Annals of Vascular Surgery
Volume 23, Issue 5 , Pages 583-597, September 2009

Morbidity and Mortality Caused by Cardiac Adverse Events after Revascularization for Critical Limb Ischemia

  • H.C. Flu

      Affiliations

    • Department of Vascular Surgery, St. Elisabeth Hospital, Tilburg, The Netherlands
  • ,
  • J.H.P. Lardenoye

      Affiliations

    • Department of Vascular Surgery, Leiden University Medical Center, Leiden, The Netherlands
    • Corresponding Author InformationCorrespondence to: J.H.P. Lardenoye, MD, Ph.D, Department of Vascular Surgery, Leiden University Medical Center, Albinusdreef 2, PO Box 9600, 2300 RC Leiden, The Netherlands
  • ,
  • E.J. Veen

      Affiliations

    • Department of Vascular Surgery, St. Elisabeth Hospital, Tilburg, The Netherlands
  • ,
  • A.E. Aquarius

      Affiliations

    • Center of Research on Psychology in Somatic Diseases, Department of Medical Psychology, Tilburg University, Tilburg, The Netherlands
  • ,
  • D.P. Van Berge Henegouwen

      Affiliations

    • Department of Vascular Surgery, St. Elisabeth Hospital, Tilburg, The Netherlands
  • ,
  • J.F. Hamming

      Affiliations

    • Department of Vascular Surgery, Leiden University Medical Center, Leiden, The Netherlands

Article Outline

Background

We assessed cardiac adverse events (AEs) after primary lower extremity arterial revascularization (LEAR) for critical lower limb ischemia (CLI) in order to evaluate the impact of cardiac AEs on the clinical outcome. We created an optimized care protocol concerning CLI patients' preoperative work-up as well as intra- and postoperative surveillance according to recent important literature and guidelines.

Methods

We conducted a prospective analysis of clinical outcome after LEAR using patient-related risk factors, comorbidity, surgical therapy, and AEs. This cohort was divided into patients with and without AEs. AEs were categorized according to predefined standards: minor, surgical, failed revascularization, and systemic. The consequences of AEs were reoperation, additional medication, irreversible physical damage, and early death.

Results

There were 106 patients (Fontaine III n=49, 46%, and Fontaine IV n=57, 56%) who underwent primary revascularization by bypass graft procedure (n=67, 63%) or balloon angioplasty (n=39, 37%). No difference in comorbidity was registered between the two groups. Eighty-four AEs were registered in 34 patients (32%). Patients experiencing AEs had significantly less antiplatelet agents (without AEs n=63, 88%, vs. with AEs n=18, 53%; p=0.000) and/or β-blockers (without AEs n=66, 92%, vs. with AEs n=16, 47%; p=0.000) compared to patients without AEs. The two most harmful consequences of AEs were irreversible physical damage (n=3) and early death (n=8). Sixty percent (n=9) of systemic AEs were heart-related. The postprocedural mortality rate was 7.5%, with a 75% (n=6) heart-related cause of death.

Conclusion

AEs occur in >30% of CLI patients after LEAR. The most harmful AEs on the clinical outcome of CLI patients were heart-related, causing increased morbidity and death. Significant correlations between prescription of β-blockers and antiplatelet agents and prevention of AEs were observed. A persistent focus on the prevention of systemic AEs in order to ameliorate the outcome after LEAR for limb salvage remains of utmost importance. Therefore, we advise the implementation of an optimized care protocol by discussing patients in a strict manner according to a predetermined protocol, to optimize and standardize the preoperative work-up as well as intra- and postoperative patient surveillance.

 

Back to Article Outline

Introduction 

Lower extremity peripheral arterial obstructive disease (PAOD) is a common syndrome that affects a large part of most adult populations in the Western world;1, 2, 3, 4, 5, 6, 7 it affects about 5% of the population aged between 55 and 74 years.8, 9 The clinical manifestations of PAOD are a major cause of acute and chronic illness. In addition, PAOD is associated with decrements in functional capacity, decreased quality of life, and increased risk of death.

Patients undergoing primary lower extremity arterial revascularization (LEAR), for critical limb ischemia (CLI) represent a dynamic challenge for the anesthetist and the surgeon that extends beyond the intricacies of the planned operation. These patients frequently have arterial disease affecting several vascular beds and suffer from other significant comorbidities such as diabetes, respiratory disease, and renal disease. Also, CLI patients have an even greater risk of experiencing cardiovascular ischemic events.10, 11, 12, 13 Undergoing LEAR, they are at increased risk of life-threatening peri- and postoperative cardiac adverse events (AEs), such as myocardial infarction.14, 15, 16 Fifty percent of patients operated for CLI die within 5 years,11, 17, 18 mainly due to cardiovascular events.19, 20, 21

In order to improve the postoperative outcome of patients undergoing primary LEAR, the pre-, intra-, and postoperative hemodynamic optimization, cardiac management, and timely detection of postoperative AEs could be one of the main goals during endovascular or surgical definitive treatment of these high-risk CLI patients.

Prospective evaluation of AEs is helpful and necessary to obtain a good insight into the occurrence of AEs after treatment for CLI in vascular surgery; it can be used as an indicator of quality in surgery and care.22, 23, 24, 25, 26, 27, 28, 29 It is important to gain insight into the causes and consequences of AEs in patients after LEAR for CLI. Therefore, the objectives of the present study were (1) to assess the occurrence of AEs after LEAR for CLI and (2) to examine the impact of AEs on the clinical outcome of CLI patients' general health.

Back to Article Outline

Materials and Methods 

Patients 

A 2-year survey was performed on 106 consecutive patients without a history of LEAR or amputations. They were admitted for the first time with CLI and underwent primary LEAR. Criteria for inclusion in the study population was CLI, ischemic rest pain (Fontaine stage III) with a resting ankle pressure of <50mm HG, and gangrene or nonhealing ischemic ulceration (Fontaine stage IV) with a resting ankle pressure of <70mm HG. This corresponds with categories 4, 5, and 6 of the Society of Vascular Surgery/North American Chapter of the International Society for Cardiovascular Surgery (SVS/ISCVS) standards30, 31 and the Trans-Atlantic Inter-Society Consensus (TASC) Document on Management of Peripheral Arterial Disease.1, 2 The included femoral popliteal lesions were according to TASC type B, C, or D for plaque morphology.1, 2 The cohort was divided into patients with AEs and without AEs during admission.

Risk Factors and Comorbidity 

Risk factors and comorbidities were registered prospectively for all patients during their admission intake. Smoking, hypertension, cardiac disease, hyperlipidemia, diabetes mellitus, renal disease, pulmonary disease, carotid disease, and age were classified according to the SVS/ISCVS and TASC reporting standards. The risk factor and comorbidity management, according to TASC and American Heart Association/American College of Cardiology (AHA/ACC) reporting standards, was conducted by either a vascular specialist or a cardiologist preoperatively in the outpatient clinic or during admission before operation when urgent intervention was indicated. Also the body mass index (BMI)32 of the patients was determined, divided into normal (18.5-24.9kg/m2), overweight (25.0-29.9kg/m2), and adipose (>30kg/m2). Data on risk factors and comorbidities are listed in Table I.

