Methods: Between February 2009 and October 2010, seven cases (3 males, 4 females; mean age 43.8±18.5 years; range 25 to 73 years) who were operated on due to APE and CTPHT were included in this observational and retrospective study. The preand postoperative mean pulmonary artery pressure (mPAP), New York Heart Association (NYHA) functional class, and length of stay in the intensive care unit (ICU) and hospital along with the demographic, clinical and operational characteristics of the patients were recorded. Statistical analyses were performed using nonparametric tests due to the limited number of cases. Wilcoxon’s test was used to compare the groups.
Results: The mPAP reduced by 20 mmHg (range 5-53) following surgery, and the mPAPs in all the patients, except for the sixth case, decreased below 30 mmHg. The pre- and postoperative mPAPs were 43 mmHg (range 33-68) and 23 mmHg (range 15-37), respectively. This indicated that a significant reduction occurred following surgery (z=-2.36; p=0.018). In addition, the NYHA functional class of the patients improved by one unit following surgery (range I-III). The patients pre- and postoperative NYHA classes were III (II-III) and II (I-II), respectively. The improvement after surgery was significant with a decline in the NYHA class (z=-2.26; p=0.024). The patients also averaged a stay of three days in the ICU (range 2-14) and 9.5 days (range 5-27) in the hospital.
Conclusion: Our study results suggest that physicians should not be reluctant to choose the surgical option and should endeavor to improve the quality of life of their patients through a detailed preoperative assessment and proper patient selection.
This type of hypertension, in which pulmonary vasculopathy is the major pathophysiological mechanism, is a rare complication of an APE episode and has an incidence rate ranging from 0.5-3.8%.[5] Echocardiographic evaluation of survivors of the first episode of APE at one year revealed a 44% persistence rate of PHT and right ventricular (RV) dysfunction.[6] In cases with a mean pulmonary artery pressure (mPAP) of more than 50 mmHg, the two-year survival rate was less than 20%.[7] Kunieda et al.[8] stated the survival rate in cases with an mPAP of 50 mmHg as 6.8 years. While Matsuda et al.[9] reported a 7.8% in-hospital mortality rate after a pulmonary thromboendarterectomy (PTEA), the survival rate, including in-hospital death was 90.9% at three years. Together with hemodynamic improvement, Saouti et al.[10] also pointed out the improvement in New York Heart Association (NYHA) class.
Persistent PHT after PTEA is believed to result from concomitant pulmonary vasculopathy.[11] Post-PTEA PHT not only remains a critical and consistent determinant of perioperative risk but also predicts long-term survival.[12,13] The type of disease is another predictor of outcome. For example, when type 3 and 4 disease is compared with type 1 and 2, a longer need for inotropic support and length of hospital stay is required and higher levels of mPAP and pulmonary vascular resistance occur.[14] In cases with symptomatic CTPHT, the reported perioperative mortality rate for PTEA ranges from 5-11%, but these ratios are lower in medical centers with experience performing this procedure.[15,16] W hile P TEA i s the only option that provides an immediate and permanent cure for this devastating disease, it is rarely performed today.[9,10,15,17,18]
Although currently there is an unwillingness to perform this troublesome surgical procedure, the aim of this article is to present PTEA as a viable alternative for selected patients with low functional capacity in which an obvious improvement in hemodynamic compromise is possible.
Statistical analyses were performed with the Statistical Package for the Social Sciences version 15.0 (SPSS Inc., Chicago, Illionois, USA). Due to the inadequate number of cases, nonparametric tests were performed. The results of descriptive statistical analysis are stated as median with minimum and maximum values. The comparison between the two groups was commenced using the Wilcoxon test. Values of p less than 0.05 were considered statistically significant.
Seven cases (two with type 2 disease, two with type 1, one with type 4, and two with APE) had undergone surgery. Case 2 had a postoperative surgical embolectomy after surgery for type 1 disease. The clinical and operative characteristics of the cases along with the demographics are revealed in Table 1. All cases were treated with lifelong warfarin after discharge with a targeted international normalized ratio (INR) range of 2.5-3.5.
