(Circulation. 1995;91:379-385.)
© 1995 American Heart Association, Inc.
Articles |
From the Departments of Thoracic and Cardiovascular Surgery (F.W.M., V.F., R.A., A.D., B.S., M.V., B.F., J.G., H.D.) and Anesthesiology (A.W.), Georg-August University, Göttingen, Germany.
Correspondence to Prof Dr F.W. Mohr, Universitätsklinik für Kardiovaskularchirurgie, Herzzentrum Leipzig, Russenstr. 19, 04289, Leipzig, FRG.
| Abstract |
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Methods and Results In 25 patients (24 men) with a mean age of 69.4 years (range, 55 to 80 years), we performed combined open heart and intra-abdominal aortic surgery. Eighteen patients had severe three-vessel disease and impaired left ventricular function (ejection fraction, <35%). In addition, 3 of these patients had severe aortic valvular stenosis and/or insufficiency. Seven patients had one- or two-vessel disease with a low left ventricular ejection fraction in the range of 15% to 30%. All patients were in New York Heart Association functional class III or IV. Twenty-one of 25 patients had symptomatic infrarenal AAA (perianeurysm hematoma was present in 9 patients, and 12 patients had signs of beginning perforation). Four patients with aortoiliac occlusive disease and limb ischemia were simultaneously operated on. The surgical procedure started with the performance of coronary artery bypass graft surgery. After completion of myocardial revascularization, aortic aneurysm repair was performed while extracorporeal circulation was continued for mechanical cardiac assist until aortic surgery was fully accomplished. An average of 3.3 (3 to 5) coronary bypass grafts were placed, including 17 internal thoracic artery grafts. In addition, three aortic valves were replaced. In the abdominal aortic position, 12 straight tube grafts and 13 bifurcation grafts were implanted, and three renal and two carotid arteries were simultaneously repaired. The total time of surgery varied from 2.3 to 8.5 hours, with a mean time of 3.9±1.4 hours. One intraoperative myocardial infarction occurred despite open grafts. Intensive care unit treatment lasted 1 to 13 days, with a mean of 3.6±2.5 days. Three patients (12%) died after surgery1 because of acute renal failure induced by an adverse reaction to heparin, 1 because of myocardial infarction, and 1 because of multiorgan failure. One-year actuarial survival rate was 88%, which compares favorably with survival after isolated AAA surgery in this high-risk patient subgroup and equals survival in patients with severe CAD and severely depressed myocardial function.
Conclusions One-stage surgery is a possible approach to highly symptomatic patients with severe multivascular disease and has acceptable early morbidity and mortality. Patients with severely impaired left ventricular function and unstable CAD carry a high risk of left heart failure and/or myocardial infarction during abdominal aortic surgery. Extracorporeal circulation protects the heart from the hemodynamic changes after aortic clamping or declamping during abdominal aortic surgery. The present study demonstrates that one-stage procedure is a reasonable option for this patient subgroup.
Key Words: coronary disease aneurysm bypass ventricles
| Introduction |
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The incidence of CAD in patients with AAA is reported to be as high as 50%.4 In patients with suspected CAD who undergo peripheral vascular surgery, the perioperative mortality rate is approximately four times higher than that in those without CAD. Perioperative cardiac death accounts for 40% to 60% of early postoperative death in these patients.5
Approximately 30% of all patients scheduled for aortic aneurysm resection, lower extremity revascularization, or extracranial reconstruction present with severe concomitant CAD, which warrants myocardial revascularization or is inoperable.6
Improvements in medical therapy, coronary artery bypass graft surgery (CABG), and percutaneous transluminal coronary angioplasty (PTCA) before the vascular procedure as well as improvements in intraoperative monitoring have clearly decreased both early and late mortality in these patients.7 8 Myocardial revascularization and PTCA are consequently performed first in patients with severe CAD and accompanying peripheral vascular disease (PVD) to obtain maximum cardiac protection (staged procedure).9 However, symptomatic AAA left untreated carries a high risk of rupture and is therefore associated with a high mortality.10 In a series of 38 patients who underwent prophylactic CABG, 10.5% of the patients had their AAA rupture while they were awaiting the second procedure.11 A combined procedure, ie, simultaneous CABG and AAA repair, has therefore been advocated by some for patients with both severe CAD and symptomatic AAA or aortoiliac occlusive disease (AOD).12 13 Acceptable early and late results of combined procedures have been reported for patients with critical coronary and peripheral vascular ischemia.
