Therapy of Coronary Heart Disease - Current Standpoint. Conservative Medical Therapy vs. PTCA/ STENT and CABG (Bypass Surgery)

01.07.2010

Englisch

9783837412314

UNI-MED

UNI-MED Science

Nein

Dietrich Strödter

320

1

Gebundene Ausgabe

1. From Primary to Secondary Prevention 16 1.1. Definition 16 1.2. Risk factors for atherosclerosis 17 1.3. Aims of secondary prevention 17 1.4. Primary versus secondary prevention 18 1.5. Blood pressure/HbA1c goals 19 1.6. HbA1c target in diabetics 21 1.7. Lipids 21 1.8. Non-pharmacological therapeutic measures 22 1.9. Summary 23 1.10. References 23 2. Manifestations and Prognosis of CAD 25 2.1. Manifestations of atherosclerosis 25 2.2. Manifestations of CAD 25 2.3. Prognosis in CAD 26 2.4. Prognosis and gender 27 2.5. Prognosis in renal insufficiency 28 2.6. Prognosis and diabetes 28 2.7. Prognosis and type of medical care 29 2.8. Prognosis in STEMI versus NSTEMI 29 2.9. Decrease in CAD mortality? 29 2.10. Summary 30 2.11. References 31 3. From the Endothelial Defect to Myocardial Infarction 32 3.1. The importance of the endothelium 32 3.2. The acetylcholine test as a method to demonstrate endothelial dysfunction 33 3.3. Clinical impact of endothelial dysfunction during stress 33 3.4. Endothelial dysfunction as a prognostic indicator 34 3.5. Endothelial progenitor cells 34 3.6. Atherosclerosis in the coronary region 35 3.7. From atherothrombosis to the acute syndrome 37 3.8. Remodelling of the left ventricle after myocardial infarction 38 3.9. Summary 38 3.10. References 39 4. Pathophysiology of CAD and Strategies for Secondary Prevention 41 4.1. Coronary insufficiency 41 4.2. Determinants of the myocardial O2 requirement 42 4.3. Strategies for secondary prevention 42 4.4. Therapeutic priorities depending on the form of presentation of CHD 43 4.5. Summary 44 4.6. References 44 5. Nitrates and Other Antianginal Agents 46 5.1. Mechanism of action of nitrates 46 5.2. Nitrate drugs 46 5.3. Do nitrates prolong survival in CAD? 47 5.4. Nitrates in secondary prevention 48 5.5. Molsidomine 48 5.6. Trapidil 48 5.7. Potassium channel openers (nicorandil) 49 5.8. Ranolazine 49 5.9. Summary 50 5.10. References 51 6. Beta-Blockers 53 6.1. Mechanism of action of beta-blockers 53 6.2. Classification of beta-blockers 53 6.3. Differences between beta-blockers 53 6.4. Treatment aims on beta-blockers 54 6.5. Beta-blockers in post-infarct patients 54 6.6. Who benefits most? 55 6.7. Do all beta-blockers have a secondary prevention effect? 57 6.8. Can beta-blockers be used for secondary prevention in CAD without infarction? 57 6.9. Beta-blockers in heart failure 57 6.10. Third-generation beta-blockers 58 6.11. Beta-blockers in LV dysfunction after infarction, the CAPRICORN study 58 6.12. 2007 AHA/ACC Guidelines 59 6.13. The 2008 ESC guidelines 59 6.14. Summary 59 6.15. References 60 7. Calcium Antagonists 62 7.1. Mechanism of action of calcium antagonists 62 7.2. Differences between the calcium antagonists 62 7.3. Calcium antagonists in stable angina 62 7.4. Dihydropyridines in postinfarct patients 63 7.5. Diltiazem in postinfarct patients 63 7.6. Verapamil in postinfarct patients 64 7.7. Hypertensive versus normotensive postinfarct patients 65 7.8. Third-generation calcium antagonists in CAD 65 7.9. Summary 67 7.10. References 68 8. ACE Inhibitors 70 8.1. Mechanism of action 70 8.2. Pathophysiological basis of ACE inhibitor treatment 70 8.3. ACE inhibitors and aspirin 72 8.4. Postinfarction studies with ACE inhibitors 73 8.5. ACE inhibitors and risk of atrial fibrillation 76 8.6. The HOPE study 76 8.7. ACE inhibitors and rate of infarction 78 8.8. ACE inhibitors in association with and after PTCA – the QUIET study 78 8.9. ACE inhibitors in association with and after CABG – the QUO VADIS study 79 8.10. ACE inhibitors in CAD patients with a lower risk 79 8.11. 2006/2007 ACC/AHA guidelines 81 8.12. Summary 82 8.13. References 82 9. AT1 Receptor Blockers 85 9.1. The mechanism of action 85 9.2. AT1 receptor blockers and pleiotropic effects 85 9.3. Clinical studies in CAD 86 9.4. Combination of ACE inhibitor plus AT1 receptor blocker 89 9.5. 