Evidence-Based Treatment in Cardiology - Erstausgabe

EAN (ISBN-13): 9783837451733
Erscheinungsjahr: 2009
Herausgeber: UNI-MED Verlag AG
360 Seiten
Sprache: eng/Englisch

Buch in der Datenbank seit 2010-06-21T23:17:46+02:00 (Berlin)
Detailseite zuletzt geändert am 2022-11-05T07:19:33+01:00 (Berlin)
ISBN/EAN: 9783837451733

ISBN - alternative Schreibweisen:
978-3-8374-5173-3
Alternative Schreibweisen und verwandte Suchbegriffe:
Autor des Buches: dietrich

---

Daten vom Verlag:

Autor/in: Dietrich Strödter; Frans Santosa
Titel: UNI-MED Science; Evidence-Based Treatment in Cardiology
Verlag: UNI-MED
360 Seiten
Erscheinungsjahr: 2009-09-04
DE
Sprache: Englisch
39,80 € (DE)
66,00 CHF (CH)
Not available (reason unspecified)

EA; E107; Nonbooks, PBS / Medizin/Klinische Fächer; Klinische und Innere Medizin; BB

1. Evidence-based medicine 1.1. Definition and importance 1.1.1. Rational and efficient medicine 1.1.2. Aims of evidence-based medicine 1.2. Sources of evidence-based medicine 1.2.1. Hierarchy of scientific evidence 1.3. Terms relating to risk reduction 1.3.1. The relative risk reduction (RRR) 1.3.2. The absolute risk reduction (ARR) 1.3.3. Number needed to treat (NNT) 1.3.4. The NNT applied to the same time period 1.3.5. Calculation for person-years 1.3.6. Survival gain 1.4. A class effect in the case of benefit/harm? 1.5. Preventive cardiology 1.6. Programme of the book—Evidence-Based Treatment in Cardiology 1.7. References 2. The treatment of hypertension 2.1. Definition and clinical significance 2.2. Systolic versus diastolic blood pressure as a predictor of prognosis 2.2.1. Systolic blood pressure 2.2.2. Pulse pressure 2.2.3. Systolic blood pressure in patients with type 2 diabetes 2.2.4. Central aortic blood pressure 2.3. Isolated systolic hypertension 2.4. Risk reduction as a result of the treatment of hypertension 2.4.1. Treatment outcomes in mild/moderate hypertension 2.4.1.1. HDFP study 2.4.1.2. Australian Study 2.4.1.3. MRC study 2.4.2. The meta-analysis by Collins et al. 2.4.3. Moderate cardiac risk reduction 2.4.4. Risk reduction in elderly hypertensive individuals 2.4.5. Antihypertensive therapy in patients ³80 years? The HYVET study 2.4.6. All are the main antihypertensive classes suitable as primary therapeutic agents? 2.5. How far should the blood pressure be lowered? The question of the J curve 2.5.1. The HOT study 2.5.1.1. Quality of life and blood pressure reduction 2.5.1.2. Hypertensive diabetics in the HOT study 2.5.2. Strict versus moderate BP lowering—the UKPDS study 2.5.2.1. No lowering of diastolic BP below 60 mmHg 2.6. Recent intervention studies in hypertension 2.6.1. The CAPPP study 2.6.2. The STOP II study 2.6.3. The ALLHAT study 2.6.3.1. The diuretic and alpha blocker arm 2.6.3.2. The chlorthalidone, amlodipine and lisinopril arm 2.6.4. The NORDIL study 2.6.5. The INSIGHT study 2.6.6. Blood Pressure Lowering Treatment Trialists' Collaboration 2.6.7. The HOPE study 2.6.8. The PROGRESS study 2.6.9. The LIFE study 2.6.10. The ANBP 2 study 2.6.11. The VALUE study 2.6.12. ASCOT-BPLA study 2.6.13. The FEVER study 2.6.14. The CONVINCE study 2.6.15. ACE inhibitors versus calcium antagonists—a meta-analysis 2.6.16. ACE inhibitors versus AT1 receptor blockers versus a combination of both—the ONTARGET study 2.7. Studies on the treatment of the hypertensive diabetic patient 2.7.1. The UKPDS study—beta-blocker versus captopril 2.7.2. The ABCD study 2.7.3. The FACET study 2.7.4. The PRIME programme 2.7.4.1. The IRMA II study 2.7.4.2. The IDNT study 2.7.5. The RENAAL study 2.7.6. The Lewis study in patients with type 1 diabetes 2.7.7. Diabetics in the LIFE study 2.7.8. The ADVANCE study 2.8. Intervention studies in isolated systolic hypertension (ISH) 2.8.1. The SHEP study 2.8.1.1. Results in the overall population 2.8.1.2. Results of the SHEP study in non-insulin-dependent