Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002962 (angina)
 21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Experimental data in animals indicate that coronary vasoconstriction occurs following blockade of the beta-adrenergic receptors or alpha-receptors activation. The vasomotor effects of these maneuvers in man are unclear. Therefore we investigated whether and to which extent alpha-stimulation (cold pressor test: CPT) and beta-blockade (propranolol) cause coronary vasoconstriction; whether this effect involves the resistance arterioles as well as the large epicardial branches, and, within these, whether the normal and stenotic tracts are involved. Patterns in patients with effort angina were compared with those in patients with Prinzmetal angina. We studied 19 cases with classic and 15 cases with Prinzmetal angina. The systemic, pulmonary and coronary hemodynamics (pressure, flow and resistance) and the vasomotor pattern of normal and stenotic epicardial branches (quantitative angiography) were evaluated in the baseline condition, during CPT, after propranolol (5 mg iv) and during CPT repeated after propranolol. We observed that: changes of the coronary flow due to beta-blockade and to CPT are related to the variations of the myocardial oxygen consumption, induced by the inhibition and activation of adrenergic receptors and not to the concomitant vasomotor reaction of the stenotic vascular tract; beta-blockade does not affect homogeneously the lumen of the stenotic lesions in effort angina and invariably increases the lumen in the Prinzmetal form; influences of CPT, in the absence as well as in the presence of beta-receptor blockade, on the lumen diameter of both normal vessels and stenotic lesions are minimal in either form of angina.
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PMID:[Activation and inhibition of adrenergic effects on the coronary vessels of patients with different forms of angina pectoris]. 255

It is now clear that the availability of different metabolic substrates can have a profound influence on the extent of damage incurred during episodes of cardiac ischaemia, and on cardiac functional recovery on reperfusion following ischaemia. In particular, increases in fatty acid availability and oxidation, compared to glucose oxidation, under such conditions leads to a worsening of outcome. Therefore metabolic interventions aimed at enhancing glucose utilisation and pyruvate oxidation at the expense of fatty acid oxidation is a valid therapeutic approach to the treatment of myocardial ischaemia. In particular, the development of agents which will promote full glucose oxidation as opposed to glycolysis alone, offer clear advantages. This can be accomplished by different means, including direct or indirect inhibition of CPT-I or inhibition of fatty acid beta-oxidation, or by direct or indirect activation of PDH. It is not yet clear which of these approaches offers the best treatment of cardiac ischaemia. To date, trimetazidine and carnitine have received limited approval in Europe for the treatment of angina; large scale clinical trials with the other agents mentioned above have not been completed. The increasing availability of agents affecting these specific sites, and the increasingly sophisticated techniques for assessing myocardial metabolism, should allow elucidation of the optimum metabolic targets and development of novel pharmacological agents for the treatment of ischaemic heart disease.
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PMID:Regulation of myocardial carbohydrate metabolism under normal and ischaemic conditions. Potential for pharmacological interventions. 907 87

The goals of pharmacological treatment of stable angina pectoris are to improve quality of life by reducing the severity and/or frequency of symptoms and also the long-term prognosis. Patients with coronary artery disease have viable but dysfunctional myocardium. The metabolism of the ischemic myocardium is characterized by a shift from fatty acid to glucose as a preferred substrate and a decline in the levels of ATP. Targeting myocardial metabolism as a pharmacologic approach for chronic angina is based on the concept that metabolic adaptive mechanisms during ischemia resemble fetal energy metabolism by shifting substrate use towards glucose metabolism. Potential pharmacologic approaches should target i) the suppression of lipolysis and the plasma fatty acid levels and subsequent uptake and oxidation by the heart, ii) direct inhibition of the enzymes of fatty acid beta-oxidation, iii) inhibition of carnitine palmitoyl transferase- I (CPT-1). Currently, there are no approved medications directly targeting myocardial metabolism. However, in the last two years a number of medications indirectly targeting cardiac metabolism have been tested in small clinical trials, and some of them appear to be promising potential therapies for stable angina. This review summarizes the main aspects of myocardial metabolism and focuses on the therapeutic approaches that could offer clinical benefit in patients with stable angina.
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PMID:Targeting myocardial metabolism for the treatment of stable angina. 2301 16