This article summarizes our results of combined surgery for both CAD and symptomatic AAA or AOD in patients with unstable angina and/or impaired left ventricular function.
| Methods |
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Four
patients with LVEF of <20% presented with ischemia of the
lower limbs (pain at rest and ischemic ulcerations) caused by severe
AOD. In addition, 2 of those patients with AOD presented with renal
artery stenosis. Cerebrovascular disease caused by symptomatic
extracranial carotid artery stenosis was encountered in another 2
patients. The cardiovascular and surgical risk factors are given in
Table 1
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Preoperative Diagnostic Procedures
All patients underwent
cardiac catheterization, abdominal CT
scanning, and, if necessary, additional aortic and peripheral
angiography. Preoperative and intraoperative echocardiography was
performed whenever possible to evaluate valve morphology and function
and left ventricular wall motion abnormalities. In patients with
suspected renovascular disease, selective renal angiography was
obtained.
Surgical Technique
The operation was performed by an
experienced team of
cardiovascular surgeons and anesthesiologists who routinely perform
open heart and vascular surgery. Standard intraoperative monitoring for
open heart surgery was followed and included use of a Swan-Ganz
catheter. Intravenous anesthesia was administered to all patients;
induction of anesthesia was with etomidate, fentanyl, and midazolam.
Pancuronium was used for muscle relaxation. To maintain analgesia and
amnesia, fetanyl and midazolam were administered continuously. For
infection prophylaxis, each patient received cefazoline
perioperatively. After median sternotomy, the left internal thoracic
artery was dissected and mobilized as a wide pedicle that included the
endothoracic fascia and saphenous vein was harvested simultaneously.
Cardiopulmonary bypass (CPB) was initiated using moderate hypothermia
(32°C). After aortic cross-clamping, the heart was arrested using
cold crystalloid cardioplegic solution (30 mL/kg body wt, Bretschneider
HTK). After completion of the distal coronary anastomoses, the aortic
cross-clamp was released, and the proximal anastomoses were performed
with the heart beating.
During reperfusion, abdominal aortic surgery was carried out. The sternotomy incision was extended down to the pubic symphisis, and the aorta was exposed down to the iliac arteries using limited dissection to minimize intraoperative blood loss. When aortobifemoral bypass was anticipated, the femoral arteries were dissected simultaneously. After aortic and iliac artery clamping, the aneurysm was opened. The lumbar vessels and the inferior mesenteric artery were ligated. Aneurysm repair was performed using standard graft inclusion technique with a collagen-coated Dacron tube or bifurcation grafts (Hemashield, Meadox). After completion of the distal anastomoses, patients were weaned off CPB, and heparinization was reversed with protamine. Blood lost during the abdominal procedure was collected into the CPB and a cell salvage system. Chest and abdominal wounds were closed simultaneously.
In addition to CABG, we performed three aortic valve replacements using porcine xenografts in 2 patients (1 Intact bioprothesis and 1 SJM Toronto Stentless valve) and a mechanical valve (Carbomedics) in 1 patient, two carotid endarterectomies, and three renal artery revascularizations (in 2 patients) using autologous vein grafts. In 1 patient, an aortobifemoral bypass had to be extended by adding a femoropopliteal bypass to achieve lower limb circulation in a patient with end-stage PVD.
Perioperative and Postoperative Control
Repeat ECG recordings
and chest radiographs completed the
continuous hemodynamic monitoring (including pulmonary capillary wedge
pressure and cardiac output measurements) during the early
postoperative period. Standard laboratory data, including cardiac
enzymes, were measured until discharge. A complete physical
examination, including a thorough neurological examination, was carried
out before discharge. The surgical complication and death rates were
assessed at 30 days after surgery.
Follow-up of patients was by visit in our outpatient clinic and/or by questionnaire and telephone interview.
Statistical Analysis
Data were collected by a detailed
protocol and processed using
the EXCEL 5.0 database (Microsoft Inc). Data are
presented as absolute and relative frequencies and mean and SD
values. Actuarial survival was calculated using the Kaplan-Meier method
(SPSS 5.01 statistical package, SPSS Inc).
| Results |
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The total time of surgery varied from 2.3 to 8.5 hours with a mean of 3.9±1.4 hours. Aortic cross-clamp and total bypass times were 131±32 and 42±21 minutes, respectively. Intraoperative and postoperative blood loss varied between 1500 and 2700 mL. Patients required a mean of 4.7 U of packed red blood cells and a mean of 3.8 U of fresh frozen plasma for blood replacement. Perianeurysm hematoma confined to the retroperitoneum as shown on CT in 8 patients was confirmed intraoperatively in 9 patients. In addition, in 4 patients, the back wall of the aneurysm was extremely thin and had direct contact with the vertebral bodies. In the remaining 8 patients, the aortic wall was intact but had a thin devascularized anterior wall and typical signs of beginning perforation.
