Acute Coronary Syndrome.ppt

1. Acute Coronary Syndromes Prof. Bernard C. Nkum MD FRCP FWACP School of Medical Sciences Hon. Consultant Cardiologist KATH

2. Objectives • To understand the role of inflammation in the pathogenesis of atherosclerosis • To distinguish between stable and vulnerable plaque • To become acquainted with the pathophysiology of coronary thrombus • To become familiar with the systemic and diffuse nature of atherosclerosis • To diagnose and manage ACS • To appreciate that therapy must address stabilization of vulnerable plaques in addition to revascularizing fixed stenosis

3. Coronary Circulation • Right coronary Artery (RCA) – Posterior Descending Coronary Artery (PDA) • Left Main Coronary Artery (LM ) – Left Anterior Descending Coronary Artery (LAD) – Left Circumflex Coronary Artery (LCx) Delineation (4 epicardial aa-base. septum)

4. External Heart: Anterior View Figure 18.4b

5. External Heart: Posterior View Figure 18.4d

6. Coronary Tree Anatomy-Additional Branches •As you can see by the diagram on the right, there are multiple branches that we have not discussed in detail. •Most of these derive from the left coronaries. •Two important ones to mention are: •Diagonal Arteries (Diag) •Derive off the LAD •Obtuse Marginal (OM1, OM2) •Derive off the Circumflex

7. Circulation cont’d Collateral Circulation • In obstruction dilate providing an avenue for significant blood flow beyond the stenoses • Most numerous – Vent septum (between septal perforators of the LAD and PDA) – Vent apex (between LAD septal perforators) – Ant R vent free wall (between LAD and RCA( • The most common sites for plaques are the proximal one-half of the LAD and the LCx and the origin and entire length of the RCA

8. Physiology of the Coronary Circulation • Heart requires continuous O2 supply • Never stops beating • Myocardial O2 consumption (MVO2) is 8-15 ml/min/100g. Skeletal muscle resting MVO2 is 0.3ml/min/100g • Major determinants are related to contraction: heart rate, wall stress (chamber pressure x chamber vol / myocardial wall thickness), and contractility

9. Coronary Vascular Bed

12. Coronary Blood Flow Regulation: Unique Features • Energy is supplied by aerobic metabolism- continuous source of O2 required • O2 extraction cannot be increased appreciably. Extra need supplied by augmenting blood flow • Autoregulation in resistance arterioles less effective in subendocardium than subepicardium • NO pathway for vasodilatation impaired in CAD • Sympathetic activation leads to vasoconstriction and parasympathetic to vasodilatation

13. Normal Arterial Wall Lumen Media: Smooth muscle cell Matrix proteins Internal elastic membrane Endothelium Intima: External elastic membrane

14. Pathogenesis of Atherosclerotic Plaques Protective response results in production of cellular adhesion molecules Monocytes and T lymphocytes attach to ‘sticky’ surface of endothelial cells Migrate through arterial wall to subendothelial space Lipid-rich foam cells Endothelial damage Macrophages take up oxidised LDL-C Fatty streak and plaque

15. Endothelium • Normal endothelium regulates many processes that are key for the maintenance of vascular structure and function, including vascular tone, growth, haemostasis, inflammation, and redox state. Endothelial dysfunction is involved in the vasomotor dysfuction of coronary arteries. • Excessive production of oxygen free radicals and subsequent metabolism of NO results in oxidative stress. • Overproduction of oxygen free radicals counteracts the effects of NO and stimulates the expression of adhesion molecules, which facilitates the attachment of leukocytes to the vascular endothelium. This process results in acute inflammation, proliferation of smooth muscle cells, and synthesis of extracellular matrix molecules, all of which contribute to the development of CVD

16. ‘activated’ endothelium CELLULAR ADHESION MOLECULES induces cell proliferation and a prothrombic state attracts monocytes and T lymphocytes which adhere to endothelial cells cytokines (eg. IL-1, TNF-) chemokines (eg.MCP-1, IL-8) growth factors (eg. PDGF, FGF) Koenig W. Eur Heart J Suppl 1999;1(Suppl T);T19-26. The ‘Activated’ Endothelium