diabetics 2.8.2. The SYST-EUR study 2.8.2.1. Results in the overall population 2.8.2.2. Results of the SYST-EUR study in diabetics 2.8.2.3. Comparison of SHEP and SYST-EUR 2.8.3. The LIFE substudy in ISH 2.8.4. The ACCOMPLISH study 2.9. Antihypertensives and left ventricular hypertrophy (LVH) 2.9.1. Definition of LVH and LVH as a risk predictor 2.9.2. Improvement in prognosis as a result of LVH regression 2.9.3. Differences in LVH regression 2.10. Differences in nephroprotection 2.10.1. Microalbuminuria / proteinuria / raised creatinine as risk predictors 2.10.2. Antihypertensive agents in diabetic nephropathy 2.10.2.1. Evidence from study data so far 2.10.2.2. The DETAIL study 2.10.2.3. The AVOID study 2.10.3. Nephroprotection in non-diabetic nephropathy 2.10.3.1. The REIN study 2.10.3.2. The AIPRI study 2.10.3.3. Results of the meta-analysis in non-diabetics 2.10.4. Nephroprotection in mixed populations 2.10.4.1. The IMPROVE-IT study 2.10.4.2. Result of a recent meta-analysis 2.11. Antihypertensives and surrogate parameters for cardiovascular end organ damage 2.12. Antihypertensives and the development of diabetes 2.12.1. Development of diabetes less common 2.12.2. Higher incidence of the development of diabetes 2.13. Differentiated treatment of hypertension 2.14. Antihypertensive drugs 2.14.1. Classification of antihypertensive drugs 2.14.2. Characteristics of the antihypertensive drug classes 2.14.2.1. Diuretics 2.14.2.2. Beta-blockers 2.14.2.3. Calcium antagonists 2.14.2.4. ACE inhibitors 2.14.2.5. AT1 receptor blockers 2.14.2.6. Post-synaptic alpha-1 blockers 2.14.2.7. Centrally acting antihypertensives 2.14.2.8. The renin inhibitor 2.14.3. The trough-to-peak ratio 2.14.4. Differentiated treatment of hypertension (ESH / ESC 2007) 2.15. Rational combinations 2.15.1. Additive blood pressure-lowering effect 2.15.2. Increase in the responder rate as a result of a combination 2.15.3. Are fixed combinations sensible? 2.15.4. Treatment of hypertension in high-risk patients 2.16. Aims of the treatment of hypertension today 2.17. Non-pharmacological therapeutic measures 2.17.1. Diet 2.17.2. Low-salt diet 2.17.3. Weight reduction 2.17.4. Physical activity 2.17.5. Alcohol consumption 2.18. Aspirin in hypertensives? 2.18.1. Results of the HOT study with aspirin 2.18.2. Results of the study by Meade et al. 2.18.3. Results of the Primary Prevention Project 2.19. Summary 2.20. References 3. Primary prevention through lipid lowering 3.1. Hyperlipoproteinaemia as a cardiovascular risk factor 3.2. Situation prior to the statin era 3.2.1. The LRC-CPPT study with cholestyramine 3.2.2. The Helsinki Heart Study with the fibrate gemfibrozil 3.3. Primary prevention studies with statins 3.3.1. The WOSCOP study 3.3.2. The AFCAPS/TexCAPS study 3.3.3. For risk stratification, LDL is just one factor 3.4. Triglycerides as a risk factor 3.5. The 2004 NCEP (ATP III) guidelines 3.6. The situation in diabetics 3.6.1. Lipid targets for treatment 3.6.2. The CARDS study 3.7. HMG-CoA reductase inhibitors in hypertensive patients 3.7.1. The ASCOT-LLA study 3.7.2. The ALLHAT lipid arm 3.8. Statins and CRP, the JUPITER study 3.9. Summary 3.10. References 4. Treatment in stable CAD and post-infarct patients 4.1. Treatment strategies in CAD 4.2. Treatment priorities depending on the way CAD presents 4.2.1. Chronic stable CAD 4.2.2. Unstable angina 4.2.3. Acute myocardial infarction 4.2.4. After CABG or PTCA 4.2.5. CAD patients with ventricular arrhythmias 4.2.6. Summary 4.3. Nitrates and other antianginal agents 4.3.1. Do nitrates prolong survival in CAD? 4.3.1.1. The ISIS-4 study 4.3.1.2. The GISSI-3 study 4.3.1.3. The meta-analysis in ISIS-4 4.3.1.4. Nitrates in secondary prevention 4.3.2. Molsidomine 4.3.2.1. The ESPRIM study 4.3.2.2. The ACCORD study 4.3.3. Trapidil 4.3.3.1. The STARC study 4.3.4. Potassium