Table I. Baseline characteristics of the total sample (n=106) stratified by patients with and without AEs
CharacteristicsTotalWithout AEWith AEp
Gender 0.987a
Male56 (53)38 (53)18 (53)
Female50 (47)34 (47)16 (47)
Age (years) 0.412a
<5514 (13)9 (13)5 (15)
55–6930 (28)23 (32)7 (20)
70–7943 (41)25 (35)18 (53)
>8019 (18)15 (21)4 (12)
BMI32 0.788a
Normal60 (57)41 (57)19 (56)
Overweight40 (38)26 (36)14 (41)
Adiposity6 (6)5 (7)1 (3)
Comorbidity
Cardiac disease52 (49)32 (44)20 (59)0.167a
Pulmonary disease33 (31)21 (29)12 (35)0.525a
Renal disease33 (31)23 (32)10 (29)0.793a
Diabetes mellitus44 (42)23 (32)11 (32)0.426a
Hypertension60 (57)40 (56)20 (59)0.751a
Tobacco use65 (61)44 (61)21 (62)0.129a
Hyperlipidemia46 (43)34 (47)12 (35)0.247a
Carotid disease24 (23)13 (18)11 (32)0.101a
SVS-ISCVS risk score30, 31
Mean (SD)0.78 (0.59)0.74 (0.62)0.87 (0.52)0.299a
(min–max)(0–2.3)(0–2.3)(0–2.1)
Risk factors
Median (SD)3.0 (1.9)3.0 (1.9)3.5 (1.8)0.270b
(min–max)(1–8)(1–8)(1–8)
Secondary prevention
Antiplatelet agent81 (76)63 (88)18 (53)0.000a
ß-blocker82 (77)66 (92)16 (47)0.000a
HMG-CoA reductase inhibitor91 (86)61 (85)30 (88)0.628a

Data are presented as n and percentages, unless otherwise specified. SD, standard deviation.

aChi-squared test.

bMann-Whitney U-test.

Medication 

Medication use according to the TASC and AHA/ACC reporting standards was listed by the patients at baseline; secondary prevention prescribed drugs, recorded at admission for purposes of analysis, were reviewed and classified according to the following categories: antiplatelet agents, β-blockers, and HMG-CoA reductase inhibitors.

Revascularization 

The vascular treatment (LEAR) consisted of percutaneous transluminal angioplasties (PTAs) and bypass graft procedures. The PTAs were carried out by conventional balloon dilatation of the lesion with or without stent placement and under regional anesthesia. Patients were prescribed with a daily dose of acetylsalicylic acid/aspirin after the PTA was performed. The bypass graft procedure (BGP) was performed according to standard vascular techniques, using preferably reversed vein for femoral popliteal (supra- and infragenual) and crural BGPs and under general anesthesia. Patients were prescribed a daily dose of coumarin after the BGP was performed. The patency of a BGP was determined by duplex ultrasound examination and ankle-brachial indices in all patients 4 weeks after LEAR. The definition of primary and secondary patency, the decision to intervene, and the type of intervention were driven by the SVS/ISCVS and TASC reporting standards. The nonvascular treatment consisted of drainage/debridement, a minor amputation (defined as toe or foot amputation), and a major amputation (defined as an amputation above or below the level of the knee). All operations were performed by or under the supervision of a vascular surgeon.

Adverse Events 

In The Netherlands, the Association of Surgeons of the Netherlands (ASN) has agreed on one common definition of AEs.33, 34, 35, 36, 37 This definition differs from that used in other studies because it has been chosen with the explicit aim of excluding subjective judgment on cause and effect, as well as right and wrong. The definition of an AE is “an unintended and unwanted event or state occurring during or following medical care, that is so harmful to a patient's health that (adjustment of) treatment is required or that permanent damage results. The AE may be noted during hospitalization, until 30 days after discharge or transfer to another department. The intended result of treatment, the likelihood of the adverse outcome occurring, and the presence or absence of a medical error causing it, is irrelevant in identifying an adverse outcome.”37 This definition did not change during the study period.

In 1993 a fully automated registration system (self-developed Microsoft Access application with an Oracle database as back-end) was implemented in the surgical department of the St. Elisabeth Hospital in Tilburg, The Netherlands. In 1995 total coverage was reached, and registration of AEs was also possible in the intensive care unit, operating room, emergency department, and outpatient clinic. Since 1995 the system has been based on an elaborated list of criteria developed by the ASN (Appendices I and II). AEs are registered immediately by the physician who diagnoses them. The registered AEs are evaluated and discussed during a weekly meeting with all senior surgeons, surgical residents, and interns. As shown in Figure 1 and Appendix I, patients with AEs were subdivided into four groups: minor, surgical, failed revascularization, and systemic.

  • View full-size image.
  • Fig. 1 

    Patients divided by the most important AEs that occurred during the postoperative period resulting in their consequences. All data are presented as percentages, unless otherwise specified. Group 1, minor; group 2, surgical; group 3, failed revascularization; group 4, systemic; I, no consequences; II, additional transfusion/medication; III, reoperation; IV, irreversible physical damage; V, death.

Registration and Statistical Analysis 

Patient information was registered prospectively in an electronic patient file (Oracle database) used for all patients during their admission intake. The review was retrospective, and this material was entered in a specifically designed computerized analysis database for vascular patients, developed in Access (Office XP from Microsoft, Redmond, WA). Statistical analyses were performed through a computerized software package, using Excel (Office XP from Microsoft) and SPSS 16.0 for Windows (SPSS, Inc., Chicago, IL). Following completion of the data collection, univariate analyses were performed using chi-squared and unpaired Student's t-test. The secondary procedures and AEs were analyzed with the Mann-Whitney U-test. Univariate and multivariate analyses were performed using AEs (minor, surgical, systemic, and failed revascularization) as dependent variables, adjusting for gender, age, BMI, cardiac disease, pulmonary disease, renal disease, diabetes mellitus, hypertension, tobacco use, hyperlipidemia, carotid disease, SVS-ISVCS risk score, antiplatelet agents, β-blockers, and HMG-CoA reductase inhibitors. For all statistical analyses, p<0.05 was considered statistically significant. The life-table analysis, constructed as described by SVS-ISCVS standards, was used to investigate differences in primary patency, secondary patency, limb salvage, and survival rates.

Back to Article Outline

Results 

Patients, Risk Factors, and Comorbidity 

A total of 56 men (53%) and 50 women (47%) underwent LEAR because of CLI. Mean ages were 72 and 70 years, respectively (range 47-93). Indication for LEAR was Fontaine III in 49 patients (44%) and Fontaine IV in 57 patients (56%). Mean duration of admission was 9 and 13 days, respectively (range 2-82). These patients suffered from cardiac disease (n=52, 49%), pulmonary disease (n=33, 31%), renal disease (n=33, 31%), diabetes mellitus (n=39, 38%), and hypertension (n=60, 57%), resulting in a mean patient risk score of 0.8. In the patient group, 46 patients (43%) were overweight or obese. A summary of the risk factors and disease characteristics is listed in Table I; no significant differences in risk factors were found between patients with and those without AEs.

Medication 

Univariate analysis 

Concerning secondary prevention, a difference was present concerning prescription drugs: antiplatelet agents (total n=81, 76%; without AEs n=63, 88%, vs. with AEs n=18, 53%; p<0.000) and β-blockers (total n=82, 77%; without AEs n=66, 92%, vs. with AEs n=16, 47%; p<0.000). No difference was present concerning HMG-CoA reductase inhibitors (total n=91, 86%; without AEs n=61, 85%, vs. with AEs n=30, 88%; p=0.628). Concerning secondary prevention, 75-86% of CLI patients were on target with the TASC and AHA/ACC reporting guidelines.

Multivariate analysis 

Not prescribing β-blockers and antiplatelet agents was associated with the occurrence of AEs (odds ratio [OR]=0.017, p=0.000, and OR=19.808, p=0.000, respectively). Subsequently, not prescribing β-blockers was associated with the occurrence of the subcategory of systemic AEs (OR=0.00, p=0.000).