Mean ventilation time was 20.8±10.1 hours. Four patients required ventilation times of longer than 36 hours. Intensive care unit treatment lasted from 1 to 13 days with a mean of 3.6±2.5 days per patient. Mean length of hospital stay was 19.6±8.3 days and ranged from 8 to 34 days. One patient sustained intraoperative myocardial infarction and developed subsequent right-side heart failure. The implantation of a mechanical assist device was not rewarding in this situation. Despite extensive reperfusion on CPB, the patient died from irreversible heart failure. Another patient died from multiple artery thrombosis in association with heparin-induced thrombocytopenia ("white clot formation"),14 and 1 patient died from multiorgan failure. Thus, the 30-day mortality rate was 12% (3 of 25).
Postoperative complications were encountered in 10 patients. One
patient underwent repeat thoracotomy for continuous bleeding from the
chest drains. One patient developed small bowel obstruction requiring
surgical intervention. In 1 patient, repeat surgery for hemorrhage at a
femoral artery anastomosis had to be performed. Lower limb ischemia
persisted in 1 patient with AOD and severe PVD despite distal
revascularization (ischemic ulcerations), and the patient subsequently
underwent fasciotomy and, later, below-knee amputation. Another patient
with AAA developed postoperative lower limb ischemia due to
intraoperative embolization and underwent crural revascularization
after unsuccessful embolectomy. Acute renal failure requiring
continuous venovenous filtration for 3 days developed in 1 patient with
preoperative chronic renal insufficiency. Transient neurological
deficits (cerebrovascular insufficiency) were encountered in 3 patients
with aortic valve replacement and preexisting CVI. Two of these
patients had minor peripheral sensory deficits, and 1 developed
hemiparesis. Cranial CT scan demonstrated multiple lesions in the left
parietal lobe. Three patients developed atrial fibrillation after
surgery that was converted to sinus rhythm in 2 patients with
conventional antiarrhythmic treatment. Table 2
summarizes the early postoperative complications.
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Follow-up was between 4 and 34 months after surgery. Completeness of
recovery and continued survival were assessed by both clinical visit
and telephone questionnaire. The actuarial 1-year survival rate was
88% (Fig 1
). One patient died 13 months after surgery
from the complications of a stroke. All survivors did well and returned
at least to their preoperative health status. Twelve patients were in
New York Heart Association functional class I or II at the time of
their last visit, and 9 patients were in functional class III. All
patients were free from angina.
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During the same time period, CABG was performed in 3020 patients and 198 patients underwent AAA repair. A cardiac history and a 12-lead ECG were obtained in all patients undergoing AAA repair. One hundred twelve of the 198 patients (56.6%) had evidence of CAD and subsequently underwent thallium scintigraphy followed by cardiac catheterization (if redistribution deficits were detected) or direct cardiac catheterization, respectively. Of the 56 patients managed medically, 10.7% died because of cardiac failure (2), hemorrhage (1), and multiorgan failure (3). Four of these patients were operated on emergently for ruptured aneurysms; the situation did not allow further cardiac evaluation.
In 13 of 112 patients (11.6%) with one- or two-vessel disease, uncomplicated lesions, and normal left ventricular function, PTCA was performed before vascular surgery. All patients in this subgroup of patients survived subsequent aneurysmectomy without cardiac complications. Eighteen patients with asymptomatic aneurysms underwent elective coronary revascularization before AAA repair at a 3- to 12-week interval (two-stage procedure). In this patient cohort, 3 patients died after aortic surgery (16.7%), two because of cardiac complications.
The remaining 25 patients (22.3%) discussed in this article
underwent a combined one-stage procedure (Fig 2
). In
comparison to the other patient cohorts, this group of patients
represented a negative selection with respect to multivessel
disease, unstable symptoms, and poor ventricular function. Finally,
they underwent a more extensive operation by thoracoabdominal
exposure.
