r wave. These changes occur at variable times and so can occur within minutes or can be delayed. Development of a pathological Q wave is the only proof of infarction. As the Q wave forms the ST elevation is reduced and after 1 week the ST changes tend to revert to normal, but the reduction in R wave voltage and the abnormal Q waves usually persist. The late change is the inversion of the T wave and in a non-Q wave myocardial infarct, when there is no pathological Q wave, this T wave change may be the only sign of infarction. Months after an MI the T waves may gradually revert to normal, but the abnormal Q waves and reduced voltage R waves persist. In terms of diagnosing AMI in time to make thrombolysis a life-saving possibility, the main change to look for on the ECG is ST segment elevation.
- Location of infarction and its relation to the ECG: anterior infarction As was discussed in the previous module, the different leads look at different aspects of the heart, and so infarctions can be located by noting the changes that occur in different leads. The precordial leads (V1–6) each lie over part of the ventricular myocardium and can therefore give detailed information about this local area. aVL, I, V5 and V6 all reflect the anterolateral part of the heart and will therefore often show similar appearances to each other. II, aVF and III record the inferior part of the heart, and so will also show similar appearances to each other. Using these we can define where the changes will be seen for infarctions in different locations. Anterior infarctions usually occur due to occlusion of the left anterior descending coronary artery resulting in infarction of the anterior wall of the left ventricle and the intraventricular septum. It may result in pump failure due to loss of myocardium, ventricular septal defect, aneurysm or rupture and arrhythmias. ST elevation in I, aVL, and V2–6, with ST depression in II, III and aVF are indicative of an anterior (front) infarction. Extensive anterior infarctions show changes in V1–6 , I, and aVL.
- Location of infarction and its relation to the ECG: inferior infarction ST elevation in leads II, III and aVF, and often ST depression in I, aVL, and precordial leads are signs of an inferior (lower) infarction. Inferior infarctions may occur due to occlusion of the right circumflex coronary arteries resulting in infarction of the inferior surface of the left ventricle, although damage can be made to the right ventricle and interventricular septum. This type of infarction often results in bradycardia due to damage to the atrioventricular node.
- Location of infarction and its relation to the ECG: lateral infarction Occlusion of the left circumflex artery may cause lateral infarctions. Lateral infarctions are diagnosed by ST elevation in leads I and aVL.
- Location of infarction: combinations The previous slides discussed the changes that occur in typical anterior, inferior and lateral infarctions. However, the area infarcted is not always limited to these areas and infarctions can extend across two regions. For example, an anterior infarction which is also on the lateral side of the heart is known as an anterolateral infarction. ST segment elevation in leads I and aVL represent a lateral infarction Anteroseptal infarctions show ST segment elevation in leads V1 to V4. ST elevation in V4 to V6 is typical of an anterolateral infarction ST elevation in II, III and aVF is typical of inferior infarction.
- Diagnostic criteria for AMI Myocardial infarction is the loss of viable, electrically active myocardium. Diagnosis can therefore be made from the ECG. However, only changes in QRS complexes can provide a definite diagnosis. Changes in each of the leads must be noted, along with symptoms, as both are important in making a diagnosis. Excluding leads aVR and III, Q wave duration of more than 0.04 seconds or depth of more than 25% of the ensuing r wave are proof of infarction. Other criteria are the development of QS waves and local area low voltage r waves. Although these are useful diagnostic features, there are additional features that are associated with myocardial infarction as have been described in the previous slides. These include ST elevation in the leads facing the infarct, ST depression (reciprocal) in the opposite leads to the infarct, deep T wave inversion overlying and adjacent to the infarct, abnormally tall T waves facing the infarct, and cardiac arrhythmias. These extra features may aid in the diagnosis of myocardial infarction from an ECG.
- This study evaluated the lipid profile in young Indian patients with angiographically proven CHD. Total cholesterol was found to be elevated in 54% of patients. Interestingly an equal proportion of patients had elevated triglycerides, HDL was found to be low in 60% of patients, while Lp(a) levels were elevated in 61% of patients. Thus the atherogenic phenotype B which is believed to be characteristic of diabetic patients seems to be prevalent even among Indian patients with CHD.