Revascularization 

Primary procedures 

Concerning the TASC type of femoral popliteal lesion stratified by patients with and those without AEs, no difference was seen (TASC B, without AEs n=26, 36%, vs. with AEs n=13, 38%; TASC C, without AEs n=12, 17%, vs. with AEs n=4, 12%; TASC D, without AEs n=34, 47%, vs. with AEs n=17, 50%; p=0.805). Concerning the PTAs stratified by patients with or without AEs, no difference was seen (total n=39, 37%; without AEs n=26, 36%, vs. with AEs n=13, 38%; p=0.345). There was a total of 67 primary BGPs (63%): reversed vein in 57 (85%) and polytetrafluoroethylene (PTFE) in 10 (15%). Concerning the type of BGP stratified by patients with or without AEs, no difference was seen (femoral popliteal supragenual total n=16, 15%, and without AEs n=12, 17%, vs. with AEs n=4, 12%; femoral popliteal infragenual total n=30, 28%, and without AEs n=20, 28%, vs. with AEs n=10, 29%; femoral crural total n=21, 20%, and without AEs n=14, 19%, vs. with AEs n=7, 21%; p=0.822).

Secondary procedures 

Secondary procedures occurred only in patients with AEs (total n=23, 40%, p=0.000; vascular n=8, 35%, p=0.000; nonvascular n=15, 65%, p=0.000). As listed in Table II, no difference (p=0.817) was seen in primary LEAR (PTA p=0.345, BGP p=0.822) in all patients stratified by the occurrence of AEs. The total 30-day cumulative life-table primary and secondary patency rates of all BGPs and limb salvage rates were 89%, 97%, and 99%, respectively.

Table II. Summary of Fontaine and TASC classifications and primary and secondary procedures of all patients with primary CLI stratified by those with and without AEs
CharacteristicsTotalWithout AEWith AEp
Fontaine classification30, 31 0.257a
III49 (46)36 (50)13 (38)
IV57 (54)36 (50)21 (62)
TASC classification1, 2
Femoral popliteal lesions 0.805a
Type B39 (37)26 (36)13 (38)
Type C16 (15)12 (17)4 (12)
Type D51 (48)34 (47)17 (50)
Primary procedures106 (82)72 (100)34 (60)0.817a
PTA39 (37)26 (36)13 (38)0.345a
Femoral popliteal67 (63)46 (64)21 (62)
Type B lesion 0.822a
BGP16 (15)12 (17)4 (12)
Femoral popliteal SG30 (28)20 (28)10 (29)
Femoral popliteal IG21 (20)14 (19)7 (21)
Femoral crural
Secondary procedures23 (18)0 (0)23 (40)0.000b
Vascular8 (35)0 (0)8 (35)0.000b
RoBGP5 (17)0 (0)5 (17)
RiBGP1 (3)0 (0)1 (3)
Hemorrhage2 (7)0 (0)2 (7)
Nonvascular15 (65)0 (0)15 (65)0.000b
Wound drainage2 (7)0 (0)2 (7)
Skin grafting2 (3)0 (0)2 (3)
Necrotectomy3 (10)0 (0)3 (10)
Minor amputation6 (20)0 (0)6 (20)
Major amputation2 (7)0 (0)2 (7)
Patients withsecondary procedures16 (15)0 (0)16 (47)0.000a

Data are presented as n and percentages, unless otherwise specified. SG, supragenual; IG, infragenual; RoBGP, revascularization of bypass graft; RiBGP, removal of infected bypass graft.

aChi-squared test.

bMann-Whitney U-test.

Adverse Events 

Thirty-four patients (men n=18, 53%, and women n=16, 47%) experienced AEs. Sixty-five percent of the patients were 70 years or older. Indication for LEAR was Fontaine III in 13 (38%) and Fontaine IV in 21 (62%) patients.

As listed in Table III, Table IV, a total of 48 AEs (during admission n=43, 90%, and postdischarge in the outpatient clinic n=5, 10%) were registered: 50% were categorized as minor/surgical and 50% as failed revascularization/systemic AEs, resulting in secondary procedures as listed in Table IV. In Figure 1, the AEs are related to their short-term outcomes. Minor AEs resulted equally in no consequence or in additional transfusion/medication. Surgical AEs resulted almost equally in additional transfusion/medication (56%) and in reoperation (44%) because of postoperative hemorrhage (n=2) or wound drainage (n=2). Patients categorized as failed revascularization underwent a reoperation to restore patency in 100% of cases. Five failed BGPs resulted in three embolectomies and two PTAs of the BGP and were performed to achieve assisted primary patency in the postoperative period. In two patients the reoperation was not successful and an amputation of the affected limb was needed (one below-knee and one above-knee).

Table III. Summary of AEs of all patients with primary CLI: stratified by primary revascularization (PTA vs. BGP)
CharacteristicsTotal (n=106)PTA (n=39)BGP (n=67)p
Cause
Minor other8 (33)5 (28)3 (10)0.247a
Surgical16 (27)7 (39)9 (30)0.338a
Systemic15 (25)6 (33)9 (30)0.738a
Failed revascularization9 (15)0 (0)9 (30)0.001a
Patients with AEs34 (32)13 (33)21 (31)0.832a
Total AEs48 (100)18 (38)30 (62)0.757a

Data are presented as n and percentages, unless otherwise specified.

aMann-Whitney U-test.

Table IV. AEs (n=48) after primary revascularization for CLI of the total sample (n=106)
Characteristics
Minor
Phlebitis1 (2)
Urinary tract infection6 (13)
Deep venous thrombosis1 (2)
Total8 (17)
Surgical
Wound dehiscence1 (2)
Wound infection7 (15)
Hemorrhage7 (15)
Other1 (2)
Total16 (33)
Failed revascularization
BGP infection1 (2)
Failed BGP8 (17)
Total9 (19)
Systemic
Pneumonia2 (4)
Respiratory failure1 (2)
Arrhythmia1 (2)
Cardiac arrest2 (4)
Cardiogenic shock3 (2)
Congestive heart1 (2)
failure
Myocardial infarction2 (4)
Stroke3 (4)
Total15 (31)
Total AEs48 (100)

Data are presented as n and percentages, unless otherwise specified.

As listed in Table III, patients undergoing minimally invasive revascularization procedures (PTA) as well as open surgical procedures (BGP) had an equal chance (total n=34, 37%; PTA n=13, 33%, vs. BGP n=21, 31%; p=0.832) of experiencing an AE. Also, no difference in the occurrence of the total AEs (PTA n=18, 30%, vs. BGP n=30, 62%; p=0.757) was seen, stratified by types of primary LEAR.

All systemic AEs resulted in irreversible physical damage (n=3, 27%) or, even worse, in the death of the patient (n=8, 73%). Causes of death included arrhythmia (n=1), cardiac arrest (n=2), myocardial infarction (n=1), cardiogenic shock (n=2), hemorrhage (n=1), and cerebrovascular accident (n=1) and resulted in a 30-day overall mortality rate of 7.5%.

Back to Article Outline

Discussion 

The primary goal of this study was to assess the occurrence of AEs after primary LEAR for CLI. The secondary goal of the study was to evaluate the impact of AEs on the clinical outcome of CLI patients' general health.

AEs are associated with poorer health outcomes for patients and increase the average estimated total costs in the treatment for PAOD.38 The registration of AEs is a helpful tool to gain insight into the incidence and type of AEs that might occur after revascularization for CLI. It optimizes our awareness of all unwanted developments in the illness of the patients and in the treatment of illnesses that occurred in the vascular department and their (possibly preventable) causes. Furthermore, it gives us the opportunity to evaluate the quality of the work done and compare it with outcomes in the literature. However, uniformity of these AE registration systems is necessary, to compare the results between different health-care facilities.

