Impact of residual pulmonary hypertension on long-term outcomes after pulmonary endarterectomy in the modern era.

Residual pulmonary hypertension (PH) negatively impacts long-term results following pulmonary endarterectomy (PEA) for chronic thromboembolic pulmonary hypertension (CTEPH). We sought to reveal whether modern PH therapy with PH-targeted medicine and balloon pulmonary angioplasty (BPA) improved long-term results of residual PH after PEA. Long-term findings of 80 patients who survived PEA between 2011 and 2019 were retrospectively investigated. One month after PEA, 30 patients developed residual PH defined as mean pulmonary artery pressure (mPAP) ≥25 mmHg, of whom 23 were treated by PH-targeted medicine and 9 by BPA. Patients with residual PH acquired considerably better functional status and exercise capacity after PEA, however, exhibited significantly worse survival rates than those without. Eleven patients died during follow-up: 8 patients with residual PH and 3 controls. Among patients with residual PH, the deceased had a significantly lower %decrease in mPAP from 1 month to 1 year following PEA (7.4 [-32.6 to 8.0] % vs. 10.4 [3.7-27.8] %, p = 0.03) and higher mPAP at 1 year following PEA (39.5 [33.25-42.5] vs. 27 [26-34] mmHg, p < 0.01) despite PH-targeted medicine than the survived. No patients passed away from right heart failure, and there was no difference between the groups in CTEPH-related mortality. Modern PH therapy was used to address the majority of residual PH. Long-term survival after PEA was negatively impacted by residual PH, but it appeared that long-term mortality was also correlated with unrelieved residual PH despite PH-targeted medicine. Modern PH therapy may have enhanced functional status and excercise capacity, and averted fatal right heart failure.

Modification of pulmonary endarterectomy to prevent neurologic adverse events.

PURPOSE: Neurologic adverse events (NAEs) are a major complication after pulmonary endarterectomy (PEA) performed under periods of deep hypothermic circulatory arrest (HCA) for chronic thromboembolic pulmonary hypertension. We modified the PEA strategy to prevent NAEs and evaluated the effectiveness of these modifications. METHODS: We reviewed the surgical outcomes of 87 patients divided into the following three groups based on the surgical strategy used: group S (n = 49), periods of deep HCA with alpha-stat strategy; group M1 (n = 19), deep HCA with modifications of slower cooling and rewarming rates and the pH-stat strategy for cooling: and group M2 (n = 13), multiple short periods of moderate HCA. RESULTS: PEA provided significant improvement of pulmonary hemodynamics in each group. Sixteen (29%) of the 49 group S patients suffered NAEs, associated with total circulatory arrest time (cutoff, 57 min) and Jamieson type I disease. The Group M1 and M2 patients did not suffer NAEs, although the group M1 patients had prolonged cardiopulmonary bypass (CPB) and more frequent respiratory failure. CONCLUSIONS: NAEs were common after PEA performed under periods of deep HCA. The modified surgical strategy could decrease the risk of NAEs but increase the risk of respiratory failure. Multiple short periods of moderate HCA may be useful for patients at risk of NAEs.

Preoperative soluble cluster of differentiation 40 ligand level is associated with outcome of pulmonary endarterectomy.

