Ann Thorac Surg 2005;80:995-999
© 2005 The Society of Thoracic Surgeons
Original article: Cardiovascular
Enhanced Aortic Pressure Wave Reflection in Patients After Repair of Aortic Coarctation
Tomoaki Murakami, MD, PhD
*
,
Atsuhito Takeda, MD, PhD
Department of Pediatrics, Hokkaido University, Graduate School of Medicine, Sapporo, Japan
Accepted for publication March 16, 2005.
* Address reprint requests to Dr Murakami, Department of Pediatrics, Hokkaido University, Graduate School of Medicine, N-15, W-7, Kita-ku, Sapporo, 060-8638 Japan (Email: murat{at}med.hokudai.ac.jp).
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Abstract
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BACKGROUND: Despite the relative successes in cardiac surgical repair, early onset of heart disease (hypertension, myocardial infarction, cardiac failure, and sudden death) is a common late complication in patients who have undergone repair of occlusive aortic vessels. Many hypotheses for the cause of this complication have been proposed, but these mechanisms are still controversial.
METHODS: We enrolled 20 patients who had undergone arch repair for coarctation or interruption of the aortic arch. We analyzed the ascending and descending aortic pressure waveforms using a pressure sensor mounted catheter during mid-term or long-term follow-up cardiac catheterization. We compared the pressure waveforms with those of age-matched control subjects who had never undergone aortic arch surgery.
RESULTS: In patients after an arch repair, the inflection time was short (0.095 ± 0.024 vs 0.19 ± 0.05 s; p < 0.0001) and the augmentation index increased (27.5 ± 15.4 vs –3.47 ± 8.8 %; p < 0.0001). Moreover, they demonstrated high systolic blood pressure (105.2 ± 12.2 vs 94.7 ± 11.7 mm Hg; p = 0.0018) and a greater range in pulse pressure variation (40.4 ± 7.2 vs 32.7 ± 5.3 mm Hg; p = 0.0004).
CONCLUSIONS: Our results show the early return of the pressure wave reflection and augmented ascending aortic pressure wave in patients after repair of the aortic arch. The elevated ventricular afterload resulting from the enhanced pressure wave reflection may contribute to subsequent late cardiovascular complications (hypertension, myocardial infarction, cardiac failure, and sudden death) in patients after repair of the aortic defects.
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Introduction
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Despite apparently successful surgical repair of aortic coarctations, subsequent cardiovascular complications have been frequently encountered [1–6]. Although many of the complications are related to anatomical problems (restenosis, aneurysm formation, and so forth), there are some complications that are directly unrelated to the morphological problems of the reconstructed aorta. One such complication is the early onset of cardiovascular diseases (hypertension, myocardial infarction, cardiac failure, and sudden death). It has been reported that problems occur, even if the arch repair is completely satisfactory [7–9]. Cohen and colleagues [5] demonstrated that the most important predictor of a long-term survival and hypertension in patients after a repair of aortic coarctation was the age at the time of the initial repair. These findings suggest that preoperative cardiovascular damage might have some affects on the patient’s postoperative condition. However, O’Sullivan and colleagues [9] reported that after an early and successful repair of aortic coarctation a high proportion of patients also showed hypertension. To explain this phenomenon, many hypotheses have been proposed, but controversy persists.
Much evidence supports the proposal that an enhanced pressure wave reflection contributes to an increase in cardiovascular diseases [10–14]. In patients after coarctation repair, the distensibility of the reconstructed aorta is somehow impaired [15, 16]. This regional arterial stiffness may create an impedance mismatch and lead to a partial reflection of an advancing pressure wave [17]. Thus we hypothesize that the enhanced pressure wave reflection, which is generated on the reconstructed site, contributes to the late vascular complications after coarctation repair. To clarify the hypothesis, we investigated the pressure wave reflection in patients after coarctation repair.
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Patients and Methods
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In our study population (see Table 1), we enrolled 20 patients who had undergone an aortic arch repair for coarctation of the aorta or interruption of the aortic arch after obtaining written informed consent (16 patients with coarctation and 4 with interruption). The institutional review board approved the study protocol. All patients were in good health, had no subjective sign of cardiovascular dysfunction, and were not taking any medication. None of them were diagnosed as suffering from Turner syndrome. The mean age was 10.1 ± 4.8 years (range, 4 to 19 years). They underwent the arch repair at 1.1 ± 3.0 years (range, 11 days to 13 years). The arch repair method was done by extended end-to-end anastomosis in 11 patients (55%), by subclavian flap in 8 (40%), and by patch angioplasty in 1 (5%). Their aortic arches were reconstructed using their native tissues, except for the patient who was repaired by patch an-gioplasty. Five patients (3 after extended end-to-end anastomosis and 2 after subclavian flap) subsequently underwent balloon angioplasty for re-stenosis of the reconstructed site. Eleven patients had other cardiac anomalies (10 patients with ventricular septal defect and 1 with atrial septal defect). They underwent intracardiac repair at the mean ages of 0.82 ± 0.66 years (range, 2 months to 2 years).