Our results showed that 32% of the primary revascularized CLI patients underwent 48 AEs in the 30-day perioperative period. As outlined in Table III, Table IV, 31% of the AEs were systemic, of which 47% were of cardiac cause. Cardiac AEs are the leading cause of morbidity and mortality in patients undergoing vascular surgery.39 Numerous reports have also confirmed that patients undergoing vascular reconstruction have an increased risk of perioperative cardiac AEs.40, 41, 42 As shown in Figure 1, profound impacts on patient morbidity and mortality were observed after systemic AEs; and these should be prevented during the pre-, peri-, and postoperative periods. It is important to stress that the cause of death was cardiac in 75% of the patients, resulting in a 30-day overall mortality rate of 7.5% compared to up to 3.9-8% mortality in the previous literature.43, 44, 45, 46, 47, 48, 49, 50

There were no significant differences in risk factors, comorbidity, BMI, and Fontaine classification between patients with or without AEs. This could be explained by the fact that CLI is accompanied by extensive comorbid conditions in almost all patients.

Detailed analysis of variables correlated with the occurrence of AEs revealed that patients without AEs were treated more often with β-blockers compared to patient with AEs. Guidelines on perioperative care recommend that high-risk cardiac patients should receive a β-blocker.3, 4, 5, 51, 52, 53, 54, 55 However, available data also suggest that β-blockers are underused in patients undergoing revascularization,56, 57, 58, 59 which was also the case with the CLI patients suffering from cardiac AEs in this study. According to the literature,51, 60, 61, 62, 63, 64, 65, 66 the use of β-blockers 1 or 2 weeks prior to surgery and continuing beyond surgery is advised to achieve adequate heart rate control, ultimately resulting in a decrease of the incidence of perioperative cardiovascular AEs, and to offer long-term survival benefit. Also, the withdrawal of β-blockers prior to major surgery is associated with an increased incidence of cardiovascular morbidity and mortality. Furthermore, detailed analysis revealed that patients with antiplatelet agents experience fewer AEs compared to patients without this medication. The use of antiplatelet agents is indicated as secondary cardiovascular prevention in patients presenting with PAOD.60, 67, 68, 69 A patient who has withdrawn antiplatelet agents prior to the event has a worse outcome than one who either continues on antiplatelet agents or has never received this therapy.

No difference was seen in primary revascularization (PTA vs. BGP) in all CLI patients stratified by the occurrence of AEs. This indicates that the widely accepted hypothesis that minimally invasive revascularization procedures (PTA) are accompanied by fewer AEs compared to BGP should not be accepted. A possible explanation for the relatively high percentage of AEs in the PTA group could be the extensive comorbid status of the CLI patients with their subsequent susceptibility for hemodynamic imbalance after use of contrast agents. Another explanation could be found in the fact that in this study, in contrast to most AE studies, postdischarge AEs in the outpatient clinic were also included.

In order to reduce AEs and thereby patient morbidity and mortality, we suggest that the pre-, intra-, and postoperative cardiac management should be one of the main important goals during endovascular and surgical treatment of these high-risk CLI patients.

Preoperative Multidisciplinary Meeting 

When considering a patient for revascularization, a careful preoperative clinical risk evaluation (Fig. 2) is essential. Extensive cardiac preoperative assessment and optimization according to the TASC and ACC/AHA guidelines is of utmost importance to reduce perioperative cardiac AEs. Second, as already stated, guidelines on perioperative care recommend that high-risk cardiac patients should receive a β-blocker.3, 4, 5, 51, 52, 53, 54, 55 Third, blood pressure-lowering therapy leads to reduction in cardiovascular events in patients with PAOD.60, 70, 71, 72, 73, 74, 75 Fourth, the use of HMG-CoA reductase inhibitors may reduce the risk of perioperative myocardial infarction and the risk of major vascular events. Cessation of HMG-CoA reductase inhibitors is associated with significantly poorer outcomes compared to patients who continue their therapy or those who have never been on a HMG-CoA reductase inhibitor.60, 76, 77, 78, 79, 80, 81, 82, 83, 84, 85, 86, 87, 88, 89, 90, 91, 92 Fifth, the use of antiplatelet agents is indicated as secondary cardiovascular prevention in patients presenting with PAOD.

  • View full-size image.
  • Fig. 2 

    Preoperative multidisciplinary meeting; clinical risk evaluation and subsequent risk-reduction strategies. aPTT, activated partial thromboplastin time; PT, prothrombin time; DUE, duplex ultrasound examination; ABI, ankle-brachial index; AP, arterial pressure; INR, international normalized ratio; Hgb, hemoglobin; Ht, hematocrit; LDL, low-density lipoprotein; HDL, high-density lipoprotein; ACE, angiotensin-converting enzyme; NYHA, New York Heart Association; PTCA, percutaneous transluminal coronary angioplasty; CABG, coronary artery bypass grafting; PTA, percutaneous transluminal angioplasty; CEA, carotid endarterectomy; EA, endarterectomy; BGP, bypass graft; BMI, body mass index; WHO/ISH, World Health Organization/International Society of Hypertension; NCEP, National Cholesterol Education Program; ICU, intensive care unit; NKF-DOQI, National Kidney Foundation-Disease Outcomes Quality Initiative; COPD, chronic obstructive pulmonary disease; GOLD, Global Initiative on Obstructive Lung Diseases; TMA, transmetatarsal amputation; BKA, below-knee amputation; TKA, through-knee amputation; AKA, above-knee amputation; PIER, percutaneous intentional extraluminal revascularization; TE, thromboembolectomy; EA, endarterectomy.

Intraoperative Patient Surveillance 

The intraoperative patient surveillance is shown in Figure 3. First, prevent intraoperative hypothermia and myocardial ischemic burden; they are independent predictors of perioperative morbid cardiac AEs.93, 94, 95, 96, 97, 98 Intraoperative and postoperative ST-segment monitoring and troponin T release can be useful to monitor patients with single or multiple risk factors for coronary artery disease, with known coronary artery disease, or undergoing vascular surgery.97, 98, 99, 100, 101, 102, 103, 104, 105, 106 Second, hyperglycemia is an independent predictor of cardiovascular risk; the severity of hyperglycemia is directly related to mortality rate during myocardial ischemia.107, 108, 109, 110, 111 Blood glucose concentration should be controlled during the perioperative period in patients with diabetes mellitus or acute hyperglycemia who are at high risk for myocardial ischemia when undergoing major revascularization procedures.96, 97

  • View full-size image.
  • Fig. 3 

    Flowchart of preoperative multidisciplinary vascular meeting and clinical risk evaluation, intraoperative patient surveillance, and postoperative patient management. ABI, ankle-brachial index; LEAR, lower extremity arterial revascularization; PIER, percutaneous intentional extraluminal revascularization; PTA, percutaneous transluminal angioplasty; TE, thromboembolectomy; EA, endarterectomy; BGP, bypass graft procedure; PTFE, polytetrafluoroethylene; TMA, transmetatarsal amputation; BKA, below-knee amputation; TKA, through-knee amputation; AKA, above-knee amputation; DM, diabetes mellitus; HL, hyperlipidemia; ECG, electrocardiogram; TASC, Trans-Atlantic Inter-Society Consensus; AHA/ACC, American Heart Association/American College of Cardiology; AIM, Annals of Internal Medicine clinical guidelines; ACCP, American College of Chest Physicians; NKF-DOQI, National Kidney Foundation–Disease Outcomes Quality Initiative; ICU, intensive care unit; Hgb, hemoglobin; RBC, red blood cells; FFP, fresh frozen plasma; aPTT, activated partial thromboplastin time; PT, prothrombin time; INR, international normalized ratio.