Objective: Soluble CD40 ligand (sCD40L) is associated with some pathobiological states. However, whether sCD40L in patients with chronic thromboembolic pulmonary hypertension (CTEPH) who underwent pulmonary endarterectomy (PEA) is associated with perioperative pulmonary hemodynamics and surgical outcomes has not been elucidated. Here we aimed to investigate whether sCD40L is a useful serologic biomarker of poor surgical outcome of PEA in patients with CTEPH. Methods: Ninety patients with CTEPH who underwent PEA were enrolled. Independent preoperative parameters were examined, including sCD40L related to lower cardiac index (CI), higher pulmonary vascular resistance (PVR), and poor surgical outcomes after PEA, according to the multivariate logistic regression analysis. In addition, the area under the curve (AUC) value of sCD40L to predict poor surgical outcomes was compared with the AUCs of D-dimer and C-reactive protein (CRP). The generalizability of this study model was tested by a 5-fold cross-validation analysis. Results: Multivariate logistic regression analysis showed that high sCD40L level was related to postoperative lower CI, higher PVR, and poor surgical outcomes independent of other preoperative parameters. The AUC value of sCD40L to predict poor surgical outcomes was higher than those of D-dimer and CRP. A sCD40L cutoff value of 1.45 ng/mL predicted poor surgical outcomes with 79.3% sensitivity and 67.3% specificity. The 5-fold cross-validation analysis showed the effectiveness of our model's performance. Conclusions: Preoperative sCD40L level could be a promising serologic biomarker associated with poor surgical outcomes in CTEPH. In addition to known preoperative parameters, the biomarker might have the potential to identify patients at high risk of PEA, thereby reducing the mortality rates.

The extent of enlarged bronchial arteries is not correlated with the development of reperfusion pulmonary edema after pulmonary endarterectomy in patients with chronic thromboembolic pulmonary hypertension.

This study investigated whether dilated bronchial arteries are associated with reperfusion pulmonary edema in patients with chronic thromboembolic pulmonary hypertension. Results showed that the extent of enlarged bronchial arteries was not associated with the development of reperfusion pulmonary edema, whereas the residual pulmonary hypertension had a significant association.

Involvement of pulmonary arteriopathy in the development and severity of reperfusion pulmonary edema after pulmonary endarterectomy.

Reperfusion pulmonary edema (RPE) is a common complication after pulmonary endarterectomy (PEA) in patients with chronic thromboembolic pulmonary hypertension (CTEPH). However, the precise mechanisms underlying the development of RPE remain unclear. To evaluate the effects of pulmonary vasculopathy on RPE, the severity of the pulmonary arteriopathies and venopathies of lung tissues biopsied during PEA were pathologically quantified in 33 CTEPH patients. The severity of RPE was classified from grade 0 (no RPE) to 4 (death due to RPE) based on the arterial oxygen tension/inspiratory oxygen fraction (P/F ratio) and necessity of respiratory management. Among the 33 patients (27 women; mean age = 63.3 years), 17 (51.5%) patients developed RPE. The severity of pulmonary arteriopathy (obstruction ratio) correlated with the grade of RPE (r = 0.576, P = 0.0005). The obstruction ratio also correlated with the P/F ratio (r = -0.543, P = 0.001) and the perioperative mean pulmonary arterial pressure (r = 0.445, P = 0.009). Multivariate logistic regression analysis revealed that the obstruction ratio was a significant independent determinant for the development of RPE (odds ratio = 15.7; 95% confidence interval = 2.29-108.00, P = 0.005). In conclusion, pulmonary arteriopathy could be a determinant of the development and severity of RPE after PEA.

Long-Term Outcome of Chronic Thromboembolic Pulmonary Hypertension at a Single Japanese Pulmonary Endarterectomy Center.

BACKGROUND: Several new treatments for chronic thromboembolic pulmonary hypertension (CTEPH) have appeared in recent years, which have led to changes in the treatment algorithm. Changes in survival rates and prognostic factors, however, have not been estimated so far.Methods and Results:Two hundred and eighty patients were diagnosed with CTEPH at Chiba University Hospital between June 1986 and June 2016. Survival rate was investigated by date of treatment initiation (group 1, 1986-1998; group 2, 1999-2008; group 3, 2009-2016). Survival rates were also evaluated by treatment strategy: balloon pulmonary angioplasty (BPA), pulmonary endarterectomy (PEA), and medical treatment. Group 3 had significantly better disease-specific survival than groups 1 and 2 (5-year survival: 91.9% vs. 67.1%, 77.0%, respectively). For the non-PEA (BPA+medication) strategy, group 3 had better disease-specific survival than groups 1 and 2 (5-year survival: 94.9% vs. 54.6%, 74.2%, respectively). The PEA strategy had significantly better survival than the medication strategy in groups 1 and 2, whereas no difference was observed between the BPA, PEA, and medication strategies in group 3. CONCLUSIONS: Survival in CTEPH in the recent era has significantly improved, especially in non-PEA patients. BPA and selective pulmonary vasodilators could improve survival in the non-PEA group. In the present study, no difference in survival was found between PEA and non-PEA.

