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

Editat de Dietrich Strödter, Frans Santosa
en Limba Engleză Hardback – 30 iun 2010
The treatment of coronary artery disease (CAD) encompasses many strategies all of which aim to improve symptoms and prognosis. While in the acute coronary syndrome, early revascularisation (usually by means of PCI and stent implantation) is the urgent goal of treatment, drug therapy initially has only a supportive role here but is also important for improving prognosis. The situation is reversed in the case of the treatment of chronic stable CAD: here conservative drug therapy has the dominant role and if implemented optimally is so successful that the prognosis cannot be further improved with additional PCI and stent implantation. Nevertheless, optimised drug therapy is often only used suboptimally, while interventional therapy is often used too frequently and is viewed as the modern and only correct therapy. The evidence presented aims to finally dispel all this!This book is therefore a critical presentation of the benefit of treatment strategies in the different forms of CAD. In addition to the value of lifestyle changes, it deals with the evaluation of the various drug therapies, invasive procedures such as PCI and stent implantation, bypass surgery and electrotherapeutic measures with ICD, CRT and cardiac pacemakers. The authors have succeeded in producing a textbook that is not just of interest to the attending doctor but also for patients affected by the disease. A textbook from the viewpoint: What is optimal? What is economic? What is evidence-based?
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Specificații

ISBN-13: 9783837412314
ISBN-10: 3837412318
Pagini: 320
Dimensiuni: 179 x 246 x 20 mm
Greutate: 0.73 kg
Editura: Uni-Med Verlag Ag
Seria UNI-MED SCIENCE


Cuprins

1. From Primary to Secondary Prevention 161.1. Definition 161.2. Risk factors for atherosclerosis 171.3. Aims of secondary prevention 171.4. Primary versus secondary prevention 181.5. Blood pressure/HbA1c goals 191.6. HbA1c target in diabetics 211.7. Lipids 211.8. Non-pharmacological therapeutic measures 221.9. Summary 231.10. References 232. Manifestations and Prognosis of CAD 252.1. Manifestations of atherosclerosis 252.2. Manifestations of CAD 252.3. Prognosis in CAD 262.4. Prognosis and gender 272.5. Prognosis in renal insufficiency 282.6. Prognosis and diabetes 282.7. Prognosis and type of medical care 292.8. Prognosis in STEMI versus NSTEMI 292.9. Decrease in CAD mortality? 292.10. Summary 302.11. References 313. From the Endothelial Defect to Myocardial Infarction 323.1. The importance of the endothelium 323.2. The acetylcholine test as a method to demonstrate endothelial dysfunction 333.3. Clinical impact of endothelial dysfunction during stress 333.4. Endothelial dysfunction as a prognostic indicator 343.5. Endothelial progenitor cells 343.6. Atherosclerosis in the coronary region 353.7. From atherothrombosis to the acute syndrome 373.8. Remodelling of the left ventricle after myocardial infarction 383.9. Summary 383.10. References 394. Pathophysiology of CAD and Strategies for Secondary Prevention 414.1. Coronary insufficiency 414.2. Determinants of the myocardial O2 requirement 424.3. Strategies for secondary prevention 424.4. Therapeutic priorities depending on the form of presentation of CHD 434.5. Summary 444.6. References 445. Nitrates and Other Antianginal Agents 465.1. Mechanism of action of nitrates 465.2. Nitrate drugs 465.3. Do nitrates prolong survival in CAD? 475.4. Nitrates in secondary prevention 485.5. Molsidomine 485.6. Trapidil 485.7. Potassium channel openers (nicorandil) 495.8. Ranolazine 495.9. Summary 505.10. References 516. Beta-Blockers 536.1. Mechanism of action of beta-blockers 536.2. Classification of beta-blockers 536.3. Differences between beta-blockers 536.4. Treatment aims on beta-blockers 546.5. Beta-blockers in post-infarct patients 546.6. Who benefits most? 556.7. Do all beta-blockers have a secondary prevention effect? 576.8. Can beta-blockers be used for secondary prevention in CAD without infarction? 576.9. Beta-blockers in heart failure 576.10. Third-generation beta-blockers 586.11. Beta-blockers in LV dysfunction after infarction, the CAPRICORN study 586.12. 