No abstract

A60-year-old man with a history of ischaemic heart disease, myocardial infarction and previous coronary bypass grafting was admitted to hospital with sustained monomorphic ventricular tachycardia. He was treated with intravenous amiodarone and was later discharged on oral amiodarone 200 mg once a day in addition to his usual antianginal therapy, angiotensin-converting enzyme inhibitor and diuretic. Approximately 6 months afterwards, he presented with profound tiredness, somnolence, weight gain constipation and fluid retention. He described fluctuating disorientation in time as well as vivid visual hallucinations of people and animals. He had also experienced auditory hallucinations of the voices of his relatives conversing with him in the second person. Transient secondary delusions were evident. In particular, on the night before his readmission he became convinced that he had lost his pituitary and enlisted his wife to help search for it in the bed. Thyroid function tests (TFTs) revealed a free thyroxine level of 2 pmol/litre (normal range 11–25 pmol/litre) and markedly raised thyroid-stimulating hormone (TSH) of more than 150 mU/litre (normal range 0.35–5.00 mU/litre). Microsomal thyroid antibodies were present — 670 IU/ml (normal range 0–200 IU/ml). Amiodarone was stopped and he was given thyroxine, with gradual dose titration up to 150 μg per day. On reviewing his medical notes it was discovered that a diagnosis of hypopituitarism was made in 1984, and he had briefly been treated with steroid, testosterone and thyroxine replacement therapy. This diagnosis had later been refuted. Of relevance is that a thyrotropinreleasing hormone test was normal at this time. Plain X-ray of the skull showed an asymmetrical sella, and a diagnosis of ‘empty sella syndrome’ was made. There was no previous psychiatric history. Interestingly his basal TFTs at the time of amiodarone initiation showed a normal thyroxine level of 16 pmol/litre but TSH was not measured. A month later his free thyroxine was still 16 pmol/litre and TSH was noted to be elevated at 8.9 mU/litre. He appeared euthyroid and no changes were made to his treatment. Following the treatment of his hypothyroidism his angina worsened, while his psychiatric symptoms settled within a matter of weeks and his TFTs showed adequate replacement after 5 months. To date there has been no recurrence of his arrhythmia.

SUMMARYPlatelets play a key role in the pathogenesis of atherothrombotic conditions, e.g. acute coronary syndromes, cerebrovascular and peripheral vascular events. Antiplatelet agents interfere with platelet activation and aggregation and, as such, would be expected to modify the natural history of cardiovascular disease. In this review we explore the evidence to support the use of such drugs, singly or in combination, in a variety of situations characterised by thrombosis and summarise some of the concerns inherent in their use.

Atherothrombotic disease places a huge financial and social burden on the nation, and antiplatelet therapy is important in preventing this. Aspirin is most widely used but newer compounds are valuable, especially on top of standard therapy in patients with unstable angina or non-ST segment elevation myocardial infarction. This article reviews the changing use of antiplatelets.