channel openers (nicorandil) 4.3.4.1. The IONA study 4.3.5. Summary 4.3.6. References 4.4. Beta-blockers 4.4.1. Mechanism of action of beta-blockers 4.4.2. Classification of beta-blockers 4.4.2.1. Differences between beta-blockers 4.4.2.2. Treatment aims on beta-blockers 4.4.3. Beta-blockers in post-infarct patients 4.4.3.1. The Norwegian Timolol Study 4.4.3.2. Beta-blocker Heart Attack Trial (BHAT) 4.4.3.3. The metoprolol meta-analysis 4.4.3.4. Beta-blockers in the meta-analysis by Yusuf 4.4.4. Who benefits most? 4.4.4.1. Patients with compensated heart failure 4.4.4.2. Patients with reduced ejection fraction 4.4.4.3. Older patients benefit more from beta-blockers 4.4.4.4. Diabetics and beta-blockers 4.4.4.5. Beta-blockers in COPD patients? 4.4.5. Do all beta-blockers have a secondary prevention effect? 4.4.6. Can beta-blockers be used for secondary prevention in CAD without infarction? 4.4.6.1. Beta-blocker studies in CAD without infarction 4.4.6.2. Prognosis of myocardial infarction on beta-blockers 4.4.7. Beta-blockers in heart failure 4.4.8. Third-generation beta-blockers 4.4.9. Beta-blockers in LV dysfunction after infarction, the CAPRICORN study 4.4.10. 2007 AHA/ACC Guidelines 4.4.11. Summary 4.4.12. References 4.5. Calcium antagonists 4.5.1. Mechanism of action of calcium antagonists 4.5.2. Differences between the calcium antagonists 4.5.3. Calcium antagonists in stable angina 4.5.4. Dihydropyridines in postinfarct patients 4.5.5. Diltiazem in postinfarct patients 4.5.5.1. The Diltiazem reinfarction study 4.5.5.2. The MDPIT study 4.5.5.3. The INTERCEPT study 4.5.6. Verapamil in postinfarct patients 4.5.6.1. The DAVIT II study 4.5.6.2. DAVIT II study versus MDPIT study 4.5.6.3. The CRIS study 4.5.7. Hypertensive versus normotensive postinfarct patients 4.5.8. Third-generation calcium antagonists in CAD 4.5.8.1. Characteristics of third-generation calcium antagonists 4.5.8.2. The PREVENT study with amlodipine in CAD 4.5.8.3. The CAPARES study with amlodipine after PTCA 4.5.8.4. The CAMELOT study 4.5.9. Summary 4.5.10. References 4.6. ACE inhibitors 4.6.1. Mechanism of action 4.6.2. Pathophysiological basis of ACE inhibitor treatment 4.6.2.1. Left ventricular remodelling 4.6.2.2. Cardiac and systemic compensatory mechanisms after infarction 4.6.2.3. Vascular effects of ACE inhibitors 4.6.3. ACE inhibitors and aspirin 4.6.4. Postinfarction studies with ACE inhibitors 4.6.4.1. The SAVE study 4.6.4.2. The AIRE study 4.6.4.3. The TRACE study 4.6.4.4. The meta-analysis of the ACE inhibitor studies in postinfarct patients 4.6.4.5. Review of ACE inhibitor studies in and after MI 4.6.5. ACE inhibitors and risk of atrial fibrillation 4.6.6. The HOPE study 4.6.6.1. Results in the overall population 4.6.6.2. Results in diabetics (MICRO-HOPE) 4.6.6.3. Effects of ramipril independent of a reduction in blood pressure 4.6.6.4. Evaluation of the HOPE study 4.6.6.5. ACE inhibitors and HMG-CoA reductase inhibitors—HOPE subgroup analysis 4.6.7. ACE inhibitors and rate of infarction 4.6.8. ACE inhibitors in association with and after PTCA—the QUIET study 4.6.9. ACE inhibitors in association with and after CABG—the QUO VADIS study 4.6.10. ACE inhibitors in CAD patients with a lower risk 4.6.10.1. The EUROPA study 4.6.10.2. The PEACE study 4.6.10.3. HOPE versus EUROPA versus PEACE 4.6.10.4. The meta-analyses of ACE inhibitor studies with preserved LV function 4.6.11. 2006/2007 ACC/AHA guidelines 4.6.12. Summary 4.6.13. References 4.7. AT1 receptor blockers 4.7.1. The mechanism of action 4.7.2. AT1 receptor blockers and pleiotropic effects 4.7.3. Clinical studies in CAD 4.7.3.1. The OPTIMAAL study 4.7.3.2. The VALIANT study 4.7.3.3. The ONTARGET study 4.7.3.4. The TRANSCEND study 4.7.3.5. The PROFESS study 4.7.4. Combination of ACE inhibitor plus AT1 receptor blocker 4.7.5. 