Abstract The cardiac pathology of the nine case with transvenous pacemakers was reviewed. Thrombosis which developed along the wire of the pacemakers was organized into a tight fibrous sheath adherent to the tricuspid valve or chordae tendineae, which may hinder replacement of the pacemakers. After inflammation subsided around the tip of the electrode, gradual fibrous thickening of the underlying endocardium occurred that may result in increased pacemaker threshold. Initial inflammation and thrombosis was noted in the SA node area which may be of no clinical significance. Complications of pulmonary embolism and perforation of the apex were also observed.