A prospective, randomized study of inhaled prostacyclin versus nitric oxide in patients with residual pulmonary hypertension after pulmonary endarterectomy.

OBJECTIVES: Pulmonary endarterectomy (PEA) is an effective treatment for chronic thromboembolic pulmonary hypertension (CTEPH), but postoperative residual hypertension leads to in-hospital mortality. Inhaled epoprostenol sodium (PGI2) and NO are administered for pulmonary hypertension after cardiothoracic surgery. This prospective study provides the first comparative evaluation of the effects of inhaled PGI2 and NO on pulmonary hemodynamics, systemic hemodynamics, and gas exchange in patients developing residual pulmonary hypertension after PEA. METHODS: Thirteen patients were randomized to receive either NO (n = 6) or PGI2 (n = 7) inhalation when pulmonary hypertension persisted after weaning from cardiopulmonary bypass. Hemodynamic and respiratory variables were measured before inhalation of the agent (T0); 30 min (T1), 3 h (T2), and 6 h after inhalation (T3); and the next morning (T4). The NO dose was started at 20 ppm and gradually tapered until extubation, and PGI2 was administered at a dose of 10 ng kg-1 min-1. RESULTS: In both groups, mean pulmonary artery pressure (PAP) and pulmonary vascular resistance (PVR) significantly decreased over time until T4 (mean PAP: p < 0.0001; PVR: p = 0.003), while mean systemic arterial blood pressure significantly increased (p = 0.028). There were no significant between-group differences in patient characteristics, cardiac index, left atrial pressure, or ratio of arterial oxygen tension to fraction of inspired oxygen. There were no in-hospital deaths. CONCLUSIONS: Both inhaled PGI2 and NO significantly reduced PAP and PVR without adverse effects on systemic hemodynamics in patients who developed residual pulmonary hypertension after PEA. Inhaled PGI2 can be offered as alternative treatment option for residual pulmonary hypertension.

Severe Pulmonary Arteriopathy Is Associated with Persistent Hypoxemia after Pulmonary Endarterectomy in Chronic Thromboembolic Pulmonary Hypertension.

BACKGROUND: Chronic thromboembolic pulmonary hypertension (CTEPH) is characterized by occlusion of pulmonary arteries by organized chronic thrombi. Persistent hypoxemia and residual pulmonary hypertension (PH) following successful pulmonary endarterectomy (PEA) are clinically important problems; however, the underlying mechanisms remain unclear. We have previously reported that residual PH is closely related to severe pulmonary vascular remodeling and hypothesize that this arteriopathy might also be involved in impaired gas exchange. The purpose of this study was to evaluate the association between hypoxemia and pulmonary arteriopathy after PEA. METHODS AND RESULTS: Between December 2011 and November 2014, 23 CTEPH patients underwent PEA and lung biopsy. The extent of pulmonary arteriopathy was quantified pathologically in lung biopsy specimens. We then analyzed the relationship between the severity of pulmonary arteriopathy and gas exchange after PEA. We observed that the severity of pulmonary arteriopathy was negatively correlated with postoperative and follow-up PaO2 (postoperative PaO2: r = -0.73, p = 0.0004; follow-up PaO2: r = -0.66, p = 0.001), but not with preoperative PaO2 (r = -0.373, p = 0.08). Multivariate analysis revealed that the obstruction ratio and patient age were determinants of PaO2 one month after PEA (R2 = 0.651, p = 0.00009). Furthermore, the obstruction ratio and improvement of pulmonary vascular resistance were determinants of PaO2 at follow-up (R2 = 0.545, p = 0.0002). Severe pulmonary arteriopathy might increase the alveolar-arterial oxygen difference and impair diffusion capacity, resulting in hypoxemia following PEA. CONCLUSION: The severity of pulmonary arteriopathy was closely associated with postoperative and follow-up hypoxemia.