2007 AHA/ACC Guidelines 596.13. The 2008 ESC guidelines 596.14. Summary 596.15. References 607. Calcium Antagonists 627.1. Mechanism of action of calcium antagonists 627.2. Differences between the calcium antagonists 627.3. Calcium antagonists in stable angina 627.4. Dihydropyridines in postinfarct patients 637.5. Diltiazem in postinfarct patients 637.6. Verapamil in postinfarct patients 647.7. Hypertensive versus normotensive postinfarct patients 657.8. Third-generation calcium antagonists in CAD 657.9. Summary 677.10. References 688. ACE Inhibitors 708.1. Mechanism of action 708.2. Pathophysiological basis of ACE inhibitor treatment 708.3. ACE inhibitors and aspirin 728.4. Postinfarction studies with ACE inhibitors 738.5. ACE inhibitors and risk of atrial fibrillation 768.6. The HOPE study 768.7. ACE inhibitors and rate of infarction 788.8. ACE inhibitors in association with and after PTCA - the QUIET study 788.9. ACE inhibitors in association with and after CABG - the QUO VADIS study 798.10. ACE inhibitors in CAD patients with a lower risk 798.11. 2006/2007 ACC/AHA guidelines 818.12. Summary 828.13. References 829. AT1 Receptor Blockers 859.1. The mechanism of action 859.2. AT1 receptor blockers and pleiotropic effects 859.3. Clinical studies in CAD 869.4. Combination of ACE inhibitor plus AT1 receptor blocker 899.5. 2006/2007 ACC/AHA- and 2008 ESC-guidelines 899.6. Summary 899.7. References 9010. Statins (HMG-CoA Reductase Inhibitors) 9110.1. Situation before the statin era 9110.2. Mechanism of action of the statins 9110.3. A comparison of statins 9110.4. Statins and dose-effect relationship 9310.5. Statins in secondary prevention - the evidence from studies 9310.6. The time for using an HMG-CoA reductase inhibitor during and after acute coronary syndrome 9810.7. Statins and number of revascularisations 9810.8. ACE inhibitors after CABG and PTCA 9910.9. HMG-CoA reductase inhibitors in PTCA 10010.10. Who benefits from LDL lowering? Younger or older patients? 10110.11. Additional vascular effects of HMG-CoA reductase inhibitors 10210.12. LDL lowering and cardiac risk - the greater the LDL reduction, the better 10710.13. LDL treatment targets today 11010.14. Statins in high-risk patients 11210.15. Fibrates in secondary prevention 11310.16. 2006/2007 ACC/AHA guidelines 11410.17. Summary 11510.18. References 11511. Antiplatelet Agents 11911.1. Antiplatelet agents - an overview 11911.2. Mechanism of action of antiplatelet agents 11911.3. Molecular target of the thienopyridines 12011.4. Prasugrel versus clopidogrel 12011.5. Clopidogrel and interaction with PPIs 12111.6. Rebound phenomena and resistance 12211.7. Ticagrelor and cangrelor 12311.8. Glycoprotein IIb/IIIa Receptor Inhibitors 12311.9. Aspirin (acetylsalicylic acid, ASS) 12311.10. Aspirin plus low-dose coumarins 12511.11. Clopidogrel 12611.12. Clopidogrel plus aspirin 12711.13. Oral glycoprotein IIb/IIIa receptor inhibitors 13111.14. Current guidelines 13111.15. Summary 13311.16. References 13312. Anticoagulants 13712.1. The Sixty Plus study in the elderly 13712.2. The WARIS-1 study 13712.3. The ASPECT-1 study 13712.4. The ASPECT-2 study 13812.5. The WARIS-2 study 13812.6. The APRICOT-2 study 13812.7. Indications for coumarins today 13812.8. Antithrombotic treatment in atrial fibrillation 13912.9. Dabigatran in atrial fibrillation - the RE-LY study 14112.10. Summary 14212.11. References 14213. Antihypertensive Agents 14413.1. Hypertension and risk in CAD 14413.2. The HOPE study 14413.3. Subgroup analysis of the CAD patients in the HOT study 14413.4. Isolated systolic hypertension (ISH) 14513.5. The RENAAL study and IDNT study 14513.6. The INVEST study 14513.7. The VALUE study 14613.8. Blood pressure versus change in plaque size 14613.9. Which combination therapy - the ACCOMPLISH study 14713.10. Target blood pressure values in CAD 14813.11. Calcium antagonists plus ACE inhibitors in chronic stable CAD 14813.12. Summary 14913.13. References 14914. Omega-3 Fatty Acids 15014.1. The GISSI Prevention study 15014.2. Recommendations of the ESC, AHA, NICE 15114.3. The OMEGA study 15214.4. Summary 15214.5. References 15215. Ivabradine, the If Channel Blocker 15415.1. The BEAUTIfUL study 15415.2. Summary 15515.3. References 15516. Unstable Angina Pectoris/Non-Q-Wave Infarction (NSTEMI) 15716.1. Definition 15716.2. The prognosis in unstable angina/non-Q-wave infarction 15716.3. Aims of treatment 15816.4. Nitrates in unstable angina/non-Q-wave infarction 15816.5. Beta-blockers 15816.6. Calcium antagonists 15916.7. Aspirin 15916.8. Heparin in unstable angina/NSTEMI 15916.9. Pentasaccharides 16116.10. Bivalirudin 16116.11. GP IIb/IIIa receptor inhibitors in unstable angina 16116.12. Clopidogrel plus aspirin in unstable angina/non-Q-wave infarction 16316.13. Prasugrel versus clopidogrel 16716.14. Statins in