Clinical and anatomic outcomes after carotid endarterectomy.

OBJECTIVE: The purpose of this study was to examine 30-day and long-term outcomes after carotid endarterectomy (CEA) in a contemporary series and to identify variables associated with stroke and death after CEA. METHODS: This was a retrospective review of patients undergoing an isolated CEA at a single institution between January 1989 and December 2005. Primary study end points were 30-day and long-term overall stroke, ipsilateral stroke, and death. Secondary end points were recurrent stenosis (>70% stenosis) and reintervention. Kaplan-Meier analysis was used to create survival curves for the long-term study end points. Multivariate models were created to identify variables associated with the study end points. RESULTS: During the study period, 3014 CEAs were performed on 2644 patients (mean age, 71.0 ± 8.9 years; 60.9% male; 33.5% symptomatic; 37% primary closure), with mean follow-up of 7.0 years. The 30-day ipsilateral stroke, death, and combined ipsilateral stroke/death rates were 1.3%, 1.1%, and 2.2%, respectively. Previous ipsilateral CEA or neck dissection for cancer (hazard ratio [HR], 3.68; P = .0081) and symptomatic disease (HR, 2.45; P = .0071) were predictive of 30-day ipsilateral stroke. Stroke-free survival was 93.8% at 4 years and 86.9% at 10 years. Diabetes (HR, 1.94; P < .0001), symptomatic disease (HR, 1.75; P < .0001), female gender (HR, 1.34; P = .035), and increasing age (HR, 1.02; P < .0001) were predictors of long-term overall stroke. Ipsilateral stroke-free survival was 97.6% at 5 years and 94.6% at 10 years, respectively. Contralateral occlusion (HR, 2.06; P = .025) and symptomatic disease (HR, 1.87; P = .003) were predictors of ipsilateral stroke, whereas antilipid therapy was protective (HR, 0.65; P = .049). Overall survival was 70.1% at 5 years and 42.2% at 10 years, with no difference between symptomatic and asymptomatic patients. Although a variety of comorbidities were associated with inferior late survival, as anticipated, female gender (HR, 0.89; P = .016) and lipid-lowering therapy (HR, 0.69; P < .0001) were protective. Reintervention was 3.4% at 5 years and 6.6% at 10 years, with primary closure (vs patch angioplasty/eversion) increasing the risk of reintervention (HR, 1.72; P = .007). CONCLUSIONS: CEA has favorable perioperative and long-term clinical and anatomic outcomes with respect to its goal of stroke prevention for symptomatic and asymptomatic patients. Adjuvant medical therapy (antilipid) has increased overall and ipsilateral stroke-free survival.

A propensity-matched comparison of outcomes for fenestrated endovascular aneurysm repair and open surgical repair of complex abdominal aortic aneurysms.

OBJECTIVE: The benefit of fenestrated endovascular aortic aneurysm repair (FEVAR) compared with open surgical repair (OSR) of complex abdominal aortic aneurysms (CAAAs) is unknown. This study compares 30-day outcomes of these procedures from two high-volume centers where FEVAR was undertaken for high-risk patients. METHODS: Patients undergoing FEVAR with commercially available devices and OSR of CAAAs (total suprarenal/supravisceral clamp position) were propensity matched by demographic, clinical, and anatomic criteria to identify similar patient cohorts. Perioperative outcomes were evaluated using univariate and multivariate methods. RESULTS: From July 2001 to August 2012, 59 FEVAR and 324 OSR patients were identified. After 1:4 propensity matching for age, gender, hypertension, congestive heart failure, coronary disease, chronic obstructive pulmonary disease, stroke, diabetes, preoperative creatinine, and anticipated/actual aortic clamp site, the study cohort consisted of 42 FEVARs and 147 OSRs. The most frequent FEVAR construct was two renal fenestrations, with or without a single mesenteric scallop, in 50% of cases. An average of 2.9 vessels were treated per patient. Univariate analysis demonstrated FEVAR had higher rates of 30-day mortality (9.5% vs. 2%; P = .05), any complication (41% vs. 23%; P = .01), procedural complications (24% vs. 7%; P < .01), and graft complications (30% vs. 2%; P < .01). Multivariable analysis showed FEVAR was associated with an increased risk of 30-day mortality (odds ratio [OR], 5.1; 95% confidence interval [CI], 1.1-24; P = .04), any complication (OR, 2.3; 95% CI, 1.1-4.9; P = .01), and graft complications (OR, 24; 95% CI, 4.8-66; P < .01). CONCLUSIONS: FEVAR, in this two-center study, was associated with a significantly higher risk of perioperative mortality and morbidity compared with OSR for management of CAAAs. These data suggest that extension of the paradigm shift comparing EVAR with OSR for routine AAAs to patients with CAAAs is not appropriate. Further study to establish proper patient selection for FEVAR instead of OSR is warranted before widespread use should be considered.

