The survival rate of 2256 patients with pacemakers was analyzed. Patients paced for Adams-Stokes equivalents (e.g. dizziness) showed a significantly better survival rate than did patients with pacemakers implanted for Adam-Stokes attacks or heart failure (P less than 0.0001). The estimated survival of the latter two groups did not differ significantly. Of the deceased patients who had received a pacemaker for the treatment of heart failure, 54% died due to this condition despite pacemaker implantation. The relative percentage of cases of sudden death after pacemaker implantation was high in the groups with Adams-Stokes attacks (12%) and Adams-Stokes equivalents (13%). In patients paced for Adams-Stokes attacks, sudden death occurred more frequently in the first year after pacemaker implantation (P less than 0.015) than during the following years. Therefore, increased efforts should be made to monitor patients carefully after pacemaker implantation to enable prompt detection of malignant tachyarrhythmias, probably the cause of sudden death in a substantial number of patients with pacemakers.

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In 2 male patients (35 and 38 years) presenting with myocardial infarction an abnormal conversion of exogenous 14C-arachidonic acid by the patients' platelets, incubated in vitro, was observed. Neither patient's platelets showed evidence of a lipoxygenase pathway. Platelet thromboxane formation from exogenous and endogenous substrate was high, while the platelet aggregation responses were normal. A myeloproliferative syndrome was excluded by bone marrow puncture. Similar defects have only been described so far in patients with myeloproliferative syndrome. This defect may be causative for the onset of clinical thrombotic events. It is speculative whether in vivo therapy with r-IFN alpha 1c might be able to eradicate the pathological platelet clone.

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