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Ann Thorac Surg 2002;73:762-766
© 2002 The Society of Thoracic Surgeons
a Second Medical Clinic (Department of Cardiology), Johannes Gutenberg- University, Mainz, Germany
b Clinic for Cardiothoracic and Vascular Surgery, Johannes Gutenberg- University, Mainz, Germany
Accepted for publication November 15, 2001.
* Address reprint requests to Dr Menzel, Weichselstrasse 14, D-81677 Munich, Germany
e-mail: menzel{at}mail.uni-mainz.de
| Abstract |
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Methods. The indices were derived for 24 patients (aged 54 ± 14 years) before and after PTE. Calculation of these indices was based on the duration of two time intervals using the formula (A - B)/B, where A is the interval between cessation and onset of mitral inflow (or tricuspid inflow) and B is LV or RV ejection time. In addition, LV and RV end-diastolic and end-systolic chamber areas were determined using two-dimensional echocardiography, and systolic function was calculated. Mean pulmonary artery pressure was determined invasively.
Results. PTE led to a significant reduction of mean pulmonary artery pressure (46 ± 10 versus 25 ± 6 mm Hg; p < 0.05). LV and RV indices were abnormally high before surgery, declined significantly afterwards, and then almost matched normal values (0.61 ± 0.26 versus 0.37 ± 0.18; p < 0.05 and 0.55 ± 0.22 versus 0.37 ± 0.13; p < 0.05). Geometric assessment of the left and right ventricle also showed impaired systolic function before PTE, with significant improvement after surgery.
Conclusions. LV and RV Tei indices allow a quantitative assessment of ventricular function in patients undergoing PTE. Lower indices after surgery reflect an improvement of the previously impaired cardiac function. Our results emphasize the value of PTE in the treatment of chronic thromboembolic pulmonary hypertension.
| Introduction |
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As has been shown before, pulmonary thromboendarterectomy (PTE) results in significantly lower RV afterload, a rapid decrease of RV size, and improvement of systolic function [13]. Hemodynamic and cardiac changes have proven to be partially reversible, even in cases of long-standing disease [1, 310].
Echocardiography is an important noninvasive tool in the diagnostic procedures undertaken for patients with CTEPH before and after PTE. RV dilatation and increased wall thickness, an abnormal septal motion, and marked tricuspid regurgitation, which are the typical signs of severe CTEPH, are detectable by means of two-dimensional and Doppler echocardiography. However, the alteration of ven-tricular shape makes it difficult to determine the size and function of LV as well as RV in severe pulmonary hypertension. The LV and RV myocardial performance indices ([MPI] or Tei indices) are based on nongeometric assessment and thus compensate difficulties in the geometric assessment of LV and RV function [11, 12, 13]. MPI can easily be derived from values obtained during routine investigation and it has been demonstrated before this investigation that MPI correlate with other indicators of systolic as well as diastolic function [14]. Determinations of MPI have recently been evaluated for patients with dilated cardiomyopathy, amyloidosis, Ebsteins anomaly, and primary pulmonary hypertension in comparison with normal subjects and they proved to be valuable predictors of clinical outcome for the diseases in question [1113, 15, 16]. We evaluated the utility of MPI in comparison with other hemodynamic variables in patients with severe CTEPH undergoing PTE.
| Patients and methods |
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Pulmonary thromboendarterectomy
The criteria for offering PTE were a pulmonary vascular resistance (PVR) of greater than 300 dynes x sec/cm5, thromboembolic lesions considered surgically accessible (main, lobar, or segmental arteries), NYHA functional class II, III, or IV, and unsuccessful anticoagulation therapy over a 6-month period.
The endarterectomy of pulmonary arteries was performed using a standardized technique [8] as follows: intrapericardial central incision of both pulmonary arteries; endarterectomy performed exclusively under circulatory arrest, with a mean circulatory arrest time of 34 minutes (range 14 to 50); prolonged reperfusion to 37°C body temperature, resulting in a mean total operation time of 6.7 hours (range 2.3 to 10); pressure-controlled high-positive end-expiratory pressure (10 cm H2O) ventilation; nitric oxide inhalation for persistent pulmonary hypertension in the early postoperative phase; modified vasopressor therapy with low-dose dobutamine and arterenol through a left atrial catheter and maintenance of the cardiac index between 2.0 and 3.0 L · min-1 · m-2; and early extubation with a mean postoperative ventilation time of 11.5 hours (range 6.5 to 25).