2006/2007 ACC/AHA- and 2008 ESC-guidelines 89 9.6. Summary 89 9.7. References 90 10. Statins (HMG-CoA Reductase Inhibitors) 91 10.1. Situation before the statin era 91 10.2. Mechanism of action of the statins 91 10.3. A comparison of statins 91 10.4. Statins and dose-effect relationship 93 10.5. Statins in secondary prevention – the evidence from studies 93 10.6. The time for using an HMG-CoA reductase inhibitor during and after acute coronary syndrome 98 10.7. Statins and number of revascularisations 98 10.8. ACE inhibitors after CABG and PTCA 99 10.9. HMG-CoA reductase inhibitors in PTCA 100 10.10. Who benefits from LDL lowering? Younger or older patients? 101 10.11. Additional vascular effects of HMG-CoA reductase inhibitors 102 10.12. LDL lowering and cardiac risk – the greater the LDL reduction, the better 107 10.13. LDL treatment targets today 110 10.14. Statins in high-risk patients 112 10.15. Fibrates in secondary prevention 113 10.16. 2006/2007 ACC/AHA guidelines 114 10.17. Summary 115 10.18. References 115 11. Antiplatelet Agents 119 11.1. Antiplatelet agents – an overview 119 11.2. Mechanism of action of antiplatelet agents 119 11.3. Molecular target of the thienopyridines 120 11.4. Prasugrel versus clopidogrel 120 11.5. Clopidogrel and interaction with PPIs 121 11.6. Rebound phenomena and resistance 122 11.7. Ticagrelor and cangrelor 123 11.8. Glycoprotein IIb/IIIa Receptor Inhibitors 123 11.9. Aspirin (acetylsalicylic acid, ASS) 123 11.10. Aspirin plus low-dose coumarins 125 11.11. Clopidogrel 126 11.12. Clopidogrel plus aspirin 127 11.13. Oral glycoprotein IIb/IIIa receptor inhibitors 131 11.14. Current guidelines 131 11.15. Summary 133 11.16. References 133 12. Anticoagulants 137 12.1. The Sixty Plus study in the elderly 137 12.2. The WARIS-1 study 137 12.3. The ASPECT-1 study 137 12.4. The ASPECT-2 study 138 12.5. The WARIS-2 study 138 12.6. The APRICOT-2 study 138 12.7. Indications for coumarins today 138 12.8. Antithrombotic treatment in atrial fibrillation 139 12.9. Dabigatran in atrial fibrillation – the RE-LY study 141 12.10. Summary 142 12.11. References 142 13. Antihypertensive Agents 144 13.1. Hypertension and risk in CAD 144 13.2. The HOPE study 144 13.3. Subgroup analysis of the CAD patients in the HOT study 144 13.4. Isolated systolic hypertension (ISH) 145 13.5. The RENAAL study and IDNT study 145 13.6. The INVEST study 145 13.7. The VALUE study 146 13.8. Blood pressure versus change in plaque size 146 13.9. Which combination therapy – the ACCOMPLISH study 147 13.10. Target blood pressure values in CAD 148 13.11. Calcium antagonists plus ACE inhibitors in chronic stable CAD 148 13.12. Summary 149 13.13. References 149 14. Omega-3 Fatty Acids 150 14.1. The GISSI Prevention study 150 14.2. Recommendations of the ESC, AHA, NICE 151 14.3. The OMEGA study 152 14.4. Summary 152 14.5. References 152 15. Ivabradine, the If Channel Blocker 154 15.1. The BEAUTIfUL study 154 15.2. Summary 155 15.3. References 155 16. Unstable Angina Pectoris/Non-Q-Wave Infarction (NSTEMI) 157 16.1. Definition 157 16.2. The prognosis in unstable angina/non-Q-wave infarction 157 16.3. Aims of treatment 158 16.4. Nitrates in unstable angina/non-Q-wave infarction 158 16.5. Beta-blockers 158 16.6. Calcium antagonists 159 16.7. Aspirin 159 16.8. Heparin in unstable angina/NSTEMI 159 16.9. Pentasaccharides 161 16.10. Bivalirudin 161 16.11. GP IIb/IIIa receptor inhibitors in unstable angina 161 16.12. Clopidogrel plus aspirin in unstable angina/non-Q-wave infarction 163 16.13. Prasugrel versus clopidogrel 167 16.14. Statins in acute coronary syndrome 172 16.15. Invasive versus non-invasive approach in unstable angina/NSTEMI 174 16.16. The importance of GP IIb/IIIa receptor inhibitors in PCI 177 16.17. The combination of GP IIb/IIIa inhibitors, aspirin, heparin, clopidogrel 178 16.18. Improvement in prognosis in NSTE-ACS 178 16.19. Approach in unstable angina/NSTEMI (2007/2009 ESC and ACC/AHA guidelines) 178 16.20. Algorithm in the case of ACS – 2007 ESC guidelines 182 16.21. The GRACE risk score 182 16.22. Ticagrelor in ACS 182 16.23. Summary 184 16.24. References 186 17. The