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Clinical and laboratory risk factors of thrombotic complications after pacemaker implantation: a prospective study
Petri Korkeila1, Pirjo Mustonen, Juhani Koistinen
1Department of Internal Medicine, Turku University Hospital, Kiinamyllynkatu 4-8, PL 52, FIN-20521 Turku, Finland. petri.korkeila@tyks.fi
Insights
Pacemaker implantation can cause venous lesions and thromboembolism (VTE). While it induces a temporary hypercoagulable state, patient risk factors, not procedure details, are key to developing these complications.
Area of Science:
- Cardiology
- Vascular Medicine
- Medical Device Research
Background:
- Venous lesions, including obstruction and venous thromboembolism (VTE), are recognized complications following pacemaker implantation.
- Identifying risk factors is crucial for preventing these adverse events.
Purpose of the Study:
- To prospectively assess patient and procedure-related risk factors for venous lesions and VTE after pacemaker implantation.
Main Methods:
- A prospective venography-based study of 150 pacemaker implantations with 6-month follow-up.
- Case-control analysis of 47 patients with new venous lesions versus matched controls.
- Evaluation of surgical factors, VTE risk factors, and plasma markers of coagulation and endothelial activation.
Main Results:
- No procedure-related variables predicted VTE.
- Transient increases in plasma markers (vWF, F1+2, DD) occurred equally in cases and controls.
- Clustering of classic VTE risk factors, not individual factors, was associated with venous lesions.
Conclusions:
- Pacemaker implantation causes a transient hypercoagulable state, but its severity does not predict VTE.
- Endothelial damage markers did not predict VTE.
- The multifactorial etiology of venous lesions involves a clustering of classic thrombotic risk factors.
Aims:
Venous lesions, including obstruction and thromboembolism (VTE), are not uncommon after pacemaker implantation. The purpose of this prospective study was to assess the role of various patient and procedure-related risk factors in the development of these complications.
Methods And Results:
A prospective venography-based study of 150 consecutive pacemaker implantations with a 6-month follow-up was conducted. Current case-control study included all cases (n = 47) with a new venous lesion, and their matched controls. Several surgical and technical factors, i.e. lead burden, choice of venous access, operator experience and procedure duration, as well as patient-related classic risk factors of VTE were assessed. Plasma markers of coagulation and endothelial activation [prothrombin fragment 1 + 2 (F1 + 2), D-dimer (DD), von Willebrand factor (vWF), thrombomodulin (Tm)] were used to evaluate the extent of acute surgical trauma. All cases with venous lesions were also screened for thrombophilia. None of the procedure-related variables were predictive of VTE. Mean levels of vWF, F1 + 2 and DD increased significantly (P < 0.001) and equally in both cases and controls. No single clinical factor predicted venous lesions, but significant (P < 0.05) clustering of classic clinical VTE risk factors was seen among the cases. Thrombophilia was overrepresented in patients with symptomatic pulmonary embolism (2/5, 40%).
Conclusion:
Pacemaker implantation induces a transient hypercoagulable state, but its degree does not predict subsequent venous thromboembolism, and neither did the grade of endothelial damage as reflected by plasma markers. The aetiology of these lesions seems to be multifactorial, and clustering of classic thrombotic risk factors plays a role in the pathogenesis.
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