Although the parameters relating to the pressure wave reflection are strongly age-dependent, there is no such data available about normal children for ethical reasons. Thus we measured the parameters in patients without aortic arch anomalies (12 patients with atrial septal defects, 2 with ventricular septal defects, 1 with congenital mitral regurgitation, and 5 with Kawasaki disease without coronary complications) as presumed "normal" controls. The age of these subjects was 10.0 ± 4.9 years (range, 4 to 19 years). The indications for cardiac catheterization were a preoperative evaluation for patients with congenital heart diseases and a coronary angiography for patients with Kawasaki disease. The cardiac catheterization was performed after obtaining informed written consent. The patients with atrial septal defects showed a pulmonary-to-systemic flow ratio of 2.0 ± 0.7, and no patient demonstrated any pulmonary hypertension. For patients with ventricular septal defects, their pulmonary-to-systemic flow ratios were 1.0 and 1.8, and both of them demonstrated deformation of their aortic valves (a prolapse on the right and noncoronary cusps). They had never received any surgical procedures, and they had no patent ductus, aortic regurgitation, or other abnormalities of the proximal aorta. Coronary angiography was undertaken for 5 patients with Kawasaki disease, and no coronary complications were detected. All control subjects were also in good health, had no subjective signs of cardiovascular dysfunction, and were not taking medications. Due to the fact that in these patients their cardiac outputs were normal (3.8 ± 0.7 L/min/m2) and they had normal arterial trees, we have adopted these data as "normal" controls. We then compared the parameters relating to the pressure wave reflection with patients after arch repair with those of age-matched normal controls.
Data Acquisition
Data were obtained from middle-term or long-term follow-up cardiac catheterizations and angiographic investigations. The interval between arch repair and the cardiac catheterization was 9.0 ± 3.9 years (range, 4.4 to 17.4 years). After conventional right and left side cardiac catheterization, their ascending and descending aortic pressure waveforms were recorded using a pressure sensor mounted catheter (Millar, SPC-464D; Millar Instruments, Inc, Houston, TX) before injection of any contrast material. The ascending aortic pressure waveform was recorded at one vertebral body thickness higher than the aortic valve. The descending aortic pressure waveform was recorded at the level of the diaphragm. The waveform was recorded on a hard disk through an analog-digital converter, simultaneously recorded with the electrocardiogram.
Data Analysis
From the recorded pressure waveforms, we measured systolic blood pressure, diastolic blood pressure, mean blood pressure, and pulse pressure in each patient. Using the pressure waveform, the inflection time was measured and an augmentation index was calculated for each patient (Fig 1). To determine the inflection point, we differentiated the pressure waveforms twice [17]. The augmentation index became negative when the peak systolic pressure precedes the inflection point. It is well known that the augmentation index is strongly influenced by heart rate. Thus we also calculated the corrected augmentation index, which is equivalent for the augmentation index at a heart rate of 75 beats per minute using this formula [18]:
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Fig 1. Schematic representation of augmentation index and inflection time. The augmentation index is the ratio of augmentation to the pulse pressure. The inflection time is defined as the interval between the onset of a systolic blood pressure waveform and the inflection point.
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Statistical Analysis
All data were presented as mean value ± standard deviation. All parameters were compared with those of age-matched controls using the Wilcoxon signed rank test. A p value less than 0.05 was considered statistically significant.
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Results
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Cardiac catheterization demonstrated that only 2 patients who had undergone coarctation repair had peak pressure differences between the ascending and descending aorta (Table 1). Figure 2 compares the actual pressure waveforms of an aortic repair patient and control subject. Comparing the ascending aortic pressure waveform with an age-matched control (Fig 2C), the inflection time of the ascending aortic pressure waveform of the patient after a coarctation repair (Fig 2A) was shorter than the control. The patient’s ascending aortic pressure waveform (Fig 2A) resembled the pressure waveform at the descending aorta of the control subject (Fig 2D) rather than that at the ascending aorta (Fig 2C).
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Fig 2. (A) An ascending aortic pressure waveform in patient after extended end-to-end anastomosis of the aorta (6 years old). (B) Descending aortic pressure waveform in a patient after coarctation repair (same patient as in fig 2A). (C) Ascending aortic pressure waveform in patient with an atrial septal defect (6 years old). (D) Descending aortic pressure waveform in the same patient with atrial septal defect (same patient as in fig 2C).
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Height, which strongly affects the aortic pressure waveform, and weight measurements of patients in this study versus control groups were not significantly different. Table 2
shows the parameters from their ascending aortic pressure waveforms. The systolic blood pressure was high and the range of pulse pressure was greater in patients after an aortic arch repair compared with age-matched controls, although diastolic blood pressure showed no difference. The inflection time in the patients was shorter than that in the controls. The patient’s augmentation index after aortic arch repair was significantly higher than that in the controls. The corrected augmentation index in patients after a repair of coarctation was also significantly higher.
