Introduction With synchrony of ventricular contraction already restored by cardiac resynchronisation therapy (CRT), optimisation of atrioventricular (AV) delay relies on improving filling. Although when AV delay is improved blood pressure immediately rises, there is a subsequent partial decline. Is this secondary decline because (1) non-invasive measurements are unreliable, (2) cardiac function increment is short-lived or (3) peripheral vasodilatation occurs? We conducted invasive experiments to distinguish between these hypotheses.
Methods Nine patients with heart failure and CRT underwent changes in programmed AV delay from 40 ms to 120 ms. We simultaneously measured beat-by-beat invasive aortic pressure and flow, and non-invasive pressure (Finometer). Triplicate sets of experiments were performed and averaged to minimise the impact of noise.
Results There was an immediate increment in invasive blood pressure of +14.7±2.0 mm Hg (p=0.0001), but after ∼10 beats there was a secondary progressive decline to a lower plateau of +8.0±1.8 mm Hg (p=0.004), Abstract 004 figure 1. The initial increment was caused by an immediate rise in flow by +9.1±2.4% (p=0.007) which did not drop later. The secondary decline in pressure was caused by a delayed gradual decline in total peripheral resistance. Finometer-derived non-invasive blood pressure tracked invasive pressure closely (r=0.97).
Conclusion When AV delay is made more favourable, only the instant pressure increment is caused by increase in stroke volume. The secondary pressure decline is caused by systemic vasodilatation. Design of AV optimisation protocols, which face severe challenge of signal vs noise, might benefit from recognition that not all beats are equally informative: the first few after a transition are most signal-rich.
- Cardiac resynchonisation therapy
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