17. Upregulation of endothelial adhesion molecules Increased endothelial permeability Migration of leucocytes into the artery wall Leucocyte adhesion Lipoprotein infiltration Endothelial Dysfunction in Atherosclerosis

18. Types of Atherosclerotic Plaque • Fatty streak • Fibrous plaque • Complex (Complicated) plaque • Ulcerative lesions • Intraplaque haemorrhage

19. Formation of foam cells Adherence and entry of leucocytes Activation of T cells Migration of smooth muscle cells Adherence and aggregation of platelets Fatty Streak Formation in Atherosclerosis

20. Formation of the fibrous cap Accumulation of macrophages Formation of necrotic core Formation of the Complicated Atherosclerotic Plaque

21. Libby P. Circulation 1995;91:2844-2850. The Synthesis and Breakdown of Atheromatous Plaques

22. The Pathophysiology Of Atherosclerosis • Arterial wall structure – Elastic vs. muscular arteries – Histologic layers: Endothelium/ Intima /Media /Adventitia Cells: Platelets (adhesion, activation, aggregation /Macrophages /SMCs Regulatory substances of mitogenic and other functions: CRP induces expression of adhesion molecules (VCAM-1); monocyte chemoattractant protein-1, macrophage colony stimulating factor (M- CSF) Atherosclerotic plaque: Fatty streak /Fibrous plaque /Fibrous cap or layered

25. Antiplatelet Mechanisms

29. Risk Factors Associated with Impaired Endothelium Dependent Vasodilatation • Dyslipidaemia • Hypertension • Diabetes Mellitus • Cigarette Smoking • Aging • Menopause • Family History of premature CAD/1st degree rel • Risk factors cause endothelial damage and do so rapidly

30. Less Reliable but Probable Risk Factors • Physical inactivity • Excess alcohol ingestion • Insufficient fruits and vegetables in the diet • Emotional stress • Elevated cardiac CT scan calcium scores • Positron emission tomography (PET) scanning

31. Atherogenic Influence of Risk Factors Biology Dyslipi HBP Smoke FHx DM End inj + + + - + Monoc ++ - - ++ ++ Platelet + - ++ - ++ SMC + + - ++ ++ Plaque ++ + - ++ - Throm + - ++ + ++ Micova + ++ + - ++

32. The Progression from CV Risk Factors to Endothelial Injury and Clinical Events Risk factors Oxidative stress Endothelial dysfunction NO Local mediators Tissue ACE-Ang II PAI-1 VCAM ICAM cytokines Endothelium Growth factors matrix Proteolysis LDL-C BP Heart failure Smoking Diabetes Vasoconstriction Vascular lesion and remodelling Plaque rupture Inflammation Thrombosis Clinical endpoints NO Nitric oxide Gibbons GH, Dzau VJ. N Engl J Med 1994;330;1431-1438.

33. Unified Hypothesis for the Pathogenesis of Atherosclerosis • Plaques occur in the intima • Acceleration by dyslipideamia. Lipid lowering improve by anti-inflammation • Mediation through macrophages and smooth muscle cells • The functional state of the atheroma, not merely its size or the luminal degree of encroachment, determines ACS development

34. • An inflammatory component in the subendothelial area further weakens and predisposes the plaque to rupture. Speed of blood flow, turbulence and vessel anatomy may be contributory factors.

