Driveline infection remains a common complication of ventricular assist device (VAD) therapy. These infections often progress from the exit site through the subcutaneous tract to the deeper tunnel and, in severe cases, the pocket, underscoring the vulnerability of the driveline–tissue interface. In this review, we examine the biological and mechanical factors governing tissue-driveline interactions and their implications for tissue integration of the implanted driveline. Dysregulated inflammation, impaired vascular maturation, abnormal extracellular matrix remodeling, repetitive micromotion and traction, and biomaterial–tissue mismatch may all compromise optimal tissue ingrowth of the driveline. Insufficient tissue integration can lead to the formation of microgaps within the driveline tunnel, providing a potential niche for microbial colonization and biofilm formation, thereby contributing to persistent driveline infections. Recognizing the potential association between inadequate tissue integration and the occurrence of driveline infection shifts the focus from microbial eradication alone toward optimizing driveline–tissue interactions across different segments of the driveline. Such an approach may help reduce the incidence of driveline infections in patients requiring long-term VAD support. Finally, strategies to promote tissue integration and long-term driveline stability, including driveline surface engineering, modulation of physicochemical properties, and optimization of surgical techniques, are discussed.
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Qiu et al. (2026) studied this question.
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