2006/2007 ACC/AHA guidelines 4.7.6. Summary 4.7.7. References 4.8. Statins (HMG-CoA reductase inhibitors) 4.8.1. Situation before the statin era 4.8.2. Mechanism of action of the statins 4.8.3. A comparison of statins 4.8.3.1. Pharmacological differences 4.8.3.2. Statins and extent of LDL reduction 4.8.4. Statins and dose-effect relationship 4.8.5. Statins in secondary prevention—the evidence from studies 4.8.5.1. The 4-S study 4.8.5.2. The CARE study 4.8.5.3. The LIPID study 4.8.5.4. A comparison of the 3 lipid studies 4.8.5.5. The Heart Protection Study (HPS) 4.8.6. The time for using an HMG-CoA reductase inhibitor during and after acute coronary syndrome 4.8.7. Statins and number of revascularisations 4.8.8. ACE inhibitors after CABG and PTCA 4.8.8.1. The Post-CABG study 4.8.8.2. The CARE subgroup of revascularisation patients 4.8.8.3. The FLARE study 4.8.9. HMG-CoA reductase inhibitors in PTCA 4.8.9.1. The study by Chan et al. 4.8.9.2. The LIPS study 4.8.10. Who benefits from LDL lowering? Younger or older patients? 4.8.10.1. HMG-CoA reductase inhibitors in elderly postinfarct patients 4.8.10.2. The PROSPER study 4.8.11. Additional vascular effects of HMG-CoA reductase inhibitors 4.8.11.1. Plaque regression 4.8.11.2. From an unstable plaque to a stable plaque 4.8.11.3. The improvement in vasomotor function 4.8.11.4. HMG-CoA reductase inhibitors and clotting 4.8.11.5. Anti-inflammatory effects 4.8.11.6. Anti-atherosclerotic effects as a result of HMG-CoA reductase inhibitors 4.8.11.7. HMG-CoA inhibitors and change in the plaque 4.8.12. LDL lowering and cardiac risk—the greater the LDL reduction, the better 4.8.12.1. The AVERT study 4.8.12.2. The REVERSAL study 4.8.12.3. The ASTEROID study 4.8.12.4. The PROVE-IT study 4.8.12.5. The TNT study 4.8.12.6. The IDEAL study 4.8.12.7. Should statins be used if the LDL is <60 mg/dl? 4.8.13. LDL treatment targets today 4.8.13.1. The 2001/2004 NCEP guidelines (ATP III) 4.8.14. Statins in high-risk patients 4.8.14.1. The ASCOT-LLA study 4.8.14.2. The CARDS study 4.8.15. Fibrates in secondary prevention 4.8.15.1. What should be done in CAD with an LDL of about 100 mg/dl and a low HDL? 4.8.15.2. The BIP study 4.8.16. 2006/2007 ACC/AHA guidelines 4.8.17. Summary 4.8.18. References 4.9. Antiplatelet agents 4.9.1. Mechanism of action of antiplatelet agents 4.9.2. Aspirin (acetylsalicylic acid, ASS) 4.9.2.1. The meta-analysis of the APTs' Collaboration in postinfarct patients 4.9.2.2. Aspirin after CABG and PTCA 4.9.2.3. The SAPAT study—aspirin in stable CAD 4.9.2.4. The aspirin dosage 4.9.2.5. On the optimal aspirin dose 4.9.2.6. An aspirin rebound phenomenon? 4.9.2.7. Aspirin in primary prevention 4.9.2.8. Aspirin resistance 4.9.3. Aspirin plus low-dose coumarins 4.9.3.1. The CARS study 4.9.3.2. The CHAMP study 4.9.4. Clopidogrel 4.9.4.1. An overview of the CAPRIE study 4.9.4.2. Subgroup analyses of the CAPRIE study 4.9.5. Clopidogrel plus aspirin 4.9.5.1. Clopidogrel after stenting—the CLASSICS study 4.9.5.2. Clopidogrel versus ticlopidine after stenting—results of a meta-analysis 4.9.5.3. How long after BMS should clopidogrel plus aspirin be given for? 4.9.5.4. Clopidogrel plus aspirin with DES 4.9.5.5. Clopidogrel plus aspirin after brachytherapy 4.9.5.6. Aspirin plus clopidogrel after STEMI 4.9.5.7. Aspirin plus clopidogrel during urgent intervention 4.9.5.8. A clopidogrel rebound phenomenon? 4.9.5.9. Is there clopidogrel resistance? 4.9.6. Oral glycoprotein IIb/IIIa receptor inhibitors 4.9.7. Current guidelines 4.9.7.1. 2007 ACC/AHA guidelines 4.9.7.2. 2007 ESC guidelines 4.9.7.3. 2008 ESC guidelines (STEMI) 4.9.7.4. 2007 ACC/AHA guidelines 4.9.7.5. 