Table 1: Demographic, clinical and operative characteristics of cases
All surgical procedures began through median sternotomy. The surgical plan depended on the type of disease. Total cardiopulmonary bypass (CPB) was not performed nor was an aortic cross-clamp applied in cases with type 1 CTPHT and APE, except for the patient in case 2. This variance in surgical management was due to the difference in management protocols of the attending surgeons. In cases with type 2 and 4 disease, surgery was performed under deep hypothermic total circulatory arrest. Again, the deviations in core temperature (moderate hypothermic to normothermic) used during surgery for APE was due to the different management protocols of attending surgeons. Pulmonary arteriotomies in all cases were initiated from the pulmonary trunk 1-2 cm above the pulmonary valve and were extended through the left pulmonary artery beyond the pericardial reflexion until the subsegmental level was reached. A right pulmonary arteriotomy was initiated as a separate incision between the aorta and the superior vena cava and was extended beyond the pericardial reflexion identical to the one on the left side.
The reason for admission for case 1 was dyspnea over a period of six months without a history of venous thromboembolism (VTE). Arterial blood gas (ABG) analysis revealed the following: pH: 7.46, pO2: 71.8, pCO2: 33.7, and O2 saturation: 95.3%. Doppler ultrasonographic evaluation of the lower extremities showed a lack of deep vein thrombosis (DVT). A transthoracic echocardiographic (TTE) evaluation revealed typical bounce movement at the base of the interventricular septum and a D-shaped pattern along with an mPAP of 70 mmHg. Upon right heart catheterization, the cardiac index was 2.3 l/min/m2, the mPAP was 68 mmHg, the pulmonary vascular reactivity test with adenosine was negative, and pulmonary vascular resistance was 598.47 dyn-sn-cm-5. As revealed in Figure 1, filling defects at the bilateral pulmonary arterial tree on computed tomography (CT) angiogram together with the bilateral endarterectomy material indicated type 2 disease.
Case 2 was referred to us for etiological evaluation
of syncope. He had been complaining of paroxysmal
dyspnea for three months. Arterial blood gas analysis
showed to following: pH: 7.5, pO2: 63.1, pCO2: 21.1, and
O2 saturation: 92%. A TTE evaluation (Figures 2a, b)
determined an mPAP of 48 mmHg, a D-shaped pattern,
and a heterogen mobile right atrial density which was
prolabing to the right ventricle (RV) at diastole. As shown in Figure 2c, CT angiogram revealed filling defects
at the bilateral pulmonary arterial and lobal levels.
The surgical procedure began with a right atriotomy,
followed by a right ventriculotomy and a pulmonary
arteriotomy due to the association of a mobile right atrial
density due to the pulmonary vascular filling defects.
During the right atriotomy, no thrombus material was
detected, and it was thought that it had progressed
into the RV. When it was not detected through a right
ventriculotomy, it was thought to have embolized into
the pulmonary vasculature, and the operation carried
on with standard pulmonary arteriotomies. Bedside
TTE on postoperative day five revealed an mPAP of 32
mmHg and a partially improved D-shaped pattern. Due
to his clinical situation, inhaled nitric oxide (NO) was
supplied throughout the course of the intubation period.
Under heparinization on postoperative day seven, left
lower limb swelling developed. Doppler evaluation
pointed to an acute thrombus at the calf and popliteal
level. On postoperative day nine, sudden onset dyspnea,
desaturation, and hemodynamic compromise developed. Emergent CT angiogram showed filling defects in the
main pulmonary arteries (Figure 2d) and an emergency
surgical embolectomy was performed together with the
implantation of an inferior vena cava filter (Figure 3). The
case was heterozygous for methylenetetrahydrofolate
reductase (MTHFR) A1298C.
Figure 3: Thrombectomy material (a) and inferior vena cava filter (b) of case 2.
In case 3 with portal vein thrombosis, selective
thrombolysis through superior mesenteric artery
catheterization had been performed previously. On
the third day of thrombolysis and the seventh day of
heparinization, retroperitoneal hematoma along with
left lower limb swelling developed. He had a history
of VTE along with heterozygous Factor V Leiden
(FVL) and prothrombin G20210A (PT) mutations.