36. Fibrous Cap Fissuring

41. Vulnerable Patient Unstable coronary atheromata are often not the “tight” stenoses • Lipid profile • Active inflammation in coronary arteries • LVEF • LV hypertrophy • Long QT, wide QRS, NSVT • Serologic markers of vulnerability

42. Libby P. Circulation 1995;91:2844-2850. The Vulnerable Atherosclerotic Plaque SMC – smooth muscle cell HDL-DR – transplantation antigen indicating ‘activation’ of SMCs

43. Vulnerable plaque • Warm plaque • Thin cap surface • Acidic plaque • Soft plaque • Adventitious inflammation • Adjacent lipid pool

44. Pathophysiology cont’d • Mechanism -plaque fissuring or rupture/thrombus formation Presentation depends on: -rapidity of vessel occlusion -extent of occlusion -recruitment of distal collaterals by infarct-related artery -transient occlusion with recurrent cycles of thromboses and spontaneous lyses that may allow time for conditioning and the dpt of collaterals

45. Imaging Techniques Used to Assess Atherosclerosis • Invasive techniques – Intravascular ultrasound (IVUS) – Coronary angiography • Non-invasive techniques – Magnetic resonance imaging (MRI) – Computed tomography (CT) – Ultrasound (B-mode)

46. Intravascular Ultrasound (IVUS) Showing Atheromatous Plaque Reproduced from Circulation 2001;103:604–616, with permission from Lippincott Williams & Wilkins. Angiogram IVUS atheroma normal vessel

47. Computed Tomography (CT) Showing Atherosclerotic Artery

48. Spectrum of ACS • UA • NSTEMI • STEMI • Non-Q wave MI • Q wave MI • Sudden cardiac death

53. WHO Criteria for Acute MI • STEMI – Chest pain or classic symptoms ≥30min – ST ↑of .1mV in 2 contiguous leads or new LBBB – ↑Cardiac enzyme levels • NSTEMI – Chest pain or classic symptoms ≥30min – ST ↓ or T inv – ↑Cardiac enzyme levels

54. Angina • Angina is likely to occur under the ff circumstances: – Brisk walking outdoors on a cold windy day – Exertion after a heavy meal – Working under the pressure of a deadline – Speaking in public – During sexual activity – During worry, tension or anger

55. Triggers of ACS • Physical exertion • Anger • Sexual activity • Cocaine use • Bereavement

65. Definitions • Angina: Discomfort in the chest with or without radiation to the arms, neck or back which is caused by myocardial ischemia and can se associated with a disturbance of myocardial function but not with necrosis • Ischemia: Recurrent chest discomfort considered to be probable or definite angina that is at least 10min in duration

66. Unstable Angina • Sudden acceleration in the severity of previously stable angina, rest angina or post-MI angina • Pathologically characterized by incomplete or transient coronary artery occlusion • Initial thrombus platelet-derived with vaso- constrictive response

67. UA Definition • Angina pectoris or equivalent ischaemic discomfort with at least one of 3 features – It occurs at rest or with minimal exertion usually lasting >10 min – It is severe and of new onset (i.e. within the prior 4-6wk) – It occurs with a crescendo pattern ( i.e. distinctly more severe, prolonged, or frequent than previously

68. STEMI vs. NSTEMI • Myocardial damage /in-hospital prognosis • Fibrin- (red) vs. platelet (grey) -rich thrombus • Benefit from thrombolysis • Angiographic occlusion by thrombus • Single vessel CAD and plaque < 50% vs. more extensive CAD and more developed collaterals

70. Diagnosis of UA/NSTEMI • Spectrum of ACS • ECG changes (12 lead ECG every 8h X3) • Cardiac Biomarkers (CK, CK-MB, Troponin I)

71. Protein Molecular mass (kD) First detection Duration of detection Sensiti vity Specifi city Myoglobin 16 1.5–2 h 8–12 h +++ + CK-MB 83 2–3 h 1–2 d +++ +++ Troponin I 33 3–4 h 7–10 d ++++ ++++ Troponin T 38 3–4 h 7–14 d ++++ ++++ CK 96 4–6 h 2–3 d ++ ++ Biochemical Markers

