Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:4.1.1.6 (CAD)
 4,420 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Exercise myocardial-thallium scintigraphy plays a fundamental role in the diagnosis of coronary artery disease. Once exercise is not always feasible, pharmacological stress became a possible alternative. The authors review the mechanism of action, administrations protocols, indications and side effects of the drugs used for this purpose: dipyridamole, adenosine and dobutamine. Dipyridamole causes coronary hyperemia by increasing the interstitial levels of endogenous adenosine. Perfusion defects result from the mismatch of coronary reserve in different coronary territories. The drug administration is classically performed with a 0.142 mg/kg/min dosage e.v. for 4 minutes, total of 0.56 mg/kg. It is possible to use a greater dose of 0.84 mg/kg e.v. for 10 minutes, increasing sensitivity without loss of specificity for diagnosis of coronary artery disease. Oral dipyridamole protocols with 300 and 400 mg were used with similar results for sensitivity and specificity. The oral protocol has the disadvantage of delayed onset and longer action. Including several dipyridamole studies, 87% was obtained for sensitivity and 84% for specificity, in the diagnosis of CAD. Dipyridamole scintigraphy has been applied to myocardial infarction risk stratification, cardiac risk evaluation of patients proposed to noncardiac surgery and therapeutic efficacy evaluation of reperfusion techniques (angioplasty and surgery). The secondary effects of dipyridamole are frequent, however mild and well tolerated. They occur in half the patients, the most frequent, facial flushing (2%), dizziness (5%), nausea (4%), vomiting (1%), headaches (11%) and chest pain (26%). Some important complications were reported although rare: myocardial infarction, ventricular fibrillation and bronchospasm.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Role of pharmacologic stimulation with myocardial perfusion scintigraphy in the evaluation of patients with ischemic cardiopathy]. 129 Jun 55

The ventricular fibrillation is still the main cause of a sudden cardiac death, even though it was described 155 years ago in experiment (M. Hoffa 1849) and its therapy--defibrillation--has been known since 1947 (C. Beck). In Europe 2500 inhabitants suffer from cardiac arrest daily and 90% is caused by ventricular fibrillation. A key interval for an effective defibrillation seems to be 3-8 minutes from the begining of a cardiac arrest. Automated (automatized) external defibrillators (AED) have been used for last 15 years, especially in USA. However it is still unclear how many devices will be needed and where to place them. We don't know if they improve the prognosis of patients with out of hospital cardiac arrest during ventricular fibrillation. The individualisation of the risk of a sudden cardiac death has brought a new method to the clinical practise--implantation of cardioverter-defibrillator (ICD). Their efficacy in reduction of total mortality was verified first in the field of secondary prevention--in patients after cardiac arrest (AVID study) and than in the field of primary prevention--in patients with risk markers (left ventricle dysfunction, non sustained ventricular tachycardias) but without sustained malignant arrhythmia in anamnesis (MUSTT, CIDS, MADIT I, MADIT II). Defibrillators (external, automated, implantable) obviously don't mean the end of the sudden cardiac death. The incidence of sudden cardiac death can be reduced significantly with prevention (nutrition, prevention of CAD) and one attention should be drawn to the fact even in the future.
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PMID:[Defibrillators--end of sudden cardiac death?]. 1565 Nov 43