Figure 3
demonstrated the relationships between age and augmentation indices in the ascending and descending aorta. The diagram demonstrates the apparent increase in corrected augmentation index (Fig 3A) in patients after a repair of the aortic arch. However, there is no difference in the descending aorta data (Fig 3B).
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Fig 3. Relationship between age and the corrected augmentation indices in the ascending aorta (left) z = –3.883; p = 0.0001, and the descending aorta (right) z = –0.579; p = 0.5628) (normal control after arch repair). (AAo = ascending aorta; DAo = descending aorta.)
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Comment
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In present study, we found an enhanced aortic pressure wave reflection in patients after a coarctation repair. It is well known that the early return of pressure wave reflection is one of the most important risk factors for several cardiovascular diseases [10–14]. The backward pressure wave returns sooner toward the heart and appears during the systolic phase (and not the diastolic phase) of the ascending aortic blood pressure curve, thus causing a higher systolic peak pressure and a greater range in pulse pressure. This process would increase the contractile workload of the left ventricle and make the ventricle potentially more vulnerable to any number of forms of heart diseases, especially ischemic heart disease. In the present study, the aortic arch repair patient’s ascending aortic pressure waveform demonstrated the early return of the reflecting wave (ie, short inflection time, increased augmentation index, high systolic pressure, and wide range in pulse pressure). These findings have a potential relevance to the development of subsequent complications in patients with coarctation of the aorta after successful repair [7, 8].
We would like to propose a possible mechanism for the cause of the enhanced aortic pressure wave reflection in patients after coarctation repair. It is well known that the distensibility of the reconstructed portion in patients after a repair of coarctation is decreased [15, 16]. Wave reflections arise from any discontinuity in elastic properties along the arterial tree in which there is a change (or mismatch) in impedance [17]. Therefore the reconstructed aortic portion could generate a reflection wave that traveled backward toward the ascending aorta. Figure 4
shows the pressure waveforms during pull-back of the catheter from the ascending to descending aorta in patients with atrial septal defects and after the repair of coarctation. Pressure waveforms in patients with atrial septal defects usually show a reduced inflection time. This means that the pressure sensor gradually got closer to a major reflecting point that generally exists in the region of the main aortic bifurcation [10]. Conversely the pressure waveform in patients after aortic arch repair demonstrates that the reflection point looks different between the ascending and descending aorta. Namely, the arterial system is divided into two parts with respect to pulse-blood flow properties. This may mean that the pressure sensor passed through a major reflecting point. We believe that the major pressure wave reflecting point, which was observed in the ascending aortic pressure waveform, often comes from the reconstructed site of the aortic arch in patients after an arch repair.
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Fig 4. Pressure waveforms during pull-back of the catheter from the ascending to the descending aorta in a control subject (patient with atrial septal defect) (top graph), and a patient after repair of coarctation at the inflection point (bottom graph).
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Structural and functional abnormalities in the pre-coarctation vessels in patients after aortic arch repair have been highlighted by recent studies [19–22]. They concluded that these abnormalities might be caused by preoperative systolic hypertension, even though the coarctation was repaired usually much earlier in the neonatal period. Damage to the pre-coarctation vessels certainly could cause the early return of a pressure wave reflection. The fact that the major risk factor for postoperative systemic hypertension is the duration of preoperative hypertension [2, 23] supports this hypothesis. However, it is difficult for us to agree with other groups about our patients, because more than half of our patients harbored ductus arteriosus-dependent conditions before arch repair. They were diagnosed as suffering from coarctation or interruption just after birth, and were infused with prostaglandins to keep the ductus open before closing the arterial duct. Therefore, their pre-coarctation vessels were never exposed to any hypertensive load. On the other hand, Markel and colleagues proposed that hemodynamics after successful repair of coarctation had a greater influence on the pre-coarctation vessels. They demonstrated that exercise-induced hypertension was greater in patients after a successful coarctation repair [24]. One of the causes of exercise-induced hypertension may be the impaired elastic property of the reconstructed site.
We believe that preoperative hypertension may be the most important cause of subsequent cardiovascular complications in patients with coarctation of the aorta after a successful repair. However, surgical repair during infancy does not prevent later cardiovascular complications, because the decreased distensibility of the repair site generates a pressure reflection wave. In other words, an impaired cushioning function of the aorta causes subsequent cardiovascular disease. O’Rourke and colleagues [25] demonstrated that not only conduit function, but also cushioning function was impaired in patients with coarctation of aortic arch. The present study has proved that the surgical repair of an aortic coarctation improved the conduit function, but the cushioning function remained impaired.
In conclusion, aortic pressure wave reflection is greater in patients after repair of coarctation. This may be one of the causes of subsequent cardiovascular complications. Long-term tracking studies are needed to clarify the relationship between the enhanced pressure wave reflection and the occurrence of cardiovascular diseases in these patients.
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Abstract
Introduction
