Calcium Antagonists
A Critical Review
(Sprache: Englisch)
Our research at the Freiburg Physiological Institute over the past 25 years has demonstrated that specific calcium antagonists interfere with all physiological and pathophysiological reactions involving the heart and vessels in which an elevated inflow of...
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Our research at the Freiburg Physiological Institute over the past 25 years has demonstrated that specific calcium antagonists interfere with all physiological and pathophysiological reactions involving the heart and vessels in which an elevated inflow of calcium ions across the potential-dependent slow membrane channels into the cells is a decisive factor. From the outset, our therapeutic interest has centred on the possibility of inhibiting excessively high levels of transmembrane cal cium influx and thereby reducing the pathogenic consequences of intra cellular calcium overload. For example, all excessive calcium influx evokes contractile hyperactivity, which manifests itself in the myocardial fibres as hyperkinetic reactions and an uneconomic rise in oxygen de mand and, analogously, in vascular smooth muscle cells as increased tonus and spasm. The therapeutic use of calcium antagonists to inhibit excessive mechanical and metabolic activity in the myocardium and to achieve prophylaxis and lysis in smooth muscle spasm was therefore a logical step. The highest potencies of calcium antagonists were found in the vas cular smooth musculature (coronary, cerebral, mesenteric and renal arteries and other systemic resistance vessels). Consequently, calcium antagonists were recognized as the agents of choice for numerous indica tions for vascular therapy. It is well established that calcium ions are also essential for the generation of impulses in cardiac pacemaker cells and for the conduc tion of electrical charges.
Inhaltsverzeichnis zu „Calcium Antagonists “
1 Physiological Significance of Calcium: Calcium Antagonism.- 1.1 Physiological Significance of Calcium.- 1.1.1 Action Potential and Cardiac Pacemaker Cells.- 1.1.2 Excitation-Contraction Coupling in the Myocardium.- 1.1.2.1 Action Potential in the Myocardial Cell.- 1.1.2.2 Anatomy of the Myocardial Cell.- 1.1.2.3 Cellular and Subcellular Calcium Movements.- 1.1.2.4 Molecular Mechanism of Muscle Contraction.- 1.1.3 Excitation-Contraction Coupling in Smooth Muscle.- 1.2 Calcium Antagonism.- 1.2.1 Definition of Calcium Antagonists.- 1.2.2 Basic Effects on the Heart.- 1.2.3 Basic Effects on Smooth Muscle.- 1.2.4 Mechanism and Site of Action.- 1.2.5 Classification of Calcium Antagonists.- References.- 2 Chemical Structure and Pharmacokinetics of Calcium Antagonists.- 2.1 Chemical Structure.- 2.1.1 Verapamil Group.- 2.1.2 Diltiazem.- 2.1.3 Dihydropyridine Group.- 2.1.4 Other Calcium Antagonists.- 2.2 Pharmacokinetics.- 2.2.1 Verapamil Group.- 2.2.2 Diltiazem.- 2.2.3 Dihydropyridine Group.- 2.2.4 Other Calcium Antagonists.- 2.2.5 Dosage Guidelines for Galium Antagonists: Individualized Dosage.- 2.2.6 Generics: Sustained-Release Preparations.- References.- 3 Pharmacological Effects of Calcium Antagonists.- 3.1 Cardiovascular System.- 3.1.1 Preliminary Remarks.- 3.1.2 Pacemaker and Conduction System.- 3.1.3 Myocardium.- 3.1.4 Cardioprotection.- 3.1.5 Vascular System.- 3.1.5.1 Coronary Vessels.- 3.1.5.2 Other Vessels.