Correction: Evaluation of the Microcirculation in Chronic Thromboembolic Pulmonary Hypertension Patients: The Impact of Pulmonary Arterial Remodeling on Postoperative and Follow-Up Pulmonary Arterial Pressure and Vascular Resistance.

[This corrects the article DOI: 10.1371/journal.pone.0133167.].

Evaluation of the Microcirculation in Chronic Thromboembolic Pulmonary Hypertension Patients: The Impact of Pulmonary Arterial Remodeling on Postoperative and Follow-Up Pulmonary Arterial Pressure and Vascular Resistance.

BACKGROUND: Chronic thromboembolic pulmonary hypertension (CTEPH) is generally recognized to be caused by persistent organized thrombi that occlude the pulmonary arteries. The aim of this study was to investigate the characteristics of small vessel remodeling and its impact on the hemodynamics in CTEPH patients. METHODS AND RESULTS: Hemodynamic data were obtained from right heart catheterization in 17 CTEPH patients before pulmonary endarterectomy (PEA). Lung tissue specimens were obtained at the time of PEA. Pathological observations and evaluation of quantitative changes in pulmonary muscular arteries and veins were performed using light microscopy on 423 slides in 17 patients. The relationship between the results and the hemodynamics of CTEPH was investigated. Pulmonary arteriopathy and venopathy were recognized in most cases, although no plexiform lesions and no capillary-hemangiomatosis-like lesions were detected in any of the specimens. The severity of pulmonary arteriopathy was correlated with pulmonary vascular resistance (PVR) in the postoperative and follow-up periods. The PVR and mean pulmonary arterial pressure were significantly higher in the high-obstruction group than in the low-obstruction group. The findings in pulmonary venopathy were similar to the findings seen in pulmonary veno-occlusive disease in some cases, although severe venopathy was only observed in a portion of the pulmonary veins. There was a significant correlation between the extent of pulmonary arteriopathy and venopathy, although an effect of pulmonary venopathy to hemodynamics, including pulmonary arterial wedged pressure (PAWP), could not be identified. CONCLUSION: The vascular remodeling of the pulmonary muscular arteries was closely associated with the hemodynamics of CTEPH. Severe pulmonary arteriopathy might be related to residual pulmonary hypertension after PEA. Those altered pulmonary arteries might be a new target for the persistent PH after the operation.

Perioperative anticoagulation management in antiphospholipid syndrome.

Patients with antiphospholipid syndrome are at increased risk of developing thrombotic and hemorrhagic complications after cardiac surgery, and may have abnormal coagulation tests and develop thrombocytopenia after invasive procedures, which can complicate the perioperative management of anticoagulant therapy. We describe a patient with chronic thromboembolic pulmonary hypertension and antiphospholipid syndrome, who presented with prolonged activated partial thromboplastin and activated clotting times, and developed thrombocytopenia after the catheterization workup. We performed pulmonary endarterectomy and successfully managed anticoagulation by restricting heparin use at the time of surgery and monitoring the heparin effect by measuring heparin concentrations during cardiopulmonary bypass.

Successful staged operation for acute aortic dissection and chronic thromboembolic pulmonary hypertension.

We describe surgical treatment for a patient with chronic thromboembolic pulmonary hypertension who developed acute type A aortic dissection. Acute aortic dissection is a life-threatening disease and must be operated emergently, and chronic thromboembolic pulmonary hypertension can be treated only by pulmonary endarterectomy. We performed a staged procedure consisting of hemiarch replacement with antegrade cerebral perfusion first and pulmonary endareterectomy with periods of deep hypothermic circulatory arrest a week later. We used extracorporeal membrane oxygenation after aortic surgery as a bridge to pulmonary endarterectomy. Our strategy was useful for patients with chronic thromboembolic pulmonary hypertension who require complicated aortic surgery.

Wound complications of the retroperitoneal approach for the abdominal aortic aneurysm repair-an evaluation of abdominal bulge formation-.