2007 ESC guidelines 4.9.8. Summary 4.9.9. References 4.10. Anticoagulants 4.10.1. The Sixty Plus study in the elderly 4.10.2. The WARIS-1 study 4.10.3. The ASPECT-1 study 4.10.4. The ASPECT-2 study 4.10.5. The WARIS-2 study 4.10.6. The APRICOT-2 study 4.10.7. Indications for coumarins today 4.10.8. Antithrombotic treatment in atrial fibrillation 4.10.8.1. Coumarins versus aspirin in atrial fibrillation 4.10.8.2. Aspirin plus clopidogrel versus warfarin—the ACTIVE W study 4.10.8.3. The ACTIVE A study 4.10.8.4. Risk stratification in atrial fibrillation 4.10.9. Summary 4.10.10. References 4.11. Antihypertensive agents 4.11.1. Hypertension and risk in CAD 4.11.2. The HOPE study 4.11.3. Subgroup analysis of the CAD patients in the HOT study 4.11.4. Isolated systolic hypertension (ISH) 4.11.5. The RENAAL study and IDNT study 4.11.6. The INVEST study 4.11.7. Target blood pressure values in CAD 4.11.8. Summary 4.11.9. References 4.12. Omega-3 fatty acids 4.12.1. The GISSI Prevention study 4.12.2. Recommendations of the ESC, AHA, NICE 4.12.3. The OMEGA study 4.12.4. Summary 4.12.5. References 4.13. Ivabradine, the If channel blocker 4.13.1. The BEAUTIFUL study 4.13.2. Summary (ivabradine) 4.13.3. References 4.14. Optimal secondary prevention as the key to success 4.14.1. Conservative treatment versus PCI in stable CAD 4.14.1.1. The COURAGE study 4.14.1.2. The open artery hypothesis 4.14.2. Should all agents for secondary prevention be used simultaneously? 4.14.3. Pharmacological versus different interventional therapies 4.14.4. Summary 4.14.5. References 5. Unstable angina pectoris/non-Q-wave infarction (NSTEMI) 5.1. Definition 5.2. The prognosis in unstable angina/non-Q-wave infarction 5.3. Aims of treatment 5.4. Nitrates in unstable angina/non-Q-wave infarction 5.5. Beta-blockers 5.6. Calcium antagonists 5.6.1. Meta-analysis by Held 5.6.2. The HINT study 5.6.3. The Diltiazem Reinfarction study 5.7. Aspirin 5.8. Heparin in unstable angina/NSTEMI 5.8.1. Unfractionated heparin 5.8.2. Low-molecular-weight heparin 5.8.2.1. The ESSENCE study 5.8.2.2. The TIMI 11B study 5.8.2.3. The TIMI 11B ESSENCE meta-analysis 5.8.2.4. The INTERACT study (ACC Atlanta, March 2002) 5.8.2.5. The SYNERGY study 5.8.2.6. The A to Z study 5.8.3. Pentasaccharides 5.8.3.1. The OASIS-5 study 5.8.4. Bivalirudin 5.9. Glycoprotein IIb/IIIa receptor inhibitors in unstable angina 5.9.1. The PRISM study 5.9.2. The PRISM-PLUS study 5.9.3. The PURSUIT study 5.9.4. The meta-analysis of studies with GP IIb/IIIa inhibitors 5.9.5. Glycoprotein IIb/IIIa receptor inhibitors—diabetics versus non-diabetics 5.10. Clopidogrel plus aspirin in unstable angina/non-Q-wave infarction 5.10.1. The CURE study 5.10.2. The PCI-CURE results 5.10.3. Benefit of clopidogrel in relation to risk 5.10.4. The ARMYDA-2 study 5.10.5. Interaction with PPI 5.10.6. New guidelines on clopidogrel 5.11. Prasugrel versus clopidogrel 5.11.1. Comparison of efficacy 5.11.2. The TRITON-TIMI 38 study 5.12. Statins in acute coronary syndrome 5.12.1. The MIRACL study 5.12.2. The A to Z study 5.12.3. Discontinuation of statins unfavourable—retrospective analysis of the PRISM study 5.13. Invasive versus non-invasive approach in unstable angina/NSTEMI 5.13.1. The FRISC II study 5.13.2. The TACTICS study 5.13.3. The RITA-3 study 5.13.4. The ICTUS study 5.14. The importance of glycoprotein IIb/IIIa receptor inhibitors in PCI 5.14.1. The CAPTURE study 5.14.2. The RESTORE study 5.15. The combination of GP IIb/IIIa inhibitors, aspirin, heparin, clopidogrel 5.16. Improvement in prognosis in NSTE-ACS 5.17. Approach in unstable angina/NSTEMI (2007 ESC and ACC/AHA guidelines) 5.17.1. Type of therapeutic approach 5.17.2. For antiplatelet drugs 5.17.3. For heparin 5.17.4. On lipid-lowering 5.17.5. Timings during treatment of NSTEMI-ACS 5.17.5.1. Early versus delayed PCI (TIMACS) 5.17.5.2. When should eptifibatide be used in NSTEMI? (EARLY ACS) 5.18. Algorithm in the case of ACS—2007 ESC guidelines 5.19. Summary 5.20. References 6. The treatment of acute myocardial infarction 6.1. The effect of