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

Dietrich Strödter, Frans Santosa (Autoren)

Buch | Hardcover

320 Seiten

2010 | 1., st edition
UNI-MED (Verlag)
978-3-8374-1231-4 (ISBN)

Infos

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?

Inhalt

1.From Primary to Secondary Prevention16
1.1.Definition16
1.2.Risk factors for atherosclerosis17
1.3.Aims of secondary prevention17
1.4.Primary versus secondary prevention18
1.5.Blood pressure/HbA1c goals19
1.6.HbA1c target in diabetics21
1.7.Lipids21
1.8.Non-pharmacological therapeutic measures22
1.9.Summary23
1.10.References23
2.Manifestations and Prognosis of CAD25
2.1.Manifestations of atherosclerosis25
2.2.Manifestations of CAD25
2.3.Prognosis in CAD26
2.4.Prognosis and gender27
2.5.Prognosis in renal insufficiency28
2.6.Prognosis and diabetes28
2.7.Prognosis and type of medical care29
2.8.Prognosis in STEMI versus NSTEMI29
2.9.Decrease in CAD mortality?29
2.10.Summary30
2.11.References31
3.From the Endothelial Defect to Myocardial Infarction32
3.1.The importance of the endothelium32
3.2.The acetylcholine test as a method to demonstrate endothelial dysfunction33
3.3.Clinical impact of endothelial dysfunction during stress33
3.4.Endothelial dysfunction as a prognostic indicator34
3.5.Endothelial progenitor cells34
3.6.Atherosclerosis in the coronary region35
3.7.From atherothrombosis to the acute syndrome37
3.8.Remodelling of the left ventricle after myocardial infarction38
3.9.Summary38
3.10.References39
4.Pathophysiology of CAD and Strategies for Secondary Prevention41
4.1.Coronary insufficiency41
4.2.Determinants of the myocardial O2 requirement42
4.3.Strategies for secondary prevention42
4.4.Therapeutic priorities depending on the form of presentation of CHD43
4.5.Summary44
4.6.References44
5.Nitrates and Other Antianginal Agents46
5.1.Mechanism of action of nitrates46
5.2.Nitrate drugs46
5.3.Do nitrates prolong survival in CAD?47
5.4.Nitrates in secondary prevention48
5.5.Molsidomine48
5.6.Trapidil48
5.7.Potassium channel openers (nicorandil)49
5.8.Ranolazine49
5.9.Summary50
5.10.References51
6.Beta-Blockers53
6.1.Mechanism of action of beta-blockers53
6.2.Classification of beta-blockers53
6.3.Differences between beta-blockers53
6.4.Treatment aims on beta-blockers54
6.5.Beta-blockers in post-infarct patients54
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 failure57
6.10.Third-generation beta-blockers58
6.11.Beta-blockers in LV dysfunction after infarction, the CAPRICORN study58
6.12.2007 AHA/ACC Guidelines59
6.13.The 2008 ESC guidelines59
6.14.Summary59
6.15.References60
7.Calcium Antagonists62
7.1.Mechanism of action of calcium antagonists62
7.2.Differences between the calcium antagonists62
7.3.Calcium antagonists in stable angina62
7.4. Dihydropyridines in postinfarct patients63
7.5.Diltiazem in postinfarct patients63
7.6.Verapamil in postinfarct patients64
7.7.Hypertensive versus normotensive postinfarct patients65
7.8.Third-generation calcium antagonists in CAD65
7.9.Summary67
7.10.References68
8.ACE Inhibitors70
8.1.Mechanism of action70
8.2.Pathophysiological basis of ACE inhibitor treatment70
8.3.ACE inhibitors and aspirin72
8.4.Postinfarction studies with ACE inhibitors73
8.5.ACE inhibitors and risk of atrial fibrillation76
8.6.The HOPE study76
8.7.ACE inhibitors and rate of infarction78
8.8.ACE inhibitors in association with and after PTCA – the QUIET study78
8.9.ACE inhibitors in association with and after CABG – the QUO VADIS study79
8.10.ACE inhibitors in CAD patients with a lower risk79
8.11.2006/2007 ACC/AHA guidelines81
8.12.Summary82
8.13.References82
9.AT1 Receptor Blockers85
9.1.The mechanism of action85
9.2.AT1 receptor blockers and pleiotropic effects85
9.3.Clinical studies in CAD86
9.4.Combination of ACE inhibitor plus AT1 receptor blocker89
9.5.2006/2007 ACC/AHA- and 2008 ESC-guidelines89
9.6.Summary89
9.7.References90
10.Statins (HMG-CoA Reductase Inhibitors)91
10.1.Situation before the statin era91
