Time to coronary reperfusion and acute kidney injury (AKI) are powerful prognostic markers in patients with ST-segment elevation myocardial infarction (STEMI) who underwent percutaneous coronary intervention (PCI); however, no information to date is present regarding the association between time to reperfusion and AKI. We evaluated whether time to reperfusion predicts the risk of developing AKI in patients with STEMI who underwent primary PCI. Medical records of 417 patients admitted to our department from January 2008 to July 2013, for STEMI, and treated with primary PCI were reviewed. Patients were stratified by time to coronary reperfusion tertiles, and their records were assessed for the occurrence of AKI after PCI. Mean age was 61 ± 13 years, and 346 patients (83%) were men. The cut-off points for the time to reperfusion tertiles were <120, 120 to 300, and >300 minutes. Patients having longer time to reperfusion had significantly more AKI complicating the course of STEMI (3% vs 11% vs 13%, p = 0.007) and had significantly higher serum creatinine change throughout hospitalization (0.13 vs 0.18 vs 0.21 mg/dl, p = 0.003). In a multivariable regression model, time to coronary reperfusion emerged as an independent predictor of AKI and to the maximal change in serum creatinine. In conclusion, longer time to coronary reperfusion is an independent risk factor for the development of AKI in patients with STEMI who underwent primary PCI.
Acute kidney injury (AKI) frequently complicates the course of acute ST-segment elevation myocardial infarction (STEMI) and is associated with adverse outcomes. The worsening of renal function throughout hospitalization in patients with STEMI is multifactorial, although the most important reason is considered to be contrast-induced nephropathy, related mainly to the amount of contrast material delivered and to preprocedural renal function. Additional important reasons for AKI in the setting of STEMI include hemodynamic state, drugs admitted (especially blockers of the renin-angiotensin axis), and the occurrence in parallel of sepsis, bleeding, atheroembolic disease, and acute hyperglycemia. Time to coronary reperfusion is a powerful prognostic marker in patients with STEMI, and major efforts are devoted to minimize the total ischemic duration to improve survival after STEMI. No trial do date, however, examined the relation between time to coronary reperfusion and the risk for developing AKI in patients with STEMI who underwent primary percutaneous coronary intervention (PCI). We hypothesized that prolonged time to reperfusion, through its acute effect on cardiac output and hemodynamics, may decrease renal perfusion, thus, leading to AKI development.
Methods
We performed a retrospective, single-center observational study at the Tel-Aviv Sourasky Medical Center, a tertiary referral hospital with a 24/7 primary PCI service. Included were all 1,367 consecutive patients admitted from January 2008 to December 2013 to the Cardiac Intensive Care Unit with the diagnosis of acute STEMI. Excluded were 28 patients who were treated either conservatively or by thrombolysis and 63 patients whose final diagnosis on discharge was other than STEMI (e.g., myocarditis or Takotusubo cardiomyopathy). Also excluded were patients who died within 24 hours of admission (n = 12) because we presumed there was insufficient time for AKI development and patients requiring chronic peritoneal or hemodialysis (n = 4) treatment. Finally, as information regarding the amount of contrast volume used during PCI was not available in 843 patients, they were excluded from the cohort. The final study population included 417 patients whose baseline demographic, cardiovascular history, clinical risk factors, treatment characteristics, and laboratory results were retrieved from their medical files. Diagnosis of STEMI was established by a typical chest pain history, diagnostic electrocardiographic changes, and serial elevation of cardiac biomarkers. Primary PCI was performed in patients with symptoms ≤12 hours in duration and in patients with symptoms lasting 12 to 24 hours in duration if the symptoms continued to persist at the time of admission. Coronary artery stenosis was defined by angiography as luminal diameter narrowing ≥70%. Coronary artery blood flow was defined according to standardized Thrombolysis In Myocardial Infarction (TIMI) grades 0 to 3. A culprit artery was defined as one with an identifiable thrombotic lesion on an angiogram corresponding to electrocardiographic changes. Successful reperfusion was defined as <30% residual stenosis and TIMI grade 3 flow. Time to coronary reperfusion was defined as the time from symptom onset (usually chest pain or discomfort), recorded on admission, to the restoration of TIMI grade 3 flow in the infarct artery, as reported in the catheterization laboratory report. Critical state patients were defined as those in whom intra-aortic balloon counterpulsation was inserted or mechanically ventilated. After primary PCI, left ventricular ejection fraction was assessed in all patients within the first 48 hours of admission. The study protocol was approved by the local institutional ethics committee.
The serum creatinine (sCr) was determined on hospital admission, before primary PCI, and at least once a day during the Cardiac Intensive Care Unit stay and was available for all analyzed patients. The estimated glomerular filtration rate (eGFR) was estimated using the abbreviated Modification of Diet in Renal Disease equation. Baseline renal insufficiency was categorized as admission eGFR of ≤60 ml/min/1.73 m 2 . AKI was determined using the AKI Network criteria and defined as an abrupt (within 48 hours) reduction in kidney function defined as an absolute increase in sCr level of 0.3 mg/dl or a percentage increase in sCr level of 50% (1.5-fold from baseline).
All data were summarized and displayed as mean (±SD) for continuous variables and as number (percentage) of patients in each group for categorical variables. Patients groups were stratified into tertiles according to the time to reperfusion. The p values for the categorical variables were calculated with the chi-square test. Continuous variables were compared using the analysis of variance or Kruskal-Wallis tests. The identification of the independent predictors of AKI and the sCr change was assessed using logistic and linear regressions, respectively. We adjusted for age, gender, hypertension, diabetes mellitus, left ventricular ejection fraction, admission eGFR, critical state, volume of contrast use, and time to reperfusion as a continuous variable. A 2-tailed p value of <0.05 was considered significant for all analyses. All analyses were performed with the SPSS software (SPSS Inc., Chicago, Illinois).