thrombolysis 6.1.1. The ISIS-2 study 6.1.2. The GUSTO-I study 6.1.3. The meta-analysis of the Fibrinolytic Therapy Trialists' Collaborative Group 6.1.4. Problems of thrombolytic therapy in MI 6.1.5. Combination of thrombolytic agents and GP IIb/IIIa receptor inhibitors 6.2. Aspirin 6.2.1. The ISIS-2 study with aspirin 6.2.1.1. The meta-analysis of the Antiplatelet Trialists' Collaboration 6.3. Clopidogrel/prasugrel 6.3.1. The CLARITY-TIMI-28 study 6.3.2. The COMMIT/CCS 2 study 6.3.3. The ACOS Registry 6.3.4. Prasugrel in STEMI – TRITON-TIMI 38 6.4. Anticoagulation 6.4.1. Unfractionated heparin 6.4.1.1. The meta-analysis of 21 heparin studies 6.4.1.2. The ISIS-3 study 6.4.1.3. Heparin plus rt-PA 6.4.2. Low-molecular-weight heparin 6.4.3. Fondaparinux 6.4.4. Bivalirudin 6.5. Nitrates 6.5.1. The meta-analysis by Yusuf 6.5.2. The ISIS-4 study 6.5.3. The GISSI-3 study 6.5.4. The meta-analysis in ISIS-4 6.5.5. Indication for nitrate therapy 6.6. Beta-blockers 6.6.1. The MIAMI study 6.6.2. The ISIS-1 study 6.6.3. The meta-analysis by Yusuf 6.6.4. Beta-blockers in MI in diabetics 6.7. ACE inhibitors/AT1 receptor blockers 6.7.1. The GISSI-3 study 6.7.2. The ISIS-4 study 6.7.3. The SMILE study 6.7.4. Systematic analysis of several ACE inhibitor studies 6.7.5. AT1 receptor blockers 6.8. Calcium antagonists 6.9. Antiarrhythmics (lidocaine prophylaxis) 6.10. PTCA in acute infarction 6.10.1. Immediate PTCA versus lysis with t-PA 6.10.2. Immediate PTCA versus lysis with t-PA in GUSTO IIb 6.10.3. The DANAMI-2 study (lysis versus PCI) 6.10.4. Immediate PTCA versus lysis in the long term 6.10.5. The PRAGUE-2 study 6.10.6. PTCA versus PTCA plus stent 6.10.7. PTCA versus thrombolysis in diabetics versus non-diabetics 6.10.8. PTCA plus stent plus GP IIb/IIIa inhibitor 6.10.8.1. The ADMIRAL study 6.10.8.2. The CADILLAC study 6.10.9. Results of meta-analyses 6.10.10. Rescue PCI/facilitated PCI 6.11. National differences in the hospitalisation time 6.12. The prognosis in STEMI 6.13. The new classification of infarction 6.14. 2007/2004 guidelines of the ACC/AHA and ESC 6.15. Summary 6.16. References 7. Elective revascularisation procedures in CAD 7.1. Bypass surgery 7.1.1. Venous versus arterial bypass 7.1.2. CABG versus conservative therapy 7.1.2.1. Results of VA, ECSS and CASS study 7.1.2.2. The meta-analysis by Yusuf: CABG versus conservative therapy 7.1.2.3. Depression as a prognostic indicator after CABG 7.1.2.4. 2004 ACC/AHA guidelines 7.2. PTCA 7.2.1. PTCA versus conservative therapy 7.2.1.1. The RITA-2 study 7.2.1.2. The meta-analysis of 6 PTCA studies 7.3. Stents 7.3.1. Studies on stent implantation 7.3.1.1. BMS stents 7.3.1.2. Drug-eluting stents 7.3.1.3. BMS versus DES 7.3.1.4. Sirolimus versus paclitaxel 7.4. PTCA versus CABG 7.4.1. The BARI study 7.4.2. PTCA plus stent versus bypass surgery in multivessel disease 7.4.3. Meta-analysis on CABG versus PCI 7.4.4. The meta-analysis of 10 studies 7.4.5. The SYNTAX study with DES 7.5. PTCA versus atherectomy 7.5.1. The CAVEAT I study 7.5.2. The BOAT study 7.5.3. Venous graft stenosis 7.5.3.1. The CAVEAT II study 7.5.3.2. PCI in venous graft stenosis and GP IIb/IIIa receptor inhibitors 7.6. Transmyocardial laser revascularisation 7.6.1. The ATLANTIC study 7.6.2. The PACIFIC study 7.6.3. Result of a meta-analysis 7.7. Beta-blockers before CABG 7.8. PCI versus conservative treatment in chronic stable CAD 7.8.1. The COURAGE study 7.8.2. Result of a meta-analysis 7.8.3. Pharmacological versus different interventional therapies 7.8.4. The BARI 2D study 7.9. Coronary angiography versus fractional flow reserve as a parameter for indicating PCI—the FAME study 7.10. Surgical ventricle reconstruction in CABG—the STICH study (Hypothesis 2) 7.11. Summary 7.12. References 8. Treatment of chronic systolic heart failure 8.1. Treatment aims and pathophysiological bases 8.2. Diuretics 8.2.1. Pathophysiology and mechanism of action 8.2.2. Dose-effect relationship of diuretics 8.2.3. Value of diuretics in heart failure 8.2.4. Evidence from studies 8.2.5. Thiazide or loop diuretic? 