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Eur J Cardiothorac Surg 2001;19:771-776
© 2001 Elsevier Science NL

Pulmonary thromboendarterectomy – risk factors for early survival and hemodynamic improvement

^a Deptartment of Thoracic and Cardiovascular Surgery, University Hospital Homburg, Homburg, Germany
^b Department of Pneumonology, University Hospital Homburg, Homburg, Germany
^c Department of Medical Biometrics, University Hospital Homburg, Homburg, Germany

Received 10 October 2000; received in revised form 2 March 2001; accepted 14 March 2001.

Corresponding author. Tel.: +49-6841-162501; fax: +49-6841-162788
e-mail: chhjsc{at}med-rz.uni-sb.de

	Abstract

Top Abstract 1. Introduction 2. Material and methods 2.1. Statistics 3. Results 4. Discussion Appendix. Conference discussion References

 
Objective: Pulmonary thromboendarterectomy (PTE) for chronic thromboembolic pulmonary hypertension is a challenging procedure with a considerable mortality. The aim of this investigation was to identify risk factors influencing mortality and operative results. Methods: Between October 1995 and August 2000, 69 patients (age 54 years; 34 women; mean New York Heart Association (NYHA) stage 3.4) underwent PTE. The preoperative pulmonary vascular resistance (PVR) was 988±554 dynesxsxcm^-5, mean pulmonary artery pressure 50±12 mmHg, right atrial pressure (RAP) 11.5±4 mmHg. Hospital mortality was 10.1% (n=7/69). Mean postoperative PVR on the 2nd day was 324±188 dynesxsxcm^-5. Pulmonary angiography was reviewed for number of involved segments (mean 9.3±2) and bronchial arteries diameter (BAD; mean 4.6±1.6 mm). A univariate and multivariate analysis was performed to determine preoperative risk factors for hospital death and inadequate hemodynamic improvement. Results: By univariate analysis, mortality was influenced by age (P=0.04), right atrial pressure (P=0.009), NYHA (P=0.02) and the number of angiographically involved segments (P=0.02). Sex, left ventricular function, presence of coronary artery disease and bronchial artery diameter did not show correlation with mortality. Inadequate hemodynamic improvement in a dichotomized analysis (PVR500 dynesxsxcm^-5, n=11, and PVR <500 dynesxsxcm^-5, n=58), assessed by univariate analysis, was significantly influenced by age (P=0.02), preoperative PVR (P=0.01), NYHA (P=0.002), RAP (P=0.02) and female sex (P=0.02). Multivariate analysis identified age (P=0.1), RAP (P=0.002) and female sex (P=0.007) as risk factors for inferior hemodynamic improvement. Conclusions: Preoperative parameters can be utilized to assess postoperative mortality and hemodynamic improvement after pulmonary thromboendarterectomy. Patient age and clinical deterioration of pulmonary hypertension are considerable preoperative factors influencing hospital mortality. Inadequate postoperative hemodynamic improvement is affected by severity of disease and female sex.

Key Words: Chronic pulmonary thromboembolism • Pulmonary hypertension • Pulmonary thromboendarterectomy

	1. Introduction

Top Abstract 1. Introduction 2. Material and methods 2.1. Statistics 3. Results 4. Discussion Appendix. Conference discussion References

 
Obstruction of major pulmonary vessels with organized thrombemboli is a rare sequela of acute pulmonary embolism. Over the past decades, the description of this clinical entity has evolved from an autopsy finding to a recognized cause of chronic pulmonary hypertension [1–3]. Persistent embolic obstruction of pulmonary arteries can initiate remodeling of pulmonary arterial wall in areas that are not involved in embolic occlusion. These alterations in conjunction with pulmonary arterial obstruction ultimately result in pulmonary hypertension [4–7].

