The recent success of transcatheter aortic valve implantation (TAVI) has been associated with a heightened awareness of the potential risks, particularly stroke. Recent meta-analyses report 30-day stroke rates of 3% to 4%,1,2 and diffusion-weighted MRI studies have revealed new, clinically silent, cerebral lesions in 68% to 84% of patients undergoing TAVI.3–5 Although the majority of patients undergoing TAVI benefit greatly in terms of quality of life and functional status, concerns about neurological disability remain. Transcranial Doppler (TCD) has been extremely helpful in clarifying the central role of cerebral embolism as the major cause of intraprocedural stroke. As Kahlert et al4 report, cerebral microembolism occurs in essentially all patients undergoing TAVI. High-intensity transient signals, largely reflecting particulate emboli, are routinely detected during many invasive cardiac procedures. Nevertheless, it has been difficult to demonstrate that high-intensity transient signals correlate directly with stroke, and attempts to correlate high-intensity transient signals with biomarkers of neuronal injury have been inconsistent.3,6 Importantly, TCD has provided considerable information about the relative contributions of the various elements of the TAVI procedure to the risk of cerebral embolization. 1. Initial passage of wires and catheters into the ascending aorta. This seems relatively benign in the great majority of patients. 2. Crossing of the diseased native valve with a wire and diagnostic catheter carries a significant but modest risk of microembolic TCD signals and new MRI lesions.7 Unless necessary, crossing a diseased native valve should be avoided, and when necessary, crossing should be accomplished with as much care and skill as possible.4,7 3. Balloon valvuloplasty disrupts both the endothelial covering and underlying friable calcific material within the diseased valve. Disruption of the valve is progressive; least with balloon dilation, greater yet with repeated …