8.2.5.1. Furosemide versus torasemide 8.2.6. Practical approach with diuretic treatment 8.2.7. Sequential nephron blockade 8.2.8. Interactions with non-steroidal anti-inflammatory drugs 8.2.9. Potassium-sparing diuretics 8.2.10. Summary (diuretics) 8.2.11. References 8.3. Positive inotropic drugs 8.3.1. Mechanism of positive inotropic substances 8.3.2. Digitalis 8.3.2.1. Pharmacological data on cardiac glycosides 8.3.2.2. Clinical studies 8.3.2.3. Digitalis after infarction in symptomatic heart failure 8.3.2.4. 2008 ESC guidelines 8.3.2.5. Summary (digitalis) 8.3.3. Dobutamine 8.3.4. Phosphodiesterase inhibitors 8.3.5. Xamoterol 8.3.6. Vesnarinone 8.3.7. Ibopamine 8.3.8. Pimobendan 8.3.9. Levosimendan 8.3.10. Summary (positive inotropic agents) 8.3.11. References 8.4. ACE inhibitors 8.4.1. Pathophysiological basis of ACE inhibitor treatment 8.4.2. Mechanism of action 8.4.3. Pharmacological data on ACE inhibitors 8.4.4. Clinical use of ACE inhibitors 8.4.4.1. Gradual uptitration of dosage 8.4.4.2. Right dosage 8.4.4.3. Doses in the intervention studies 8.4.4.4. Dosage recommendations of the manufacturers 8.4.4.5. The ATLAS study 8.4.5. Kidney and heart failure 8.4.6. ACE inhibitors and NSAIDs 8.4.6.1. ACE inhibitors and aspirin 8.4.7. Clinical heart failure studies with ACE inhibitors 8.4.7.1. The CONSENSUS I study 8.4.7.2. The V-HeFT II study 8.4.7.3. The SOLVD Treatment arm 8.4.7.4. The SOLVD Prevention arm 8.4.7.5. X-SOLVD 8.4.7.6. Cause of death: acute cardiac death versus pump failure 8.4.8. Summary (ACE inhibitors) 8.4.9. References 8.5. AT1 receptor blockers 8.5.1. Mechanism of action 8.5.2. Comparison of AT1 receptor blockers 8.5.3. Clinical studies 8.5.3.1. The ELITE I study 8.5.3.2. The RESOLVD study 8.5.3.3. The ELITE II study 8.5.4. AT1 receptor blockers versus/plus ACE inhibitors 8.5.4.1. The Val-HeFT study 8.5.4.2. The CHARM study 8.5.4.3. Combination of ACE inhibitor plus sartan? 8.5.4.4. Triple therapy? 8.5.5. Summary (sartans) 8.5.6. References 8.6. Other vasodilators 8.6.1. Hydralazine 8.6.1.1. The V-HeFT I study 8.6.1.2. The V-HeFT II study 8.6.1.3. The A-HeFT study 8.6.2. Alpha-1 blockers 8.6.3. Nitrates 8.6.4. Epoprostenol 8.6.5. Flosequinan 8.6.6. Summary (vasodilators) 8.6.7. References 8.7. Calcium antagonists 8.7.1. Mechanism of action 8.7.2. Clinical studies in heart failure 8.7.2.1. The V-HeFT III study 8.7.2.2. The PRAISE I study 8.7.2.3. The PRAISE II study 8.7.2.4. The MACH I study 8.7.3. Summary (Calcium antagonists) 8.7.4. References 8.8. Beta-blockers 8.8.1. Clinical background 8.8.2. Pathophysiological background 8.8.3. Beta-blockers—from contraindication to indication 8.8.4. Possible mechanisms of beta-blockers in heart failure 8.8.5. Type of beta-blocker and negative inotropism 8.8.6. Clinical studies with beta-blockers in heart failure 8.8.6.1. The US Carvedilol study 8.8.6.2. The CIBIS II study 8.8.6.3. The MERIT-HF study 8.8.6.4. Comparison of the results of the three large beta-blocker studies in NYHA class II/III heart failure 8.8.7. Beta-blockers in NYHA class IV? 8.8.7.1. Evidence before the COPERNICUS study 8.8.7.2. The COPERNICUS study 8.8.8. Beta-blockers in asymptomatic LV dysfunction? 8.8.8.1. Evidence before CAPRICORN 8.8.8.2. The CAPRICORN study 8.8.9. Clinical use of beta-blockers 8.8.10. What dose of a beta-blocker should be achieved? 8.8.11. What approach should be adopted in patients with beta-blockers and cardiac decompensation? 8.8.12. Dangers during beta-blocker treatment 8.8.13. Beta-blockers should be started during the inpatient phase—the IMPACT-HF study 8.8.13.1. Which beta-blocker in heart failure? 