Background. Hypercoagulable disorders can lead to deep vein thrombosis (DVT), arterial thrombosis or embolization, and early or recurrent bypass graft failure. The purpose of this study was to identify whether diabetes increased the likelihood of heparin-induced platelet factor 4 antibodies in at risk vascular patients. Methods. We reviewed clinical data on 300 consecutive patients. A hypercoagulable workup was performed if patients presented with (1) early bypass/graft thrombosis (<30 days), (2) multiple bypass/graft thrombosis, and (3) a history of DVT, pulmonary embolus (PE), or native vessel thrombosis. Relevant clinical variables were analyzed and compared between patients with diabetes (DM) and without diabetes (nDM). Results. 85 patients (47 women; age 53 ± 16 years, range 16–82 years) had one of the defined conditions and underwent a hypercoagulable evaluation. Screening was done in 4.7% of patients with early bypass graft thrombosis, 60% of patients were screened because of multiple bypass or graft thrombosis, and 35.3% had a previous history of DVT, PE, or native vessel thrombosis. Of the 43 patients with DM and 42 nDM evaluated, 59 patients (69%) had an abnormal hypercoagulable profile. An elevated heparin antibody level was present in 30% of DM and 12% of nDM patients (chi-squared test P < 0.04). Additionally, DM was associated with a higher likelihood of arterial complications while nDM was associated with a higher rate of venous adverse events (chi-squared test P < 0.003). Conclusions. Diabetes is associated with a higher likelihood of developing heparin-induced antibodies and an increased combined incidence of arterial complications that include early or multiple bypass/graft thrombosis. This finding may influence the choice of anticoagulation in diabetic patients at risk with vascular disease.

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Placement of ICDs, permanent pacemakers, and biventricular devices is performed under fluoroscopic guidance. Implantable device leads can cause tricuspid regurgitation (TR) when they interfere with leaflet motion. In the past, we had the experience of 2 cases with RV lead who had severe TR; one had lead repositioning and the other needed surgery. Aim: Evaluation of TR after right ventricular (RV) permanent lead implantation to check if echocardiographic guidance is needed for adequate lead positioning. Methods: Seventy six patients had trans-thoracic Doppler echocardiographic studies before and after implantation of permanent RV leads. Results: Before RV lead implantation 96% of patients had TR, grade 1 in 57 patients (75%), grade 2 in 12 (16%), grade 3 and 4 in 4 (5%). After RV lead implantation 44 patients with grade 1 TR remained with the same degree (77%) while in 2 (3.5%) TR progressed to grade 2, and in the remainder the TR disappeared. Most of the patients with grade 2 TR before RV lead implantation (75%) remained in grade 2 while 25% the grade decreased to grade 1. In all the patients with grade 3 and 4 TR pre-implantation, the severity of TR decreased by one grade. In 56 patients with non-CRT device implantations, 39 (70%) had grade I TR before procedure and in 28 (72%) of them TR grade did not change and 11(28%) TR grade progressed to grade 2 after implantation. Grade 2 TR before implantation in 8 patients (14%), the TR grade decreased in3 (37.5%) and did not change in the others. In 3 (5.4%) patients with grade 3 and 4 TR before procedure, the TR decreased after procedure. Conclusions: Implantation of permanent RV leads did not worsen TR grade.