Authors:

A Saglietto¹ , S Scarsoglio² , C Gallo² , L Ridolfi³ , M Anselmino¹ , ¹Hospital 'Città della Salute e della Scienza di Torino', Division of Cardiology, Department of Medical Sciences - Turin - Italy , ²Politecnico di Torino, Department of Mechanical and Aerospace Engineering - Turin - Italy , ³Politecnico di Torino, Department of Environmental, Land and Infrastructure Engineering - Turin - Italy ,

Citation:

Background. Different mechanisms have been proposed to explain the association between atrial fibrillation (AF) and coronary flow impairment, even in absence of relevant coronary artery disease (CAD). However, the underlying hemodynamics remains unclear.

Purpose. Aim of the present work was to computationally explore whether and to what extent ventricular rate during AF affects the coronary perfusion.

Methods. AF was simulated at different ventricular rates (50, 70, 90, 110, 130 bpm) through a 0D-1D multiscale validated model, which combines the left heart-arterial tree together with the coronary circulation. Artificially-built RR stochastic extraction mimics the in vivo beating features during AF. All the hemodynamic parameters computed are based on the left anterior descending (LAD) artery and account for the waveform, amplitude and perfusion of the coronary blood flow.

Results. Increasing ventricular rates during AF significantly altered LAD flow rate waveform (p < 0.01), due to the shortening of the diastolic phase and the increasing signal variability, with a substantial relative delay of the diastolic peak (Figure, panel a) and reduction of blood volume per beat (ml/beat). As a consequence, coronary blood flow (CBF), calculated as ml/min, increased up to 90-110 bpm and then decreased, while cardiac oxygen consumption, evaluated by rate-pressure product (RPP), increases monotonically with ventricular rate, thus leading to significant imbalances in oxygen supply-demand ratio (p < 0.01) as ventricular rate increased (Figure, panel b).

Conclusions. Higher ventricular rate during AF exerts an overall coronary blood flow impairment and imbalance of the myocardial oxygen supply-demand ratio.

Figure. a) Average flow rate signals of LAD (QLAD) as function of the adimensionalized time, t, at different ventricular rates; b) Mean values (µ, solid curves) and standard deviation values (in terms of µ ± s, shaded areas) of CBF and RPP as function of HR.