Randomised controlled trial
Acyl ghrelin improves cardiac function in heart failure and increases fractional shortening in cardiomyocytes without calcium mobilization
- Randomised controlled trial
- double-blind
- placebo-controlled
Authors' conclusion
In patients with HFrEF, acyl ghrelin increased cardiac output without causing hypotension, tachycardia, arrhythmia, or ischaemia. In isolated cardiomyocytes, acyl ghrelin increased contractility independently of preload and afterload and without Ca2+ mobilization, which may explain the lack of clinical side effects.
Study context
- Population
- Patients with chronic heart failure and reduced ejection fraction (HFrEF); plus ex vivo isolated mouse cardiomyocytes
- Participants
- 31 patients
- Comparison
- Acyl ghrelin vs placebo
- Primary endpoint
- Change in cardiac output
Primary result
As reported in the abstract
Cardiac output (baseline to end of infusion)
Acyl ghrelin
4.08 ± 1.15 to 5.23 ± 1.98
L/min
Placebo
4.26 ± 1.23 to 4.11 ± 1.99
L/min
P < 0.001
Further findings
| Outcome | Acyl ghrelin | Placebo |
|---|---|---|
| Heart rate (nominal decrease) | 71 ± 11 to 67 ± 11 b.p.m. | 69 ± 8 to 68 ± 10 b.p.m. |
Stroke volume, LVEF, segmental longitudinal strain, TAPSE
- Significant increase in stroke volume with acyl ghrelin
- Nominal increases in LVEF, segmental longitudinal strain and TAPSE
Isolated mouse cardiomyocytes (mechanistic)
- Acyl ghrelin increased fractional shortening, did not affect Ca2+ transients and reduced troponin I phosphorylation
- Increase in fractional shortening and reduction in troponin I phosphorylation blocked by the antagonist D-Lys 3
Safety
BP, arrhythmias, ischaemia
- No effects on BP, arrhythmias or ischaemia
Original publication
Acyl ghrelin improves cardiac function in heart failure and increases fractional shortening in cardiomyocytes without calcium mobilization. Eur Heart J. Published 14 March 2023. doi:10.1093/eurheartj/ehad100
Summarised from the published abstract; every number is checked against it