Risk Factors and Prognosis for Clot Formation on Cardiac Device Leads

Ata Soleimani Rahbar, M.D; Peyman N. Azadani, M.D; Sindhura Thatipelli, B.A; Kirsten E. Fleischmann, M.D., M.P.H; Nhunhu Nguyen, B.A; Byron K. Lee, M.D., M.A.S.

Disclosures

Pacing Clin Electrophysiol. 2013;36(10):1294-1300. 

In This Article

Results

Characteristics of Our Study Cohort

Only 15 of 1,086 (1.4%) cardiac device patients who underwent TTE were found to have thrombus adhered to a device lead without the diagnosis of endocarditis. These 15 patients comprised our study cohort. All case patients had previous TTE studies for comparison. In each case, the thrombus or thrombi was a new finding. In the case group, 60% of patients were females. The mean patient age and device age in the case group was 59.0 ± 21.2 years and 52.0 ± 36.2 months, respectively. The shape of thrombus was string-like (having one measurable dimension) in eight patients, mass-like (having two measurable dimensions) in five patients, and a combined mass-string form (having two measurable dimensions but one dimension is significantly larger) in the other two cases. Using longest diameter in any direction, there were nine cases with medium-sized clots, five patients with small-sized clots, and only one patient had a large thrombus (small: <10 mm, medium: 10–20 mm, large: >20 mm). The mean clot size was 13.8 mm. The location of clot was in the right atrium (RA) in all the cases. We identified the lead to which thrombus or thrombi were adhered. In six of 15 cases, the clot was found to be attached to atrial lead. In eight of 15 cases, the adherent lead was the right ventricular lead. Only in one case, the clot was detected adherent to left ventricular (LV) lead. Furthermore, the distance of clot from the tricuspid valve was measured. The mean distance of clot from tricuspid valve was 2.6 ± 1.3 cm. The minimum distance was 1 cm and the maximum distance was 6 cm. We defined three categories to stratify the clots based on their distance from the tricuspid valve; near: <2 cm, midway: 2–4 cm, and far: >4 cm. According to this stratification, clots in four cases were near tricuspid, in nine cases were in the midway, and in two other cases were far from the tricuspid valve. In five patients, multiple thrombi were observed to be attached to a single cardiac device lead. No patient with multiple thrombi had clot attached to different leads.

Characteristic of the Vegetations

There were 17 patients with endocarditis and vegetation detected by TTE among those 1,086 individuals who had TTE studies after receiving implants (1.6%). Among these 17 patients, 14 individuals had mass-like vegetation, and three patients had string-like vegetation. The mean size of vegetation was 13.5 mm.

The Differences Between the Cases and Controls

Table I shows the gender, comorbidities, and number of implantable cardioverter defibrillators (ICD) versus pacemakers (PMs) in the case and control groups. Additionally, only one patient in the case group (antiphospholipid antibody syndrome) and one patient in the control group (lupus anticoagulant) had coagulopathy. Only one patient in the case group had history of hormone replacement therapy. There were no significant differences between the case cohort and the control cohort in regards to RA enlargement, left atrial enlargement, right ventricular enlargement, LV enlargement, and LV hypertrophy. Furthermore, the anticoagulant/antiplatelet usage between the cases and controls was not significantly different. Table II compares the case and control groups in terms of number of the leads, time since cardiac device implantation, international normalized ratio (INR), body mass index (BMI), partial thromboplastin time (PTT), platelet, ejection fraction, systolic pulmonary artery pressure, and percentage mode switch found at the device clinic interrogation closest to the date of TTE in which clot was discovered. The mean number of leads among the cases was 2.13 versus 2.22 in the controls (P = 0.55). Two patients among the cases had single chamber devices. Other cases had either dual chamber or biventricular devices. Device interrogation information was available in only eight of 15 cases, 39 of 45 controls. In univariate analysis, females had more than four times greater odds of having a clot on their cardiac device lead (odds ratio [OR] = 4.6, 95% confidence interval [CI]: 1.3–16.0, P = 0.024) and patients with a history of AF had an eight times greater odds (OR = 8.0, 95% CI: 2.2–29.3, P = 0.003). Additionally, among the continuous variables, percentage mode switch was associated with forming a clot (P = 0.002). For every 10% increase of mode switch, there was a 33% increase in odds of having a clot. The incidence of clot formation in patients with AF is (10/15) 66.7% and the incidence of this phenomenon in patients without AF as the major risk factor is (5/15) 33.3%. No other variables were examined, including history of malignancy, right-sided or left-sided heart failure, previous anticoagulant/antiplatelet use, or time since device implantation was associated with clot formation. In multivariate analysis after using gender, AF, previous anticoagulant/antiplatelet use, LV hypertrophy, and BMI as covariates (there were trends toward the last two variables in univariate analysis), only AF remained statistically significant (OR = 8.7, 95%CI: 1.8–41.1, P = 0.006).

Therapeutic Strategies

In the case group, seven of 15 patients had persistent AF, whereas three of 15 patients had paroxysmal AF. Follow-up data were available in nine of 15 patients in the case group ( Table III ). Before clot detection, three patients received no anticoagulant/antiplatelet drugs, one was on acetylsalicylic acid (ASA) and clopidogrel, one was taking warfarin and ASA, two patients were on ASA only, and two patients were on warfarin alone. Following clot detection, all nine patients had changes (usually intensification) to their anticoagulant and/or antiplatelet therapy; one of nine patients was switched from warfarin to dabigatran. Those three of nine patients who were already on warfarin were put on a higher dose to achieve a higher target INR that was at least 0.5 higher than the previous target INR ( Table IV ).

Natural History

The mean time to the last follow-up assessment was 269.0 ± 236.5 days.

A complete resolution or shrinkage of clot was observed in eight of nine patients. Only one of nine patients had no change in clot size during follow-up. This patient continued taking ASA alone with higher dose following clot discovery. All these changes were detected by follow-up TTE. For some cases, TEE was performed to confirm changes in thrombus size. None of the cases had known embolic phenomenon attributable to the intracardiac clot.

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