Anti-arrhythmic

The structural requirements for such activity are not very confining, as can be seen in part by comparing the structure of lorcai nide with oxi ramide (21). Anti arrhythmic oxi ramide... 

Another quaternary anti arrhythmic agent is emilium tosyl-ate (65). It is synthesized simply by quaternization of... 

A slightly more complex anti arrhythmic agent is pi rmentol (74). It is synthesized from 4-chloropropiophenone (72) by keto group protection as the dioxolane (with ethylene glycol and acid) followed by sodium iodide-mediated alkylation with cis 2,6-dimethyl pi peri dine to give 7. Deblocking with acid followed by addition of 2-1ithiopyridine completes the synthesis of pi rmentol (74). 

Several obvious variants exist. Tolbutamide, the prototypic drug, has some anti arrhythmic activity by an unknown mechanism. his side effect has become the principal action with tosifen, which itself does not in turn significantly lower blood... 

Treatment of the piperidine 74, obtainable from an aminonitrile such as 73, under N-methylation conditions leads to the dimethylamino derivative 75. The carbobenzoxy protecting group is then removed by catalytic hydrogenation. Reaction of the resulting secondary amine 76 with cyclohexene oxide leads to the alkylated trans aminoalcohol. There is thus obtained the anti-arrhythmic agent transcainide (77) [18]. 

Ventricular extrasystoles are treated only if they may degenerate into life-threatening arrhythmia. In milder forms the proarrhythmic risk of the diugs overshadows their benefits. In such cases (3-adrenoceptor antagonists may be attempted. For the treatment of ventricular extrasystoles, such as series or runs of extrasystoles, amiodarone or sotalol are used. In the absence of structural heart disease, class I anti-arrhythmic diugs can be considered an alternative. However, they may not be administered during the post-infarction period. 

Self-Monitoring Pulse Rate With Anti arrhythmic Therapy... 

ATC C01B C07A Use beta blocking agent, antianginal, anti arrhythmic... 

Uncontrolled hypertension Valvular disorders function sympathomi meti cs) Offending medications (NSAIDs, COX-2 inhibitors, steroids, lithium, (i-blockers, calcium channel blockers, anti-arrhythmics, alcohol, thiazolidinediones)... 

Vaughan-Williams Classification of Anti-arrhythmic Drugs... 

Monitor patients for adverse effects of adenosine or any other anti-arrhythmic agents administered (Table 6-6). 

Amenorrhea or problems with menstrual period Cardiac arrhythmias or current anti-arrhythmic Aripiprazole, quetiapine, clozapine NOT ziprasidone or clozapine Olanzapine, ziprasidone... 

Vardenafil can cause QT-interval prolongation this effect in combination with certain anti-arrhythmic agents can lead to life-threatening arrhythmias. CYP, cytochrome P-450 isoenzyme. 

Disopyramide anti-arrhythmic S(+)-isomer more strongly protein bound... 

Which of the following is an anti arrhythmic agent that has relatively few electro physiologic effects on normal myocardial tissue hut suppresses the arrhythmogenic tendencies of ischemic myocardial tissues ... 

A 68-year-old female has AF, which is treated with an anti arrhythmic agent that blocks Na+ channels. On a recent office visit, she complained of recurrent attacks of feeling faint and of experiencing an episode of loss of consciousness. An EKG showed marked prolongation of the QT interval. Plasma concentration of the drug was in the therapeutic range. 

It is customary today to classify anti arrhythmic drugs according to their mechanism of action. This is best defined by intracellular recordings that yield monophasic action potentials. In the accompanying figure, the monophasic action potentials of (A) slow response fiber (SA node) and (B) fast Purkinje fiber are shown. For each description that follows, choose the appropriate drug with which the change in character of the monophasic action potential is likely to be associated... 

I88-E89. The answers arc 188-g 189-b. (Hardman, pp 858-859, 864-865.) It is widely accepted that anti arrhythmic drugs are best classified according to their electro physio logic attributes. This is best accomplished by relating the effects of the different drugs to their actions on Na and Ca channels, which are reflected by changes in the monophasic action potential. Amiodarone blocks Na, Ca, and K currents and markedly prolongs repolarization, particularly in depolarized cells. Hecainide is related... 

Dosing with beta-blockers and anti-arrhythmics (CYP 2D6)... 

It is also very important, if possible, to discontinue or lower the doses of drugs with anticholinergic effects antihistamines, antipsychotics, antidepressants, uro-logic spasmolytics, anti-arrhythmics, drugs for Parkinson s disease and more. Prophylactic treatment against Candida infection, bacteria and caries can also be useful (Mouly et al. 2007). 

Enkaid (4 years on market) Anti arrhythmic Cardiovascular (sudden cardiac death)... 

Lidocaine (lignocaine, 4.128, Fig. 4.5) is a typical representative of the class of aminoacylanilides. Lidocaine is a local anesthetic and an anti-arrhythmic agent that is very resistant to chemical hydrolysis even in strongly acidic or basic media. Only at higher temperature does lidocaine... 

De Ponti, F., Poluzzi, E., and Montanaro, N., Organising evidence on QT prolongation and occurrence of Torsades de pointes with non-anti-arrhythmic drugs a call for consensus, Eur. J. Clin. Pharmacol, 57,185-209, 2001. 

Amiodarone is an anti-arrhythmic drug indicated in supraventricular and ventricular arrhythmias. One of the main side-effects is photosensitivity and patients are advised to avoid exposure to sunlight and use sun protection factors. 

Substrates for CYP2D6 include tricyclic antidepressants, p-blockers, class 1 anti-arrhythmics. In brief, the structural similarities of many of the substrates and inhibitors in terms of position of hydroxylation, overall structure (aryl-alkylamine) and physicochemistry (ionized nitrogen at physiological pH), have allowed template models such as that illustrated as Figure 7.3 to be constructed. 

Preliminary studies [241, 249, 250] of the cardiovascular and sympatholytic properties of prenylamine demonstrated that coronary blood flow and oxygenation could be increased under experimental conditions (in dogs) and that the drug interacted in complex fashion with sympathetically innervated organs, but the picture presented was someudiat confused because of the many uncontrolled variables and limitations of the actual techniques used. Anti-arrhythmic activity of potency comparable with that of quinidine, plus local anaesthetic properties, were also demonstrated [251] but the same worker was notable to reproduce these effects in intact live animals with any consistency. Large doses of the drug actually provoked cardiac fibrillation in some cases. 

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