While dipyridamole has no role in congestive heart failure, it is being discussed here for the sake of convenience. Dipyridamole is a coronary vasodilator. It is an antithrombotic agent most often used to modify platelet function. It is also used intrave-nously as a non-nitrate coronary vasodilator for non-invasive stress thallium cardiac imaging.
· Long-term prevention of coronary insufficiency.
· For coronary dilatation, and to improve collateral circula-tion following myocardial infarction.
· For inhibition of platelet aggregation.
· Dipyridamole is well absorbed orally, and peak plasma concen-trations are achieved in 70 to 75 minutes. Oral absorption is from 30 to 70% of the dose ingested. It is extensively protein-bound (99%), and the volume of distribution is approximately 2 L/kg. After undergoing an enterohepatic recirculation, dipyridamole is mainly excreted in the faeces. 86 to 92% of the dose is recovered in the faeces. Elimination half-life is 10 to 16 hours.
Dipyridamole acts by inhibiting adenosine transport with consequent accumulation in plasma, inhibiting cyclic AMP and phosphodiesterase, and stimulating prostaglandin I2 synthesis.
· Gastrointestinal disturbances, headache, vertigo, facial flushing, and skin rash are common.
· In some cases there may be significant hypotension.
· Intravenous use can cause cardiac arrhythmias and wors-ening of angina.
· Intravenous dipyridamole can induce severe bronchospasm in asthmatic patients.
· Allergic reactions are rare, but have occurred.
· Dipyridamole can be combined with aspirin in the preven-tion of thromboembolic phenomena.
· It potentiates the effects of oral anticoagulants and anti- arrhythmic agents.
· Heparin given concomitantly can induce bleeding.Aminophylline may reverse its vasodilating effect.
Symptoms and signs of overdose include headache, facial flushing, drowsiness, weakness, fainting, nausea with GI distress, hypotension, and brady- or tachycardia. Fatalities are rare. Angina has been reported as a side effect and may occur following overdose in patients with underlying myocardial ischaemia.
Blood pressure should be monitored for at least 3 to 4 hours. Patients with uderlying cardiac disease or a history of asthma may require more intensive monitoring.
· Activated charcoal may be beneficial.
· Haemodialysis and haemoperfusion are ineffective, since dipyridamole is highly protein-bound.
o Atropine for bradycardia.
o Anginal symptoms usually respond to sublingual nitro-glycerine therapy. If this is ineffective, IV theophylline can be tried.
o Severe chest pain following dipyridamole administra-tion responds to aminophylline and anti-anginal medi-cation. Thrombolysis may be required.
o For hypotension: Infuse 10 to 20 ml/kg of isotonic fluid and place in Trendelenburg position. If hypoten-sion persists, administer dopamine or noradrenaline. Consider central venous pressure monitoring to guide further fluid therapy.
o Dipyridamole produces vasodilation via inhibition of adenosine reuptake, leading to accumulation in plasma and tissues. Adenosine-mediated adverse effects, such as bronchoconstriction and angina, can be reversed with intravenous aminophylline administration.
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