Key result
Ischaemic cardiomyopathy was associated with lower pulmonary arterial capacitance (1.25 vs 1.58, p=0.002) and higher pulmonary artery pulsatility index (3.4 vs 2.5, p=0.007) than non-ischaemic etiology.
Why the study?
Heart failure aetiology may differentially affect right ventricular function and afterload, but whether PAC and PAPi differ between ICMP and NICMP in end-stage heart failure was unclear.
Does ischaemic versus non-ischaemic aetiology affect pulmonary arterial capacitance and pulmonary artery pulsatility index in end-stage heart failure?
Observational (n=215)
Does ischaemic versus non-ischaemic aetiology affect pulmonary arterial capacitance and pulmonary artery pulsatility index in end-stage heart failure?
In end-stage heart failure, an ischaemic aetiology is associated with higher right ventricular afterload (lower PAC) and better right ventricular function (higher PAPi) compared to a non-ischaemic aetiology.
Ischaemic etiology linked to distinct RV-pulmonary coupling in end-stage HF; hypothesis-generating for prognosis and device selection.
Background The aetiology of heart failure may have different effects on right ventricular (RV) function, pulmonary pressures and RV afterload. Pulmonary arterial capacitance (PAC) and pulmonary artery pulsatility index (PAPi) are novel haemodynamic indices used in determining RV afterload and RV function, respectively. We aimed to investigate whether there was a difference in PAC and PAPi between ischaemic cardiomyopathy (ICMP) and non-ischaemic cardiomyopathy (NICMP) in patients with end-stage heart failure.Methods and results A total of 215 subjects undergoing evaluation for heart transplantation or left ventricular (LV) assist device were classified into two groups: ICMP (n = 101) and NICMP (n = 114). The patients with LV ejection fraction ≤ 25% were included in the study. ICMP group had lower PAC and higher PAPi values compared to NICMP group [1.25 (0.82–1.86) vs. 1.58 (1.02–2.21), p = 0.002 and 3.4 (2.2–5.0) vs. 2.5 (1.7–4.0); p = 0.007]. Pulmonary vascular resistance, pulmonary artery systolic and mean pressure were higher in ICMP group compared to NICMP group [3.5 ± 1.8 vs. 2.9 ± 2.3, p = 0.004; 59.0 (42.0–73.0) vs. 46.0 (37.0–59.0), p < 0.001, 35.0 (27.0–46.0) vs. 31.0 (23.0–39.0), p = 0.002]. The patients with ICMP had higher tricuspid annular plane systolic excursion and less RV dilatation. ICMP was an independent risk factor for pulmonary hypertension (OR: 4.02, 95% CI: 1.13-14.24, p = 0.031).Conclusion ICMP was associated with lower PAC and higher PAPi. These results indicated that an ischaemic aetiology is associated with higher RV afterload and better RV function in the end-stage heart failure.
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Bayram et al. (2021) conducted an observational in End-stage heart failure (n=215). Ischaemic cardiomyopathy (ICMP) vs. Non-ischaemic cardiomyopathy (NICMP) was evaluated on Pulmonary arterial capacitance (PAC) (p=0.002). Ischaemic cardiomyopathy was associated with lower pulmonary arterial capacitance (1.25 vs 1.58, p=0.002) and higher pulmonary artery pulsatility index (3.4 vs 2.5, p=0.007) than non-ischaemic etiology.
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