Surgical specimens, haemodynamics and long-term outcomes after pulmonary endarterectomy

Nika Skoro-Sajer, Gabriel Marta, Christian Gerges, Gerald Hlavin, Patrick Nierlich, Shahrokh Taghavi, Roela Sadushi-Kolici, Walter Klepetko, Irene Marthe Lang, Nika Skoro-Sajer, Gabriel Marta, Christian Gerges, Gerald Hlavin, Patrick Nierlich, Shahrokh Taghavi, Roela Sadushi-Kolici, Walter Klepetko, Irene Marthe Lang

Abstract

Background: Chronic thromboembolic pulmonary hypertension is surgically curable by pulmonary endarterectomy (PEA). It is unclear whether PEA impacts primarily steady state right ventricular afterload (ie, pulmonary vascular resistance (PVR)) or pulsatile right ventricular afterload (ie, pulmonary arterial compliance (C(PA))). Our objectives were to (1) quantify PEA specimens and measure the impact of PEA on PVR and C(PA) in a structure/function study and (2) analyse the effects of haemodynamic changes on long-term survival/freedom of lung transplantation in an outcome study.

Methods: Thrombi were laid out, weighed, photographed and measured. PVR, C(PA) and resistance times compliance (RC-time) were assessed at baseline, within 4 days after PEA ('immediately postoperative') and 1 year after PEA, in 110 consecutive patients who were followed for 34.5 (11.9; 78.3) months.

Results: Lengths and numbers of PEA specimen tails were inversely correlated with immediate postoperative PVR (p<0.0001, r=-0.566; p<0.0001, r=-0.580). PVR and C(PA) normalised immediately postoperatively while RC-time remained unchanged. Immediate postoperative PVR was the only predictor of long-term survival/freedom of lung transplantation (p<0.0001). Patients with immediate postoperative PVR<590 dynes.s.cm(-5) had better long-term outcomes than patients with PVR≥590 dynes.s.cm(-5) (p<0.0001, respectively).

Conclusions: PEA immediately decreased PVR and increased C(PA) under a constant RC-time. However, immediate postoperative PVR was the only predictor of long-term survival/freedom of lung transplantation. Our study confirms the importance of a complete, bilateral surgical endarterectomy. Low PVR measured immediately postoperative predicts excellent long-term outcome.

Keywords: Primary Pulmonary Hypertension; Pulmonary Embolism.

Figures

Figure 1
Figure 1
Illustration of how numbers and lengths of tails were accounted for. Tails were defined as dissectates not exceeding 2 mm in thickness and at least 2 mm in length (measured tails in this specimen are pointed out by white double-headed arrows). For the analysis, thrombus tails were counted and their total length was expressed in centimetres. The following two examples represent a ‘good’ (A) and a ‘poor’ (B) surgical specimen. (A) Surgical specimen of patient #101 with an immediate postoperative pulmonary vascular resistance (PVR) of 190 dynes.s.cm−5 and 19 thrombus tails (total tail length 24.5 cm). (B) Surgical specimen of patient #14 with an immediate postoperative PVR of 640 dynes.s.cm−5 and only four thrombus tails (total tail length 8.1 cm).
Figure 2
Figure 2
Scatter plots of immediate postoperative pulmonary vascular resistance (PVR) against the cumulative length of surgically extracted thrombus tails in centimetres (p

Figure 3

Box plots of steady and…

Figure 3

Box plots of steady and pulsatile flow parameters at baseline, immediately postoperative and…

Figure 3
Box plots of steady and pulsatile flow parameters at baseline, immediately postoperative and at 1-year follow-up (FU). (A) Pulmonary vascular resistance (PVR) decreased from preoperative 770.4 (583.2; 1011) to 368.5 (250.5; 516) immediately postoperative, and to 280 (186.3; 472) dynes.s.cm−5 at 1-year FU (p<0.001, p<0.001, ie, respective changes from baseline). (B) Pulmonary arterial compliance (CPA) changed from 1.0 (0.8; 1.4) to 2.1 (1.5; 3.2) immediately postoperative, and to 2.7 (1.4; 3.8) mL/mm Hg at 1-year FU (p<0.001 and p<0.001). (C) Resistance times compliance (RC-time) did not change significantly during the observation period: RC-time=0.72+0.71 s (baseline), RC-time=0.60+0.3 s (immediately postoperatively) and RC-time=0.59+0.34 s (1-year FU; p=0.13 and p=0.32). (D) Stroke volume (SV) increased from preoperative 58.4±16.8 to 61.1±20.9 immediately postoperative and to 71.6±18.6 mL at 1-year FU (p=NS and p<0.001).