OBJECTIVE: To evaluate the incidence of wound complications after the retroperitoneal approach for abdominal aortic aneurysm (AAA) repair, and to ascertain the cause of abdominal bulge (AB). SUBJECTS AND METHODS: Forty-three patients with AAA repair via the retroperitoneal space were retrospectively investigated. Wound complications and their incidence were studied by chart review. The thickness of the abdominal wall muscle was measured by follow-up computed tomography films. Compound muscle action potentials (CMAPs) of the abdominal rectus muscle were examined for three bulge patients and three non-bulge patients. RESULTS: Wound hypoesthesia (30%), wound numbness (21%), AB (7%), and wound pain (2%) were found in these patients. The thickness of the abdominal wall muscle was reduced in the incision side. CMAP of abdominal rectus muscle in the incision side disappeared only in AB patients. CONCLUSIONS: (1) Wound hypoesthesia and numbness displayed a high incidence. (2) Atrophy of the abdominal wall muscle in the incision side was found in these patients. (3) The cause of AB is considered to be muscle atrophy induced by denervation injury of an 11th intercostal nerve. (4) To avoid an eleventh intercostal nerve injury must be deemed the most effective method for preventing AB.

The role of matrix metalloproteinase in the intimal sarcoma-like cells derived from endarterectomized tissues from a chronic thromboembolic pulmonary hypertension patient.

Sarcoma-like cells (SCLs) were derived from endarterectomized tissue of a single chronic thromboembolic pulmonary hypertension (CTEPH) patient during incubation of those thrombi at second passage as described at our previous report. These cells had malignant potential, with an increased expression of matrix metalloproteinase-14 (MMP-14), leading to tumor emboli within pulmonary arteries in in vivo studies. The purpose of this study was to perform a more detailed evaluation of the characteristics of SCLs, and to elucidate the role of the increased expression of MMP-14 expression in the growth and death of these cells. In order to elucidate the characteristics of SCLs and to confirm the protein expression of MMP-14, three-dimentional culture, invasion assays, a Western blot analysis and immunohistochemical studies were performed. To examine the role of MMP-14 in tumorigenesis, the metalloproteinase inhibitor, batimastat, was administered to SCID mice which were subcutaneously injected with SCLs. Those mice were sacrificed on day 14 and the tumor volume was evaluated. A Western blot analysis showed the increased expression of MMP-14 in comparison to the expression in lung adenocarcinoma cells (A549). Immunohistochemistry showed that SCLs were positive for vimentin, MMP-14, MMP-2 and CD44. However, endothelial markers, such as CD31 and von Willebrand factor (vWF), were negative. The in vivo studies demonstrated that batimastat could suppress the growth of the subcutaneous tumors formed by the SCLs. This study suggested that MMPs had critical roles on the pathological activities of SCLs and that batimastat might have anti-proliferative and anti-invasive effects on these cells.

Characterization of sarcoma-like cells derived from endarterectomized tissues from patients with CTEPH and establishment of a mouse model of pulmonary artery intimal sarcoma.

In general, intravascular thrombus formation in the pulmonary arteries is considered to be the most common cause of chronic thromboembolic pulmonary hypertension (CTEPH). The current mainstay of therapy for patients with CTEPH is pulmonary endarterectomy (PEA). Recently, the existence of myofibroblast-like cells in endarterectomized tissues has been demonstrated. At the 2nd passage of these myofibroblast-like cells, a pleomorphic cell type was isolated. Pulmonary intimal sarcoma is a very uncommon neoplastic tumor thought to originate from subendothelial-mesenchymal cells of the pulmonary vascular wall. Because these pleomorphic cells were isolated from the pulmonary vascular beds, it is believed that the analysis of these cells may contribute to the understanding of pulmonary intimal sarcoma. We isolated cells from the endarterectomized tissue from patients with CTEPH and identified one type as sarcoma-like cells (SCLs). The SCLs were characterized as hyperproliferative, anchorage-independent, invasive and serum-independent. Moreover, C.B-17/lcr-scid/scidJcl mice injected subcutaneously with SCLs developed solid, undifferentiated tumors at the site of injection, and those injected intravenously with SCLs via the tail vein developed tumors which grew along the intimal surface of the pulmonary vessels, thus, demonstrating the high tumorigenic potential of these cells. The behavior of SCLs indicated that these cells may have a vascular cell-like potential which can affiliate them with the intimal surface of the pulmonary artery, and which may be shared with pulmonary intimal sarcoma. A further investigation of this mouse model with SCLs may elucidate the mechanism(s) underlying the development of pulmonary intimal sarcoma.

