Pacemaker/ICD Patients: To Anticoagulate or Not To Anticoagulate?

Abstract

Patients with atherosclerosis, valvular, ischemic, and dilatative cardiomyopathies, or atrial fibrillation, and those with a cardiac valvular prothesis, by-pass, pacemaker, or ICD, may be subject to thrombotic or thromboembolic events (TEEs). TEEs associated with the implantation or chronic presence of permanent pacing leads have been described in many case reports but are actually considered a relatively uncommon complication of cardiac pacing [1]. TEEs have traditionally been reported as a late problem (more than 1 month after implantation of a pacemaker or ICD), and embolic complications have been reported as occurring at any time following implantation. However, venous obstruction can also occurr soon after implantation [2, 3]. Venous stenosis and thrombosis after permanent cardiac pacing are probably more common than previously thought because most patients remain asymptomatic and the condition remains undetected. An understanding of the thromboembolic complications of transvenous cardiac pacing is important because prompt diagnosis and therapy may diminish the potential for morbidity and mortality. The pathogenesis of venous thrombosis after implantation of a permanent transvenous pacemaker or ICD has not been clearly determined. Possible causes of early thrombosis include the following:

• 1. Extrusion of thrombus from the ligated vein (especially with the cephalic vein approach)

• 2. Lead entry site

• 3. Lead-induced endothelial trauma, which causes local release of coagulation factors

• 4. Hypercoagulability induced by the surgical procedure

• 5. Atrioventricular asynchronism that causes numerous atrial contractions against closed atroventricular valves (this mechanism is even more significant in patients with 1:1 ventricular retrograde conduction)

• 6. Presence of the lead in the right ventricle

• 7. Old age in patients with pacemaker or ICD

• 8. Interventricular and intraventricular asynchronism of contraction. Venous thrombosis that occurs more than 1 year after implantation of a permanent transvenous pacemaker is usually associated with underlying venous stenosis, which may result from fibrosis of preexistent venous thrombi. The long-term residence of a permanent lead in the venous system may also act a continuing nidus for formation of a thrombus [4–6]. The presence of multiple transvenous pacemaker leads, especially if one is severed, also increases the risk of thrombosis [7, 8]. In addition, the pacing lead may produce a foreign-body type of reaction and subsequent inflammation and fibrosis along the course of the lead. In some reports on the evaluation of antiplatelet therapy and platelet aggregability in patients with pacing [9,10], Fazio et al. have shown an increase of TEEs (fatal and nonfatal stroke, fatal and nonfatal myocardial infarction, inferior limb thromboembolism) in patients treated with antiplatelet therapy compared to those not so treated (p < 0.05) [9]; they have shown a significant increase of β-Tromboglobulin (β-Tg) in paced patients with respect to controls. Even if their data do not conclusively demonstrate a precise causal relationship between platelet activation and increase of TEEs in patients with pacemakers or ICDs, they strongly suggest that antiplatelet drugs could represent a pathogenic treatment in these patients.