Transformation of S1S2 CV restitution curves to steady state restitution curves
Atrial fibrillation (AF) is the prevailing arrhythmic disease. AF leads to a distortion of the normal heart function and depending on the severity of the disease can suppress blood flow in certain heart regions leading to coagulation which in turn can cause serious consequences like stroke. To prevent this from happening, minimally invasive catheter procedures are used to measure electrical signals by placing electrode arrays on the cells of the inner wall of the atria. Depending on the measured voltage, information about the underlying substrate can be deduced. Furthermore, by measuring a multitude of points, conduction paths and conduction velocities (CV) of the depolarization wave can be traced, aiding the physician in planning ablation therapies. Additionally, the substrate properties CV and amplitude depend on the stimulation rate activating the cells. Therefore, the rate dependency of these properties is measured, yielding restitution information. In clinical practice, measurements using pacing protocols at continuously short cycle lengths as well as measuring ERP restitution is not possible due to the high health risks involved. To overcome this, we use a special measurement protocol called the S1S2 stimulation protocol, in which a single beat of a shorter cycle length is used to measure restitution information. In general, CV restitution is understood as the dependency of CV to a steady state at a basic cycle length. This leads to the following question. Does the single S1S2 beat measurement accurately reproduce the situation of a continuous pacing in the patient, or is there a transient effect for the CV?
To answer this question, we aim for a simulation setup which will reproduce tissue characteristics and changes.
The aim of this thesis is to find out if there is a difference when measuring patient substrate CV with the S1S2 protocol vs. measuring with a continuous pacing (PCL). The current hypothesis is that there is no change when plotting over the diastolic interval (DI). This means when plotting over the stimulation cycle length the shift of both stimulation protocols to each other is only due to the APD change of the previous beat. If this holds true, it is possible to find a transformation between the measured S1S2 protocol and the steady state measurement (BCL). For this transformation, the change of APD with stimulation rate has to be measured or estimated. Since it is not measurable in patients, a simulation study is the best approach.