Characterization of myofibroblasts in chronic thromboembolic pulmonary hypertension.

BACKGROUND: It has been generally accepted that chronic thromboembolic pulmonary hypertension (CTEPH) results from pulmonary embolism arising from deep vein thrombosis. An unresolved question regarding the etiology of CTEPH is why pulmonary thromboemboli are stable and resistant to effective anticoagulation. Recently non-resolving pulmonary thromboemboli in CTEPH have been shown to include myofibroblasts. This study investigates the cellular characteristics of myofibroblasts included in the organized thrombotic tissues of CTEPH. METHODS: Organized thrombotic tissues of patients with CTEPH were obtained following pulmonary endarterectomy. We isolated cells from endarterectomized tissue from patients with CTEPH and identified them as endothelial-like cells and myofibroblast-like cells. RESULTS: Myofibroblast-like cells were characterized as hyperproliferative, anchorage-independent, invasive and serum-independent. CONCLUSIONS: Here we report the presence of active myofibroblast-like cells in endarterectomized tissue of CTEPH. We suggest that the formation of myofibroblasts with a high growth potential in the organized thrombotic tissues may be an important event in the pathobiology of this disease.

Subpleural perfusion as a predictor for a poor surgical outcome in chronic thromboembolic pulmonary hypertension.

BACKGROUND: Small vessel disease is a major determinant of poor outcome after pulmonary endarterectomy for chronic thromboembolic pulmonary hypertension (CTEPH). Out-of-proportion pulmonary vascular resistance (PVR) may indicate the presence of small vessel disease, but it is a very subjective evaluation. We investigated poor subpleural perfusion as a marker for small vessel disease and assessed its association with disease severity and surgical outcome of CTEPH. METHODS: We assessed the subpleural perfused area in the capillary phase of pulmonary angiography in 104 consecutive patients, including 45 who underwent surgery, and then divided the patients into either the well-perfused group (the subpleural space in at least one segment was well perfused [n = 75]) or the poorly perfused group (subpleural spaces were either unperfused or minimally perfused in all segments [n = 29]). We compared the pulmonary hemodynamics, degree of distal thrombi, and surgical outcome between these two groups. RESULTS: The poorly perfused group had significantly higher PVR (937 ± 350 dyne/s/cm(5) vs 754 ± 373 dyne/s/cm(5), P = .02) and more distal thrombi, resulting in fewer surgically treated patients (27.6% vs 49.3%, P = .04) compared with the well-perfused group. This group showed a higher surgical mortality (62.5% vs 2.7%) and higher postoperative PVR (656 ± 668 dyne/s/cm(5) vs 319 ± 223 dyne/s/cm(5), P = .04). Even in a multivariate analysis, poor subpleural perfusion was associated with surgical mortality. CONCLUSIONS: Poor subpleural perfusion in the capillary phase of pulmonary angiography might be related to small vessel disease and a poor surgical outcome of CTEPH.

Long-term outcome after pulmonary endarterectomy for chronic thromboembolic pulmonary hypertension.