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| Discussion |
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Myocardial infarction is the leading cause of postoperative death after AAA repair and accounts for as many as 50% of all postoperative deaths.16 17 The 5-year mortality rate from myocardial infarction in patients who had preoperative evidence of heart disease is four times higher than that for patients without CAD.18 The cumulative incidence of cardiac events in perioperative survivors with suspected or overt CAD at 8 years is 61% compared with 15% in patients without evidence of CAD.19
Survival of patients with diminished left ventricular function who
undergo major vascular surgery is even worse. A 75% to 80% incidence
of perioperative myocardial infarction and a 12% to 20% incidence of
death from cardiac causes after major vascular surgery have been
reported in patients with impaired left ventricular function (LVEF,
27% to 35%).20 21 Kazmers et al22
reported
a 29% incidence of perioperative cardiac complications in patients
with an LVEF of
35% who underwent major vascular surgery. Patients
in their study had a 10% perioperative early mortality rate after
direct AAA repair and a 40% mortality rate at follow-up (410±390
days). Most late deaths (71%) occurred within the first 6 months of
surgery and were exclusively due to cardiovascular complications.
Survival after 12 months was only 30% in the subgroup of patients with
an LVEF of <29%.22 Our results compare favorably with
these results as at 1 year, our follow-up survival rate was 88%. Only
one patient died later, so the actuarial survival rate of our cohort is
81% at 2 years after surgery.
In a preoperative radionuclide study of patients undergoing AAA repair by Mosley et al,23 all 3 patients with an LVEF of <30% died of refractory myocardial failure after surgery. In contrast, McCann and Wolfe24 reported no significant difference in mortality for patients with low or high LVEF who underwent abdominal aneurysm repair. They concluded that reduced left ventricular function alone is not sufficient clinical ground on which to deny a patient aneurysm resection. In their series, however, half of the patients were in New York Heart Association functional class I, and no statement was made concerning the severity of concomitant CAD.
It is generally accepted that the repair of an abdominal aneurysm requires optimal monitoring and maintenance of cardiac performance. Careful fluid management, including preoperative volume loading, is essential to prevent hemodynamic changes after aortic clamping in patients with underlying cardiac disease. However, there is only a small margin between optimal fluid therapy and overhydration in patients with reduced left ventricular function,25 which makes postoperative management very difficult.
During aortic cross-clamping, the heart is challenged with a sudden rise in peripheral vascular resistance and an increase in afterload.26 27 In patients with severe CAD, pulmonary capillary wedge pressure rises after aortic cross-clamping, indicating cardiac dysfunction.1 Fiser et al28 demonstrated a decrease in cardiac index along with an increase in systemic vascular resistance at the time of aortic cross-clamping. Harpole et al2 used serial intraoperative radionuclide angiocardiography and transesophageal echocardiography to determine left ventricular function (LVEF) during infrarenal aortic cross-clamping. They found a significant decrease in LVEF, a rise in left ventricular end-diastolic volume and pulmonary blood volume, and an increase in meridional end-systolic wall stress. Not surprisingly, LVEF and cardiac output were lower and end-diastolic and end-systolic volumes were higher in a subgroup of patients with concomitant CAD. They pointed out that among the hemodynamic effects of aortic occlusion, increased ventricular wall stress was the most important because it may eventually lead to myocardial ischemia secondary to reduced subendocardial perfusion. However, myocardial ischemia was not observed in the patients with CAD and impaired LVEF. Because mean LVEF in this group of patients with both CAD and AAA was near normal at 42% and the severity of CAD was not described in detail, conclusions regarding the safety of AAA in the patient with severe CAD and poor LVEF cannot be drawn from this study.
Hypotension after declamping is due to a sudden fall in peripheral vascular resistance. Coronary perfusion eventually decreases, leading to myocardial ischemia in patients with severe coronary artery stenoses.29 If hypotension occurs, it is usually corrected with aggressive volume replacement in an attempt to maintain sufficient filling pressure. This treatment, in turn, may also adversely affect cardiac function in patients with reduced LVEF because dilated ventricles do not adequately respond to volume overload. Furthermore, declamping can cause metabolic acidosis by the release of vasodepressor substances that have accumulated in the lower limbs during clamping or, in case of AOD, in ischemic limbs, resulting in myocardial depression.
It has been shown that the risk of vascular surgery is lower in patients who have previously had CABG,8 20 and the protective effect of CABG in patients who undergo elective vascular surgery has been demonstrated.7 Subsequently, patients with severe correctable CAD have been advised in the past to undergo myocardial revascularization before AAA repair.30 The effectiveness of preoperative screening and selective coronary revascularization before AAA repair has been recently noted by Suggs et al.31 They found a low cardiac complication rate of 2.4% in a series of 263 patients using a screening algorithm for CAD similar to the one used in the present study. With optimal medical therapy and selective coronary revascularization by PTCA or prior CABG, we also saw a lower overall mortality rate in patients undergoing AAA repair during the past.
