Left ventricular beat-to-beat performance in atrial fibrillation: Contribution of frank-starling mechanism after short rather than long RR intervals

Abstract

Cycle length-dependent contractile mechanisms, including postextrasystolic potentiation and mechanical restitution, determine the varying left ventricular systolic performance during atrial fibrillation over the entire range of intervals. Beat-to-beat changes in preload, consistent with the Frank-Starling mechanism, also play a role, but their influence is diminished after long preceding and short prepreceding intervals.

Autocorrelation Patterns in the Left-Ventricular Pressure Course of Isolated Working Hearts at Sinus Rhythm

“…It was used to analyse electrical fluctuations in acute atrial fibrillation [13], to auto-recognise tachycardia and fibrillation [14], and to access ventricular performance at random RR intervals [15] or in chronic atrial fibrillation [16]. Some standard heart rate variability indices are mathematically related to the autocorrelation within RR-interval time series [7].…”

“…The response curve is adjusted (shifted) by other regulatory pathways and attributed to Ca 2+ sensitivity of the myocardial filament which increases with precontraction sarcomere length (length dependent activation) [20,22,23,24]. As standing to reason, this effect has been thoroughly investigated by sudden preload changes [25,26] and in the presence of spontaneous [16] or artificially induced ventricular arrhythmia [27,28]. Physiological importance of Frank-Starling's law is acknowledged in attuning right and left cardiac output [21]; apart of that, it is considered somewhat to compensate for lacking neuro-humoral regulation (elderly [19]), transplant recipients [5]) or arrhythmia [16,28].…”

“…The pacing experiments were originally done to exclude possible intrinsic RR fluctuations as a cause for mechanical BI fluctuations, but a contrariant effect emerges. Obviously, pacing at constant cardiac inflow immediately unloads ventricular enddiastolic filling and, consequently, diminishes ejection fraction [16] and stroke volume. Thus, ventricular contraction becomes seemingly downregulated to a highly sensitive part of the FrankStarling response curve, with compensation at the next following beat, as mean cardiac inflow and BI length remain constant.…”

“…As standing to reason, this effect has been thoroughly investigated by sudden preload changes [25,26] and in the presence of spontaneous [16] or artificially induced ventricular arrhythmia [27,28]. Physiological importance of Frank-Starling's law is acknowledged in attuning right and left cardiac output [21]; apart of that, it is considered somewhat to compensate for lacking neuro-humoral regulation (elderly [19]), transplant recipients [5]) or arrhythmia [16,28]. It has been stated that Starling's law cannot readily been demonstrated even by gross volume changes in healthy subjects, due to autonomic nervous counteraction [25]; subsequent studies relativised this notion [22,26].…”

“…Heterometric autoregulation is the most pertinent (if not only) mechanism providing an immediate, viz., end-diastole-to-systole regulation of LVP development [16,19,20]. It remains effective Left-ventricular pressure curves (sinus rhythm) are lagged to autocorrelation windows of 1 to 24 seconds width (see Table) by 1 to 20,000 ms, covering nBI beats (median, with central 90% range).…”