Impact of severe chronic kidney disease on outcomes of infrainguinal peripheral arterial intervention.

OBJECTIVE: Patients with severe chronic kidney disease (CKD) and peripheral vascular disease are at increased risk of major adverse limb events (MALEs) and death; however, patients with end-stage renal disease have been excluded in current objective performance goals. We evaluated the effect of severe (class 4 and 5) CKD on outcomes after infrainguinal endovascular arterial interventions. METHODS: All primary peripheral vascular interventions (PVIs) performed at a single institution (January 2002 through December 2009) were included. End points were defined by Society for Vascular Surgery objective performance goals for critical limb ischemia (CLI), which include all-cause mortality, reintervention, and composite end points of death or amputation and MALEs (reintervention or amputation). Univariate and multivariable analysis was used to examine the effect of severe CKD on study end points. RESULTS: A total of 879 PVIs were performed, with severe CKD in 125 (14%). Severe CKD patients were significantly (P < .05) more likely to have diabetes (64% vs 46%), CLI (72% vs 11%), and need a multilevel PVI (34% vs 19%) or tibial intervention (35% vs 20%) compared with the remainder of the cohort. Distribution of TransAtlantic Inter-Society Consensus C and D lesions were similar (19% severe CKD vs 15%; P = .2). Severe CKD predicted perioperative (30-day) reintervention (odds ratio [OR], 2.3; 95% confidence interval [CI], 1.5-4; P = .05), amputation or death (OR, 3.1; 95% CI, 1.1-9; P = .04), and MALEs (OR, 2.8; 95% CI, 1.3-6.1; P = .04), which was independent of CLI in multivariable regression analysis. On Kaplan-Meier analysis, severe CKD was significantly (log-rank P < .05) associated with death (31% ± 4% vs 7% ± 1%), amputation (14% ± 3% vs 3% ± 1%), and MALEs (40% ± 5% vs 26% ± 2%) at 1 year. Freedom from reintervention was similar at 1 year (70% ± 5% severe CKD vs 75% ± 2%; P = .23). Risk-adjusted (age, CLI, diabetes, coronary artery disease) Cox proportional hazards regression showed that severe CKD increased the risk of late mortality (hazard ratio [HR], 2.4; 95% CI, 1.8-3.2; P < .01), amputation (HR, 2.1; 95% CI, 1.1-3.9; P = .02), and death or amputation (HR, 1.8; 95% CI, 1.3-2.4; P = .04), without increasing the risk of late reinterventions or MALEs. CONCLUSIONS: CKD independently predicts early and late adverse events after a PVI, in particular, excessive mortality. CKD should figure prominently in clinical decision making for patients with peripheral vascular disease.

A risk prediction model for determining appropriateness of CEA in patients with asymptomatic carotid artery stenosis.