However, few patients present with both unstable CAD and
symptomatic AAA or AOD. In this situation, selective myocardial
revascularization is not safe because the risk of rupture does not
allow for a delay in AAA repair. A combined, one-stage approach has
therefore been advocated by some authors (see Table 3
).
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In 1980, Whittemore et al32 reported 2 patients with severe angina and impending rupture of their abdominal aneurysms who underwent combined cardiac and aortic surgery. Both patients survived. This approach was later adopted by Ruby et al.9 In their series of 227 patients who had elective or emergency repair of nonruptured AAA, 6 patients had unstable angina and symptomatic AAA and subsequently underwent combined surgery. In both studies, CABG was completed first and AAA repair was started without cardiac support by extracorporeal circulation. The authors reported no associated morbidity or mortality for the combined approach.
David33 pointed out that in addition to achieving good surgical results, the combined approach is cost effective. The average cost for combined cardiac and abdominal aortic surgery was only slightly more than one half of the cost of the two separate operations. Furthermore, the total times spent in the operating room and intensive care unit as well as the length of the hospital stay were significantly shorter for patients who underwent the combined procedure compared with those who underwent a staged approach.
Of a series of 255 patients reported by Reul et al7 who underwent simultaneous CABG and peripheral vascular surgery, 33 had symptomatic AAA (11) or severe AOD (22). Indications for concomitant AAA repair were tender aneurysm with suspicion of impending rupture, a recent dissecting aneurysm of the abdominal aorta, or an extremely large aneurysm. In some patients with large abdominal aneurysms and unstable vital signs, CPB was continued during AAA repair to provide stable hemodynamics during aortic cross-clamping and removal. Patients who underwent aortofemoral bypass had the highest mortality rate in the group with combined procedures (9.1%). Interestingly, the rate of pulmonary complications was not increased in the group of patients undergoing the combined procedure despite large abdominal and thoracic wounds. Also, the incidence of cerebrovascular and renal complications as well as local wound infection was not more frequent in this subgroup than in patients who had their vascular operation at the same or separate admission. It was concluded that the increased risk in patients undergoing simultaneous or same-admission procedures was related to the severity of the underlying disease and not to the combined procedure. In our limited experience with 4 patients with rest pain due to AOD and PVD, we observed only minimal hemodynamic changes during the operation. In contrast, we observed an aggravation of ischemia in the involved limbs despite successful revascularization in 2 patients (with highly elevated creatine kinase levels). This further reduction in peripheral limb perfusion was due to extracorporeal circulation with continuous flow. Indication for combined surgery in the case of severe AOD with critical or no lower limb perfusion is therefore critical and in our opinion justified only if myocardial revascularization is absolutely mandatory and limb salvage requires peripheral revascularization. Vein harvesting in an ischemic limb may also lead to combined surgery to achieve wound healing.
Two successful combined procedures were reported by Emery et al34 in 1988. In 1991, Carrel et al12 reported 32 patients who underwent the combined procedure for severe PVD and CAD. Of these, 10 patients had bifurcation prostheses implanted or aortofemoral bypasses performed along with CABG. Aortic surgery was performed after the patients had been weaned from CPB. Overall 30-day mortality rate for all combined procedures (including aortoiliac and femoroiliac endarterectomies and femoropopliteal bypass implantation) was 3.1%. Mean intubation time, recovery time in the intensive care unit, and average hospitalization time were not different for patients undergoing combined procedures than for those undergoing isolated CABG. The calculated actuarial survival rate at 8 years also did not differ from the survival rate of patients after isolated CABG but was superior to the 8-year survival rate of patients after AAA repair or peripheral revascularization.12 However, exact figures for early and late survival in the subgroup of patients undergoing simultaneous AAA repair or surgery for symptomatic AOD are not provided in that study. Despite the fact that all patients were classified as being in New York Heart Association class III or IV, 81% of the patients had normal left ventricular function. Furthermore, patients in this study were relatively young (mean age, 58.4 years).