Figure 4

Δ Pulmonary vascular resistance (PVR)…

Figure 4

Δ Pulmonary vascular resistance (PVR) and Δ pulmonary arterial compliance (C PA )…

Figure 4
Δ Pulmonary vascular resistance (PVR) and Δ pulmonary arterial compliance (CPA) represented as vectors from the origin, indicating changes in both PVR and CPA between catheterisations at baseline and immediately postoperative. All patients’ vectors with persistent/recurrent pulmonary hypertension (PH) in the left-upper quadrant are localised within the circled area (representing cases with only a minor improvement in CPA and PVR).

Figure 5

Receiver operator characteristics curve identifying…

Figure 5

Receiver operator characteristics curve identifying an immediate postoperative pulmonary vascular resistance (PVR) of…

Figure 5
Receiver operator characteristics curve identifying an immediate postoperative pulmonary vascular resistance (PVR) of 590 dynes.s.cm−5 as the PVR threshold with greatest areas under the curve for likelihood of survival at 1, 3 and 5-year follow-ups.

Figure 6

(A) Kaplan–Meier survival curves in…

Figure 6

(A) Kaplan–Meier survival curves in patients with operated chronic thromboembolic pulmonary hypertension (CTEPH)…

Figure 6
(A) Kaplan–Meier survival curves in patients with operated chronic thromboembolic pulmonary hypertension (CTEPH) and immediate postoperative pulmonary vascular resistance (PVR)≥590 dynes.s.cm−5 compared with patients with immediate postoperative PVR<590 dynes.s.cm−5. Patients with immediate postoperative PVR<590 dynes.s.cm−5 had a better long-term outcome than patients with PVR≥590 dynes.s.cm−5 (p<0.0001). (B) Kaplan–Meier survival curves in patients with operated CTEPH by tertiles of immediate PVR (p<0.001, respectively).
Figure 3
Figure 3
Box plots of steady and pulsatile flow parameters at baseline, immediately postoperative and at 1-year follow-up (FU). (A) Pulmonary vascular resistance (PVR) decreased from preoperative 770.4 (583.2; 1011) to 368.5 (250.5; 516) immediately postoperative, and to 280 (186.3; 472) dynes.s.cm−5 at 1-year FU (p<0.001, p<0.001, ie, respective changes from baseline). (B) Pulmonary arterial compliance (CPA) changed from 1.0 (0.8; 1.4) to 2.1 (1.5; 3.2) immediately postoperative, and to 2.7 (1.4; 3.8) mL/mm Hg at 1-year FU (p<0.001 and p<0.001). (C) Resistance times compliance (RC-time) did not change significantly during the observation period: RC-time=0.72+0.71 s (baseline), RC-time=0.60+0.3 s (immediately postoperatively) and RC-time=0.59+0.34 s (1-year FU; p=0.13 and p=0.32). (D) Stroke volume (SV) increased from preoperative 58.4±16.8 to 61.1±20.9 immediately postoperative and to 71.6±18.6 mL at 1-year FU (p=NS and p<0.001).
Figure 4
Figure 4
Δ Pulmonary vascular resistance (PVR) and Δ pulmonary arterial compliance (CPA) represented as vectors from the origin, indicating changes in both PVR and CPA between catheterisations at baseline and immediately postoperative. All patients’ vectors with persistent/recurrent pulmonary hypertension (PH) in the left-upper quadrant are localised within the circled area (representing cases with only a minor improvement in CPA and PVR).
Figure 5
Figure 5
Receiver operator characteristics curve identifying an immediate postoperative pulmonary vascular resistance (PVR) of 590 dynes.s.cm−5 as the PVR threshold with greatest areas under the curve for likelihood of survival at 1, 3 and 5-year follow-ups.
Figure 6
Figure 6
(A) Kaplan–Meier survival curves in patients with operated chronic thromboembolic pulmonary hypertension (CTEPH) and immediate postoperative pulmonary vascular resistance (PVR)≥590 dynes.s.cm−5 compared with patients with immediate postoperative PVR<590 dynes.s.cm−5. Patients with immediate postoperative PVR<590 dynes.s.cm−5 had a better long-term outcome than patients with PVR≥590 dynes.s.cm−5 (p<0.0001). (B) Kaplan–Meier survival curves in patients with operated CTEPH by tertiles of immediate PVR (p<0.001, respectively).