Treatment of Acute Myocardial Infarction (STEMI) 190 17.1. The effect of thrombolysis 190 17.2. Aspirin 193 17.3. Clopidogrel 195 17.4. Prasugrel vs clopidogrel in STEMI – the TRITON-TIMI 38 study 196 17.5. Anticoagulation 197 17.6. Nitrates 198 17.7. Beta-blockers 200 17.8. ACE inhibitors/AT1 receptor blockers 201 17.9. AT1 receptor blockers 203 17.10. Calcium antagonists 203 17.11. Antiarrhythmics (lidocaine prophylaxis) 203 17.12. PTCA in acute infarction (STEMI) 203 17.13. Lysis versus transport to a PCI centre 204 17.14. PTCA versus PTCA plus stent 205 17.15. PTCA plus stent plus GP IIb/IIIa inhibitor 205 17.16. Rescue PCI/facilitated PCI 206 17.17. National differences in the hospitalisation time 207 17.18. The prognosis in STEMI 207 17.19. The new classification of infarction 207 17.20. 2009 and 2008 guidelines of the ACC/AHA and ESC 207 17.21. DES versus BMS in STEMI – the HORIZONS-AMI study 209 17.22. Summary 209 17.23. References 211 18. Elective Revascularisation Procedures in CAD 216 18.1. Bypass surgery 216 18.2. PTCA 218 18.3. Stents 219 18.4. PTCA versus CABG 222 18.5. PTCA versus atherectomy 223 18.6. Transmyocardial laser revascularisation 224 18.7. Beta-blockers before CABG 225 18.8. Coronary angiography versus fractional flow reserve as a parameter for indicating PCI – the FAME study 225 18.9. Surgical ventricle reconstruction – the STICH study 225 18.10. Adherence to guidelines for PCI and CABG 226 18.11. Measures in refractory angina 226 18.12. CABG versus minimally invasive surgery 227 18.13. Summary 227 18.14. References 228 19. Conservative Therapy Versus Interventional/Surgical Therapy 232 19.1. Current secondary prevention and targets 232 19.2. Additive effects with four secondary prevention agents? 232 19.3. Individual conservative measures in chronic stable CAD versus PCI 235 19.4. Optimised secondary prevention versus PCI with stent 236 19.5. Is late reperfusion worthwhile? The open artery hypothesis 238 19.6. Optimised secondary prevention vs PCI in diabetes – the BARI 2D study 238 19.7. Meta-analyses on optimised secondary prevention vs PCI 239 19.8. No successes with low risk 240 19.9. Conservative versus interventional/surgical therapy 241 19.10. The problem and a suggested solution 242 19.11. COURAGE and Wall Street – a controversial subject 242 19.12. Summary: prioritising before rationing 244 19.13. Summary 244 19.14. References 245 20. Postinfarction Failure 248 20.1. Pathophysiological background 248 20.2. Spironolactone in NYHA class III and IV 248 20.3. Eplerenone after acute myocardial infarction with LV dysfunction 248 20.4. Guidelines on aldosterone antagonists after myocardial infarction 249 20.5. 2006/2007 ACC/AHA guidelines and 2008 ESC guidelines 249 20.6. Summary 250 20.7. References 250 21. Antiarrhythmic Drugs 251 21.1. Pathophysiological background 251 21.2. The pro-arrhythmogenic effect in relation to the ejection fraction 251 21.3. Clinical studies in ventricular extrasystoles 251 21.4. Amiodarone in heart failure 252 21.5. Amiodarone in post-infarct patients 253 21.6. Antiarrhythmics in atrial fibrillation 254 21.7. Summary 259 21.8. References 260 22. ICD, CRT, Cardiac Pacemakers 262 22.1. The implantable defibrillator (ICD) 262 22.2. Resynchronisation therapy (CRT) 268 22.3. Programmed stimulation for risk identification 272 22.4. Cardiac pacemaker therapy 272 22.5. Summary 273 22.6. References 274 23. Lifestyle, Body Weight, Smoking, Alcohol, Physical Activity and Rehabilitation 277 23.1. Diet 277 23.2. Normalisation of body weight 279 23.3. Smoking 281 23.4. Alcohol 284 23.5. Physical activity and rehabilitation 287 23.6. When should lifestyle changes begin? 289 23.7. Summary 289 23.8. References 290 24. HDL, Triglycerides, Lp(a), the Forgotten Lipid Fractions 294 24.1. Hyperlipoproteinaemias, an overview 294 24.2. Associations between lipids 294 24.3. Lipid-lowering drugs 296 24.4. HDL 296 24.5. Triglycerides 301 24.6. What do the guidelines say? 305 24.7. Lipoprotein (a) 306 24.8. All lipid fractions are important 307 24.9. Summary 307 24.10. Literatur 309 25. Abbreviations 312 Index 314

240 mm

17 cm