OBJECTIVES: Pulmonary endarterectomy is the treatment of choice for chronic thromboembolic pulmonary hypertension. Although several reports demonstrated excellent medium-term survival after pulmonary endarterectomy, long-term outcomes remain unclear. We reviewed long-term outcomes and determined risk factors for early and late adverse events. METHODS: Seventy-seven patients were studied. Mean pulmonary arterial pressure was 47±10 mm Hg and pulmonary vascular resistance was 868±319 dyne·s·cm(-5). Disease was classified as chronic thromboembolic pulmonary hypertension type 1 (n=61), type 2 (n=12), or type 3 (n=4). Median and maximum follow-up periods were 5.6 and 20 years, respectively. RESULTS: There were 11 in-hospital deaths. Nonsurvivors had significantly higher mean pulmonary arterial pressure and pulmonary vascular resistance than did survivors (54±10 vs 46±10 mm Hg; P=.02; 1124±303 vs 824±303 dyne·s·cm(-5); P<.01). In multivariate analysis, preoperative pulmonary vascular resistance was associated with in-hospital death (odds ratio, 1.003; 95% confidence interval, 1.001-1.005; P<.01). During follow-up, there were 10 all-cause deaths, including 5 related to chronic thromboembolic pulmonary hypertension. Freedom from adverse events, including disease-specific death or New York Heart Association functional class III, was 70% at 10 years. In the Cox proportional hazard model, postoperative mean pulmonary arterial pressure was associated with adverse events (hazard ratio, 1.12; 95% confidence interval, 1.03-1.21; P<.01). Receiver operating characteristic curve analysis showed mean pulmonary arterial pressure of 34 mm Hg as cutoff for adverse events. CONCLUSIONS: Pulmonary endarterectomy had sustained favorable effects on long-term survival. High pulmonary vascular resistance was associated with in-hospital death, and postoperative mean pulmonary arterial pressure was an independent predictor of adverse events.

Improvement of tricuspid regurgitation after pulmonary thromboendarterectomy.

Chronic thromboembolic pulmonary hypertension causes right ventricular dilation with various degrees of tricuspid regurgitation, leading to right heart failure. Pulmonary thromboendarterectomy can substantially improve pulmonary hemodynamics and right ventricular dilation. The aim of this study was to determine whether the reduction of tricuspid regurgitation persists during follow-up. We studied 26 patients undergoing pulmonary thromboendarterectomy without repair of tricuspid regurgitation; 24 were followed up for 7 to 59 months after surgery (mean, 33 months). Echocardiographic and right heart catheterization data were obtained before and early after surgery. Severity of tricuspid regurgitation and tricuspid pressure gradient were evaluated at follow-up. Two patients died early after surgery, but none died during follow-up. Pulmonary thromboendarterectomy substantially improved pulmonary hemodynamics and right ventricular dilation. Tricuspid regurgitation graded severe in 5 patients and moderate in another 5, improved to trivial or mild postoperatively. The decreases in tricuspid pressure gradient and regurgitation early after surgery persisted during follow-up.

Mid-term results of surgery for chronic thromboembolic pulmonary hypertension.

Pulmonary thromboendarterectomy is an effective surgical treatment for chronic thromboembolic pulmonary hypertension (CTEPH). In this study, we review our short- and mid-term results in the recent series of patients undergoing pulmonary thromboendarterectomy. Twenty-three patients (54+/-12 years) were re-evaluated 7-59 months (mean, 34 months) after surgery. Nine patients were in New York Heart Association functional class II, 11 patients in class III and three patients in class IV. All patients used supplemental oxygen therapy. After surgery, pulmonary hemodynamics were significantly improved: pulmonary vascular resistance (PVR) decreased from 925+/-342 to 337+/-260 dynes x s x cm(-5) (P<0.01); mean pulmonary artery pressure (MPAP) decreased from 47+/-12 to 25+/-10 mmHg (P<0.01). Three patients developed severe residual pulmonary hypertension and one of them died soon after surgery. During the follow-up period there were no deaths, but one recurrence of pulmonary embolism. Nineteen patients (86%) were in New York Heart Association functional class I or II and thirteen patients (59%) were weaned from oxygen therapy. In conclusion, pulmonary thromboendarterectomy provided remarkable early and late results with acceptable hospital mortality rate, normalization of pulmonary hemodynamics, and improvement in clinical functional status with relief of hypoxemia.