- 3.1.6 Integrated Haemodynamic Response.- References.- 3.2 Smooth Muscle.- 3.2.1 Gastrointestinal Tract.- 3.2.2 Respiratory Tract.- 3.2.3 Urogenital Tract.- References.- 3.3 Other Organ Systems.- 3.3.1 Kidney.- 3.3.2 Metabolism - Endocrinology.- 3.3.3 Erythrocytes - Thrombocytes - Mast Cells.- 3.3.4 Eye.- 3.3.5 Bone-Mineral Metabolism.- 3.3.6 Central Nervous System.- References.- 3.4 Atherosclerosis - Antiatherogenic Effects.- References.- 4 Indications for Calcium Antagonists.- 4.1 Coronary Heart Disease.- 4.1.1 Presenting Forms: Coronary Physiology.- 4.1.2
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Stable Angina Pectoris.- 4.1.2.1 Monotherapy with Calcium Antagonists.- 4.1.2.2 Mechanism of Action.- 4.1.2.3 Combination Therapy with Calcium Antagonists.- 4.1.2.4 Practical Considerations.- References.- 4.1.3 Unstable Angina Pectoris.- 4.1.3.1 Prinzmetal's Angina Pectoris.- 4.1.3.2 Syndrome X.- References.- 4.1.4 Myocardial Infarction (MI).- 4.1.4.1 Primary Prevention of MI.- 4.1.4.2 Calcium Antagonists in the Acute Phase of MI.- 4.1.4.3 Long-Term Therapy with Calcium Antagonists Following Acute MI (Secondary Prevention).- References.- 4.1.5 Arrhythmias in Coronary Heart Disease.- References.- 4.1.6 Silent Myocardial Ischaemia - Therapy with Calcium Antagonists.- References.- 4.2 Hypertension.- 4.2.1 Fundamentals of Antihypertensive Therapy with Calcium Antagonists.- 4.2.1.1 Definition.- 4.2.1.2 Hypertension as a Risk Factor or Risk Indicator.- 4.2.1.3 Stepped Care Versus Individualized Therapy.- 4.2.1.4 Discovery of the Antihypertensive Action of Calcium Antagonists.- References.- 4.2.2 Mechanism of Antihypertensive Action of Calcium Antagonists.- References.- 4.2.3 Monotherapy with Calcium Antagonists in Hypertension 123 References.- 4.2.4 Calcium Antagonists in Antihypertensive Combination Therapy (with Inclusion of Special Treatment Criteria).- 4.2.4.1 Combination with ?-Receptor Blockers.- 4.2.4.2 Combination with Diuretics.- 4.2.4.3 Combination with Other Antihypertensives.- 4.2.4.4 Special Treatment Criteria and Marginal Indications 132 References.- 4.2.5 Calcium Antagonists in Hypertensive Emergencies 134 References.- 4.3 Cardiac Arrhythmias.- 4.3.1 Mechanism of Antiarrhythmic Action of Calcium Antagonists.- 4.3.1.1 Mechanism of Action in Supraventricular Arrhythmias.- 4.3.1.2 Mechanisms of Action in Ventricular Arrhythmias.- 4.3.2 Supraventricular Arrhythmias.- 4.3.2.1 Sinus Tachycardia.- 4.3.2.2 Paroxysmal Supraventricular Tachycardia.- 4.3.2.3 Atrial Fibrillation.- 4.3.2.4 Atrial Flutter.- 4.3.2.5 Supraventricular Extrasystoles.- 4.3.3 Wolff-Parkinson-White Syndrome.- 4.3.4 Ventricular Arrhythmias.- 4.3.5 Digitalis-Induced Arrhythmias.- 4.3.6 Drug Interactions in Antiarrhythmic Combination Therapy.- References.- 4.4 Cardiomyopathies.- 4.4.1 Pathophysiological Classification of Cardiomyopathies According to Haemodynamic Criteria.- 4.4.2 Haemodynamics and Diagnosis of Hypertrophic Cardiomyopathy.- 4.4.3 Therapy of Hypertrophic Cardiomyopathy with Calcium Antagonists.- 4.4.4 Haemodynamics and Diagnosis of Dilated Cardiomyopathy.- 4.4.5 Treatment of Dilated Cardiomyopathy with Calcium Antagonists.- References.- 4.5 Other Cardiac Indications.- 4.5.1 Congestive Heart Failure.- 4.5.1.1 Fundamentals of Therapy with Vasodilators.- 4.5.1.2 Therapy of Congestive Heart Failure with Calcium Antagonists.- 4.5.2 Aortic Regurgitation.