Transthoracic echocardiography
Examinations were performed using standard techniques on commercially available equipment (Sonos 2500 with a 2.0/2.5 MHz transducer or Sonos 5500 with S4 Ultraband transducer [2 to 4 MHz]; Hewlett-Packard, Andover, MA). Images were obtained with the patient in the left lateral position. Measurements were performed in end-expiration.
The Doppler-derived RV MPI was calculated as described previously [17] using the length of two intervals in the formula (A - B)/B, where A equals the time between cessation and onset of tricuspid inflow and B is the ejection time of RV outflow.
The time from cessation to onset of tricuspid flow was measured using the duration of the tricuspid regurgitation flow signal. Continuous-wave Doppler recording of the tricuspid regurgitation signal was obtained from the apical window. RV ejection time was determined as the interval between the onset and cessation of RV outflow. RV outflow was recorded from the parasternal short-axis view with the pulsed-wave Doppler sample volume positioned immediately proximal to the pulmonary valve.
As described by Tei and colleagues [14] LV MPI was calculated on the duration of two intervals using the formula (A - B)/B, whereby A is the time between cessation and onset of mitral inflow and B is the ejection time of LV outflow.
The mitral inflow pattern was recorded from the apical four-chamber view with the pulsed-wave Doppler sample volume positioned between the tips of the mitral leaflets. The LV outflow velocity pattern was recorded from the apical long-axis view with the pulsed-wave Doppler sample volume positioned just below the aortic valve. LV ejection time was determined as the interval between the onset and cessation of LV outflow.
Right ventricular end-diastolic (RV-EDA) and end- systolic (RV-ESA) cavity areas were determined planimetrically in the apical four-chamber view. Fractional area change was calculated as RV-FAC = (RV-EDA - RV-ESA)/RV-EDA x 100 [18]. Left ventricular end-diastolic (LV-EDA) and end systolic (LV-ESA) cross-sectional areas were determined planimetrically in parasternal short-axis view (at the level of the mitral valve and chordae tendinae transition). Instead of the ejection fraction, LV fractional area change (LV-FAC) calculated as (LV-EDA - LV-ESA)/LV-EDA x 100 was employed to measure systolic function. End-diastole was defined as peak of the R wave in the QRS complex, and the point of maximum LV posterior wall thickening defined the end-systole [2].
Heart catheterization
All of the patients underwent invasive determination of pulmonary vascular resistance (PVR) and mean pulmonary artery pressure (mPAP) before and after surgery.
Statistical methods
The Statistical Analysis System (version 6.12, SAS Institute, Cary, NC) was employed to process the study results. Continuous variables were averaged from three consecutive measurements and expressed as mean value ± 1 SD. Preoperative and postoperative continuous variables were compared by the Wilcoxon signed-rank test. The Spearman correlation coefficients test was used to correlate the continuous variables such as CI, PVR, mPAP, LV-FAC, RV-FAC as well as the nominal variable NYHA with RV MPI and LV MPI. We analyzed preoperative variables versus preoperative MPI, postoperative variables versus postoperative MPI, and changes of variables versus changes of the MPI. Potential influences on the indices due to gender, age, and duration of symptoms were also investigated, using the Spearman correlation coefficients. For all tests, a p value less than 0.05 was considered to be statistically significant.
| Results |
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Systolic LV and RV function determined by two-dimensional echocardiography
Before surgery, the RV area measurements indicated enlarged cavities (mean values were EDA = 28 cm2 ± 6 cm2; ESA = 22 cm2 ± 5 cm2), and systolic function was impaired in all cases (FAC = 21% ± 7%). On examination after surgery, end diastolic and end systolic areas had both decreased and systolic function as reflected in the mean value of fractional area change had improved (EDA = 20 cm2 ± 5 cm2; ESA = 13 cm2 ± 4 cm2; FAC = 35% ± 9%; p < 0.05; Fig 1).
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No other relevant variables were found to correlate with the MPI or with the preoperative to postoperative change of these indices. It is noteworthy that no relation was found between preoperative LV MPI and LV systolic function or between the preoperative RV MPI and RV systolic function. Neither did the postoperative results show a relation between LV MPI or RV MPI compared with the respective LV and RV systolic function after surgery.
Hemodynamic variables
Mean values for PVR and mPAP were elevated in preoperative measurements. After PTE a marked decrease could be shown for PVR (839 ± 332 versus 281 ± 148 dynes x sec/cm5; p < 0.05) and for mPAP (46 ± 10 versus 25 ± 6 mm Hg; p < 0.05; Fig 3).