OBJECTIVE: The benefit of carotid endarterectomy (CEA) over medical therapy in patients with asymptomatic carotid artery stenosis is predicated upon a life expectancy of at least 5 years after the procedure. The goal of this study was to create a scoring system for prediction of 5-year survival after CEA that can be used to triage patients with ACAS. METHODS: All patients who underwent CEA for severe asymptomatic carotid stenosis from 1989 to 2005 were identified. Long-term survival was determined by a review of hospital records and the social security death index. Because all patients had at least 5-year follow-up, a logistic regression of predictors of survival at 5 years was performed and the odds ratios associated with particular significant comorbidities were used to create a scoring system to predict survival. The scoring system was then validated within the cohort using the Hosmer-Lemeshow Test and a derivation/validation receiver operating characteristic (ROC) curve. RESULTS: There were 2004 CEA performed in 1791 patients. The average follow-up was 130 ± 49 months. The clinical profile of the cohort data included 84% hypertension, 56% coronary artery disease (CAD), 24% diabetes, and 71% on statins. The 30-day stroke rate was 1.1% and the death rate was 0.7%. The actual 5-year survival was 73%. Logistic regression yielded the following predictors of mortality: age (by decade) (odds ratio [OR] = 1.8, P < 0.0001), CAD (OR = 1.5, P = 0.0007), chronic obstructive pulmonary disease (OR = 2.5; P < 0.0001), diabetes (OR = 1.7, P < 0.0001), neck radiation (OR = 2.6, P = 0.005), no statin (OR = 2.1, P < 0.0001), and creatinine more than 1.5 (OR = 2.6, P < 0.0001). These variables were then assigned a hierarchal point scoring system in accordance with the OR value. The 5-year survival based on the scoring system was as follows: 0 to 5 points = 92.5%, 6 to 8 points = 83.6%, 9 to 11 points = 63.7%, 12 to 14 points = 46.5%, and more than 15 points = 33.8%. The Hosmer-Lemeshow test validated the scoring system (P = 0.26) and there was no difference in the ROC curves (C statistic = 0.74 vs 0.73). CONCLUSIONS: This validated scoring system can be a useful tool for determining which patients are likely to benefit most from CEA based on the probability of long-term survival. Given that the 5-year survival of patients in the medical arm of the asymptomatic CEA trials was 60% to 70%, it is reasonable to conclude that patients who score 0 to 8 points are excellent candidates for CEA whereas most patients with ≥12 points should be managed with medical therapy alone.

Progression of asymptomatic carotid stenosis despite optimal medical therapy.

BACKGROUND: Despite level 1 evidence in support of carotid endarterectomy vs medical therapy in selected asymptomatic patients, an alternative posture is that optimal medical therapy (OMT) has not been adequately studied and that such OMT has reduced stroke risk in asymptomatic patients to levels wherein carotid endarterectomy is no longer justified. The goal of this study was to determine the natural history of patients with asymptomatic moderate (50%-69%) carotid artery stenosis (AMCAS) in a contemporary cohort as a function of their associated medical therapy. METHODS: Patients with AMCAS determined by duplex ultrasound (DUS) from 2005-2006 were identified in our hospital database. Patients were included in the cohort if they had at least one additional DUS during the 6-year follow-up interval. Patient characteristics including medication history and lipid levels were collected. Patients were considered to have OMT if they were on aspirin and a statin with a low-density lipoprotein level that was always <100 mg/dL. Study end points included progression of carotid disease by DUS to severe stenosis (70%-100%), development of ipsilateral neurologic symptoms (INS) such as stroke or transient ischemic attack, and death. RESULTS: There were 900 carotid arteries in 794 patients in the study cohort. The average age was 72.5 years, 77.2% had hypertension, 59.6% had coronary artery disease, and 87.1% were on a statin throughout the study. The low-density lipoprotein cholesterol level was always normal (<100 mg/dL) in 37.8% and accordingly, 241 (30.3%) had OMT as defined above. The 5-year actuarial survival was 81.9% ± 1.3% with no advantage seen with OMT. Multivariate analysis of survival showed statins were protective (hazard ratio [HR], 0.50; confidence interval [CI], 0.34-0.73; P = .0004). The 5-year freedom from plaque progression was 61.2% ± 2.1% with no benefit from OMT vs the control group. Multivariate predictors of plaque progression were chronic kidney disease (HR, 2.1; CI, 1.2-3.7; P = .009), aspirin use (HR, 1.9; CI, 1.2-3.0; P = .01), and the use of calcium channel blockers (HR, 1.4; CI, 1.1-1.8; P = .007). There were 90 (11.3%) patients who developed INS during follow-up (58% of these were strokes), and the 5-year freedom from INS was 88.4% ± 1.5%. Multivariate predictors of INS were diabetes (HR, 2.3; CI, 1.5-3.6; P = .0002) and warfarin use (HR, 1.9; CI, 1.2-2.9; P = .009); while statin use (HR, 0.37; CI, 0.22-0.65; P = .0005) was protective against symptom development. CONCLUSIONS: At the 5-year of follow-up, OMT failed to prevent carotid disease progression or development of ipsilateral symptoms in 45% of patients with AMCAS.