Postoperative Patient Management 

The postoperative patient management is shown in Figure 3. Because the majority of cardiac events in noncardiac surgical patients occur postoperatively, the postoperative period may be the time during which ablation of stress, adverse hemodynamics, and hypercoagulable responses are most critical. Epidural anesthesia/analgesia result in lower opiate dosages, a better ablation of the catecholamine response, and a reduction of hypercoagulability.112, 113, 114 Second, anemia and hematocrit <28-30% impose stress on the cardiovascular system that may exacerbate myocardial ischemia and aggravate heart failure.115, 116, 117, 118, 119, 120, 121 Third, hyperviscosity and hypercoagulability have also proven to be markers of poor prognosis.1, 2, 3, 4, 5, 121

Limitations 

Because of its retrospective nature, our study has limitations, which should be considered when interpreting the results. The number of patients in the present study does not permit further analyses in depth. Patients with previous surgical treatment for CLI were excluded in this study to reduce the influence of previous AEs on the outcome of the current treatment. The sample was composed exclusively of patients with CLI, and our results may not generalize to other patient samples. It should be appreciated that our results were obtained in one high-volume hospital and that cardiac event rates might differ in other centers.

Back to Article Outline

Conclusion 

AEs occur in >30% of CLI patients after LEAR. The most harmful AEs on the clinical outcome of CLI patients were heart-related, causing increased morbidity and death. Significant correlations between prescription of β-blockers and/or antiplatelet agents and prevention of AEs were observed. A persistent focus on the prevention of systemic AEs in order to ameliorate the outcome after LEAR for limb salvage remains of utmost importance.

Back to Article Outline

Appendix 

Appendix 1. Classification of AEs and explanation of causes
CategoryaCause of the AEb (groups 1–4)Outcome (categories I–V)
Cardiac1 MinorI No consequence
Pulmonary2 SurgicalII Additional transfusion/medication
Neurology3 Failed RevascularizationIII Reoperation
Renal4 SystemicIV Irreversible physical damage
(subcutis, muscles/skeleton, hematology, vascular management) V death

aThese categories were further subdivided as listed in Appendix II.

bExplanation and definition of the causes of perioperative complications: minor, an AE such as urinary tract infection or deep venous thrombosis; surgical, an AE due to surgical treatment, such as abscess, wound infection, wound necrosis, wound dehiscence, hemorrhage; failed revascularization, when a primary bypass graft occluded or at risk for occlusion and surgical or endovascular reintervention was performed or when an anatomical arterial segment occluded after a PTA was performed on that same segment; systemic, potential life-threatening AEs, such as pneumonia, respiratory failure, arrhythmia, cardiac arrest, cardiogenic shock, congestive heart failure, myocardial infarction, shock, stroke.

Appendix II. Subdivision of specific AE categories
Cardiac
Congestive Heart Failure
Arrhythmia
Cardiac arrest
Myocardial infarction
Endocarditis/pericarditis
Cardiogenic shock
Hypertension/hypotension
Tachycardia/bradycardia
Pulmonary
Respiratory insufficiency
Aspiration/pneumonia
Pleural fluid
Atelectasis
Embolism
Neurology
Cerebrovascular accident
Transient ischaemic attack
Neuropraxia
Renal
Renal failure
End-stage renal disease
Urinary tract infection
Urinary retention
Pyelonephritis/hydronephritis
(Sub)Cutis
Blister/ulcer
Abscess
Epidermiolysis
Seroma
Cellulites
Wound hematoma
Wound infection
Wound dehiscence
Necrosis/unexpected tissue loss
Muscles/skeleton
Compartmental syndrome
Osteomyelitis
Hematology
Spontaneous hemorrhage
Heparin-induced thrombocytopenia
Transfusion reaction
Decreased hemoglobin
Thrombosis from ATIII or protein C or S deficiency
Septicemia
Fluid and electrolytes
Vascular management
Line infection
Deep venous thrombosis
Infection BGP
Stenosis BGP/anatomical segment after PTA
Occlusion BGP/anatomical segment after PTA
Anastomotic pseudoaneurysm/anatomical segment after PTA
Hemorrhage
General management
Error in medication, diagnosis, judgment, or technique
Delay to OR, in MD response, or in diagnosis
Incomplete hospital record

BGP=bypass graft procedure; PTA=percutaneous transluminal angioplasty; OR=operating room; MD=medical doctor.