Results
Our final study population included 417 patients (mean age 61 ± 13 years, range 30 to 93, 83% men). Table 1 presents the baseline demographic, clinical, laboratory, and angiographic characteristics of patients according to the time to coronary reperfusion tertiles. The cut-off points for the time to reperfusion tertiles were <120, 120 to 300, and >300 minutes. Patients with longer time delay to coronary reperfusion were more likely to be older, women, with more co-morbidities, and had both longer symptom duration before hospital admission and longer door to balloon time. Table 2 compares the occurrence of AKI and sCr changes, between time to reperfusion tertiles. Patients having longer time to reperfusion had more AKI complicating the course of STEMI (3% vs 11% vs 13%, p = 0.007) and had significantly higher sCr change throughout hospitalization (p = 0.003). No significant difference between groups regarding the amount of contrast volume delivered during PCI was observed. In multivariate regression models ( Table 3 ), time to coronary reperfusion emerged as an independent predictor of AKI (p = 0.04) and to the sCr change throughout hospitalization (R² = 0.109, p = 0.003).
| Variable | Time to Perfusion (minutes) | p | ||
|---|---|---|---|---|
| <120 (n = 142) | 120–300 (n = 134) | >300 (n = 141) | ||
| Age (years) | 59 ± 11 | 61 ± 14 | 63 ± 13 | 0.01 |
| Men | 126 (89%) | 109 (81%) | 111 (79%) | 0.06 |
| Diabetes mellitus | 25 (18%) | 36 (27%) | 28 (20%) | 0.155 |
| Dyslipidemia | 50 (35%) | 64 (48%) | 75 (53%) | 0.007 |
| Hypertension | 46 (32%) | 64 (48%) | 73 (52%) | 0.002 |
| Smoker | 84 (59%) | 70 (52%) | 72 (81%) | 0.336 |
| Family history of CAD | 28 (20%) | 26 (19%) | 21 (15%) | 0.492 |
| Previous myocardial infarction | 18 (13%) | 20 (15%) | 17 (12%) | 0.765 |
| No. of narrowed coronary arteries: | ||||
| 1 | 72 (51%) | 61 (45%) | 63 (45%) | 0.691 |
| 2 | 40 (28%) | 37 (28%) | 42 (30%) | |
| 3 | 30 (21%) | 36 (27%) | 35 (25%) | |
| Critical state at admission | 5 (3%) | 9 (7%) | 4 (3%) | 0.261 |
| Time to ED (minutes) (median ± SD) | 56 ± 15 | 143 ± 48 | 760 ± 451 | <0.001 |
| Door to balloon time (minutes) (median ± SD) | 41 ± 12 | 47 ± 16 | 55 ± 26 | <0.001 |
| Admission CRP (mg/l) (mean ± SD) | 6.0 ± 9.3 | 8.4 ± 13.4 | 18.9 ± 38 | <0.001 |
| LV ejection fraction (mean ± SD) | 47 ± 7 | 46 ± 7 | 47 ± 8 | 0.285 |
| Variable | Time to Perfusion (minutes) | p | ||
|---|---|---|---|---|
| <120 (n = 142) | 120–300 (n = 134) | >300 (n = 141) | ||
| Acute kidney injury | 5 (3%) | 15 (11%) | 18 (13%) | 0.007 |
| eGFR (ml/minute/1.73 m 2 ) (mean ± SD) | 73 ± 16 | 73 ± 20 | 70 ± 21 | 0.373 |
| Admission sCr (mg/dl) (mean ± SD) | 1.15 ± 0.19 | 1.14 ± 0.24 | 1.16 ± 0.31 | 0.490 |
| Peak sCr (mg/dl) (mean ± SD) | 1.10 ± 0.20 | 1.16 ± 0.37 | 1.23 ± 0.51 | 0.391 |
| sCr change in hospital (mg/dl) (mean ± SD) | 0.13 ± 0.20 | 0.18 ± 0.27 | 0.21 ± 0.18 | 0.003 |
| sCr at discharge (mg/dl) (mean ± SD) | 1.07 ± 0.17 | 1.10 ± 0.28 | 1.15 ± 0.39 | 0.598 |
| Contrast material amount (ml) (mean ± SD) | 150 ± 48 | 141 ± 44 | 145 ± 49 | 0.238 |
| Correlates | Model 1 for AKI ∗ | Model 2 for sCr Change † | ||
|---|---|---|---|---|
| Beta | p | Beta | p | |
| Age | 1.02 | 0.434 | 0.389 | <0.001 |
| Gender | 1.07 | 0.889 | 0.121 | 0.03 |
| Diabetes mellitus | 0.80 | 0.643 | 0.055 | 0.257 |
| Hypertension | 1.08 | 0.485 | 0.058 | 0.263 |
| eGFR ml/min/1.73 m 2 | 0.97 | 0.050 | 0.314 | <0.001 |
| LV ejection fraction (%) | 0.95 | 0.053 | 0.091 | 0.06 |
| Critical state | 2.35 | 0.237 | 0.025 | 0.614 |
| Contrast volume | 0.99 | 0.526 | 0.067 | 0.171 |
| Time to reperfusion | 1.01 | 0.04 | 0.142 | 0.003 |
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