The prognosis is poor, 5-year survival in patients with a mean pulmonary artery pressure of more than 30 mmHg is only 30% [8]. Besides lung transplantation, pulmonary thromboendarterectomy is the only effective therapeutic option for this disease. It is however associated with a considerable hospital mortality between 6.6 and 23% [9–12]. Common causes of death have been massive hemoptysis, reperfusion edema of the lung, right ventricular failure, respiratory failure and multiorgan failure [2,13,14]. In addition, pulmonary thromboendarterectomy does not always result in normalized pulmonary vascular resistance, most likely due to superimposed peripheral disease [15].

In view of the morbidity and mortality of this operation the individual decision in favor of or against pulmonary thromboendarterectomy can be difficult. It would be helpful if preoperative parameters facilitated this decision making process. In this retrospective investigation we have attempted to define preoperative predictors for early survival and hemodynamic improvement after pulmonary thromboendarterectomy.

	2. Material and methods

Top Abstract 1. Introduction 2. Material and methods 2.1. Statistics 3. Results 4. Discussion Appendix. Conference discussion References

 
Between October 1995 and August 2000, 69 patients underwent pulmonary thromboendarterectomy in our institution. Thirty-four of these were female (49%). The age ranged from 10 to 80 years with a mean age of 55±15 years. Two thirds of the patients (64%) were in New York Heart Association (NYHA) functional class III and 32% were in class IV. Ten patients had concomitant coronary artery disease (15%). Two patients (2.9%) suffered from additional combined tricuspid valve lesions, one patient (1.4%) presented with aortic valve stenosis and two patients showed a patent foramen ovale. Additional operative procedures were performed in eight of these patients (coronary artery bypass n=3, tricuspid valve reconstruction n=2, aortic valve replacement n=1, closure of patent foramen ovale n=2).

Preoperatively all patients underwent left and right heart catheterization, pulmonary angiography and CT scan of the chest. Right atrial pressure, pulmonary artery pressure and pulmonary wedge pressure were measured. Cardiac output was determined by thermodilution and pulmonary vascular resistance was calculated. The number of involved segmental arteries was counted on the basis of pulmonary angiography. CT scans of the chest were analyzed for presence of occluded or stenosed pulmonary vessels. Left heart catheterization was performed to document or rule out coronary artery disease or valve pathology. Left ventricular ejection fraction was calculated. Angiography of the descending aorta was performed for visualization of bronchial arteries, the diameter of the biggest bronchial artery was determined at the origin of the vessel.

All operations were performed by the same surgeon. The chest was opened through a median sternotomy. The patient was placed on extracorporeal circulation by bicaval and aortic cannulation and was cooled to a nasopharyngeal temperature of 18–20°C. The central pulmonary arteries were opened and a dissection plane developed which was then followed to segmental level. Hypothermic circulatory arrest was used in all procedures to achieve accurate visualization during peripheral dissection. Using head light and surgical loupes, the pulmonary arterial tree could be visualized directly approximately 2–3 cm beyond the origin of the segmental arteries. Angioscopy was not used. Repeated periods of circulatory arrest limited to 20 min were used; usually endarterectomy of one pulmonary arterial bed could be accomplished within one 20 min period. After complete endarterectomy extracorporeal circulation was resumed, and the patient rewarmed. Concomitant cardiac procedures (closure of patent foramen ovale, tricuspid valve reconstruction, aortic valve replacement or coronary bypass grafting) usually were performed during the rewarming period.

Postoperatively, hemodynamic monitoring was continued for the first 48–72 h after the operation. Decreased systemic vascular resistance was treated by norepinephrine if necessary. Residual pulmonary hypertension was treated by nitrates, inhalation of prostacyclins or iloprost. After hemodynamic stabilization the patients were weaned from ventilator support and extubated once normal gas exchange was present. Anticoagulation was started with intravenous heparin 6 h postoperatively. Oral cumadin therapy was restarted on postoperative day 1 with a target INR of 3–3.5.

