Ischaemic versus non-ischaemic: how does heart failure aetiology affect pulmonary arterial capacitance and pulmonary artery pulsatility index in end-stage heart failure?

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.

Impaired endothelium-dependent and endothelium-independent systemic vasodilatory reserve in pulmonary hypertension regardless the clinical group: A generalized dysfunction beyond the pulmonary arteries?

OBJECTIVE: Endothelium-dependent (ED) and endothelium-independent (EI) flow-mediated vasodilatation (FMD) have been used as measures of systemic arterial vasodilatory reserve. In this study, we aimed to assess both ED-FMD and EI-FMD in different groups with pulmonary hypertension (PH), and to investigate the relationship of these measures with clinical, echocardiographic, and invasive parameters of diseases severity and targeted treatment status. METHODS: Our study population comprised 41 patients with PH [28 (68.2%) women, age 46.3±19.6 years] including idiopathic pulmonary arterial hypertension, Eisenmenger syndrome, and chronic thromboembolic PH in whom diagnosis were confirmed in accordance with current guidelines and 17 age and sex-matched healthy controls. The brachial artery (BA) was used for assessment of FMD with Duplex ultrasound, and serial changes in diameter were recorded at baseline, 1, and 3 minutes after termination of 2-minute external occlusive compression for ED-FMD, and after sublingual intake of glycerol trinitrate for EI-FMD, respectively. RESULTS: Compared with controls, overall the PH group showed significantly lower ED-FMD (0.65±0.21 vs. 0.30±0.23 and 0.65±0.18 vs. 0.24±0.21) and EI-FMD (0.67±0.15 vs. 0.37±0.25 and 0.75±0.20 vs. 0.32±0.24) responses at 1st and 3rd min (p<0.001 for all). All these changes in the values of ED-FMD and EI-FMD were comparable among the PH subgroups. Neither ED-FMD nor EI-FMD were correlated with measures of PH severity and targeted therapy (TT) status (p>0.05). CONCLUSION: Our results suggest an impaired BA vasodilatory reserve in patients with PH regardless of the clinical subgroup. Although these findings seem to be consistent with systemic dysfunction, acute FMD may not reflect the severity of PH and cannot be used as a potential surrogate for outcome in this setting.

Impact of the updated hemodynamic definitions on diagnosis rates of pulmonary hypertension.

We evaluated whether updated pulmonary hypertension definitive criteria proposed in sixth World Symposium on Pulmonary Hypertension had an impact on diagnosis of overall pulmonary hypertension and pre-capillary and combined pre- and post-capillary phenotypes as compared to those in European Society of Cardiology/European Respiratory Society 2015 pulmonary hypertension Guidelines. Study group comprised the retrospectively evaluated 1300 patients (age 53.1 ± 18.8 years, female 807, 62.1%) who underwent right heart catheterization with different indications between 2006 and 2018. Mean pulmonary arterial pressure ≥25 mmHg (European Society of Cardiology) and PAMP (mean pulmonary arterial pressure) >20 mmHg (World Symposium on Pulmonary Hypertension) right heart catheterization definitions criteria were used, respectively. For pre-capillary pulmonary hypertension, pulmonary artery wedge pressure ≤15 mmHg and pulmonary vascular resistance ≥3 Wood units criteria were included in the both definitions. Normal mean pulmonary arterial pressure (<21 mmHg), borderline mean pulmonary arterial pressure elevation (21-24 mmHg), and overt pulmonary hypertension (≥25 mmHg) were documented in 21.1, 9.8, and 69.1% of the patients, respectively. The pre-capillary and combined pre- and post-capillary pulmonary hypertension were noted in 2.9 and 1.1%, 8.7 and 2.5%, and 34.6 and 36.6% of the patients with normal mean pulmonary arterial pressure, borderline, and overt pulmonary hypertension subgroups, respectively. The World Symposium on Pulmonary Hypertension versus European Society of Cardiology/European Respiratory Society definitions resulted in a net 9.8% increase in the diagnosis of overall pulmonary hypertension whereas increases in the pre-capillary pulmonary hypertension and combined pre- and post-capillary pulmonary hypertension diagnosis were only 0.8 and 0.3%, respectively. The re-definition of mean pulmonary arterial pressure threshold seems to increase the frequency of the overall pulmonary hypertension diagnosis. However, this increase was mainly originated from those in post-capillary pulmonary hypertension subgroup whereas its impact on pre-capillary and combined pre- and post-capillary pulmonary hypertension was negligible. Moreover, criteria of pre-capillary pulmonary vascular disease and combined pre- and post-capillary phenotypes were still detectable even in the presence of normal mean pulmonary arterial pressure. The obligatory criteria of pulmonary vascular resistance ≥3 Wood units seems to keep specificity for discrimination between pre-capillary versus post-C pulmonary hypertension after lowering the definitive mean pulmonary arterial pressure threshold to 20 mmHg.