Cardiac pathology of transvenous pacemakers in dogs

Fishbein, Michael C.; Tan, Kie S.; Beazell, James; Schulman, Joseph H.; Hirose, Frank M.; Criley, J. Michael

doi:10.1016/s0002-8703(77)80174-9

Cited by 39 publications

(15 citation statements)

References 20 publications

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“…Maximum lead diameter was more important than lead tip area. This may be explained by the fact that histological changes are not confined to the area where the electrode tip is positioned but also extend to other sites along the course of the electrode, such as the right atrium, the papillary muscles, and the right ventricle 1,4,16 . Steroid eluting electrodes were not shown to have an independent effect on peak CTNI levels.…”

Section: Discussionmentioning

confidence: 92%

“…Coagulation necrosis of the myocardial tissue around the electrode has been reported in the first hours after both epicardial 11 and endocardial 18 lead implantation, followed by an acute inflammatory response. Coagulation necrosis and myocytolysis have also been reported in the studies performed a few days to several weeks after lead implantation and have been attributed to focal myocardial hypoxia around the implanted leads due to proliferation of endocardial and interstitial connective tissue 1,2,4,11 . However, the kinetics of CTNI levels indicate that troponin release is the result of early histological events following electrode implantation.…”

Section: Discussionmentioning

confidence: 97%

“…Myocardial atrophy and myocytolysis have not, however, been shown to be less in areas adjacent to steroid eluting leads. Moreover, it is possible that, although inflammation may be associated with myocytolysis at later stages, 1,2,4,11 it is not so important for myocardial damage immediately after electrode implantation. The technique of lead fixation in the right atrium did not have an independent effect on peak CTNI levels.…”

Section: Discussionmentioning

confidence: 99%

“…Histological evidence from animal models has shown that the transvenous insertion of endocardial pacing leads triggers a sequence of local events as a result of the physical and immunological presence of the lead 1,2 . They consist of injury, acute and chronic inflammation, formation of granulation tissue, foreign body reaction, and fibrosis 3 .…”

Section: Introductionmentioning

confidence: 99%

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Biochemical Evidence of Cardiac Damage Following Transvenous Implantation of a Permanent Antibradycardia Pacemaker Lead

Νικολάου

Spanodimos

Tsaglis

et al. 2005

Pacing Clinical Electrophis

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Section: Discussionmentioning

confidence: 92%

Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Biochemical Evidence of Cardiac Damage Following Transvenous Implantation of a Permanent Antibradycardia Pacemaker Lead

Νικολάου

Spanodimos

Tsaglis

et al. 2005

Pacing Clinical Electrophis

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“…Reactive fibrous connective tis sue forms because insertion of an endocardia pacemaker lead irritates the endocardium, cause the local accumulation of platelets and leuko cytes, and provokes an inflammatory response The endocardium adjacent to the distal electrod of an implanted lead becomes thickened by con nective tissue containing fibroblasts, collagen and variable numbers of leukocytes. 7 The sever ity of the leukocytic infiltration and of the ensu ing connective tissue proliferation is presumed to vary among individuals. The thickness and elec trical characteristics of the nonexcitable but con ductive layer of connective tissue (peri-electrode tissue) separating the electrode from the myocar dium directly influence the magnitude of the stimulation threshold.…”

Section: Introductionmentioning

confidence: 99%

Paired Comparisons of Steroid‐Eluting and Nonsteroid Endocardial Pacemaker Leads in Dogs: Electrical Performance and Morphologic Alterations

Radovsky

Vleet

Stokes

et al. 1988

Pacing Clinical Electrophis

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The effects of steroid elution from endocardial pacemaker electrodes on electrical performance and the thickness and cellularity of the reactive fibrous connective tissue formed around the stimulating electrode (peri-electrode tissue) were determined. Comparison was made with a nonsteroid electrode implanted in the same cardiac chamber (right ventricle) in each of six dogs for 6 weeks. Paired Students' t-tests showed that steroid-eluting leads had significantly (P less than .05): (1) lower voltage stimulation thresholds (as determined in sequential measurements made on the conscious animals during the experiment and on the anesthetized dogs at termination of the study); (2) less fibrous connective tissue formation around the electrode surfaces; and (3) fewer cells per unit area of peri-electrode fibrous connective tissue. There were also fewer (P less than .10) mast cells in the reactive connective tissue surrounding steroid-eluting leads. The thinner reactive connective tissue surrounding the steroid-eluting electrodes was correlated with lower voltage stimulation thresholds (r = 0.7, P less than .01). This is consistent with the hypothesis that the effect of the peri-electrode connective tissue is to increase the virtual surface area of the electrode, decreasing current density in adjacent stimulatable tissue. The relatively fewer total cells and mast cells in the peri-electrode connective tissue of the steroid-eluting electrodes suggest that the observed differences in fibrous connective tissue thickness, and therefore voltage stimulation threshold, may be related to a relatively decreased population of inflammatory cells due to the anti-inflammatory properties of the steroid.

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Morphologic and immunohistochemical observations of tissues surrounding retrieved transvenous pacemaker leads

Esposito

Kennergren

Holmstrom

et al. 2002

J. Biomed. Mater. Res.

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Immunohistochemical and morphologic techniques were employed to evaluate the tissue response around chronically implanted pacing leads. Seventeen leads were retrieved from 12 patients. Leads were extracted by direct manual traction (1), extraction with sheaths and locking stylets (1), or with by a combination of mechanical tools and Excimer laser sheaths (15). Mean lead implantation time was 5.6 years (range 1-8 years). Frozen sections, 6-8 microm thick, were incubated with antibodies against HLA-DR antigen, endothelial cells, macrophages, T cells, plasma cells, fibrinogen, and interleukin-1beta. Prominent morphologic observations were fibrous encapsulations of the leads. Immunohistochemical analysis revealed a tissue generally devoid of inflammatory and immune cells. The fibrous capsule surrounding the lead was partially or completely covered with a monolayer of CD34 expressing endothelial cells. The results from this study provide useful information in design and material selection for pacemaker leads. Endothelialization of the fibrous encapsulation indicates a functionalization of blood-contacting surfaces around pacemaker materials, thus providing a mechanism for long-term persistence of foreign materials in the blood. The laser method allowed an efficient extraction of pacemaker leads without damage to the studied tissues, as suggested by the presence of immunolabeled cells close to the cut surfaces.

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Cardiac pathology of transvenous pacemakers in dogs

Cited by 39 publications

References 20 publications

Biochemical Evidence of Cardiac Damage Following Transvenous Implantation of a Permanent Antibradycardia Pacemaker Lead

Biochemical Evidence of Cardiac Damage Following Transvenous Implantation of a Permanent Antibradycardia Pacemaker Lead

Paired Comparisons of Steroid‐Eluting and Nonsteroid Endocardial Pacemaker Leads in Dogs: Electrical Performance and Morphologic Alterations

Morphologic and immunohistochemical observations of tissues surrounding retrieved transvenous pacemaker leads

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