72. Gheorghiade, Am J Cardiol 2005;96(suppl):18G-25G

73. Cardiac Biomarkers • Positive Cardiac Markers – cTnI>0.1, CK-MB>5, CK> 266 – CK, CK-MB every 8h x3d – cTnI X1 (at least 3h after the onset of chest discomfort) • CTnI – cTnI begins to increase 3h after ischaemia, peaks at 14-18h and remains elevated for 5-7days – cTnI levels 1.0-1.6: About 1/3 of patients previously diagnosed as unstable angina because of normal CK- MB levels actually have elevated cTnI levels and therefore are experiencing a micro MI

74. Immediate Assessment < 30min • Measure vitals/BP • Measure O2 saturation • Obtain IV access • Obtain 12 lead ECG • Perform brief targeted history and PE • Obtain initial serum cardiac marker levels • Evaluate initial electrolyte and coagulation studies • Request, review portable CXR

75. Immediate General Treatment • O2 • Aspirin 300mg • Nitroglycerin (0.4mg SL or spray) • Morphine (if pain not relieved by NTG) (Memory MONA) Bed rest

76. Nursing • Telemetry Monitoring – HR every 2h and rhythm every 4h or as patient condition warrants • O2 – O2 sat every 4h. Delivery via nasal prongs for 2-3h. Continue if low arterial sat (<90%) • Activity level – Bedrest with commode privileges for 12 h – If haemodynamically stable progress activity as tolerated with ambulation to the bathroom, bathing, and light ambulation – A patient with an uncomplicated Mi is likely to return to prior activities within 2 weeks • Exercise test – Before discharge from hospital or shortly thereafter – Submaximal at 4-7days – Symptom limited at 10-14days • X

81. Assess Initial ECG • ST segment elevation or new LBBB 1mm in 2 or more anatomically contiguous leads (0.04s after the J point, TP baseline) • ST depression or T wave inversion • Non-diagnostic or normal ECG

82. Risk Stratification in UA/NSTEMI • ECG Troponin /TIMI Risk Score / Multimarker approach (CRP, BNP) • High risk – Persistent symptoms – Recurrent ischemia – Depressed LV function – Widespread ECG changes – Prior AMI, PCI, CABG

83. UA/NSTEMI Adjunctive Rx Anti- Ischemic Rx • Nitrates • Beta blockers • ACEI • Calcium channel blockers 2nd line • Angiography – High risk – Low EF, prior PCI or CABG

85. UA/NSTEMI Adjunctive Rx (Antiplatelet/Anticoagulant) • Aspirin 300mg daily • LMWH > UFH • GP IIb/IIIa inhibitors (Check package insertion) – Inhibit the integrin glcoprotien receptor in the membrane of the platelets inhibiting platelet aggregation – Epitifibitide: 180µ/kg IV bolus then 2µ/kg/min IV infusion – Tirofiban: 0.4µ/kg/min IV for 30min, then 0.1µ/kg/min IV infusion • Clopidogrel

86. UA/NSTEMI Long-term Rx • ASA • Beta blockers • Clopidogrel < 1 year • Lipid lowering (LDL <70) • ACEI (if low EF, DM, HBP) – No benefit if CAD alone NTG prn

87. Structure of Lipoproteins Free cholesterol Phospholipid Triglyceride Cholesteryl ester Apolipoprotein

88. Types of Lipoprotein Particles • Triglyceride-rich lipoproteins – Chylomicrons – Very low-density lipoprotein (VLDL) • Cholesterol-rich lipoproteins – Low-density lipoprotein (LDL) – High-density lipoprotein (HDL)

89. Lipid Abnormalities Associated with Endothelial Dysfunction • Ox-LDL • Small dense LDL • HDL • Remnant Particles • Lp(a) • LDL

90. Additional Emerging Lipid Parameters • Apolipoprotein (Apo) B • Apo C-III • Nonfasting triglyceridews • Remnants of triglyceride-rich lipoproteins containing Apo-III • X