- Risk factors for future cardiovascular events: WHS How well does the CRP test compare with other novel and emerging risk factors for vascular disease? This issue was directly addressed in the Women's Health Study, in this direct comparison of ten putative risk factors for vascular disease. In each case, the point estimate is based on being in the top versus bottom quartile for that particular analyte, and the horizontal bars represent the 95% confidence intervals for that effect. Starting from the top, we see that lipoprotein(a) screening was not a statistically significant predictor of risk, and below that, homocysteine screening, while statistically significant, was only of modest predictive value. This plot also indicates that the predictive value for LDL cholesterol, while highly statistically significant, sits approximately midway in terms of our overall risk prediction models. Interestingly, plasma levels of soluble intercellular adhesion molecule 1 (ICAM-1), a molecular marker associated with the adhesion and transmigration of leukocytes across the endothelial wall, as well as serum amyloid A (SAA), a nonspecific marker of inflammation, were in fact better markers of risk than was the LDL cholesterol or the total cholesterol level. Also of note from a clinical perspective, the best lipid marker was the total cholesterol:HDL cholesterol ratio. This finding is highly consistent with many prior epidemiologic studies and in fact is why many preventive practices prefer to use the ratio rather than any single lipid marker. However, the critical observation in this study was that plasma levels of hs-CRP on their own were actually the single strongest predictor for future vascular events, and those data are shown in the second line from the bottom. On its own, hs-CRP screening was associated with a 4.4-fold increase in risk for future vascular events among these otherwise healthy, middle-aged women. But again, the important issue is to consider combining the inflammatory screening with the lipid screening, and that is shown in the bottom line of data on the slide, suggesting that the combination of CRP level with total cholesterol: HDL cholesterol ratio provides the best overall risk estimate. Reference: Ridker PM, Hennekens CH, Buring JE, Rifai N. C-reactive protein and other markers of inflammation in the prediction of cardiovascular disease in women. N Engl J Med 2000;342:836-843.
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- Our current understanding of the unstable coronary syndromes is that they fall on a spectrum of disease and begin with a coronary plaque rupture. The degree of thrombus determines the severity of the clinical syndrome, with total occlusion in ST elevation myocardial infarction (MI) or severe (90%) stenosis in patients with non-ST elevation MI or unstable angina. In addition, it is worthwhile to note that 99% of all plaque ruptures are clinically silent. A small degree of rupture leads to a small thrombus, which heals over, but leads to progression of the plaque—like rings on a tree. This is the understanding of how atherosclerosis progresses. This emphasizes the key role that antithrombotic therapy plays in all, patients with unstable coronary syndromes, both acutely and chronically.
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- Antman and colleagues developed a simple risk scoring system to identify patients with various responses to treatments for unstable angina and non–ST-elevated myocardial infarction. It is characterized by its broad applicability and is easily calculated at patient presentation. The 7 Thrombolysis in Myocardial Infarction (TIMI) risk-score–predictor variables are aged >65 years, unstable angina and >3 risk factors for CAD, a prior stenosis of >50%, aspirin in the past 7 days, >2 anginal events in the prior 24 hours, ST-segment deviation on ECG at presentation, and elevated troponin. Event rates increased significantly as the TIMI risk score increased in a test cohort for TIMI IIB. The adverse event rates are significantly increased with a TIMI risk score of 4. Based on a TIMI risk score of 6, this combination of features indicates a high-risk patient.
- Atherosclerotic disease is a progressive disease as shown in this slide. Many therapeutic interventions are aimed at specific cardiovascular conditions. These interventions may be directed at alleviating symptoms or preventing progression to more serious stages or both. Angiotensin-converting enzyme (ACE) inhibitors have been studied, for example, in patients with hypertension, who are at the top of this progression pathway. These studies looked only at the effects on blood pressure, however, and did not address the long-term question of risk reduction. Other clinical trials with ACE inhibitors have been designed to investigate the effects of these agents on the morbidity and mortality following an acute myocardial infarction.