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We recently observed five cases of early thrombus formation in patients undergoing anticoagulation with subcutaneous heparin following open heart surgery. The reasons prompting surgery were as follows: one mitral valve replacement, one double valve replacement, one mitral valve reconstruction, one aortic valve replacement associated with coronary bypass. In all cases, intravenous heparin was begun on the day of surgery and replaced by subcutaneous (SC) heparin on postoperative day 1. Acute thrombocytopenia was observed between the 6th and 11th postoperative day. This was interpreted as denoting an idiosyncratic reaction to heparin which was replaced by low molecular weight heparin (LMWH) in two cases and by acenocoumarol in the other cases. Massive thrombosis of the aortic valve resulted in the death of one patient. Thrombosis of the left atrium occurred in three patients (two of whom had a transient ischemic attack (TIA)). One patient had aorto-iliac thrombosis. Successful reoperation was carried out in four of the five patients. Although heparin-induced thrombocytopenia and thrombosis [HITT] is a rare complication of heparin therapy, serial platelet count monitoring and in vitro platelet aggregation tests are mandatory in the diagnosis of this syndrome. Discontinuation of heparin is indicated as soon as the syndrome is recognized and the institution of aspirin is recommended if the thromboembolic complication requires reoperation and reexposure to heparin.

Reperfusion injury remains the most uncontrolled phenomenon during cardiac surgery. Potential myocardial protection by trimetazidine was tested in a double blind placebo controlled study on 19 patients undergoing aorto-coronary bypass surgery. The trimetazidine group was composed of 10 patients and the placebo group of 9 patients. Pretreatment was started three weeks before surgery with 1 tablet (trimetazidine 20 mg) t.i.d. and the same drug was added to the cardioplegic solutions (trimetazidine: 10(-6) M). The cross clamping time was 41.1 +/- 3.8 minutes in the trimetazidine group and 39.8 +/- 2.3 minutes in the placebo group. Metabolic measurements showed that the increase of malondialdehyde measured in the coronary sinus 20 minutes after reperfusion was significantly (p = 0.014) less in the trimetazidine group (from 1.60 +/- 0.11 to 1.79 +/- 0.2 mumol/L-1) than in the placebo group (from 1.17 +/- 0.11 to 2.84 +/- 0.58 mumol/L-1). Myosin was present 4 hours after surgery in all patients in the placebo group and in 5 of the 10 of the trimetazidine group (p = 0.036). Haemodynamic measurements showed that patients pretreated with trimetazidine had a better ventricular function, as assessed by the stroke work index (SWI) significantly (p = 0.01) higher in the trimetazidine group (0.0391 +/- 0.0029 g/min/m2/beta) than in the placebo group (0.0282 +/- 0.0026 g/min/m2/beat), the evolution of SWI during surgery was not significantly different between the two groups. Thus trimetazidine seems to reduce ischaemia-reperfusion damage during cardiac surgery; moreover pretreatment with trimetazidine allows the patient to face the operation with better ventricular function.