Methods

We prospectively included 429 consecutive patients undergoing elective isolated CABG, except those on renal dialysis or with a history of renal transplantation. Secondarily, patients with poor duplex imaging quality were also excluded. Clinical data were investigated preoperatively. Chronic kidney disease (CKD) was defined as an estimated glomerular filtration rate <60 ml/min/1.73 m² according to the Modification of Diet in Renal Disease formula. PAD was defined according to the medical history and/or an ankle-brachial index ≤0.90 or ≥1.40. Cerebrovascular disease was defined by any history of stroke, transient ischemic attack, carotid revascularization, and/or carotid stenosis detected during preoperative duplex of neck arteries. Left ventricular hypertrophy measured by echocardiography was defined by the left ventricular mass/height ^2.7 formula, with thresholds set at 50 g/m ^2.7 in men and 47 g/m ^2.7 in women. Intraoperative data included the completeness of myocardial revascularization and the use of on- or off-pump surgery.

The participants underwent a systematic preoperative Doppler ultrasonography of the renal arteries (models ATL HDI 5000, ATL HDI 3000, and iE33; Philips, Bothell, Washington). We defined RAS >60% when at least 2 of the 3 following criteria were present : renal artery peak systolic velocity >180 cm/s, renorenal (peak systolic velocity) ratio >2.7, and/or renal-to-aortic peak systolic velocity ratio >3.5. The renal index was determined at the renal hilum, using the following equation:

Renal index = (peak systolic velocity − end-diastolic velocity)/peak systolic velocity.

An elevated resistive index (ERI) was defined by a renal resistance index >0.80.

The primary outcome was composite, including the occurrence of any of the following events within the first 30 postoperative days, whichever first: death, stroke, or perioperative myocardial infarction (defined by new Q waves in at least 2 contiguous leads on the postoperative electrocardiogram and/or troponin peak and creatine phosphokinase peak >10 times the ninety-ninth percentile).

A secondary postoperative outcome was defined by the occurrence of acute kidney injury, according to the risk of renal dysfunction; injury to the kidney; failure of kidney function, loss of kidney function and end-stage kidney disease injury-risk “R” criteria (serum creatinine increase of 1.5 times or 25% decrease of glomerular filtration rate compared with baseline data). Two other midterm secondary outcomes have been determined: the occurrence of death and a composite outcome (death, stroke or acute coronary syndrome, or myocardial revascularization) during the follow-up period.

Data are reported as mean (SD) and number (percentage) for continuous and categorical variables, respectively. Categorical and continuous variables were analyzed using Fisher’s exact test and the Student t test, respectively. The Kaplan-Meier survival method was used for the comparison of survival according to the presence of RAS or ERI, using the log-rank test. Multivariate analysis was performed using a logistic regression model for the 30-day events and Cox proportional hazards model for the midterm events. For this purpose, several models were run by adding sequentially baseline demographic factors, CKD, CV risk factors, co-morbidities, CV treatment, and preoperative data. Because some patients could have both conditions (RAS and ERI), these 2 variables have been assessed concomitantly in a same model, rather than taking into account the 3 patient groups. A p value <0.05 was considered statistically significant. The software used for statistical analysis was StatView, version 5.0, for Windows (SAS Institute, Cary, North Carolina).

Results

Of the 429 patients eligible for our study, 401 patients (82.5% men) had satisfactory imaging of renal vascularization by duplex and were included in the study. Table 1 lists the characteristics of the study population. The 28 excluded patients did not differ from those included except for lower rates of dyslipidemia (52% vs 71%, respectively, p = 0.03). Notably, these patients did not differ in terms of age (67.6 ± 9.1 vs 67.7 ± 10.3 years, p = NS) and prevalence of CKD (17.9% vs 15.0%, p = NS).

The rates of abnormal duplex findings are displayed in Figure 1 . Forty patients (10.0%) had RAS, including unilateral RAS in 36 patients (9.0%) and bilateral RAS in 4 patients (1.0%). The prevalence of ERI was 8.7% (35 patients). The prevalence of concomitant RAS and ERI was 2.2% (9 patients). These 9 patients were included in the RAS group. Patients with ERI were older with higher rates of co-morbidities such as diabetes, PAD, or chronic obstructive pulmonary disease and lower levels of glomerular filtration rate compared with the normal group ( Table 2 ).

Distribution of renal duplex findings.

The primary composite outcome (30-day death, stroke, and/or perioperative myocardial infarction) occurred in 40.0%, 45.7%, and 29.5%, respectively, in the RAS, ERI, and normal groups (RAS vs normal: p = NS, ERI vs normal: p = 0.056). After serial adjustments for confounders, ERI (not RAS) was independently and significantly associated with the primary outcome ( Table 3 ).

Table 3

The association between renal artery stenosis and elevated renal index with 30-day outcomes

	Model 1	Model 2	Model 3	Model 4	Model 5
Primary outcome: 30-days composite outcome
Elevated renal index	2.6 (1.32–5.08) p = 0.0058	3.1 (1.50–6.42) p = 0.0022	4.1 (1.86–9.10) p = 0.0005	4.2 (1.87–9.25) p = 0.0005	4.3 (1.87–9.89) p = 0.0006
Renal artery stenosis	1.2 (0.62–2.49) p = 0.55	1.4 (0.65–2.81) p = 0.42	1.1 (0.51–2.49) p = 0.77	1.2 (0.53–2.62) p = 0.5	1.2 (0.53–2.69) p = 0.66
Acute kidney injury
Elevated renal index	2.2 (1.07–4.66) p = 0.03	2.4 (1.07–5.24) p = 0.03	2.3 (0.99–5.34) p = 0.0517	2.3 (0.98–5.29) p = 0.0545	2.4 (1.01–5.82) p = 0.0475
Renal artery stenosis	0.7 (0.3–1.69) p = 0.44	0.7 (0.27–1.63) p = 0.37	0.8 (0.3–1.96) p = 0.58	0.8 (0.29–1.95) p = 0.56	0.7 (0.28–1.93) p = 0.54

Model 1: adjusted for age, gender, and CKD; model 2: model 1 plus hypertension, diabetes mellitus, smoking, body mass index, C-reactive protein, and hematocrit; model 3: model 2 plus chronic obstructive pulmonary disease, ejection fraction <40%, 3-vessel disease, left main coronary artery stenosis, sinus rhythm, and New York Heart Association classification; model 4: model 3 plus β blockers, angiotensin-converting enzyme inhibitors (or angiotensin receptor blockers), and statins; and model 5: model 4 plus on-pump CABG and complete revascularization.

Only gold members can continue reading. Log In or Register to continue

Share this:

• Click to share on Twitter (Opens in new window)
• Click to share on Facebook (Opens in new window)

Related

Related posts:

1. Comparison of the Efficacy of Pharmacoinvasive Management for ST-Segment Elevation Myocardial Infarction in Smokers Versus Non-Smokers (from the Trial of Routine Angioplasty and Stenting After Fibrinolysis to Enhance Reperfusion in Acute Myocardial Infarction)
2. Rate of Percutaneous Coronary Intervention for the Management of Acute Coronary Syndromes and Stable Coronary Artery Disease in the United States (2007 to 2011)
3. An Intervention to Address Secondhand Tobacco Smoke Exposure Among Nonsmokers Hospitalized With Coronary Heart Disease
4. Genetic Mechanisms Possibly Leading to Racially Different Responses to Nitrate Therapy

Stay updated, free articles. Join our Telegram channel

Join