Acute changes in microvascular resistance after treating aortic stenosis

How does the reversal of aortic stenosis by transcatheter aortic valve implantation (TAVI) acutely alter myocardial physiology? Addressing this question – as was done in the recent collaborative manuscript from three centres in Italy and Belgium1 – allows us a timely opportunity to synthesise 30 years of data with a view to clinical application.

While often written about in the singular form, the term “hyperaemic microvascular (or myocardial) resistance” actually contains two conceptual parts. First, how much flow (mL/min) results from a given coronary driving pressure (mmHg)? Second, at what coronary pressure does flow cease? The first notion corresponds to our intuition of resistance (a constant value during hyperaemia). However, the second notion reminds us that – unlike a classical electrical circuit – the system does not behave proportionally without accounting for what has been termed the zero-flow or wedge or back pressure (depending on the details of its assessment and with conceptual differences beyond the scope of this editorial). Visually, myocardial resistance can be depicted as shown in Figure 1A: a straight line linking...