Back to Article Outline

References 

  1. Dormandy JA, Rutherford RB. Management of peripheral arterial disease (PAD). TASC Working Group. TransAtlantic Inter-Society Consensus (TASC). J Vasc Surg. 2000;31:S1–S296
  2. Norgren L, Hiatt WR, Dormandy JA, et al. Inter-Society Consensus for the Management of Peripheral Arterial Disease (TASC II). Eur J Vasc Endovasc Surg. 2007;33(Suppl. 1):S1–S75
  3. Hirsch AT, Haskal ZJ, Hertzer NR, et al. ACC/AHA guidelines for the management of patients with peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal aortic): a collaborative report from the American Association for Vascular Surgery/Society for Vascular Surgery, Society for Cardiovascular Angiography and Interventions, Society of Interventional Radiology, Society for Vascular Medicine and Biology, and the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. http://www.acc.org/clinical/guidelines/pad/index.pdf.
  4. Hunt SA, Abraham WT, Chin MH, et al. ACC/AHA 2005 guideline update for the diagnosis and management of chronic heart failure in the adult: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Update the 2001 Guidelines for the Evaluation and Management of Heart Failure). http://www.acc.org/clinical/guidelines/failure//index.pdf (accessed August 17, 2005).
  5. Eagle KA, Berger PB, Calkins H, et al. ACC/AHA guideline update for perioperative cardiovascular evaluation for noncardiac surgery executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Update the 1996 Guidelines on Perioperative Cardiovascular Evaluation for Noncardiac Surgery). J Am Coll Cardiol. 2002;39:542–553
  6. Smith SC, Allen J, Blair SN, et al. AHA/ACC guidelines for secondary prevention for patients with coronary and other atherosclerotic vascular disease: 2006 update-Endorsed by the National Heart, Lung, and Blood Institute. Circulation. 2006;113:2363–2372
  7. Criqui MH, Denenberg JO, Langer RD, et al. The epidemiology of peripheral arterial disease: importance of identifying the population at risk. Vasc Med. 1997;2:221–226
  8. Fowkes FG, Housley E, Cawod EH, Macintyre CC, Ruckley CV, Prescott RJ. Edinburgh Artery Study: prevalence of asymptomatic and symptomatic peripheral arterial disease in the general population. Int J Epidemiol. 1991;20:384–392
  9. Selvin E, Erlinger TP. Prevalence of and risk factors for peripheral arterial disease in the United States: results from the National Health and Nutrition Examination Survey, 1999-2000. Circulation. 2004;110:738–743
  10. Hirsch AT, Criqui MH, Treat-Jacobson D, et al. Peripheral arterial disease detection, awareness, and treatment in primary care. J A M A. 2001;286:1317–1324
  11. Criqui MH, Langer RD, Fronek A, et al. Mortality over a period of 10 years in patients with peripheral arterial disease. N Engl J Med. 1992;326:381–386
  12. Mukherjee D, Lingam P, Chetcuti S, et al. Missed opportunities to treat atherosclerosis in patients undergoing peripheral vascular interventions: insights from the University of Michigan Peripheral Vascular Disease Quality Improvement Initiative (PVD-QI2). Circulation. 2002;106:1909–1912
  13. Grundy SM, Pasternak R, Greenland P, et al. AHA/ACC scientific statement. Assessment of cardiovascular risk by use of multiple-risk-factor assessment equations: a statement for healthcare professionals from the American Heart Association and the American College of Cardiology. J Am Coll Cardiol. 1999;34:1348–1359
  14. Mangano DT. Perioperative cardiac morbidity. Anesthesiology. 1990;72:153–184
  15. Jamieson WRJM, Miyagishima RT, Gerein AN. Influence of ischemic heart disease on early and late mortality after surgery for peripheral occlusive vascular disease. Circulation. 1982;66:I92–I97
  16. McFalls E, Ward H, Santilli S, Scheftel M, Chesler E, Doliszny K. The influence of perioperative myocardial infarction on long-term prognosis following elective vascular surgery. Chest. 1998;113:681–686
  17. Whittemore AD. Infrainguinal bypass. In:  Rutherford RB editors. Vascular Surgery. Philadelphia: WB Saunders; 1995;p. 794–814
  18. Dawson I, van Bockel JH, Brand R. Late nonfatal and fatal cardiac events after infrainguinal bypass for femoropopliteal occlusive disease during a thirty-one-year period. J Vasc Surg. 1993;18:249–260
  19. Leng GC, Lee AJ, Fowkes FGR, et al. Incidence, natural history and cardiovascular events in symptomatic and asymptomatic peripheral arterial disease in the general population. Int J Epidemiol. 1996;25:1172–1181
  20. Newman AB, Siscovick DS, Manolio TA, et al. Ankle–arm index as a marker of atherosclerosis in the cardiovascular health study. Circulation. 1993;88:837–845
  21. Hertzer NR, Beven EG, Young JR, et al. Coronary artery disease in peripheral vascular patients. A classification of 1000 coronary angiograms and results of surgical management. Ann Surg. 1984;199:223–233
  22. Kroon HM, Breslau PJ, Lardenoye JW. Can the incidence of unplanned reoperations be used as an indicator of quality of care in surgery?. Am J Med Qual. 2007;22:198–202
  23. De Waal Malefijt MC, Peeters H. Een complicatieregistratiesysteem. Ned Tijdschr Orth. 1994;1:76–83
  24. Campion FX, Rosenblatt MS. Quality assurance and medical outcomes in the era of cost containment. Surg Clin North Am. 1996;76:139–156
  25. Blumenthal D, Epstein AME. The role of physicians in the future of quality management. N Engl J Med. 1996;335:1328–1331
  26. Chassin MPH. Improving the quality of care. N Engl J Med. 1996;335:1060-1030
  27. Brook RH, Clearly PD. Part 2: Measuring quality of care. N Engl Med. 1996;335:966–970
  28. de Vries BC, Keeman JN. Quality policy of the Association of Surgeons of the Netherlands. Ped Tgdschr Gen. 1996;14:789–791
  29. Veen EJ, Janssen-Heijnen MLG, Leenen LPH, Roukema JA. The registration of complications in surgery: a learning curve. World J Surg. 2005;29:402–409
  30. Rutherford RB, Baker JD, Ernst C, et al. Recommended standards for reports dealing with lower extremity ischemia: revised version. J Vasc Surg. 1997;26:517–538
  31. Rutherford RB. Presidential address. Vascular surgery-comparing outcomes. J Vasc Surg. 1996;23:5–17
  32. Luchsinger JA, Lee W, Carrasquillo O, Rabinowitz D, Shea S. Body mass index and hospitalization in the elderly. J Am Geriatr Soc. 2003;51:1615–1620
  33. de Vries BC, Keeman JN. Quality policy of the Association of Surgeons of the Netherlands. [in Dutch] Ned Tijdschr Gen. 1996;14:789–791
  34. Roukema JA, van der Werken CHR, Leenen LPH. Registration of postoperative complications to improve the results of surgery. [in Dutch] Ned Tijdschr Gen. 1996;140:781–784
  35. de Marang-van Mheen PJ, Kievit J. Automated registration of adverse events in surgical patients in the Netherlands: the current status. [in Dutch] Ned Tijdschr Gen. 2003;147:1273–1277
  36. Kievit J, Jeekel J, Sanders FBM. Adverse outcome registration and quality improvement. [in Dutch] Med Contact. 1999;54:1363–1365
  37. Marang-van de Mheen PJ, van Hanegem N, Kievit J. Effectiveness of routine reporting to identify minor and serious adverse outcomes in surgical patients. Qual Saf Health Care. 2005;14:378–382
  38. Flu HC, van der Hage JH, Knippenberg B, Merkus JW, Hamming JF, Lardenoye JHP. Treatment for peripheral arterial obstructive disease: an appraisal of the economic outcome of complications. J Vasc Surg. 2008;48:368–376
  39. Mamode N, Scott RN, McLaughlin SC, McLellland A, Pollack JG. Perioperative myocardial infarction in peripheral vascular surgery. B M J. 1996;312:1396–1397
  40. Plecha FR, Bertin VJ, Plech EJ, et al. The early results of vascular surgery in patients 75 years of age and older: an analysis of 3259 cases. J Vasc Surg. 1985;2:769–774
  41. Krupski WC, Layug EL, Reilly LM, Rapp JH, Magano DT. Comparison of cardiac morbidity rates between aortic and infrainguinal operations: 2 year follow-up study of Perioperative Ischemia Research Group. J Vasc Surg. 1993;18:609–615
