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Thromboembolic complications of the Jarvik-7 total artificial heart: case report
Insights
The Jarvik-7 total artificial heart (TAH) can cause blood clots, leading to stroke. Thrombus formation occurred in specific TAH components, linked to patient hypercoagulability and heparin resistance.
Area of Science:
- Biomedical Engineering
- Cardiovascular Surgery
- Hematology
Background:
- The Jarvik-7 total artificial heart (TAH) is a device for end-stage heart failure.
- Cerebral embolic events are a significant complication in TAH recipients.
Observation:
- Examination of an explanted Jarvik-7 TAH revealed thrombus formation.
- Thrombotic deposition was concentrated in crevices within the aortic quick connector and around the valves.
Findings:
- Thrombus formation was observed in the aortic quick connector and around all four valves.
- The most severe deposition was on the atrioventricular valves' outflow surface and around the pulmonic valve crevices.
- The patient exhibited developing hypercoagulability and increasing resistance to heparin, correlating with the embolic event.
Implications:
- Understanding thrombus formation sites is crucial for TAH design improvements.
- Patient-specific hypercoagulability and heparin resistance may increase embolic risk.
- Further research is needed to mitigate thrombotic complications in TAH patients.
Abstract:
The Jarvik-7 total artificial heart (TAH) has now been implanted in seven patients, with four (57%) suffering cerebral embolic events. Functional recovery in two patients was impaired by subsequent intracranial hemorrhage from anticoagulant therapy. The findings of a Jarvik-7 TAH explanted following a cerebral embolus are reported here. Thrombotic deposition was seen in the inner crevice formed between the two components of the aortic quick connector. In addition, deposition was seen around all four valves in the crevice formed between the valve ring and the plastic valve housing. On the atrioventricular valves, the deposition in this crevice was most severe on the outflow surface adjacent to the minor flow orifice. On the pulmonic valve, deposition was seen around the entire circumference of both the inflow and the outflow crevices. No thrombi were seen on the diaphragm, the diaphragm-housing junction, or the housing of the left ventricle. Hypercoagulability of the patient's blood gradually developed during implant, reaching a maximum on the evening before the clinical embolus. Increasing resistance to heparin was also demonstrated by in vitro testing.