Pulmonary Artery Pulsatility Index in Acute and Chronic Pulmonary Embolism

TY - JOUR

T1 - Pulmonary Artery Pulsatility Index in Acute and Chronic Pulmonary Embolism

AU - Lyhne, Mads Dam

AU - Yuriditsky, Eugene

AU - Zochios, Vasileios

AU - Dragsbæk, Simone Juel

AU - Hansen, Jacob Valentin

AU - Andersen, Mads Jønsson

AU - Mellemkjær, Søren

AU - Kabrhel, Christopher

AU - Andersen, Asger

PY - 2025/2/19

Y1 - 2025/2/19

N2 - Background and Objectives: The pulmonary artery pulsatility index (PAPi) is an emerging marker of right ventricular (RV) injury but has not been well investigated in acute pulmonary embolism (PE) or chronic thromboembolic pulmonary hypertension (CTEPH). We aimed to investigate its discriminatory capabilities and ability to detect therapeutic effects in acute PE and CTEPH. Materials and Methods: This was a secondary analysis of data from both experimental studies of autologous PE and human studies of acute PE and CTEPH. PAPi was calculated and compared in (1) PE versus sham and (2) before and after interventions aimed at reducing RV afterload in PE and CTEPH. The correlations between PAPi, cardiac output, and RV to pulmonary artery coupling were investigated. Results: PAPi did not differ between animals with acute PE versus sham, nor was it affected by clot burden (p = 0.673) or at a 30-day follow-up (p = 0.242). Pulmonary vasodilatation with oxygen was associated with a reduction in PAPi (4.9 [3.7–7.8] vs. 4.0 [3.2–5.6], p = 0.016), whereas positive inotropes increased PAPi in the experimental PE. In humans, PAPi did not change consistently with interventions. Balloon pulmonary angioplasty did not significantly increase PAPi (6.5 [4.3–10.7] vs. 9.8 [6.8–14.2], p = 0.1) in patients with CTEPH, and a non-significant reduction in PAPi (4.3 ± 1.6 vs. 3.3 ± 1.2, p = 0.074) was observed in patients with acute PE who received sildenafil. PAPi did not correlate well with cardiac output or measures of RV to pulmonary artery coupling in either species. Conclusions: PAPi did not detect acute, experimental PE or changes as a result of therapeutic interventions in patients with hemodynamically stable acute PE or CTEPH. However, it did change with pharmacological interventions in the experimental PE. Further research should establish its utility in detecting and monitoring RV injury in different clinical phenotypes of acute PE and CTEPH.

AB - Background and Objectives: The pulmonary artery pulsatility index (PAPi) is an emerging marker of right ventricular (RV) injury but has not been well investigated in acute pulmonary embolism (PE) or chronic thromboembolic pulmonary hypertension (CTEPH). We aimed to investigate its discriminatory capabilities and ability to detect therapeutic effects in acute PE and CTEPH. Materials and Methods: This was a secondary analysis of data from both experimental studies of autologous PE and human studies of acute PE and CTEPH. PAPi was calculated and compared in (1) PE versus sham and (2) before and after interventions aimed at reducing RV afterload in PE and CTEPH. The correlations between PAPi, cardiac output, and RV to pulmonary artery coupling were investigated. Results: PAPi did not differ between animals with acute PE versus sham, nor was it affected by clot burden (p = 0.673) or at a 30-day follow-up (p = 0.242). Pulmonary vasodilatation with oxygen was associated with a reduction in PAPi (4.9 [3.7–7.8] vs. 4.0 [3.2–5.6], p = 0.016), whereas positive inotropes increased PAPi in the experimental PE. In humans, PAPi did not change consistently with interventions. Balloon pulmonary angioplasty did not significantly increase PAPi (6.5 [4.3–10.7] vs. 9.8 [6.8–14.2], p = 0.1) in patients with CTEPH, and a non-significant reduction in PAPi (4.3 ± 1.6 vs. 3.3 ± 1.2, p = 0.074) was observed in patients with acute PE who received sildenafil. PAPi did not correlate well with cardiac output or measures of RV to pulmonary artery coupling in either species. Conclusions: PAPi did not detect acute, experimental PE or changes as a result of therapeutic interventions in patients with hemodynamically stable acute PE or CTEPH. However, it did change with pharmacological interventions in the experimental PE. Further research should establish its utility in detecting and monitoring RV injury in different clinical phenotypes of acute PE and CTEPH.

KW - acute pulmonary embolism

KW - animal model

KW - chronic thromboembolic pulmonary hypertension

KW - pulmonary circulation

KW - right heart catheterization

KW - right ventricular function

UR - http://www.scopus.com/inward/record.url?scp=85219005498&partnerID=8YFLogxK

U2 - 10.3390/medicina61020363

DO - 10.3390/medicina61020363

M3 - Journal article

SN - 1010-660X

VL - 61

JO - Medicina

JF - Medicina

IS - 2

M1 - 363

ER -