8.8.13.2. Carvedilol versus metoprolol: results of a meta-analysis 8.8.13.3. The COMET study 8.8.14. The SENIORS study in the elderly 8.8.15. Start with an ACE inhibitor or beta-blocker? 8.8.15.1. The CARMEN study 8.8.15.2. The CIBIS III study 8.8.16. Dosage and titration levels of beta-blockers 8.8.17. Summary (beta-blockers) 8.8.18. References 8.9. Aldosterone antagonists in heart failure 8.9.1. The rationale of treatment with aldosterone antagonists 8.9.2. Aldosterone and spironolactone effects 8.9.3. The RALES study 8.9.4. Increased incidence of hyperkalaemia after publication of the RALES study 8.9.5. Aldosterone antagonists in postinfarction heart failure 8.9.5.1. The rationale 8.9.5.2. Aldosterone, a predictor of prognosis in acute myocardial infarction 8.9.5.3. Eplerenone in the EPHESUS study 8.9.6. When should aldosterone antagonists be used? 8.9.7. Summary (aldosterone antagonists) 8.9.8. References 8.10. Omega-3 fatty acids 8.10.1. The GISSI-HF study 8.10.2. References 8.11. Anticoagulant drugs 8.11.1. The incidence of embolism in controlled studies 8.11.2. Aspirin in heart failure 8.11.3. Anticoagulants in heart failure 8.11.4. Heparin 8.11.5. Clopidogrel 8.11.5.1. The WATCH study 8.11.6. Warfarin versus aspirin plus clopidogrel 8.11.7. ACC/AHA/ESC guidelines on atrial fibrillation and coumarin treatment 8.11.8. Summary 8.11.9. References 8.12. Evidence-based treatment in systolic heart failure—algorithms 8.12.1. Algorithms in systolic heart failure 8.12.2. Diastolic heart failure 8.12.3. Current 2009 ACC/AHA guidelines 8.12.4. References 9. Antiarrhythmic drugs 9.1. Pathophysiological background 9.2. The pro-arrhythmogenic effect in relation to the ejection fraction 9.3. Clinical studies in ventricular extrasystoles 9.3.1. The CAST studies 9.4. Amiodarone in heart failure 9.4.1. The CHF-STAT study with amiodarone 9.4.2. The GESICA study 9.5. Amiodarone in post-infarct patients 9.5.1. The EMIAT and CAMIAT study with amiodarone 9.5.2. Combination of amiodarone and beta-blockers 9.5.3. The meta-analysis of the amiodarone studies 9.5.4. Antiarrhythmics in the meta-analysis 9.6. Antiarrhythmics in atrial fibrillation 9.6.1. Atrial fibrillation and prognosis 9.6.2. Atrial fibrillation in heart failure 9.6.2.1. Atrial fibrillation as a prognostic indicator 9.6.2.2. Prognosis in the presence of atrial fibrillation depending on the cause of the heart failure 9.6.2.3. The AF-CHF study 9.6.3. The DIAMOND study 9.6.4. Dronedarone 9.6.4.1. Dronedarone in heart failure 9.6.4.2. The ATHENA study 9.6.5. Heart failure therapy and atrial fibrillation 9.6.6. Rate control versus rhythm control in atrial fibrillation 9.6.6.1. The AFFIRM study 9.6.7. The RACE study 9.7. Summary 9.8. References 10. ICD, CRT, cardiac pacemakers 10.1. The implantable defibrillator (ICD) 10.1.1. The AVID study in sustained ventricular tachycardia 10.1.2. The CASH study 10.1.3. The CIDS study 10.1.4. The MADIT I study in non-sustained ventricular tachycardia 10.1.5. The CABG-Patch study 10.1.6. The meta-analysis of the ICD studies 10.1.7. The MADIT II study 10.1.8. The SCD-HeFT study 10.1.9. In the case of ICD, VVIR or DDDR—DAVID study 10.1.10. ICD in dilated cardiomyopathy—the DEFINITE study 10.1.11. When should ICD be used after myocardial infarction? 10.1.12. Indication for prophylactic ICD 10.2. Resynchronisation therapy (CRT) 10.2.1. The MUSTIC study 10.2.2. The MIRACLE study 10.2.3. The meta-analysis of the resynchronisation studies to date 10.2.4. The COMPANION study 10.2.5. The CARE-HF study 10.2.6. CRT in atrial fibrillation? 10.2.7. Indication for CRT 10.3. Programmed stimulation for risk identification 10.4. Cardiac pacemaker therapy 10.4.1. Pacing in the case of bradycardia 10.4.2. Atrioventricular pacing (DDD) versus VVI 10.4.3. The MOST study 10.4.4. The UKPACE study 10.5. Summary 10.6. References 11. Abbreviations