Mean heart rate did not change greatly after the surgery (86 ± 15 versus 85 ± 13 beats per minute).
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| Comment |
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Successfully performed PTE decreases RV afterload and leads to the improvement of cardiac hemodynamics [1, 310]. Thus, a noninvasive evaluation of the hemodynamic state, and of the LV and RV systolic function in particular, can provide important clinical information before and after surgery. The standard echocardiographic measurements of ventricular function, however, such as two-dimensional measurement of ejection fraction or fractional area change, are difficult to perform in patients who have pulmonary hypertension because of the distortion of both LV and RV geometry. But the myocardial performance indices (MPI, or Tei indices) are based on nongeometric assessment and they make it possible to overcome difficulties inherent to the geometric assessment of LV and RV function [17, 18].
Before surgery conventional two-dimensional echocardiography revealed enlargement of RV end-diastolic as well as end-systolic chamber size and impaired systolic function in all of the patients in our study. Left ventricular end-diastolic chamber size was abnormally small before surgery and LV systolic function was also impaired. Compared with the values of normal subjects, the presurgical LV and RV performance indices ranged abnormally high in our study, which is in good agreement with findings previously described in pulmonary hypertension [12, 15].
After PTE, two-dimensional echocardiography demonstrated a decrease in both end-diastolic and end-systolic RV chamber size and systolic function had improved, although the RV fractional area change (ie, systolic function) did not reach the normal range. The abnormally low LV end-diastolic chamber size enlarged after PTE while end-systolic size remained unchanged. Thus LV systolic function showed a normalization after surgery. The increase of end-diastolic LV chamber size can be attributed to the diminishment of RV size and the corresponding normalization of previously abnormal septal motion.
After PTE we also found a significant decrease and normalization of the LV myocardial performance index, which was comparable with the improvement of systolic LV function determined by two-dimensional echocardiography. Although it did not match the normal value, the RV myocardial performance index was significantly lower after PTE and this finding was comparable with the improvement of RV fractional area change (ie, systolic function), as described above.
Using the RV MPI, Eidem and colleagues [16] could show that a worsening of RV function in Ebsteins anomaly determined semiquantitatively by two-dimensional echocardiography could well be associated with progressively increasing values of RV MPI. They stated that the RV MPI quantitatively reflects RV performance.
In our study the LV and RV MPI were not found to correlate statistically with conventionally derived LV and RV systolic function. This discrepancy in comparison to the findings of Eidem and colleagues might be explained by the difference in methods used to determine RV function, because we determined chamber size quantitatively (ie, in square centimeters), where in the other projects it was assessed in semiquantitative fashion (visual assessment). Secondly, our investigation only included a small number of patients.
Limitations of the study
One possible limitation to the conclusiveness of our statistical analysis is the small study population; a larger cohort would strengthen the impact.
We determined the LV and RV fractional area change as reference for LV and RV performance indices derived from preoperative and postoperative examinations. In pulmonary hypertension, however, it is difficult to assess RV size and systolic function with great accuracy because of the complex shape and difficulties in tracing endocardial borders. A slight rotation of the transducer or placement over either ventricular apex can make the right ventricle appear different in size.
There is a dorsal and left-lateral displacement of the left ventricle in pulmonary hypertension that renders echocardiographic determination of LV size and systolic function inaccurate from the apical position. Thus LV end-diastolic and end-systolic cross-sectional areas were determined in the parasternal short-axis view, and to measure systolic function, LV fractional area change was used instead of the ejection fraction.
Clinical implications
Currently, there are no easily measurable indicators of RV and LV systolic function in severe pulmonary hypertension owing to the distortion of ventricular shape. The indices studied in this investigation are derived from two simple measurements that are easily obtainable during Doppler echocardiographic examination. The significant decrease of both LV and RV indices in patients with severe pulmonary hypertension undergoing PTE reflects the improvement of RV and LV systolic function, as could be demonstrated by the parallel two-dimensional echocardiography. Therefore we would propose the use of these easily derived measurements.
In addition, several authors have reported that the LV MPI and RV MPI are useful predictors of adverse outcome in patients with pulmonary hypertension as well as with left-heart disease [1115]. It is strongly expected that reduced postoperative LV and RV MPI foretell a better long-term clinical outcome for patients who have undergone PTE but this remains to be investigated.
| Acknowledgments |
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| References |
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