10.2.Mechanism of action of the statins91
10.3.A comparison of statins91
10.4.Statins and dose-effect relationship93
10.5.Statins in secondary prevention – the evidence from studies93
10.6.The time for using an HMG-CoA reductase inhibitor during and after acute coronary syndrome98
10.7.Statins and number of revascularisations98
10.8.ACE inhibitors after CABG and PTCA99
10.9.HMG-CoA reductase inhibitors in PTCA100
10.10.Who benefits from LDL lowering? Younger or older patients?101
10.11.Additional vascular effects of HMG-CoA reductase inhibitors102
10.12.LDL lowering and cardiac risk – the greater the LDL reduction, the better107
10.13.LDL treatment targets today110
10.14.Statins in high-risk patients112
10.15.Fibrates in secondary prevention113
10.16.2006/2007 ACC/AHA guidelines114
10.17.Summary115
10.18.References115
11.Antiplatelet Agents119
11.1.Antiplatelet agents – an overview119
11.2.Mechanism of action of antiplatelet agents119
11.3.Molecular target of the thienopyridines120
11.4.Prasugrel versus clopidogrel120
11.5.Clopidogrel and interaction with PPIs121
11.6.Rebound phenomena and resistance122
11.7.Ticagrelor and cangrelor123
11.8.Glycoprotein IIb/IIIa Receptor Inhibitors123
11.9.Aspirin (acetylsalicylic acid, ASS)123
11.10.Aspirin plus low-dose coumarins125
11.11.Clopidogrel126
11.12.Clopidogrel plus aspirin127
11.13.Oral glycoprotein IIb/IIIa receptor inhibitors131
11.14.Current guidelines131
11.15.Summary133
11.16.References133
12.Anticoagulants137
12.1.The Sixty Plus study in the elderly137
12.2.The WARIS-1 study137
12.3.The ASPECT-1 study137
12.4.The ASPECT-2 study138
12.5.The WARIS-2 study138
12.6.The APRICOT-2 study138
12.7.Indications for coumarins today138
12.8.Antithrombotic treatment in atrial fibrillation139
12.9.Dabigatran in atrial fibrillation – the RE-LY study141
12.10.Summary142
12.11.References142
13.Antihypertensive Agents144
13.1.Hypertension and risk in CAD144
13.2.The HOPE study144
13.3.Subgroup analysis of the CAD patients in the HOT study144
13.4.Isolated systolic hypertension (ISH)145
13.5.The RENAAL study and IDNT study145
13.6.The INVEST study145
13.7.The VALUE study146
13.8.Blood pressure versus change in plaque size146
13.9.Which combination therapy – the ACCOMPLISH study147
13.10.Target blood pressure values in CAD148
13.11.Calcium antagonists plus ACE inhibitors in chronic stable CAD148
13.12.Summary149
13.13.References149
14.Omega-3 Fatty Acids150
14.1.The GISSI Prevention study150
14.2.Recommendations of the ESC, AHA, NICE151
14.3.The OMEGA study152
14.4.Summary152
14.5.References152
15.Ivabradine, the If Channel Blocker154
15.1.The BEAUTIfUL study154
15.2.Summary155
15.3.References155
16.Unstable Angina Pectoris/Non-Q-Wave Infarction (NSTEMI)157
16.1.Definition157
16.2.The prognosis in unstable angina/non-Q-wave infarction157
16.3.Aims of treatment158
16.4.Nitrates in unstable angina/non-Q-wave infarction158
16.5.Beta-blockers158
16.6.Calcium antagonists159
16.7.Aspirin159
16.8.Heparin in unstable angina/NSTEMI159
16.9.Pentasaccharides161
16.10.Bivalirudin161
16.11.GP IIb/IIIa receptor inhibitors in unstable angina161
16.12.Clopidogrel plus aspirin in unstable angina/non-Q-wave infarction163
16.13.Prasugrel versus clopidogrel167
16.14.Statins in acute coronary syndrome172
16.15.Invasive versus non-invasive approach in unstable angina/NSTEMI174
16.16.The importance of GP IIb/IIIa receptor inhibitors in PCI177
16.17.The combination of GP IIb/IIIa inhibitors, aspirin, heparin, clopidogrel178
16.18.Improvement in prognosis in NSTE-ACS178
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 guidelines182
16.21.The GRACE risk score182
16.22.Ticagrelor in ACS182
16.23.Summary184
16.24.References186
17.The Treatment of Acute Myocardial Infarction (STEMI)190
17.1.The effect of thrombolysis190
17.2.Aspirin193
17.3.Clopidogrel195
17.4.Prasugrel vs clopidogrel in STEMI – the TRITON-TIMI 38 study196
17.5.Anticoagulation197
17.6.Nitrates198
17.7.Beta-blockers200
17.8.ACE inhibitors/AT1 receptor blockers201