For identification of risk factors we analyzed the influence of preoperative parameters (age, sex, NYHA class, right atrial pressure, pulmonary artery pressure, pulmonary vascular resistance, cardiac output, number of angiographically involved segments, diameter of bronchial artery and presence of coronary artery disease,) on hospital mortality and hemodynamic improvement. Preoperative creatinine and cholinesterase were analyzed with respect to their influence on hospital mortality.

	2.1. Statistics

Top Abstract 1. Introduction 2. Material and methods 2.1. Statistics 3. Results 4. Discussion Appendix. Conference discussion References

 
All data were presented as mean±standard deviation. The results were computed on commercially available systems with the SPSS^® software. Comparison of preoperative and postoperative variables was performed by Wilcoxon sign rank test. Predictors for hemodynamic improvement and early mortality were analyzed by uni- and multivariate analysis. The univariate analysis for continuos variables were performed by t-test or nonparametric Mann–Whitney test, nominal variables by Fisher's exact test. Cut-off points for postoperative pulmonary vascular resistance were assessed with the aid of receiver operating characteristic curve. Predictors for improvement of postoperative pulmonal vascular resistance were analyzed by Spearman rank correlation, as univariate analysis and multiple linear regression as multivariate analysis. Additionally we separated two groups (PVR500 dynesxsxcm^-5 and PVR<500 dynesxsxcm^-5) for uni- and multivariate analysis.

	3. Results

Top Abstract 1. Introduction 2. Material and methods 2.1. Statistics 3. Results 4. Discussion Appendix. Conference discussion References

 
Preoperative mean pulmonary artery pressure ranged from 25 to 70 mmHg with a mean of 50±12 mmHg. Pulmonary vascular resistance was 988±554 dynesxsxcm^-5, right atrial pressure 11.5 ±3.9 mmHg. Mean left ventricular ejection fraction was 59±8%. The number of involved segmental pulmonary arteries as determined by pulmonary angiography, ranged from 2 to 12 (mean 9.3±1.9). The diameter of bronchial arteries ranged from 2.6 to 8.6 mm with a mean of 4.6±1.6 mm.

Mean duration of hypothermic circulatory arrest was 35±13 min, mean cross clamp time 97±19 min and mean total cardiopulmonary bypass time 132±25 min.

The duration of postoperative ventilator support ranged from 8 h to 20 days (mean 2.8±3.1 days). Patients stayed in the intensive care unit for an average of 5.5±3.2 days.

Early mortality was defined as death before hospital discharge or during the first 30 days after operation. Seven of the 69 patients died for a hospital mortality of 10.1%. No patient died intraoperatively. One patient died with hepatic failure, six patients with multiorgan failure 2–21 days following surgery. Preoperative creatinine in the surviving patients showed significantly lower levels compared to the patients who died early (creatinine 1.01 mg/dl versus 1.67 mg/dl P<0.001). The analysis of preoperative hepatic function (cholinesterase) showed no significant difference between survivors and non-survivors (Table 2).

In order to assess favorable or unfavorable hemodynamic response pulmonary vascular resistance was analyzed as continuous variable using Spearman's correlation test and multiple linear regression. In addition, we subdivided the patients into two groups; one group with an inadequate hemodynamic improvement defined as pulmonary vascular resistance greater than 500 dynesxsxcm^-5 (n=11) and the other group with pulmonary vascular resistance below 500 dynesxsxcm^-5 (n=58). These two groups were compared by univariate and multivariate analysis.

Increased postoperative pulmonary vascular resistance showed a significant correlation with preoperative NYHA, preoperative right atrial pressure and pulmonary vascular resistance. Preoperative mean pulmonary artery pressure, cardiac output and diameter of bronchial artery showed only a weak correlation (r<0.3) as determined by Spearman's correlation test (Table 3).