Impact of hospital volume and type on outcomes of open and endovascular repair of descending thoracic aneurysms in the United States Medicare population.

OBJECTIVE: Favorable outcomes of thoracic endovascular aortic repair (TEVAR) compared with open repair for descending thoracic aortic aneurysms (DTAs) have led to increasing TEVAR use. We evaluated the effect of case volume and hospital teaching status on clinical outcomes of intact DTA repair. METHODS: The Medicare Provider Analysis and Review (MEDPAR) data set (2004 to 2007) was queried to identify open repair or TEVAR for DTA. Hospitals were stratified by DTA volume into high volume (HV; ≥ 8 cases/y) or low volume (LV; <8 cases/y) and teaching or nonteaching. The effect of hospital variables on the primary study end point of 30-day mortality and secondary end points of 30-day complications and long-term survival after open repair and TEVAR DTA repair were studied using univariate testing, multivariable regression modeling, Kaplan-Meier survival analysis, and Cox proportional hazards regression modeling. RESULTS: We identified 763 hospitals performing 3554 open repairs and 3517 TEVARs. Overall DTA repair increased (P < .01) from 1375 in 2004 to 1987 in 2007. The proportion of hospitals performing open repair significantly decreased from 95% in 2004 to 57% in 2007 (P < .01), whereas those performing TEVAR increased (P < .01) from 24% to 76%. Overall repair type shifted from open (74% in 2004, the year before initial commercial availability of TEVAR) to TEVAR (39% open in 2007; P < .01). The fraction of open repairs at LV hospitals decreased from 56% in 2004 to 44% in 2007 (P < .01), whereas TEVAR increased from 24% in 2004 to 51% in 2007 (P < .01). Overall mortality during the study interval for open repair was 15% at LV hospitals vs 11% at HV hospitals (P < .01), whereas TEVAR mortality was similar, at 3.9% in LV vs 5.5% in HV hospitals (P = .43). LV was independently associated with increased mortality after open repair (odds ratio, 1.4; 95% confidence interval, 1.1-1.8; P < .01) but not after TEVAR. There was no independent effect of hospital teaching status on mortality or complications after open repair or TEVAR repair. CONCLUSIONS: The total number of DTA repairs has significantly increased. Operative mortality for TEVAR is independent of hospital volume and type, whereas mortality after open surgery is lower at HV hospitals, suggesting that TEVAR can be safely performed across a spectrum of hospitals, whereas open surgery should be performed only at HV hospitals.

Impact of chronic kidney disease on outcomes after abdominal aortic aneurysm repair.

OBJECTIVE: Chronic kidney disease (CKD) is associated with increased morbidity and death after open abdominal aortic aneurysm (AAA) repair (OAR). This study highlights the effect of CKD on outcomes after endovascular AAA (EVAR) and OAR in contemporary practice. METHODS: The National Surgical Quality Improvement Program (NSQIP) Participant Use File (2005-2008) was queried by Current Procedural Terminology (American Medical Association, Chicago, Ill) code to identify EVAR or OAR patients, who were grouped by CKD class as having mild (CKD class 1 or 2), moderate (CKD class 3), or severe (CKD class 4 or 5) renal disease. Propensity score analysis was performed to match OAR and EVAR patients with mild CKD with those with moderate or severe CKD. Comparative analysis of mortality and clinical outcomes was performed based on CKD strata. RESULTS: We identified 8701 patients who were treated with EVAR (n = 5811) or OAR (n = 2890) of intact AAAs. Mild, moderate, and severe CKD was present in 63%, 30%, and 7%, respectively. CKD increased (P < .01) overall mortality, with rates of 1.7% (mild), 5.3% (moderate), and 7.7% (severe) in unmatched patients undergoing EVAR or OAR. Operative mortality rates in patients with severe CKD were as high as 6.2% for EVAR and 10.3% for OAR. Severity of CKD was associated with increasing frequency of risk factors; therefore, propensity matching to control for comorbidities was performed, resulting in similar baseline clinical and demographic features of patients with mild compared with those with moderate or severe disease. In propensity-matched cohorts, moderate CKD increased the risk of 30-day mortality for EVAR (1.9% mild vs 3.2% moderate; P = .013) and OAR (3.1% mild vs 8.4% moderate; P < .0001). Moderate CKD was also associated with increased morbidity in patients treated with EVAR (8.3% mild vs 12.8% moderate; P < .0001) or OAR (25.2% mild vs 32.4% moderate; P = .001). Similarly, severe CKD increased the risk of 30-day mortality for EVAR (2.6% mild vs 5.7% severe; P = .0081) and OAR (4.1% mild vs 9.9% severe; P = .0057). Severe CKD was also associated with increased morbidity in patients treated with EVAR (10.6% mild vs 19.2% severe; P < .0001) or OAR (31.1% mild vs 39.6% severe; P = .04). CONCLUSIONS: The presence of moderate or severe CKD in patients considered for AAA repair is associated with significantly increased mortality and therefore should figure prominently in clinical decision making. The high mortality of AAA repair in patients with severe CKD is such that elective repair in such patients is not advised, except in extenuating clinical circumstances.