17.9.AT1 receptor blockers203
17.10.Calcium antagonists203
17.11.Antiarrhythmics (lidocaine prophylaxis)203
17.12.PTCA in acute infarction (STEMI)203
17.13.Lysis versus transport to a PCI centre204
17.14.PTCA versus PTCA plus stent205
17.15.PTCA plus stent plus GP IIb/IIIa inhibitor205
17.16.Rescue PCI/facilitated PCI206
17.17.National differences in the hospitalisation time207
17.18.The prognosis in STEMI207
17.19.The new classification of infarction207
17.20.2009 and 2008 guidelines of the ACC/AHA and ESC207
17.21.DES versus BMS in STEMI – the HORIZONS-AMI study209
17.22.Summary209
17.23.References211
18.Elective Revascularisation Procedures in CAD216
18.1.Bypass surgery216
18.2.PTCA218
18.3.Stents219
18.4.PTCA versus CABG222
18.5.PTCA versus atherectomy223
18.6.Transmyocardial laser revascularisation224
18.7.Beta-blockers before CABG225
18.8.Coronary angiography versus fractional flow reserve as a parameter for indicating PCI – the FAME study225
18.9.Surgical ventricle reconstruction – the STICH study225
18.10.Adherence to guidelines for PCI and CABG226
18.11.Measures in refractory angina226
18.12.CABG versus minimally invasive surgery 227
18.13.Summary227
18.14.References228
19.Conservative Therapy Versus Interventional/Surgical Therapy232
19.1.Current secondary prevention and targets232
19.2.Additive effects with four secondary prevention agents?232
19.3.Individual conservative measures in chronic stable CAD versus PCI235
19.4.Optimised secondary prevention versus PCI with stent236
19.5.Is late reperfusion worthwhile? The open artery hypothesis238
19.6.Optimised secondary prevention vs PCI in diabetes – the BARI 2D study238
19.7.Meta-analyses on optimised secondary prevention vs PCI239
19.8.No successes with low risk240
19.9.Conservative versus interventional/surgical therapy241
19.10.The problem and a suggested solution242
19.11.COURAGE and Wall Street – a controversial subject242
19.12.Summary: prioritising before rationing244
19.13.Summary244
19.14.References245
20.Postinfarction Failure248
20.1.Pathophysiological background248
20.2.Spironolactone in NYHA class III and IV248
20.3.Eplerenone after acute myocardial infarction with LV dysfunction248
20.4.Guidelines on aldosterone antagonists after myocardial infarction249
20.5.2006/2007 ACC/AHA guidelines and 2008 ESC guidelines249
20.6.Summary250
20.7.References250
21.Antiarrhythmic Drugs251
21.1.Pathophysiological background251
21.2.The pro-arrhythmogenic effect in relation to the ejection fraction251
21.3.Clinical studies in ventricular extrasystoles251
21.4.Amiodarone in heart failure252
21.5.Amiodarone in post-infarct patients253
21.6.Antiarrhythmics in atrial fibrillation254
21.7.Summary259
21.8.References260
22.ICD, CRT, Cardiac Pacemakers262
22.1.The implantable defibrillator (ICD)262
22.2.Resynchronisation therapy (CRT)268
22.3.Programmed stimulation for risk identification272
22.4.Cardiac pacemaker therapy272
22.5.Summary273
22.6.References274
23.Lifestyle, Body Weight, Smoking, Alcohol, Physical Activity and Rehabilitation277
23.1.Diet277
23.2.Normalisation of body weight279
23.3.Smoking281
23.4.Alcohol284
23.5.Physical activity and rehabilitation287
23.6.When should lifestyle changes begin?289
23.7.Summary289
23.8.References290
24.HDL, Triglycerides, Lp(a), the Forgotten Lipid Fractions294
24.1.Hyperlipoproteinaemias, an overview294
24.2.Associations between lipids294
24.3.Lipid-lowering drugs296
24.4.HDL296
24.5.Triglycerides301
24.6.What do the guidelines say?305
24.7.Lipoprotein (a)306
24.8.All lipid fractions are important307
24.9.Summary307
24.10.Literatur309
25.Abbreviations312
Index314

Produkt-Details

• Erscheint lt. Verlag: 7.12.2010
• Reihe/Serie: UNI-MED Science
• Sprache: englisch
• Maße: 170 x 240 mm
• Gewicht: 735 g
• Einbandart: gebunden
• Themenwelt: Medizin / Pharmazie ► Medizinische Fachgebiete
• Schlagworte: Herzinsuffizienz
• ISBN-10: 3-8374-1231-8 / 3837412318
• ISBN-13: 978-3-8374-1231-4 / 9783837412314
• Zustand: Neuware