As determined by a cut-off point in postoperative pulmonary vascular resistance (500 dynesxsxcm^-5) we found significant differences between the two groups for the preoperative parameters age, right atrial pressure, NYHA, preoperative pulmonary vascular resistance and sex (Tables 4 and 5). Multivariate analysis identified only age, right atrial pressure and female sex as risk factors for lower hemodynamic improvement (PVR500 dynesxsxcm^-5) after PTE (Table 6).

	4. Discussion

Top Abstract 1. Introduction 2. Material and methods 2.1. Statistics 3. Results 4. Discussion Appendix. Conference discussion References

Little is known about preoperative predictors of postoperative hemodynamic improvement and mortality.

Daily et al. [10,13] analyzed risk factors for mortality and reperfusion pulmonary edema. By univariate and multivariate analysis they identified ascites and need for blood transfusions (four units) as predictors for reperfusion pulmonary edema. Increased cardiopulmonary bypass time and failure to achieve at least 50% reduction on pulmonary vascular resistance strongly predicted hospital death [9]. Hartz et al. [11] analyzed predictors of mortality after pulmonary thromboendarterectomy. In 34 patients they identified preoperative pulmonary artery pressure and pulmonary vascular resistance as highly significant predictors for hospital mortality. In patients with a preoperative pulmonary vascular resistance greater than 1100 dynesxsxcm^-5 the risk of death was six times higher after pulmonary thromboendarterectomy compared to those with lower pulmonary vascular resistance [11]. An investigation of Bergin et al. [15] identified the evidence of extensive central vessel disease by CT scan and limited small vessel involvement as favorable factors for surgical outcome.

In order to facilitate preoperative decision making, we included demographic, preoperative hemodynamic and angiographic parameters into the statistical analysis. The severity of the pulmonary hypertension, for example increased pulmonary vascular resistance, elevated right atrial pressure and decreased cardiac output, were predictors for hospital mortality. Therefore it is not surprising that clinical evidence of deterioration (NYHA) was identified as additional significant risk factor for hospital death. In addition, the age of the patient significantly predicted hospital death. Interestingly we found no influence of concomitant cardiac disease on hospital mortality. A preoperative pulmonary vascular resistance greater than 1136 dynesxsxcm^-5 was identified as a cut-off point for highly increased hospital mortality, which is almost identical to the findings of Hartz et al. [11]. The increased hospital mortality for older patients might be explained by a higher preoperative comorbidity in these patients, although we found no influence of concomitant cardiac disease. The perioperative morbidity generated by operative trauma, extracorporeal circulation and hypothermic circulatory arrest is generally known to be severe in older patients and may result in increased perioperative mortality also in the context of pulmonary thromboendarterectomy. Due to the limited number of hospital deaths, multivariate analysis of preoperative risk factors for early mortality could not be performed. Since inadequate reduction of pulmonary vascular resistance after PTE is the most important factor for death, results can be extrapolated from the analysis for hemodynamic improvement.

Concerning the inadequate postoperative hemodynamic improvement we found somewhat different risk factors. Preoperative pulmonary vascular resistance, preoperative pulmonary artery pressure, age, and high NYHA functional class were identified as significant risk factors. Most importantly, female sex predicted elevated postoperative pulmonary vascular resistance. The reason for this imbalance of operative outcome concerning the sex of the patients is unknown. In female patients the prevalence of primary pulmonary hypertension is higher than in men [17]. Also the development of secondary pulmonary hypertension following the abuse of fenfluramine, an amphetamine-like drug used for appetite suppression primarily affected women [18]. Another reason might be the effect of estrogen on endothelium-triggered vasoconstriction in the small pulmonary vessels. Therefore it appears possible or even likely that in female patients with chronic thromboembolic hypertension the degree of peripheral, small vessel involvement is higher compared to men [16]. Finally, coexistence of thromboembolic and primary vascular pulmonary hypertension cannot be ruled out. Further studies will be necessary to identify the exact cause of this phenomenon.

