Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Traditionally when considering the pharmacologic basis of therapy in angina pectoris, attention is focussed on alterations of coronary blood flow. Yet the diseased coronary arteries in these patients often do not appear to be capable of responding to vasodilatory drugs. Since the pain of myocardial ischemia is relieved by a number of interventions without an increase in coronary blood flow, the concept herein considered is that angina pector is best viewed as an unfavorable relation between myocardial oxygen requirements and availability. Thus, the clinical value of the major antianginal agents is thought to be based importantly upon their actions to reduce myocardial oxygen consumption rather than to increase coronary blood flow. Sublingual nitroglycerin possesses a powerful dilator effect on veins which reduces venous return and thereby the size of the heart and intra-myocardial tension; thus myocardial oxygen requirements are diminished. The beta-adrenergic receptor blocking drug, propranolol (Inderal(R)), inhibits sympathetic stimulation of the heart at rest and during exercise. Thus, myocardial oxygen requirements are diminished by the reduction in heart rate and diminished contractility. As a result of this latter action, cardiac output is reduced and thereby arterial pressure and intramyocardial tension is lowered. In patients with advanced heart disease and borderline cardiac compensation, propranolol is hazardous because it removes the availability of one of the important reserve mechanisms for maintaining cardiac compensation-the sympathetic support of the failing heart. The introduction of electrical stimulation of the carotid sinus nerves as a means of therapy in patients with angina pectoris has provided a powerful tool for the treatment of patients with refractory ischemic pain.
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PMID:New trends in the treatment of angina pectoris. 498 Aug 81

The long QT syndrome (LQTS) is a cardiac disorder characterized by prolongation of the QT interval on electrocardiograms (ECGs), syncope and sudden death caused by a specific ventricular tachyarrhythmia known as torsade de pointes. LQTS is caused by mutations in ion channel genes including the cardiac sodium channel gene SCN5A, and potassium channel subunit genes KCNQ1, KCNH2, KCNE1, and KCNE2. Little information is available about LQTS mutations in the Chinese population. In this study, we characterized 42 Chinese LQTS families for mutations in the two most common LQTS genes, KCNQ1 and KCNH2. We report here the identification of four novel KCNQ1 mutations and three novel KCNH2 mutations. The KCNQ1 mutations include L191P in the S2-S3 cytoplasmic loop, F275S and S277L in the S5 transmembrane domain, and G306V in the channel pore. The KCNH2 mutations include L413P in transmembrane domain S1, E444D in the extracellular loop between S1 and S2, and L559H in domain S5. The location and character of these mutations expand the spectrum of KCNQ1 and KCNH2 mutations causing LQTS. Excitement, exercises, and stress appear to be the triggers for developing cardiac events (syncope, sudden death) for LQTS patients with KCNQ1 mutations F275S, S277L, and G306V, and all three KCNH2 mutations L413P, E444D and L559H. In contrast, cardiac events for an LQTS patient with KCNQ1 mutation L191P occurred during sleep or awakening from sleep. KCNH2 mutations L413P and L559H are associated with the bifid T waves on ECGs. Inderal or propanolol (a beta blocker) appears to be effective in preventing arrhythmias and syncope for an LQTS patient with the KCNQ1 L191P mutation.
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PMID:KCNQ1 and KCNH2 mutations associated with long QT syndrome in a Chinese population. 1244 76

Propranolol hydrochloride is a beta blocker used to treat high blood pressure, abnormal heart rhythms, heart disease, pheochromocytoma, and certain types of tremors. Propranolol is marketed by Wyeth (now a part of Pfizer) and AstraZeneca under the brand names Inderal, Inderal LA, Avlocardyl, Deralin, Dociton, Inderalici, InnoPran XL, Sumial, Anaprilium, Bedranol SR (Sandoz). It is also available generically from several manufacturers. Propranolol hydrochloride is available as tablet, capsule, and oral liquid dosage forms in several strengths. Some patients are unable to tolerate oral tablets and capsules, challenging compounding pharmacies to seek alternative dosing options; namely oral solutions and suspensions. The objective of this study was to determine the stability of propranolol hydrochloride in SyrSpend SF. The drug was compounded into a 1-mg/mL suspension using SyrSpend SF and subsequently stored in a low-actinic plastic prescription bottle at room temperature conditions. Six samples were assayed at each specific time point extending to 90 days by a stability-indicating high-performance liquid chromatography method. The method was validated for its specificity through forced-degradation studies. Based on the data collected, when protected from light at room temperature, the beyond-use date of propranolol hydrochloride in SyrSpend SF was shown to be at least 90 days.
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PMID:Stability of propranolol hydrochloride in SyrSpend SF. 2325 69