  42. L'Italien CJ, Cambria RP, Cutler BS, et al. Comparative early and late cardiac morbidity among patients requiring different vascular surgery procedures. J Vasc Surg. 1995;21:935–944
  43. Biancari F, Kantonen I, Albäck A, Mätzke S, Luther M, Lepäntalo M. Limits of infrapopliteal bypass surgery for critical leg ischemia: when not to reconstruct. World J Surg. 2000;24:727–733
  44. Biancari F, Albäck A, Kantonen I, Luther M, Lepäntalo M. Predictive factors for adverse outcome of pedal bypasses. Eur J Vasc Endovasc Surg. 1999;18:138–143
  45. Albäck A, Lepäntalo M. Immediate occlusion of in situ saphenous vein bypass grafts: a survey of 329 reconstructions. Eur J Surg. 1998;164:745–750
  46. Dawson I, van Bockel JH. Reinterventions and mortality after infrainguinal reconstructive surgery for leg ischaemia. Br J Surg. 1999;86:38–44
  47. Kantonen I, Lepäntalo P, Luther M, Salenius J, Ylönen K. Finnvasc Study Group. Factors affecting the results of surgery for chronic critical leg ischemia—a nationwide survey. J Vasc Surg. 1998;27:940–947
  48. Lam YE, Landry JG, Edwards MJ, Yeager RA, Taylor LM, Moneta GL. Risk factors for autogenous infrainguinal bypass occlusion in patients with prosthetic inflow grafts. J Vasc Surg. 2004;39:336–342
  49. Halloran BG, Lilly MP, Cohn EJ, Benjamin ME, Flinn WR. Tibial bypass using complex autologous conduit: patency and limb salvage. Ann Surg. 2001;15:634–643
  50. Virkkunen J, Heikkinen M, Lepäntalo M, Metsänoja R, Salenius JP. Diabetes as an independent risk factor for early postoperative complications in critical limb ischaemia. J Vasc Surg. 2004;40:761–767
  51. Poldermans D, Bax JJ, Schouten O, et al. Should major vascular surgery be delayed because of preoperative cardiac testing in intermediate-risk patients receiving beta-blocker therapy with tight heart rate control?. J Am Coll Cardiol. 2006;48:964–969
  52. Hoeks SE, Scholte op Reimer WJM, van Urk H, et al. Increase of 1-year mortality after perioperative beta-blocker withdrawal in endovascular and vascular surgery patients. Eur J Vasc Endovasc Surg. 2007;33:13–19
  53. Schouten O, Welten GMJM, Bax JJ, Poldermans D. Secondary medical prevention in patients with peripheral arterial disease. Eur J Vasc Endovasc Surg. 2008;35:59–60
  54. Boersma E, Poldermans D, Bax JJ, et al. Predictors of cardiac events after major vascular surgery: role of clinical characteristics, dobutamine echocardiography, and β-blocker therapy. J A M A. 2001;285:1865–1873
  55. Poldermans D, Boersma E, Bax JJ, et al. The effect of bisoprolol on perioperative mortality and myocardial infarction in high-risk patients undergoing vascular surgery. N Engl J Med. 1999;341:1789–1794
  56. Schmidt M, Lindenauer PK, Fitzgerald JL, Benjamin EM. Forecasting the impact of a clinical practice guideline for perioperative beta-blockers to reduce cardiovascular morbidity and mortality. Arch Intern Med. 2002;162:63–69
  57. Rapchuk I, Rabuka S, Tonelli M. Perioperative use of betablockers remains low: experience of a single Canadian tertiary institution. Can J Anaesth. 2004;51:761–767
  58. Lindenauer PK, Fitzgerald JL, Hoople N, Benjamin EM. The potential preventability of postoperative myocardial infarction: underuse of perioperative beta-adrenergic blockade. Arch Intern Med. 2004;164:762–766
  59. Vanderkerkhof EG, Milne B, Parlow JL. Knowledge and practice regarding prophylactic perioperative beta blockade in patients undergoing noncardiac surgery: a survey of Canadian anesthesiologists. Anesth Analg. 2003;96:1558–1565
  60. Flu WJ, Hoeks SE, van Kuijk JP, Bax JJ, Poldermans D. Treatment recommendations to prevent myocardial ischemia and infarction in patients undergoing vascular surgery. Curr. Treat. Options Cardiovasc. Med. 2009;1:33–44
  61. Fleisher LA, Poldermans D. Perioperative ß blockade: where do we go from here?. Lancet. 2008;371:www.thelancet.com
  62. Mangano DT, Layug EL, Wallace A, Tateo I. Effect of atenolol on mortality and cardiovascular morbidity after noncardiac surgery. Multicenter Study of Perioperative Ischemia Research Group. N Engl J Med. 1996;335:1713–1720
  63. Schouten O, Bax JJ, Dunkelgrun M, Feringa HHH, Poldermans D. Pro: beta-blockers are indicated for patients at risk for cardiac complications undergoing noncardiac surgery. Anesth Analg. 2007;104:8–10
  64. Hoeks SE, Scholte Op Reimer WJ, van Urk H, et al. Increase of 1-year mortality after perioperative beta-blocker withdrawal in endovascular and vascular surgery patients. Eur J Vasc Endovasc Surg. 2007;33:16–19
  65. Shammash JB, Trost JC, Gold JM, Berlin JA, Golden MA, Kimmel SE. Perioperative beta-blocker withdrawal and mortality in vascular surgical patients. Am Heart J. 2001;141:148–153
  66. Kertai M, Boersma E, Westerhout C, et al. A combination of statins and beta-blockers is independently associated with a reduction in the incidence of perioperative mortality and nonfatal myocardial infarction in patients undergoing abdominal aortic aneurysm surgery. Eur J Vasc Endovasc Surg. 2004;28:345–352
  67. Antiplatelet Trialists' Collaboration. Collaborative overview of randomised trials of antiplatelet therapy—I: prevention of death, myocardial infarction, and stroke by prolonged antiplatelet therapy in various categories of patients. B M J. 1994;308:81–106
  68. CAPRIE Steering Committee . A randomised, blinded, trial of clopidogrel versus aspirin in patients at risk of ischaemic events (CAPRIE). Lancet. 1996;348:1329–1339
  69. Collet JP, Montalescot G, Blanchet B, et al. Impact of prior use or recent withdrawal of oral antiplatelet agents on acute coronary syndromes. Circulation. 2004;110:2361–2367
  70. Kinikini D, Sarfati MR, Mueller MT, Kraiss LW. Meeting AHA/ACC secondary prevention goals in a vascular surgery practice: an opportunity we cannot afford to miss. J Vasc Surg. 2006;43:781–787
  71. Heart Outcomes Prevention Evaluation Study Investigators . Effects of ramipril on cardiovascular and microvascular outcomes in people with diabetes mellitus: results of the HOPE study and MICRO-HOPE substudy. Lancet. 2000;355:253–259
  72. Ostergren J, Sleight P, Dagenais G, et al. Impact of ramipril in patients with evidence of clinical or subclinical peripheral arterial disease. Eur Heart J. 2004;25:17–24
  73. Mehler PS, Coll JR, Estacio R, et al. Intensive blood pressure control reduces the risk of cardiovascular events in patients with peripheral arterial disease and type 2 diabetes. Circulation. 2003;107:753–756
  74. Chobanian AV, Bakris GL, Black HR, et al. The seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report. J A M A. 2003;289:2560–2571
  75. Psaty BM, Smith NL, Siscovick DS, et al. Health outcomes associated with antihypertensive therapies used as first-line agents. A systematic review and meta-analysis. J A M A. 1997;277:739–745
  76. Group SSSS . Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S). Lancet. 1994;344:1383–1389
  77. Downs J, Clearfield M, Weis S. Primary prevention of acute coronary events with lovastatin in men and women with average cholesterol levels: results of AFCAPS/TexCAPS. J A M A. 1998;279:1615–1622
  78. Heart Protection Study Collaborative Group. MRC/BHF Heart Protection Study of cholesterol lowering with simvastatin in 20536 high-risk individuals: a randomised placebo-controlled trial. Lancet. 2002;360:7–22
  79. Poldermans D, Bax J, Kertai M, et al. Statins are associated with a reduced incidence of perioperative mortality in patients undergoing major noncardiac vascular surgery. Circulation. 2003;107:1848–1851
  80. Kertai M, Boersma E, Westerhout C, et al. Association between long-term statin use and mortality after successful abdominal aortic aneurysm surgery. Am J Med. 2004;116:96–103
  81. Hindler K, Shaw AD, Samuels J, Fulton S, Collard CD, Riedel B. Improved postoperative outcomes associated with preoperative statin therapy. Anesthesiology. 2006;105:1260–1272
  82. Poldermans D, Bax JJ, Kertai MD, et al. Statins are associated with a reduced incidence of perioperative mortality in patients undergoing major noncardiac vascular surgery. Circulation. 2003;107:1848–1851
