Key result
Exercise deteriorated postexercise ventricular-arterial coupling in patients with systolic heart failure, whereas controls maintained baseline status.
Why the study?
Does exercise worsen postexercise ventricular-arterial coupling and pulsatile efficiency in patients with systolic dysfunction compared to matched controls?
Observational (n=60)
Does exercise worsen postexercise ventricular-arterial coupling and pulsatile efficiency in patients with systolic dysfunction compared to matched controls?
Exercise induces ventricular-arterial decoupling and pulsatile inefficiency that extends into the postexercise recovery phase in patients with systolic heart failure.
Answers are grounded in this paper and cite their sources.
May warrant postexercise VA monitoring in HF; leaves open whether targeting pulsatile efficiency improves recovery.
BACKGROUND: A suboptimal ventricular-arterial (VA) interaction may have a prolonged depressing effect on the failing heart after functional reserves forced to their limits under stress conditions such as exercise. The continuation of excessive load in the postexercise period may be more important than the load during exercise, because the sum of postexercise periods generally exceeds exercise time itself. We sought that exercise-induced changes in postexercise VA coupling and pulsatile efficiency in patients with heart failure (HF). METHODS: Thirty consecutive HF with reduced ejection fraction (EF) and thirty age-, sex- and peak VO2 -matched subjects with preserved EF were enrolled. Pre- and postexercise echocardiographic and tonometric measurements were taken to calculate left ventricular and arterial elastances, arterial compliance and wave reflections, and steady and pulsatile power. RESULTS: VA coupling significantly deteriorated in HF group (from 1·50 ± 0·47 to 2·00 ± 0·75 mmHg/mL, P < 0·01), but control group maintained basal favourable coupling status after exercise (from 1·04 ± 0·29 to 1·03 ± 0·24 mmHg/mL, P = 0·77). Pulsatile percentage of total power significantly increased with exercise in HF group, whereas it showed a significant decrease in control group. The change in pulsatile power fraction was correlated with the change in augmentation pressure (r = 0·41, ß = 3·00, P < 0·01) and inversely correlated with the change in total arterial compliance (r = -0·29, ß = -8·52, P = 0·02). CONCLUSION: Our data indicate that exercise-induced VA decoupling and pulsatile inefficiency extend into postexercise phase in patients with systolic dysfunction. The exact duration of these derangements requires further studies.
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Aslanger et al. (2015) conducted an observational in Heart failure with reduced ejection fraction (n=60). Exercise vs. Matched subjects with preserved EF was evaluated on Postexercise ventricular-arterial coupling (mmHg/mL) (p=<0.01). Exercise deteriorated postexercise ventricular-arterial coupling in patients with systolic heart failure, whereas controls maintained baseline status.
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