More recently, Westaby et al13 reported 8 patients undergoing simultaneous surgery for CAD and AAA. All patients in their series had significant impairment of left ventricular function and respiratory impairment. Poor respiratory function was considered one criterion with which to select patients for a combined procedure because it is a significant risk factor in major surgery, even more so if two major procedures are required. After completion of the cardiac procedure, CPB was continued during aortic surgery. Rewarming was not started until the proximal aortic anastomosis was almost completed, to protect vital organs. Mortality in this high-risk group of patients was 18% (both deaths were not cardiac related; 1 patient died from colonic ischemia and 1 from multiorgan failure after bilateral limb ischemia). All survivors were well at follow-up (3 to 18 months) and were in New York Heart Association functional class I or II.
The argument to perform aortic surgery with extracorporeal support is made because even after myocardial revascularization, a recovery period is necessary for the heart to overcome the effects of cardioplegic arrest and the risk of aortic cross-clamping persists during the short period of revascularization. Westaby et al also pointed out that continuous hypothermia during aortic repair may have a protective effect on other organs.
After CABG, acute myocardial dysfunction is a common occurrence.35 In patients with impaired ventricular function and diffuse CAD, ventricular function recovers slowly due to inadequate myocardial protection and reperfusion injury.36 It therefore cannot be expected that revascularization alone warrants cardiac protection during aortic cross-clamping, and it seems illogical to take the patient off bypass before aortic occlusion. We therefore advocate performing aortic surgery with the patient on continuous CPB for maximum mechanical cardiac support.
Our results with 25 patients undergoing combined procedures are in accordance with earlier studiesthe early mortality rate was 12% (3 of 25). At late follow-up (4 to 32 months), only 1 patient had died (noncardiac course). At follow-up, 12 patients were in New York Heart Association class I or II, whereas 9 patients were in functional class III. The hemiparesis observed in 1 patient with carotid endarterectomy, CABG, and AAA repair almost completely resolved. Respiratory insufficiency was a common postoperative complication, and mean ventilation time was higher than in comparable subgroups undergoing isolated CABG or AAA repair alone. In contrast to other reports, in our opinion, respiratory complications are related to the combined procedure itself, which requires much thoracoabdominal exposure. We therefore do not agree with Westaby et al13 and consider poor respiratory function to be a contraindication to the combined procedure.
Major blood loss due to full heparinization during aortic surgery was prevented by the use of collagen preclotted woven Dacron grafts (Hemashield, Meadox). The use of shielded vascular prostheses is mandatory for such operations. The conduct of one-stage surgery was uncomplicated in all except 1 patient, who developed acute myocardial infarction during surgery despite patent bypass grafts and died on postoperative day 3.
Postoperative adequate intensive care unit management is most critical in these patients. After combined surgery, two completely different strategies of infusion therapy have to be considered. Intra-abdominal surgery requires adequate postoperative volume replacement to compensate for volume loss by sequestration of fluid into the extravascular space and the abdominal cavity and to overcome the effect of washout acidosis. At the same time, myocardial overload is potentially harmful and should be avoided whenever possible after cardiac surgery. Complete hemodynamic monitoring, including measurements of pulmonary capillary wedge pressure, cardiac output, and mixed venous saturation, should therefore be continued for at least the first 48 hours after surgery.
Overall mortality for AAA repair in our department has substantially
decreased from 14.8% in 1986 to 6.4% in 1993 (P<.05 by
2 test). This decrease was observed for both elective
and emergency AAA repair. In addition to improvements in technique, the
more frequent use of tube grafts and coated prostheses was responsible
for these improved results. Due to a more aggressive approach in the
patient with both severe CAD and AAA using prior PTCA and two-stage and
combined one-stage procedures in selected patients, cardiac-related
mortality for AAA surgery may decrease further. It should be emphasized
that by adopting the one-stage approach, patients who had formerly been
denied surgery because of their high risk for possible cardiac-related
events underwent AAA repair. Furthermore, some patients were referred
from elsewhere for this treatment at our institution.
In conclusion, the combined procedure with aortic surgery being performed during extracorporeal circulation is safe and guarantees optimal cardiac protection. It may decrease both early and late mortality in this small but high-risk subset of patients with severe CAD, reduced left ventricular function, and AAA or AOD.
Promising new minimally invasive techniques are being introduced for the treatment of AAA37 and AOD.38 Perhaps transfemoral endovascular stenting of abdominal aneurysms will help to solve the problem of cardiac-related morbidity and mortality in patients with CAD and reduced left ventricular function who undergo surgical AAA repair. However, despite initial encouraging clinical results, these methods are still experimental and far from achieving widespread clinical application.39
Received August 4, 1994; accepted August 28, 1994.
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