  83. Heeschen C, Hamm CW, Laufs U, Snapinn S, Bohm M, White HD. Withdrawal of statins increases event rates in patients with acute coronary syndromes. Circulation. 2002;105:1446–1452
  84. Dajani AS, Bisno AL, Chung KJ, et al. Prevention of bacterial endocarditis: recommendations by the American Heart Association. J A M A. 1990;264:2919–2922
  85. Alderman M, Arakawa K, Beilin L, et al. 7th WHO-ISH Meeting on Hypertension, Fukuoka, Japan, 29 September to October, 1998: 1999 World Health Organization-International Society of Hypertension guidelines for the management of hypertension. J Hypertens. 1999;17:151–185
  86. Executive Summary of the Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). J A M A. 285:2486-2497.
  87. American Diabetes Association . Position statement. Standards of medical care for patients with diabetes mellitus. Diabetes Care. 2003;26:S33–S50
  88. Garber AJ, Moghissi ES, Bransome EDJ, et al. American College of Endocrinology position statement on inpatient diabetes and metabolic control. Endocr Pract. 2004;10:77–82
  89. Eknoyan G, Levin NW, Eschbach JW, Golper TA, Owen WF, Schwab S, et al. Continuous quality improvement: DQQI becomes K/DOQI and is updated. National Kidney Foundation's Dialysis Outcomes Quality Initiative. Am J Kidney Dis. 2001;37:179–194
  90. Pauwels RA, Buist SA, Calvery PMA, Jenkins CR, Hurd SS. Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease. NHLBI/WHO Global Initiative for Chronic Obstructive Lung Disease (GOLD) workshop summary. Am J Respir Crit Care Med. 2001;163:1256–1276
  91. Smetana GW, Lawrence VA, Cornell JE. Preoperative pulmonary risk stratification for noncardiothoracic surgery: systematic review for the American College of Physicians. Ann Intern Med. 2006;144:581–595
  92. Bapoje SR, Whitaker JF, Schulz T, Chu ES. RK Albert. Preoperative evaluation of the patient with pulmonary disease. Chest. 2007;132:1637–1645
  93. Frank SM, Fleisher LA, Breslow MJ, et al. Perioperative maintenance of normothermia reduces the incidence of morbid cardiac events. A randomized clinical trial. J A M A. 1997;277:1127–1134
  94. Frank SM, Beattie C, Christopherson R, et al. Unintentional hypothermia is associated with postoperative myocardial ischemia. The Perioperative Ischemia Randomized Anesthesia Trial Study Group. Anesthesiology. 1993;78:468–476
  95. Landesberg G, Luria MH, Cotev S, et al. Importance of long-duration postoperative ST segment depression in cardiac morbidity after vascular surgery. Lancet. 1993;341:715–719
  96. Slogoff S, Keats AS. Does perioperative myocardial ischemia lead to postoperative myocardial infarction?. Anesthesiology. 1985;62:107–114
  97. Kim LJ, Martinez EA, Faraday N, et al. Cardiac troponin I predicts short-term mortality in vascular surgery patients. Circulation. 2002;106:2366–2371
  98. Landberg G, Shatz V, Akopnik I, et al. Association of cardiac troponin, CK-MB, and postoperative myocardial ischemia with long-term survival after major vascular surgery. J Am Coll Cardiol. 2003;42:1547–1554
  99. Mangano DT, Browner WS, Hollenberg M, Li J, Tateo IM. Long-term cardiac prognosis following noncardiac surgery. The Study of Perioperative Ischemia Research Group. J A M A. 1992;268:233–239
  100. Fleisher LA, Nelson AH, Rosenbaum SH. Postoperative myocardial ischemia: etiology of cardiac morbidity or manifestation of underlying disease. J Clin Anesth. 1995;7:97–102
  101. Landesberg G. Monitoring for myocardial ischemia. Best Pract Res Clin Anaesthesiol. 2005;19:77–95
  102. Lopez-Jimenez F, Goldman L, Sacks DB, et al. Prognostic value of cardiac troponin T after noncardiac surgery: 6-month follow-up data. J Am Coll Cardiol. 1997;29:1241–1245
  103. Godet G, Dumerat M, Baillard C, et al. Cardiac troponin I is reliable with immediate but not medium-term cardiac complications after abdominal aortic repair. Acta Anaesthesiol. Scand. 2000;44:592–597
  104. Bursi F, Babuin L, Barbieri A, et al. Vascular surgery patients: perioperative and long-term risk according to the ACC/AHA guidelines, the additive role of post-operative troponin elevation. Eur Heart J. 2005;26:2448–2456
  105. Filipovic M, Jeger R, Probst C, et al. Heart rate variability and cardiac troponin I are incremental and independent predictors of one-year all-cause mortality after major noncardiac surgery in patients at risk of coronary artery disease. J Am Coll Cardiol. 2003;42:1767–1776
  106. Kertai MD, Boersma E, Klein J, van UH, Bax JJ, Poldermans D. Long-term prognostic value of asymptomatic cardiac troponin T elevations in patients after major vascular surgery. Eur J Vasc Endovasc Surg. 2004;28:59–66
  107. Ouattara A, Lecomte P, Le MY, et al. Poor intraoperative blood glucose control is associated with a worsened hospital outcome after cardiac surgery in diabetic patients. Anesthesiology. 2005;103:687–694
  108. McGirt MJ, Woodworth GF, Brooke BS, et al. Hyperglycemia independently increases the risk of perioperative stroke, myocardial infarction, and death after carotid endarterectomy. Neurosurgery. 2006;58:1066–1073
  109. Gandhi GY, Nuttall GA, Abel MD, et al. Intraoperative hyperglycemia and perioperative outcomes in cardiac surgery patients. Mayo Clin Proc. 2005;80:862–866
  110. Krinsley JS. Effect of an intensive glucose management protocol on the mortality of critically ill adult patients. Mayo Clin Proc. 2004;79:992–1000
  111. McAlister FA, Man J, Bistritz L, Amad H, Tandon P. Diabetes and coronary artery bypass surgery: an examination of perioperative glycemic control and outcomes. Diabetes Care. 2003;26:1518–1524
  112. Parker SD, Breslow MJ, Frank SM, et al. Catecholamine and cortisol responses to lower extremity revascularization: correlation with outcome variables. Perioperative Ischemia Randomized Anesthesia Trial Study Group. Crit Care Med. 1995;23:1954–1961
  113. Rosenfeld BA, Beattie C, Christopherson R, et al. The effects of different anesthetic regimens on fibrinolysis and the development of postoperative arterial thrombosis. Perioperative Ischemia Randomized Anesthesia Trial Study Group. Anesthesiology. 1993;79:435–443
  114. Christopherson R, Beattie C, Frank SM, et al. Perioperative morbidity in patients randomized to epidural or general anesthesia for lower extremity vascular surgery. Perioperative Ischemia Randomized Anesthesia Trial Study Group. Anesthesiology. 1993;79:422–434
  115. Nelson AH, Fleisher LA, Rosenbaum SH. Relationship between postoperative anemia and cardiac morbidity in high-risk vascular patients in the intensive care unit. Crit Care Med. 1993;21:860–866
  116. Carson JL, Noveck H, Berlin JA, Gould SA. Mortality and morbidity in patients with very low postoperative Hgb levels who decline blood transfusion. Transfusion. 2002;42:812
  117. Hogue CWJ, Goodnough LT, Monk TG. Perioperative myocardial ischemic episodes are related to hematocrit level in patients undergoing radical prostatectomy. Transfusion. 1998;38:924–931
  118. Wu WC, Schifftner TL, Henderson WG, et al. Preoperative hematocrit levels and postoperative outcomes in older patients undergoing noncardiac surgery. J A M A. 2007;297:2481–2488
  119. Murphy MF, Wallington TB, Kelsey P, et al. British Committee for Standards in Haematology, Blood Transfusion Standards Task Force. Guidelines for the clinical use of red cell transfusions. Br J Haematol. 2001;113:24–31
  120. Kleinman S, May AK, Silvergleid AJ, Landaw SA. Indications for red cell transfusion in the adult. UpToDate 2008. http://www.uptodate.com/patients/content/topic.do?topicKey=∼PUZnAWY5WRgXpZ.
  121. Practice guidelines for perioperative blood transfusion and adjuvant therapies: an updated report by the American Society of Anesthesiologists Task Force on Perioperative Blood Transfusion and Adjuvant Therapies. Anesthesiology. 2006;105:198–208

PII: S0890-5096(09)00138-1

doi:10.1016/j.avsg.2009.06.012

Annals of Vascular Surgery
Volume 23, Issue 5 , Pages 583-597, September 2009