acute coronary syndrome 17216.15. Invasive versus non-invasive approach in unstable angina/NSTEMI 17416.16. The importance of GP IIb/IIIa receptor inhibitors in PCI 17716.17. The combination of GP IIb/IIIa inhibitors, aspirin, heparin, clopidogrel 17816.18. Improvement in prognosis in NSTE-ACS 17816.19. Approach in unstable angina/NSTEMI (2007/2009 ESC and ACC/AHA guidelines) 17816.20. Algorithm in the case of ACS - 2007 ESC guidelines 18216.21. The GRACE risk score 18216.22. Ticagrelor in ACS 18216.23. Summary 18416.24. References 18617. The Treatment of Acute Myocardial Infarction (STEMI) 19017.1. The effect of thrombolysis 19017.2. Aspirin 19317.3. Clopidogrel 19517.4. Prasugrel vs clopidogrel in STEMI - the TRITON-TIMI 38 study 19617.5. Anticoagulation 19717.6. Nitrates 19817.7. Beta-blockers 20017.8. ACE inhibitors/AT1 receptor blockers 20117.9. AT1 receptor blockers 20317.10. Calcium antagonists 20317.11. Antiarrhythmics (lidocaine prophylaxis) 20317.12. PTCA in acute infarction (STEMI) 20317.13. Lysis versus transport to a PCI centre 20417.14. PTCA versus PTCA plus stent 20517.15. PTCA plus stent plus GP IIb/IIIa inhibitor 20517.16. Rescue PCI/facilitated PCI 20617.17. National differences in the hospitalisation time 20717.18. The prognosis in STEMI 20717.19. The new classification of infarction 20717.20. 2009 and 2008 guidelines of the ACC/AHA and ESC 20717.21. DES versus BMS in STEMI - the HORIZONS-AMI study 20917.22. Summary 20917.23. References 21118. Elective Revascularisation Procedures in CAD 21618.1. Bypass surgery 21618.2. PTCA 21818.3. Stents 21918.4. PTCA versus CABG 22218.5. PTCA versus atherectomy 22318.6. Transmyocardial laser revascularisation 22418.7. Beta-blockers before CABG 22518.8. Coronary angiography versus fractional flow reserve as a parameter for indicating PCI - the FAME study 22518.9. Surgical ventricle reconstruction - the STICH study 22518.10. Adherence to guidelines for PCI and CABG 22618.11. Measures in refractory angina 22618.12. CABG versus minimally invasive surgery 22718.13. Summary 22718.14. References 22819. Conservative Therapy Versus Interventional/Surgical Therapy 23219.1. Current secondary prevention and targets 23219.2. Additive effects with four secondary prevention agents? 23219.3. Individual conservative measures in chronic stable CAD versus PCI 23519.4. Optimised secondary prevention versus PCI with stent 23619.5. Is late reperfusion worthwhile? The open artery hypothesis 23819.6. Optimised secondary prevention vs PCI in diabetes - the BARI 2D study 23819.7. Meta-analyses on optimised secondary prevention vs PCI 23919.8. No successes with low risk 24019.9. Conservative versus interventional/surgical therapy 24119.10. The problem and a suggested solution 24219.11. COURAGE and Wall Street - a controversial subject 24219.12. Summary: prioritising before rationing 24419.13. Summary 24419.14. References 24520. Postinfarction Failure 24820.1. Pathophysiological background 24820.2. Spironolactone in NYHA class III and IV 24820.3. Eplerenone after acute myocardial infarction with LV dysfunction 24820.4. Guidelines on aldosterone antagonists after myocardial infarction 24920.5. 2006/2007 ACC/AHA guidelines and 2008 ESC guidelines 24920.6. Summary 25020.7. References 25021. Antiarrhythmic Drugs 25121.1. Pathophysiological background 25121.2. The pro-arrhythmogenic effect in relation to the ejection fraction 25121.3. Clinical studies in ventricular extrasystoles 25121.4. Amiodarone in heart failure 25221.5. Amiodarone in post-infarct patients 25321.6. Antiarrhythmics in atrial fibrillation 25421.7. Summary 25921.8. References 26022. ICD, CRT, Cardiac Pacemakers 26222.1. The implantable defibrillator (ICD) 26222.2. Resynchronisation therapy (CRT) 26822.3. Programmed stimulation for risk identification 27222.4. Cardiac pacemaker therapy 27222.5. Summary 27322.6. References 27423. Lifestyle, Body Weight, Smoking, Alcohol, Physical Activity and Rehabilitation 27723.1. Diet 27723.2. Normalisation of body weight 27923.3. Smoking 28123.4. Alcohol 28423.5. Physical activity and rehabilitation 28723.6. When should lifestyle changes begin? 28923.7. Summary 28923.8. References 29024. HDL, Triglycerides, Lp(a), the Forgotten Lipid Fractions 29424.1. Hyperlipoproteinaemias, an overview 29424.2. Associations between lipids 29424.3. Lipid-lowering drugs 29624.4. HDL 29624.5. Triglycerides 30124.6. What do the guidelines say? 30524.7. Lipoprotein (a) 30624.8. All lipid fractions are important 30724.9. Summary 30724.10. Literatur 30925. Abbreviations 312 Index 314