Abstract

Abstract Background It has been suggested that left atrial (LA) characteristics modulate the functional capacity in heart failure (HF) patients through the impact that LA cavity exerts on the pulmonary circulation and the pulsatile component of right ventricular (RV) afterload, as represented by pulmonary arterial compliance (PAC). Purpose Thus, we hypothesized that, in a HF patients' population, a larger relative contribution of LA phasic conduit function (PCF) to the left ventricular (LV) stroke volume would be associated with a heavier right ventricular hemodynamic burden and a reduced functional capacity. Methods 60 sinus rhythm HF subjects (42 males, 67±11 years, ejection fraction [EF] 39±11%, range 20% - 62%) underwent 6 minute walking test (6MWT) and routine transthoracic echocardiography, plus real time 3D acquisitions analyzed with a dedicated echo software package. LV ejection fraction (EF) was obtained from 3D echo acquisitions. LV diastolic dysfunction (DD) was assessed according to current guidelines. Computation of PCF was made by simultaneous gathering real time 3D multibeats (6 cycles) LA and LV volumes, using the formula: PCF(time) = [LV(time) − LV minimum] − [LA maximum − LA(time)] as proposed by Bowman & Kovacs (2004), with PCF expressed as % of LV stroke volume. Atrioventricular compliance (Cn) was also assessed, as proposed by Flachskampf et al. (1992): 1270*(mitral valve area/E wave downslope) and expressed in ml/mmHg. Finally, PAC was obtained as the ratio between RV stroke volume (pulmonary velocity time integral*pulmonary valve annulus area measured from the RV outflow tract diameter) and pulse pressure (obtained from pulmonary and tricuspid regurgitant envelopes) and expressed in ml/mmHg. Results Maximal LA and LV volumes averaged 69±21 ml and 147±47 ml, respectively. The mean value of PCF was 33±12% (range 7% - 58%). Mean 6MWT was 397±162 m. Mean PAC was (3.1±1.1 ml/mmHg). DD grade I, II and III were detected in 38 (63%), 18 (30%) and 4 (7%) of the patients' population, respectively. PCF was independent of LA or LV volumes and EF, but showed a strong direct relation with DD (r=0.62; p<0.0001) and a relevant inverse dependence on Cn (r=−0.48; p=0.0001). For a comparable Cn, dividing patients into tertiles according to 6MWT, it was clear that highest PCF was significantly associated with lowest functional capacity (ANCOVA, figure left). Similarly, dividing patients into tertiles according to PAC, it emerges that highest PCF is significantly associated with most deranged PAC (ANCOVA, figure right), suggesting outmost RV hemodynamic burden. Conclusion PCF is an important parameter to be quantified in HF patients that is dependent on global left heart compliance, being affected by DD, but not LV EF. Furthermore, at a given Cn, PCF is increased in HF patients with lowest functional capacity, likely because RV pulsatile afterload is highest in these subjects.

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