A Doppler ultrasonographic evaluation revealed an
acute thrombus at the calf extending to the common
femoral vein. After a short period of time, he
developed sudden onset dyspnea with hypotension.
Arterial blood gas analysis revealed the following:
pH: 7.44, pO2: 65, pCO2: 22.6, and O2 saturation of
90.5%. Transthoracic echocardiography pointed to a
thrombus bound with a slim portion of the septa to the
right atrial wall and a mobile thrombus in the main
pulmonary artery. The RV was dilated and the mPAP
was 36 mmHg. He emerged to the operating room under deep hypotension. A surgical embolectomy
revealed fresh thrombus (Figure 4).
Figure 4: Thrombectomy material of case 3.
Case 4 had complained of left calf swelling for one
month and an effort dyspnea for three days. Her Doppler
ultrasonography revealed an occluded left popliteal vein
with an acute thrombus extending to the superficial
femoral vein. A TTE evaluation showed a D-shaped
pattern with a dil-ated RV and an mPAP of 43 mmHg. A
magnetic resonance angiogram pointed to the occlusive
changes along with a loss of visualization at the left
pulmonary vasculature.
Case 5 had been admitted to the emergency
department with retrosternal pain which had been
diagnosed as acute coronary syndrome and had
been evaluated with coronary angiography that
revealed noncritical stenosis. After a while, she had
complained of chest pain and shortness of breath.
Arterial blood gas analysis revealed the following:
pH: 7.5, pO2: 66.4, pCO2: 28.4, and O2 saturation:
91%. A TTE evaluation showed RV dilatation with
a D-shaped pattern and an echogen thrombus in the
common pulmonary artery along with an mPAP of
33 mmHg. An urgent surgical embolectomy was
performed (Figure 5).
Figure 5: Thrombectomy material of case 5.
With a history of pulmonary embolism, case 6 was
referred with symptoms of NYHA class III heart failure.
A TTE evaluation revealed an mPAP of 42 mmHg along
with a D-shaped pattern and an extremely dilated RV. He
was homozygous for FVL and MTHFR C677T. At his
operation, the type 4 disease was very extensive and stiff
making it difficult to remove, and the endarterectomy
had to be extended to the segmental levels. Disconnection
from CPB was associated with serious RV failure.
Inhaled NO was commenced in the operation room, but
the patient died on postoperative day three.
Case 7 had a history of DVT and had been complaining
of progressive effort dyspnea for three years. Arterial
blood gas analysis showed the following: pH: 7.49,
pO2: 96, pCO2: 21.8, and O2 saturation: 96%. He was
homozygous for FVL. Transthoracic echocardiography
found an mPAP of 55 mmHg along with a D-shaped
pattern and RV dilatation. His CT angiogram revealed
type 2 disease. While early postoperative bedside TTE
revealed an mPAP of 38 mmHg, he was managed
with NO through the intubation period. His TTE
evaluation revealed an mPAP of 30 mmHg along with an
improvement in RV dilatation and the D-shaped pattern.
The undervaluation of a surgical embolectomy for APE seems to be due to the published high mortality rates, which make it difficult to argue for its benefits because of the natural history and the vague, aforementioned indications.[2,3] On the other hand, with rapid diagnosis, careful patient selection, and improved surgical techniques, high survival rates of 89% at 10 months have been achieved.[24] Debates continue regarding whether or not the complexity of the surgical procedure is worth the risk and whether there are enough postoperative care facilities that have sufficient experience to care for patients who undergo this procedure. Although these are legitimate concerns, they should not preclude the necessity of surgical embolectomies for certain patients.
In our cases, only case 6 died because his type 4 disease was very extensive and stiff which made it difficult to remove. Furthermore, only a 10 mmHg drop on his mPAP was achieved. Our significant results regarding the decrease in the mPAP (p=0.018) resemble those found in the literature.[10,17,25,26] Moreover, our significant improvement in the NYHA functional class (p=0.024) is also parallel with the results of Saouti et al,[10] Narayana Iyengar et al[25] and Ishida et al.[26] The inadequate number of cases in our retrospective study is a drawback; therefore, larger case series are needed for further investigation.
