Protective Effects of Calcium Antagonists Against Ischaemia and Reperfusion Damage
Autor: | Visioli O, Roberto Ferrari |
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Rok vydání: | 1991 |
Předmět: |
medicine.medical_specialty
Nifedipine Ischemia chemistry.chemical_element Coronary Disease Myocardial Reperfusion Injury Calcium Diltiazem Internal medicine Humans Medicine Pharmacology (medical) cardiovascular diseases Myocardial infarction business.industry Unstable angina Dihydropyridine Calcium Channel Blockers medicine.disease Verapamil chemistry Anesthesia cardiovascular system Cardiology business medicine.drug |
Zdroj: | Drugs. 42:14-27 |
ISSN: | 0012-6667 |
DOI: | 10.2165/00003495-199100421-00005 |
Popis: | The most positive results in this area have been those of the second Danish Study Group on Verapamil in Myocardial Infarction (1990) which assessed the benefit of treatment with verapamil from the second week after myocardial infarction. Verapamil produced a significant reduction in both mortality and reinfarction rates. Consequently, it may be concluded that treatment with calcium antagonists, such as verapamil and diltiazem, should not be used in the acute phase of myocardial infarction, but rather as prophylaxis to prevent reinfarction by protecting against myocardial ischaemia. The lack of reported cardioprotective efficacy with calcium antagonists, which contrasts with experimental predictions, can be explained by the inappropriate timing of administration and the use of dihydropyridine, which can be detrimental in myocardial infarction. These is little or no evidence to show that calcium antagonists are cardioprotective in patients with myocardial infarction or unstable angina. Thus, the randomised trials studying acute myocardial infarction reveal no overall effect of treatment on mortality in the short or long term. The prototype calcium antagonists differ in their effects on the reinfarction rate in these patients. With verapamil there is a small tendency for a reduction in reinfarction, with nifedipine a clear worsening, and with diltiazem a reduction almost reaching statistical significance. The general lack of protective efficacy is presumably a result of the drugs being administered too late after the onset of ischaemia. |
Databáze: | OpenAIRE |
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