91. LDL cholesterol • Strongly associated with atherosclerosis and CVD events • 10% increase results in an approximate 20% increase in CHD risk • Most of the cholesterol in plasma is found in LDL particles • Smaller denser LDL are more atherogenic than larger, less dense particles • Risk associated with LDL-C is increased by other risk factors: – low HDL-C – smoking – hypertension – diabetes and the metabolic syndrome

92. HDL cholesterol • HDL-C has a protective effect for risk of atherosclerosis and CHD • Epidemiological studies show the lower the HDL-C level, the higher the risk for atherosclerosis and CHD – low level (<40 mg/dL, 1 mmol/L) increases risk • HDL-C tends to be low when triglycerides are high • HDL-C is lowered by smoking, obesity and physical inactivity

93. Triglycerides • May be associated with increased risk of CHD events • Link with increased CHD risk is complex – may be direct effect of smaller TG-rich lipoproteins and/or – may be related to: • low HDL levels • highly atherogenic forms of LDL-C • hyperinsulinaemia/insulin resistance • procoagulation state • hypertension • abdominal obesity

94. 0 1 2 3 4 5 1 2 3 4 5 LDL-C CRP CRP (mg/L) (0.49) (>0.049-1.08) (>1.08-2.09) (>2.09-4.19 ) (>4.19) LDL-C (mg/dL) (97.6) (>97.6-115.4) (>115.4 –132.2) (>132.2 –153.9) (>153.9) Quintiles Ridker PM. New Engl J Med 2002;347:1557-1565. CRP is a Strong Predictor for Future CV Events: Women’s Health Study

96. Lipid Lowering Medications Range of Lipid Effects (% Change) TG HDL-C LDL-C Fibric 35-50 10-25 10-15 Bile acid - - 15-30 Nicotinic acid 25-30 10-30 10-25 Statins 20-30 5-10 20-45

98. Effect of Lipid-modifying Therapies on Lipids Therapy Bile acid sequestrants Nicotinic acid Fibrates Probucol Statins* Ezetimibe TC–total cholesterol, LDL–low density lipoprotein, HDL–high density lipoprotein, TG–triglyceride. *Daily dose of 40 mg of atorvastatin, simvastatin, pravastatin and fluvastatin. TC Down 20% Down 25% Down 15% Down 25% Down 19–37% - LDL Down 15–30% Down 25% Down 5–15% Down 10–15% Down 25–50% Down 18% HDL Up 3–5% Up 15–30% Up 20% Down 20–30% Up 4–12% Up 1% TG Neutral or up Down 20–50% Down 20–50% Neutral Down 14-29% Down 8% Patient tolerability Poor Poor to reasonable Good Reasonable Good Good Yeshurun D, Gotto AM. Southern Med J 1995;88(4):379–391. Knopp RH. N Engl J Med 1999;341:498– 511. Product Prescribing Information. Gupta EK, Ito MK. Heart Dis 2002;4:399-409.

99. Dyslipidaemia Update • Linear relationship between chol levels and CV events. Inverse for HDL • Lowering LDL with statins decreased CV events • Exetimibe (chol absorption inhibitor can be used with statins • Statins: Most potent for reducing LDL and most tolerated. Night • Fibric acid derivatives: Stimulate lipoprotein lipase which results in enhanced TG clearance – Gemfibrozil (mixed: TG, LDL) – Fenofibrate: (TG) • Atorvastatin 80mg (LDL not effective for HDL or TG); Pravastatin, Rosuvastatin, Simvastatin • Nicotinic acid: cheap; most potent for HDL; Aspirin for flushing, IGT, myopathy in combo with statin • Bile acid sequestrants: Cholestyramine: Reduce total chol and LDL. by binding positively charged bile acids in the gut to interrupt enterohepatic circulation