- 4.5.3 Application of Calcium Antagonists in Heart Surgery.- 4.5.4 Calcium Antagonists in Coronary Arteriography and Percutaneous Transluminal Coronary Angioplasty.- 4.5.5 Cardiac Involvement in Systemic Sclerosis: Hyperkinetic Heart Syndrome: Cardioprotection in Tocolysis.- References.- 4.6 Other Vascular Indications.- 4.6.1 Pulmonary Hypertension.- 4.6.2 Raynaud's Syndrome.- 4.6.3 Ergotism: Mesenteric Ischaemia: Arterial Occlusive Disease: Chronic Venous Insufficiency: Accidental Intraarterial Injection of Drugs.- 4.6.4 Atherosclerosis.- References.- 4.7 Calcium Antagonists in Neurological Disease (Claudia Trenkwalder).- 4.7.1 Migraine.- 4.7.1.1 Classification and Definition.- 4.7.1.2 Pathogenetic Factors.- 4.7.1.3 Mechanism of Action of Calcium Antagonists: Experimental Studies in Animals.- 4.7.1.4 Prophylactic Treatment of Migraine: Clinical Studies.- 4.7.1.5 Prophylactic Treatment in Childhood.- References.- 4.7.2 Vasospasm Following Subarachnoid Haemorrhage.- 4.7.2.1 Pathogenesis and Experimental Studies.- 4.7.2.2 Clinical Studies and Therapy of Vasospasm.- References.- 4.7.3 Calcium Antagonists in Cerebral Ischaemia and in Cardiopulmonary Resuscitation.- 4.7.3.1 Pathophysiology and Animal Studies.- 4.7.3.2 Clinical Studies.- References.- 4.7.4 Vertigo.- References.- 4.7.5 Epilepsy.- 4.7.5.1 Mechanism of Action of Flunarizine.- 4.7.5.2 Clinical Studies.- References.- 4.7.6 Further Indications.- References.- 4.8 Gastrointestinal Tract.- 4.8.1 Oesophagus.- 4.8.2 Small Intestine: Large Intestine.- 4.8.3 Gallbladder: Bile Ducts.- 4.8.4 Other Gastrointestinal Indications.- References.- 4.9 Respiratory Tract.- 4.9.1 Asthma.- 4.9.2 Chronic Obstructive Pulmonary Disease.- References.- 4.10 Urogenital Tract.- 4.10.1 Ureteral Spasm: Ureteral Colic: Renal Colic.- 4.10.2 Detrusor Instability (Detrusor Hyperreflexia - Irritable Bladder - Nervous Bladder).- 4.10.3 Tocolysis.- 4.10.3.1 Direct Tocolytic Action of Calcium Antagonists.- 4.10.3.2 Application of Calcium Antagonists for Cardioprotection in Tocolysis with ?-Sympathomimetics.- 4.10.4 Dysmenorrhoea.- References.- 4.11 Further Indications for Calcium Antagonists.- References.- 4.12 Calcium Antagonists in Anaesthesiology.- References.- 5 Side Effects - Overdosage - Contraindications - Drug Interactions.- 5.1 Side Effects Directly due to Blockade of Calcium-Dependent Metabolic Processes.- 5.2 Side Effects Independent of Blockade of Calcium-Dependent Metabolic Processes.- 5.3 Substance-Specific Side Effects.- 5.4 Overdosage of Calcium Antagonists: Intoxication.- 5.5 Incidence of Side Effects.- 5.6 Contraindications.- 5.7 Withdrawal of Calcium Antagonists: A Calcium Antagonists Withdrawal Syndrome?.- 5.8 Drug Interactions in Calcium Antagonist Therapy 232 References.- 6 Perspective: What Next?.- References.
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Autoren-Porträt von Helmut Lydtin, Peter Trenkwalder
Claudia Trenkwalder, Prof. Dr. med., Fachärztin für Neurologie, Chefärztin der Paracelsus-Elena-Klinik, Kassel, Zentrum für Parkinson-Syndrome und Bewegungsstörungen.
Bibliographische Angaben
- Autoren: Helmut Lydtin , Peter Trenkwalder
- 2012, Softcover reprint of the original 1st ed. 1990, XVI, 255 Seiten, Maße: 17 x 24,2 cm, Kartoniert (TB), Englisch
- Verlag: Springer, Berlin
- ISBN-10: 3642748899
- ISBN-13: 9783642748899
Sprache:
Englisch
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