References

    1. Jamieson SW, Kapelanski DP, Sakakibara N, et al. Pulmonary endarterectomy: experience and lessons learned in 1,500 cases. Ann Thorac Surg 2003;76:1457–62; discussion 1462–1454
    1. Mayer E, Jenkins D, Lindner J, et al. Surgical management and outcome of patients with chronic thromboembolic pulmonary hypertension: results from an international prospective registry. J Thorac Cardiovasc Surg 2011;141:702–10
    1. Thistlethwaite PA, Kaneko K, Madani MM, et al. Technique and outcomes of pulmonary endarterectomy surgery. Ann Thorac Cardiovasc Surg 2008;14:274–82
    1. Madani MM, Auger WR, Pretorius V, et al. Pulmonary endarterectomy: recent changes in a single institution's experience of more than 2,700 patients. Ann Thorac Surg 2012;94:97–103;discussion 103
    1. Stevens GR, Garcia-Alvarez A, Sahni S, et al. RV dysfunction in pulmonary hypertension is independently related to pulmonary artery stiffness. JACC Cardiovasc Imaging 2012;5:378–87
    1. Mahapatra S, Nishimura RA, Sorajja P, et al. Relationship of pulmonary arterial capacitance and mortality in idiopathic pulmonary arterial hypertension. J Am Coll Cardiol 2006;47:799–803
    1. Bonderman D, Martischnig AM, Vonbank K, et al. Right ventricular load at exercise is a cause of persistent exercise limitation in patients with normal resting pulmonary vascular resistance after pulmonary endarterectomy. Chest 2011;139:122–7
    1. Lankhaar JW, Westerhof N, Faes TJ, et al. Pulmonary vascular resistance and compliance stay inversely related during treatment of pulmonary hypertension. Eur Heart J 2008;29:1688–95
    1. Lankhaar JW, Westerhof N, Faes TJ, et al. Quantification of right ventricular afterload in patients with and without pulmonary hypertension. Am J Physiol Heart Circ Physiol 2006;291:H1731–1737
    1. Klepetko W, Mayer E, Sandoval J, et al. Interventional and surgical modalities of treatment for pulmonary arterial hypertension. J Am Coll Cardiol 2004;43:73S–80S
    1. Skoro-Sajer N, Hack N, Sadushi-Kolici R, et al. Pulmonary vascular reactivity and prognosis in patients with chronic thromboembolic pulmonary hypertension: a pilot study. Circulation 2009;119:298–305
    1. Robin X, Turck N, Hainard A, et al. pROC: an open-source package for R and S+ to analyze and compare ROC curves. BMC Bioinform 2011;12:77
    1. Team RDC R: A language and environment for statistical computing. R Foundation for Statistical Computing, Vienna, Austria 2011; ISBN: 3-900051-07-0.
    1. Kim NH. Assessment of operability in chronic thromboembolic pulmonary hypertension. Proc Am Thorac Soc 2006;3:584–8
    1. Thistlethwaite PA, Mo M, Madani MM, et al. Operative classification of thromboembolic disease determines outcome after pulmonary endarterectomy. J Thorac Cardiovasc Surg 2002;124:1203–11
    1. Saouti N, Westerhof N, Helderman F, et al. RC time constant of single lung equals that of both lungs together: a study in chronic thromboembolic pulmonary hypertension. Am J Physiol Heart Circ Physiol 2009;297:H2154–60
    1. Westerhof N, Bosman F, De Vries CJ, et al. Analog studies of the human systemic arterial tree. J Biomech 1969;2:121–43
    1. Stergiopulos N, Segers P, Westerhof N. Use of pulse pressure method for estimating total arterial compliance in vivo. Am J Physiol 1999;276:H424–8
    1. Moser KM, Bloor CM. Pulmonary vascular lesions occurring in patients with chronic major vessel thromboembolic pulmonary hypertension. Chest 1993;103:685–92
    1. Toshner M, Suntharalingam J, Fesler P, et al. Occlusion pressure analysis role in partitioning of pulmonary vascular resistance in CTEPH. Eur Respir J 2012;40:612–17
    1. Kim NH, Fesler P, Channick RN, et al. Preoperative partitioning of pulmonary vascular resistance correlates with early outcome after thromboendarterectomy for chronic thromboembolic pulmonary hypertension. Circulation 2004;109:18–22

Source: PubMed

Szponzorok és közreműködők

Egészségi állapot

Kábítószer-beavatkozások

3
Iratkozz fel