Management of cardiac device infections: A retrospective survey of a non-surgical approach combining antibiotic therapy with transvenous removal.

Pacemakers (PMs) and implantable cardioverter defibrillators (ICDs) have become life-saving therapeutic tools for patients with cardiac arrhythmia. Complications include thrombosis, embolism and infections at a highly variable rate. Surgical removal of the infected device has been perceived as the only way to guarantee a successful outcome and to reduce the high risk of mortality. Recently, a transvenous extraction method has been developed to remove infected intracardiac leads without sternotomy. This survey was designed to evaluate the outcome of an approach combining antibiotic therapy with non-surgical transvenous complete removal for the management of cardiac device infections (CDIs). We reviewed case-histories of 121 patients (105 with PM and 16 with ICD infections). The aim of our retrospective survey was to ascertain that a non-invasive transvenous complete removal of the infected devices is safe and effective when associated with appropriate antibiotic therapy starting 10 days before the procedure and extending to at least three weeks after. The infected devices were successfully removed in all patients with a non-surgical transvenous technique. The infections were most frequently caused by coagulase-negative staphylococci (70%), Staphylococcus aureus (14%), and Gram-negative rods (12%). Polymicrobial infections were documented in 19 patients and represent 16% of all device-related infections. The removal of the devices was done during antibiotic therapy, administered for a median of 26 days (range 23 to 45 days). Neither fatalities nor relapse of infections were recorded in the patient population during the one-year follow-up visits. According to our experience, CDIs can be treated with antibiotic therapy and non-surgical removal of the entire infected device, thus allowing a successful reimplantation. This procedure prevents recurrent infections and operative mortality.

Elevated levels of lipoprotein (a) in patients suffering from myocardial infarction with carotid atherosclerotic lesions.

The aim of the present study was to evaluate metabolic, coagulation and fibrinolytic parameters in 45 patients [31 men, 14 women, aged 56.5 +/- 3.5 years (mean +/- SD)] who had suffered myocardial infarction more than 6 months earlier, with or without carotid atherosclerotic lesions. After the extracranial carotid arteries had been evaluated using a B-mode Duplex scanning system, patients were subdivided into two groups: group 1 (n = 20) with carotid plaques or measurable intima-media thickness; and group 2 (n = 25) without carotid plaques or measurable intima-media thickness. Twenty-two age- and sex-matched subjects were recruited as controls (group 3). Groups 1 and 2 displayed significantly higher levels of total cholesterol, apolipoprotein B, human autoantibodies against oxidised low-density lipoprotein and the c fraction of the third component system, and significantly lower levels of high-density lipoprotein cholesterol and apolipoprotein A1 than group 3. However, serum levels of triglyceride and lipoprotein (a) were significantly higher in group 1 than in the control group. Moreover, groups 1 and 2 displayed significantly higher levels of factor VII, fibrinogen, fragment 1+2, thrombin-antithrombin complex and plasminogen activator inhibitor after venous occlusion, and significantly lower levels of tissue-type plasminogen activator after venous occlusion than group 3. Significantly higher levels of tissue-type plasminogen activator and plasminogen activator inhibitor before venous occlusion were observed in groups 1 and 2 and significantly lower levels of antithrombin III, protein C and protein S were observed in group 1 compared with the controls. Patients were also analysed according to levels of lipoprotein (a). The lowest levels of tissue-type plasminogen activator after venous occlusion and the highest levels fragment 1 + 2, the c fraction of the third component system, and plasminogen activator inhibitor after venous occlusion were observed in patients with the highest levels of lipoprotein (a). Our data demonstrate an activation of coagulation and deficient fibrinolysis in survivors of myocardial infarction, particularly in those with associated carotid atherosclerotic lesions. We speculate that this thrombophilic state may play a key role in the pathogenesis of atherosclerotic vascular disease and thromboembolic complications.