We conclude that preoperative parameters can be utilized to assess postoperative mortality and hemodynamic improvement after pulmonary thromboendarterectomy. Patient age and indicators of clinical deterioration of pulmonary hypertension are significant preoperative factors influencing hospital mortality. Inadequate postoperative hemodynamic improvement is affected by severity of the disease and female sex.

	Footnotes

 
Presented at the 14th Annual Meeting of the European Association for Cardio-thoracic Surgery, Frankfurt, Germany, October 7–11, 2000.

	Appendix. Conference discussion

Top Abstract 1. Introduction 2. Material and methods 2.1. Statistics 3. Results 4. Discussion Appendix. Conference discussion References

 
Dr M. Zembala (Zabrze, Poland): The group I conduct is continuously working on the PTE surgery and your and Osaka group shows similar results. Do you agree with me that we should consider our personal learning curve mortality. I don't see that in your study and in the other studies as well. It is completely different when you start your series and perhaps after one or two visits in Stuard Jamiesons Center in San Diego, you have different outcome. That's first.

Secondly, can you comment a little bit more about one of your patients, the youngest one, who lived 10 years with chronic PTE? It's very interesting and very uncommon. I would like to know this data.

Dr Schäfers: My personal learning curve started 2 1/2 years earlier when I was still in Hannover. If I include the initial operations and the fatalities, my personal hospital mortality is in the range of 13%. There is certainly some learning curve effect, I fully agree with you. I think this certainly has implications for performance of the operation, but most importantly, really decision-making, who to operate and who not to operate. I think now, we are still in the process of refining that decision-making process. We need more predictors that aid in the decision-making process, and that's really why we did this study.

To comment specifically on the 10-year-old patient, this was a kid who came from Syria in severe heart failure with tricuspid regurgitation. He had a combined tricuspid valve lesion, and on right heart catheterization, he had an occluded right intermediate pulmonary artery. So he had some combination of chronic endocarditis with calcifications in the tricuspid valve and elevated pulmonary vascular resistance due to the chronic occlusion. He was one of the patients we did tricuspid valve reconstruction on and pulmonary thromboendarterectomy. It is unusual and one must assume that he had an episode of pulmonary embolism years before presentation.

Dr M. Turina (Zurich, Switzerland): Dr Schäfers, when you put all the science aside and the odds ratio and percentage, et cetera, could you tell us your guidelines now? If you have a 60-year-old female with a central venous pressure of 20, do you do surgery or not? I'm sure you modified your guidelines.

Dr Schäfers: It depends. One of the problems is really to come up with objective criteria for what we call angiographic studies, and that really is the crucial point. If that patient had evidence of five occluded segments, three in the left lower lobe, two in the right lower lobe, and one maybe segment in the right middle lobe, she was in severe heart failure, 65, and New York Heart Class 4, I would not operate.

Dr J. Bachet (Paris, France): I think that in this matter, as in surgery in general, the technique is important. You didn't give us any detail of your technique. Do you use the Dartevelle technique, for instance, using video to go very deeply distally and be sure of taking all the distal thrombi away?

Dr Schäfers: I essentially follow the technique that has been developed by Pat Daily and continued by Stuart Jamieson. We do not use angioscopy. I find that on the right side, just by using loupes and headlight illumination, you can see far down into the segmental arteries. The only lobe that is somewhat difficult to reach is the left lower lobe, but with a little traction, you can even start dissection at the origin, at the orifice of left lower lobe segmental arteries. So far, I have seen no need and no real improvement of angioscopy over that conventional technique.

Dr Bachet: How long is the circulatory arrest in your patients?

Dr Schäfers: Thirty-five minutes, mean, but there is also some learning curve effect. Initially it was somewhere in the range of 42, mean, and now we are down to 35. The longest is 60 min for a very difficult case.

Dr Bachet: Would you like to make a few comments before closing now?

Dr Schäfers: I think PTE is a very effective treatment. We still need to study more the individual physiologic factors that are involved, and we need to be very careful, particularly in decision-making, when it comes to conservative or operative treatment.

	References

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