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

Effective management of the postinfarction patient includes early assessment of direct complications such as angina pectoris, congestive heart failure and ventricular arrhythmias. Treatment of persistent ischaemia might call for early revascularisation. Early prevention of reocclusion with aspirin is recommended. It is advisable to correct blood lipid disturbances and to treat elevated blood pressure. beta-Blocking drugs have shown worthwhile reductions of both non-fatal and fatal recurrences, whereas calcium blockers and antiarrhythmic drugs have not been found to be effective. Anticoagulants have not been definitely effective in reducing mortality but seem to have some effects on non-fatal recurrences. Platelet active drugs, among which aspirin is the best documented, reduce the incidence of both non-fatal and fatal recurrences.
 ...
PMID:Practical guidelines for drug therapy after myocardial infarction. 269 42

beta-Blocking therapy is used extensively is conditions as diverse as hypertension, angina pectoris, arrhythmias, thyrotoxicosis, hypertrophic cardiomyopathy, migraine, glaucoma, and myocardial infarction. Studies show they beneficially influence sinus node and atrioventricular conduction, but excessively high doses may cause sinus arrest or sinoatrial block. Nonselective beta-blockade in asthmatic patients may aggravate bronchoconstriction, whereas increased airways resistance is less likely with beta 1-selective, partial agonist, or alpha-beta-blocking drugs. Hypoglycemia can be prolonged; beta 1-selective or partial agonist drugs may cause less interference with glucose metabolism. beta-Blockade affects free fatty acids, lipids and lipoproteins, thyroid hormones, and parathormone. beta-Blockade may normalize abnormal platelet aggregation. Finally, the choice of the most effective drug depends on the clinician's knowledge of the various pharmacodynamic and pharmacokinetic drug profiles, allied with familiarity of the patient's medical condition.
 ...
PMID:Circulatory and metabolic aspects of beta-adrenoceptor blockade. 290 49

Early trials of beta-blocking drugs in angina indicated an increase in symptoms above pretreatment levels when placebo was substituted for active drug. This was followed by some reports of sudden death after beta-blockade withdrawal. There is evidence of increased beta-receptor sensitivity as suggested by increased responsiveness to isoprenaline after propranolol withdrawal. This may be due to an increased beta-receptor population. Other factors may be a reversal of the reduced free triiodothyroxine, of the rightward shift of the oxyhaemaglobin dissociation curve, and of reduced platelet aggregation, when the beta-blocking drug is stopped. Finally, progression of the disease process may take place during treatment, which is unmasked when treatment is withdrawn. beta-Blocking agents may differ; we have observed that in normal volunteers, withdrawal of pindolol, which has partial agonist properties, was not associated with postblockade increase in response to isoprenaline. The beta-blocker withdrawal syndrome is a real phenomenon, although overall the incidence is low. Besides stopping the beta-blocker, exertion may be a frequent prerequisite for the development of significant clinical sequelae, so exertion should be restricted when stopping a beta-blocking drug. Also the dose should be reduced gradually, particularly the final decrements.
 ...
PMID:The beta-adrenergic blockade withdrawal phenomenon. 618 21

Carvedilol (CRV) is an antihypertensive drug with both alpha and beta receptor blocking activity used to preclude angina and cardiac arrhythmias. To overcome the low, variable oral bioavailability of CRV, niosomal formulations were prepared and characterized: plain niosomes (without bile salts), bile salt-enriched niosomes (bilosomes containing various percentages of sodium cholate or sodium taurocholate), and charged niosomes (negative, containing dicetyl phosphate and positive, containing hexadecyl trimethyl ammonium bromide). All formulations were characterized in terms of encapsulation efficiency, size, zeta potential, release profile, stability, and morphology. Various formulations were administered orally to ten groups of Wistar rats (n=6 per group). The plasma levels of CRV were measured by a validated high-performance liquid chromatography (HPLC) method and pharmacokinetic properties of different formulations were characterized. Contribution of lymphatic transport to the oral bioavailability of niosomes was also investigated using a chylomicron flow-blocking approach. Of the bile salt-enriched vesicles examined, bilosomes containing 20% sodium cholate (F2) and 30% sodium taurocholate (F5) appeared to give the greatest enhancement of intestinal absorption. The relative bioavailability of F2 and F5 formulations to the suspension was estimated to be 1.84 and 1.64, respectively. With regard to charged niosomes, the peak plasma concentrations (Cmax) of CRV for positively (F7) and negatively charged formulations (F10) were approximately 2.3- and 1.7-fold higher than after a suspension. Bioavailability studies also revealed a significant increase in extent of drug absorption from charged vesicles. Tissue histology revealed no signs of inflammation or damage. The study proved that the type and concentration of bile salts as well as carrier surface charge had great influences on oral bioavailability of niosomes. Blocking the lymphatic absorption pathway significantly reduced oral bioavailability of CRV niosomes. Overall twofold enhancement in bioavailability in comparison with drug suspension confers the potential of niosomes as suitable carriers for improved oral delivery of CRV.
...
PMID:Niosomal carriers enhance oral bioavailability of carvedilol: effects of bile salt-enriched vesicles and carrier surface charge. 2625 98