In conclusion, we believe that in selected cases, a PTEA/embolectomy clearly improves the functional capacity of the patient.[25] In our opinion, reducing the mPAP below 30 mmHg is essential.[7,8,12] Pulmonary angiography can play a crucial role in optimal patient selection along with confirming the diagnosis and classification of the type of disease.[16] Close follow-up of cases who survived the APE episode with regard to their persistence of PHT is also necessary.[6,12] In cases with progressively worsening symptoms, PTEA should strictly be considered. We think that a drop of one unit in the NYHA class or a decline in the mPAP below 30 mmHg demonstrates satisfactory results and indicates improved quality of life.[12,25] As a result, with good preoperative assessment and patient selection, clinics and physicians should not be reluctant to choose PTEA.
Acknowledgement
As a correspondence, I’d like to thank to my estimable
academics in giving me the opportunity for managing
this article.
Declaration of conflicting interests
The authors declared no conflicts of interest with respect
to the authorship and/or publication of this article.
Funding
The authors received no financial support for the
research and/or authorship of this article.
1) Goldhaber SZ, Visani L, De Rosa M. Acute pulmonary
embolism: clinical outcomes in the International Cooperative
Pulmonary Embolism Registry (ICOPER) Lancet
1999;353:1386-9.
2) Doerge H, Schoendube FA, Voss M, Seipelt R, Messmer BJ.
Surgical therapy of fulminant pulmonary embolism: early
and late results. Thorac Cardiovasc Surg 1999;47:9-13.
3) Meyer G, Tamisier D, Sors H, Stern M, Vouhé P, Makowski
S, et al. Pulmonary embolectomy: a 20-year experience at
one center. Ann Thorac Surg 1991;51:232-6.
4) Yalamanchili K, Fleisher AG, Lehrman SG, Axelrod HI,
Lafaro RJ, Sarabu MR, et al. Open pulmonary embolectomy
for treatment of major pulmonary embolism. Ann Thorac
Surg 2004;77:819-23.
5) Pengo V, Lensing AW, Prins MH, Marchiori A, Davidson
BL, Tiozzo F, et al. Incidence of chronic thromboembolic
pulmonary hypertension after pulmonary embolism. N Engl
J Med 2004;350:2257-64.
6) Ribeiro A, Lindmarker P, Johnsson H, Juhlin-Dannfelt A,
Jorfeldt L. Pulmonary embolism: one-year follow-up with
echocardiography doppler and five-year survival analysis.
Circulation 1999;99:1325-30.
7) Riedel M, Stanek V, Widimsky J, Prerovsky I. Longterm
follow-up of patients with pulmonary thromboembolism.
Late prognosis and evolution of hemodynamic and respiratory
data. Chest 1982;81:151-8.
8) Kunieda T, Nakanishi N, Satoh T, Kyotani S, Okano Y,
Nagaya N. Prognoses of primary pulmonary hypertension
and chronic majorvessel thromboembolic pulmonary
hypertension determined from cumulative survival curves.
Intern Med 1999;38:543-6.
9) Matsuda H, Ogino H, Minatoya K, Sasaki H, Nakanishi N,
Kyotani S, et al. Long-term recovery of exercise ability after
pulmonary endarterectomy for chronic thromboembolic
pulmonary hypertension. Ann Thorac Surg 2006;82:1338-43.
10) Saouti N, Morshuis WJ, Heijmen RH, Snijder RJ. Longterm
outcome after pulmonary endarterectomy for chronic
thromboembolic pulmonary hypertension: a single institution
experience. Eur J Cardiothorac Surg 2009;35:947-52.
11) Hoeper MM, Mayer E, Simonneau G, Rubin LJ. Chronic
thromboembolic pulmonary hypertension. C i r c u l a t i o n
2006;113:2011-20.
12) Freed DH, Thomson BM, Berman M, Tsui SS,
Dunning J, Sheares KK, et al. Survival after pulmonary
thromboendarterectomy: effect of residual pulmonary
hypertension. J Thorac Cardiovasc Surg 2011;141:383-7.
