[show abstract][hide abstract] ABSTRACT: Heparin-induced thrombocytopenia (HIT) results from development of an antibody to a complex of heparin and platelet factor 4 (PF4) resulting in thrombocytopenia and a prothrombotic state with serious clinical consequences. The diagnosis depends on a combination of both the clinical presentation and laboratory detection of an appropriate antibody.
To determine the frequency, clinical characteristics and laboratory correlates of HIT in a tertiary care hospital.
A retrospective review of all case of HIT over a thirty month period in a tertiary care hospital was conducted.
HIT was diagnosed in 136 patients including 114/28,091 (0.48%) of those receiving only unfractionated heparin, 22/6,559 (0.33%) of those that received both unfractionated and low-molecular-weight heparin (LMWH) and in 2/2498 (0.08%) of those receiving only LMWH (P=0.02 compared to those receiving only unfractionated heparin). HIT occurred in 62/16,939 patients (0.39%) of patients receiving subcutaneous (SC) heparin or LMWH compared to 69/11,152 (0.62%) of patients receiving intravenous (IV) therapy (P=0.003). Of all patients with exposure to heparin products, 41/34,650 (0.1%) developed symptomatic thrombosis. The optical density (OD) of the ELISA was significantly higher in patients with HIT and thrombosis (1.2 +/- 0.8) compared to those without thrombosis (0.9 +/- 0.6, P=0.03).
HIT develops in approximately 0.4% of all patients exposed to heparin at a tertiary care hospital but is significantly less frequent in those treated with LMWH only than in those who receive unfractionated heparin. A higher antibody titer is associated with the development of thrombosis. The occurrence of HIT could be decreased by reducing exposure to unfractionated heparin, and the diagnosis could be improved by reporting the OD of the ELISA test result.
Thrombosis Research 03/2009; 124(2):189-92. · 3.13 Impact Factor
[show abstract][hide abstract] ABSTRACT: Venous complications of pacemaker/ implantable cardioverter defibrillator (ICD) system implantation rarely cause immediate clinical problems. The challenge starts when patients come for system revision or upgrade. Numerous reports of venous complications such as stenosis, occlusions, and superior vena cava syndrome have been published. We reviewed current knowledge of these complications, management, and their impact on upgrade/revision procedures. One study has suggested that intravenous lead infection promotes local vein stenosis. Another found that the presence of a temporary wire before implantation is associated with an increased risk of stenosis. Although data for ICD leads is based only on three studies-it suggests that the rate of venous complications is very similar to that of pacing systems, and probably data from pacing leads can be extrapolated to ICD leads. Despite 40 years of experience with transcutaneous implanted intravenous pacing systems and dozens of studies, we were unable to identify clear risk factors (confirmed by independent studies) that lead to venous stenosis. Neither the hardware (lead size, number and material) nor the access site choice (cephalic cut down, subclavian or axillary puncture) appears to affect rate of venous complications. A few factors were proposed as predictors of severe venous stenosis/occlusion: presence of multiple pacemaker leads (compared to a single lead), use of hormone therapy, personal history of venous thrombosis, the presence of temporary wire before implantation, previous presence of a pacemaker (ICD as an upgrade) and the use of dual-coil leads. Anticoagulant therapy (for other reasons than pacemaker lead) seemed to have protective antithrombotic effect.