Impacts of lesion angle on incidence and distribution of acute vessel wall injuries and strut malapposition after drug-eluting stent implantation assessed by optical coherence tomography.

AIMS: To investigate the impact of lesion angle on the incidence and distribution of acute vessel wall injuries and incomplete stent apposition (ISA) following second-generation drug-eluting stent (DES) implantation using optical coherence tomography (OCT). Several ex vivo studies demonstrated that angled arterial walls are exposed to imbalanced mechanical stress from deployed stents. METHODS AND RESULTS: We included 243 lesions treated with a single DES (148 everolimus-eluting stent and 95 zotarolimus-eluting stent). Angled lesions were defined as lesions with angle ≥45° on an angiogram (n = 58). The vessel wall injuries and ISA were evaluated by OCT. The results were compared with non-angled lesions (<45°, n = 185). The incidence of instent dissection, thrombus, and ISA was significantly higher in the angled group than in the non-angled group (84.5 vs. 63.2%, P < 0.01; 55.2 vs. 35.1%, P < 0.01; 75.9 vs. 44.9%, P < 0.001, respectively). In the angled group, the normalized tissue protrusion volume around the centre of angle (6.59 ± 6.81, mm(3) × 10(2)) was higher than in the distal sub-segment (2.21 ± 2.87, mm3 × 10(2), P < 0.001), in the proximal sub-segment (4.14 ± 5.34, mm3 × 10(2), P = 0.02), and in the non-angled group (3.30 ± 2.81, mm3 × 10(2), P < 0.001). The incidence of major adverse cardiac events within 12 months was similar between the groups. CONCLUSIONS: Angled coronary lesions had a higher incidence rate of OCT-detected vessel wall injuries and ISA compared with non-angled lesions following second-generation DES implantation. Further studies are needed to understand the long-term clinical significance of these findings.

Smoking and risk of preterm birth among predominantly Puerto Rican women.

PURPOSE: Studies of smoking during pregnancy and preterm birth among Hispanic women are sparse. Our goal was to evaluate the effect of cigarette smoking during pre-pregnancy, early pregnancy, and mid pregnancy on preterm birth among Hispanic women, the fastest growing ethnic group in the United States. METHODS: We evaluated data from a prospective cohort study of 1,041 Hispanic (predominantly Puerto Rican) women recruited between 2000 and 2004 in Springfield, Massachusetts. At recruitment (mean = 15 weeks), women reported their smoking since pregnancy awareness (early pregnancy) and in the year prior to pregnancy (pre-pregnancy). Mid pregnancy smoking was collected at a second interview (mean = 28 weeks). RESULTS: Smoking in pre-pregnancy was not associated with preterm birth. After adjustment for age, parity, education, and illicit drug use, women who smoked in early pregnancy had 1.6 times the risk of preterm birth (95% confidence interval [CI], 1.0-2.7) compared with nonsmokers. Women who smoked in mid pregnancy had 2.1 times the risk of preterm birth (95% CI, 1.0-4.2) compared with nonsmokers with a trend of increased risk of preterm birth with increasing levels of smoking (p trend, 0.03). CONCLUSIONS: Smoking in early or mid pregnancy increased the risk of spontaneous preterm birth in a Hispanic population.