13) Skoro-Sajer N, Hack N, Sadushi-Koliçi R, Bonderman
D, Jakowitsch J, Klepetko W, et al. Pulmonary vascular
reactivity and prognosis in patients with chronic
thromboembolic pulmonary hypertension: a pilot study.
Circulation 2009;119:298-305.
14) Thistlethwaite PA, Mo M, Madani MM, Deutsch R,
Blanchard D, Kapelanski DP, et al. Operative classification
of thromboembolic disease determines outcome after
pulmonary endarterectomy. J Thorac Cardiovasc Surg
2002;124:1203-11.
15) Jamieson SW, Kapelanski DP, Sakakibara N, Manecke
GR, Thistlethwaite PA, Kerr KM, et al. Pulmonary
endarterectomy: experience and lessons learned in 1,500
cases. Ann Thorac Surg 2003;76:1457-62.
16) Klepetko W, Mayer E, Sandoval J, Trulock EP, Vachiery JL,
Dartevelle P, et al. Interventional and surgical modalities of
treatment for pulmonary arterial hypertension. J Am Coll
Cardiol 2004;43:73S-80S.
17) Freed DH, Thomson BM, Tsui SS, Dunning JJ, Sheares KK,
Pepke-Zaba J, et al. Functional and haemodynamic outcome
1 year after pulmonary thromboendarterectomy. Eur J
Cardiothorac Surg 2008;34:525-9.
18) Suntharalingam J, Treacy CM, Doughty NJ, Goldsmith K,
Soon E, Toshner MR, et al. Long-term use of sildenafil in
inoperable chronic thromboembolic pulmonary hypertension.
Chest 2008;134:229-36.
19) Stoney WS. A short history of cardiac surgery. In: Stoney
WS, editor. Pioneers of cardiac surgery. Nashville: Vanderbilt
University Press; 2008. p. 1-60.
20) Opinions regarding the diagnosis and management of venous
thromboembolic disease. ACCP Consensus Committee on
Pulmonary Embolism. Chest 1996;109:233-7.
21) Opinions regarding the diagnosis and management of venous thromboembolic disease. ACCP Consensus Committee
on Pulmonary Embolism. American College of Chest
Physicians. Chest 1998;113:499-504.
22) British Thoracic Society Standards of Care Committee
Pulmonary Embolism Guideline Development Group. British
Thoracic Society guidelines for the management of suspected
acute pulmonary embolism. Thorax 2003;58:470-83.
23) Torbicki A, Perrier A, Konstantinides S, Agnelli G, Galiè
N, Pruszczyk P, et al. Guidelines on the diagnosis and
management of acute pulmonary embolism: the Task Force
for the Diagnosis and Management of Acute Pulmonary
Embolism of the European Society of Cardiology (ESC). Eur
Heart J 2008;29:2276-315.
24) Aklog L, Williams CS, Byrne JG, Goldhaber SZ. Acute
pulmonary embolectomy: a contemporary approach.
Circulation 2002;105:1416-9.
Turkish Journal of Thoracic and Cardiovascular Surgery published orginal papers on topics in cardiovascular surgery, cardiovascular anesthesia,cardiology and thoracic surgery. These encompass all relevant clinical, surgical and laboratory specialities, editorials, current and collective reviews, tecnical knowhow papers, case reports, "How to Do It" papers. All copyrights of the articles that published or will be published belongs to Turkish Journal of Thoracic and Cardiovascular Surgery and without permission of editorial board whole articles or any part of articles table pictures and graphics could not be published. Turkish Journal of Thoracic and Cardiovascular Surgery is indexed by Science Citation Index - Expanded (SCIE)
Editor of the Journal of Turkish Thoracic and Cardiovascular Surgery
Ataşehir Mah. Ataşehir Bulvarı 48 Ada Mimoza 2-2 K:2 D:6 Ataşehir - İSTANBUL - TURKEY
Phone: +90 216 456 14 54 | GSM: 0549 456 14 54 | e - Mail : dergi@tkdcd.org
www.tkdcd.org
){kind=link}
){kind=link}
){kind=link}
){kind=link}
){kind=link}
){kind=link}
){kind=link}
){kind=link}