100. NCEP ATP III Guidelines * TLC: therapeutic lifestyle changes Adapted from NCEP, Adult Treatment Panel III. JAMA 2001;285:2486-2497. Patients with Drug therapy considered if LDL-C Initiate TLC* if LDL-C LDL-C treatment goal 0-1 risk factors 160 mg/dL† 190 mg/dL (160-189 mg/dL: drug optional) <160 mg/dL† 2 risk factors (10-year risk 20%) 130 mg/dL† 10-yr risk 10-20%: 130 mg/dL 10-yr risk <10%:  160 mg/dL <130 mg/dL† CHD and CHD risk equivalents (10-year risk >20%) 100 mg/dL† 130 mg/dL (100-129 mg/dL: drug optional) <100 mg/dL† † 100 mg/dL = 2.6 mmol/L; 130 mg/dL = 3.4 mmol/L; 160 mg/dL = 4.1 mmol/L; 190 mg/dL = 5 mmol/L

101. NCEP ATP III: LDL-C Goals Adapted from NCEP, Adult Treatment Panel III, 2001. JAMA 2001:285;2486-2497. CHD or CHD risk equivalents < 2 risk factors ≥ 2 risk factors LDL-C level 100 - 160 - 130 - 190 - goal 100 mg/dL goal 130 mg/dL goal 160 mg/dL 100 mg/dL = 2.6 mmol/L; 130 mg/dL = 3.4 mmol/L; 160 mg/dL = 4.1 mmol/L

102. NCEP ATP III: LDL-C Goals (2004 proposed modifications) *Therapeutic option 70 mg/dL =1.8 mmol/L; 100 mg/dL = 2.6 mmol/L; 130 mg/dL = 3.4 mmol/L; 160 mg/dL = 4.1 mmol/L High Risk CHD or CHD risk equivalents (10-yr risk >20%) LDL-C level 100 - 160 - 130 - 190 - Lower Risk < 2 risk factors Moderately High Risk ≥ 2 risk factors (10-yr risk 10-20%) goal 160 mg/dL goal 130 mg/dL 70 - goal 100 mg/dL or optional 70 mg/dL* Moderate Risk ≥ 2 risk factors (10-yr risk <10%) goal 130 mg/dL or optional 100 mg/dL* Grundy SM et al. Circulation 2004;110:227-239. Existing LDL-C goals Proposed LDL-C goals

103. Effect of Lipid-modifying Therapies on Lipids Therapy Bile acid sequestrants Nicotinic acid Fibrates Probucol Statins* Ezetimibe TC–total cholesterol, LDL–low density lipoprotein, HDL–high density lipoprotein, TG–triglyceride. *Daily dose of 40 mg of atorvastatin, simvastatin, pravastatin and fluvastatin. TC Down 20% Down 25% Down 15% Down 25% Down 19–37% - LDL Down 15–30% Down 25% Down 5–15% Down 10–15% Down 25–50% Down 18% HDL Up 3–5% Up 15–30% Up 20% Down 20–30% Up 4–12% Up 1% TG Neutral or up Down 20–50% Down 20–50% Neutral Down 14-29% Down 8% Patient tolerability Poor Poor to reasonable Good Reasonable Good Good Yeshurun D, Gotto AM. Southern Med J 1995;88(4):379–391. Knopp RH. N Engl J Med 1999;341:498– 511. Product Prescribing Information. Gupta EK, Ito MK. Heart Dis 2002;4:399-409.

104. Effects of Statins on Lipids Statin rosuvastatin (10 mg) atorvastatin (10 mg) simvastatin (20 mg) pravastatin (20 mg) fluvastatin (20 mg) LDL-C % change -52 -39 -33 -32 -22 HDL-C % change TG % change +14 +6 +8 +2 +3 -10 -19 -19 -11 -12 US Product Data Sheets.

105. 2013 ACC/AHA Guidelines • Shift from focusing on LDL-c as primary target for cholesterol lowering therapy to the appropriate intensity of statin therapy to reduce ASCVD risk in those most likely to benefit • 4 statin benefit groups identified • High/Moderate/Low Intensity6 statin therapy

106. Groups • Clinical ASCVD – Age < 75yr - high intensity – Age >75yr - moderate • Primary prevention – >21yr LDL-c <190mg/dl – high – Ages 40-75 with DM, LDL-c 70-189mg/dl, without clinical ASCVD • Estimated 10yr ASCVD risk <7.5% - Moderate • Estimated 10yr ASCVD risk >7.5% - High

107. Groups cont,d • Primary prevention – Ages 40-75 without clinical diabetes or clinical ASCVD. Estimated 10yr ASCVD risk greater than or equal to 7.5% LDL-c 70-189 – mod to high intensity

108. Intensity of Statin Rx • High – Atorvastatin (40) – 80mg – Rosuvastatin 20 – (40)mg • Moderate – Atorvastatin 10- (20) – Rosuvastatin 5-(10) – Simvastatin 20 - 40 – Fluvastatin 40mg bd (XL 80mg) • Low –Simv, Fluva and Prava

109. STEMI Adjunctive Rx • IV Beta blocker • IV NTG • IV Heparin (start immediately and continue for 48h if tPA is used) • ACEI (after 6h or when stable)

110. Indications for Fibrinolysis • ST elevation (≥1mm in ≥2 contiguous leads) or new or presumably new LBBB strongly suspicious of injury (BBB obscuring ST analysis). • In context of signs and symptoms of MI • Time from onset of symptoms <12 hours

111. Specific Exclusion Criteria • Acute internal bleeding (except menses) within 21 days • Hx of CV, intracranial or intraspinal event within 3/12 (CVA, AV mal, neoplasm, aneurysm,recent trauma, recent surgery) • Major surgery or serious trauma within 14 days • Aortic dissection • Severe uncontrolled HTN • Known bleeding disorders • Prolonged CPR with evidence of thoracic trauma • Lumbar puncture within 7 days • Recent arterial puncture at non-compressible site • During the first 24 h of fibrinolytic therapy for acute ischaemic CVA do not administer aspirin or heparin

112. STEMI Fibrinolytic Rx • tPA (3-hour infusion) – Give 10mg IV bolus – Then 50mg in the first hour – Then 20mg/h for 2 additional hours • For AMI the total dose should not exceed 100mg; for acute CVA not exceed .90mg

113. STEMI Fibrinolytic Rx • tPA (Accelerated infusion 1.5hours( – 15mg IV bolus – Then 0.75mg/kg over the next 30min (not to exceed 50mg) – Then 0.5mg/kg over the next 60 min (not to exceed 35mg) • Streptokinase – 1.5 million IU in a 1h infusion

114. STEMI Reperfusion • Angiography • PCI (Angioplasty + stent) • Rates of restenosis within 6/12 of PCI – No stenting 30-40% – Bare met5al stent 15-30% – Drug-eluting stent <10% • CABG

115. Arrhythmias During Acute STEMI Electrical Instability • VPCs: K+, Mg2+, Beta blocker • VT: Antiarrhythmics, DC shock • AIVR: Observe unless heamodynamic compromise • NJPT: Search for cause (e.g. Dig toxicity) • It is sound clinical practice to maintain serum K+ > 4mmol/l and Mg2+ > 2mmol/l

116. Arrhythmias During Acute STEMI: AV Conduction Disturbances Proximal Distal Site of Block Intranodal Infranodal Site of Infarction Inferoposterior Anteroseptal Infarct Artery RCA (90%) LAD (septals) ECG Pattern 1O AV block Mobitz 1 IVCD Mobitz 2

117. Arrhythmias During Acute AV Conduction Disturbance Proximal Distal Escape rhythm His bundle <120 ms 45-60 Distal to His >120 ms Often < 30 Duration of AVB 2-3 days Transient Mortality Low High (HF, VT) Rx Observe PM / ICD

118. Mechanical Complications In STEMI • Ventricular septal rupture • Ventricular free wall rupture • Mitral regurgitation – Chordal /papillary muscle rupture

120. • Thank You For Your Attention

Acute Coronary Syndrome.ppt

Acute Coronary Syndrome.ppt

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