Acute kidney injury (AKI) is a common complication among patients with ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PCI), and it is associated with poor long-term clinical outcomes. No studies have yet evaluated the association between cardiac function and the risk of AKI in this patient population. We conducted a retrospective study of consecutive 386 patients with STEMI who underwent primary PCI and had a full echocardiography study performed within 72 hours of hospital admission from June 2011 to December 2013. AKI was defined as an increase of ≥0.3 mg/dl in serum creatinine within 48 hours after admission. Thirty-four patients (9.7%) developed AKI. Echocardiography demonstrated that patients with AKI had significantly lower systolic ejection fraction (EF; 48% ± 8% vs 41% ± 10%, p <0.001), lower septal (p = 0.001) and lateral (p = 0.01) e′ velocities, higher average E/e′ ratio (p = 0.006), elevated systolic pulmonary artery pressure (p <0.001), and higher right atrial pressure (p = 0.001). In multivariate regression analysis, left ventricular EF emerged as an independent predictor of AKI (odds ratio 1.1, 95% confidence interval 0.86 to 0.96; p = 0.001) for every 1% reduction in EF. In conclusion, among patients with STEMI undergoing primary PCI, left ventricular EF is a strong and independent predictor of AKI.
Among patients with ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PCI), worsening of renal function resulting in acute kidney injury (AKI) is a frequent complication, known to be associated with adverse outcomes. Although contrast-induced (CI) nephropathy is considered a major determent for this complication, other important factors among this specific patient population includes an adverse hemodynamic state resulting in reduced renal perfusion, as well as other metabolic factors. Previous reports have demonstrated that chronic congestive heart failure (CHF) especially in advanced stages of New York Heart Association class III and IV contributes to the development of CI nephropathy primarily by decreasing renal perfusion, related with systolic dysfunction and low-stroke volume. Some studies specifically demonstrated that low ejection fraction (EF <30% to 40%) is an independent predictor of AKI in patients with CHF. No studies till date examined the relation between echocardiographic parameters of left ventricular (LV) function and the risk of AKI among patients with STEMI undergoing PCI. We evaluated the relation between systolic and diastolic parameters and AKI in a large cohort of patients with STEMI undergoing PCI.
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 412 consecutive patients admitted from June 2011 to December 2013 to the cardiac intensive care unit with the diagnosis of acute STEMI. Patients who were treated either conservatively or by thrombolysis were excluded (n = 5), as were 13 patients whose final diagnosis on discharge was other than STEMI (e.g., myocarditis or Takotsubo cardiomyopathy). We also excluded patients who died within 24 hours of admission (n = 6) because we presumed there was insufficient time for AKI to occur, and patients requiring chronic peritoneal dialysis or hemodialysis (n = 2) treatment. The final study population included 386 patients whose baseline demographics, cardiovascular history, clinical risk factors, treatment characteristics, and laboratory results were all retrieved from the hospital electronic medical records. Diagnosis of STEMI was established in accordance to published guidelines including a typical chest pain history, diagnostic electrocardiographic changes, and serial elevation of cardiac biomarkers. The study protocol was approved by the local institutional ethics committee. Primary PCI was performed on patients with symptoms ≤12 hours in duration and in patients with symptoms lasting 12 to 24 hours in duration if the symptoms persisted at the time of admission. After coronary interventional procedures, physiologic (0.9%) saline solution was given intravenously at a rate of 1 ml/kg/h for 12 hours after contrast exposure. In patients with overt heart failure, the hydration rate was reduced at the discretion of the attending physician. The contrast medium used in procedures was iodixanol (Visipaque; GE healthcare, Ireland) or iohexol (Omnipaque; GE healthcare, Ireland). The serum creatinine (sCr) level 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 a sCr increase of >0.3 mg/dl, compared with admission sCr.
All patients underwent a screening echocardiographic examination within 3 days of admission. Echocardiography was performed by Philips IE-33 equipped with S5-1 transducers (Philips Healthcare, Andover, Massachusetts), and GE Vivid 7 model equipped with M4S transducer. LV diameters and interventricular septal and posterior wall widths were measured from the parasternal short axis by means of a 2-dimensional, or a 2-dimension–guided M-mode echocardiogram of the LV at the papillary muscle level using the parasternal short-axis view. LVEF was calculated by the biplane method. The 16-segment model was used for scoring the severity of segmental wall motion abnormalities according to the American Society of Echocardiography. Early transmitral flow velocity (E), late atrial contraction (A) velocity and early diastolic mitral annular velocity (e′) were measured in the apical 4-chamber view to provide an estimate of LV diastolic function. The ratio of peak E to peak e′ was calculated (mitral E/e′ ratio) from the average of at least 3 cardiac cycles and the deceleration time of the E wave was also measured. Left atrial volume was calculated using the biplane area length method at end-systole. Cardiac output was calculated as the product of LV outflow tract area, LV outflow tract flow integral, and heart rate as demonstrated on pulse-wave Doppler.
All data were summarized and displayed as mean ± SD for continuous variables and as number (percentage) of patients in each group for categorical variables. The p values for the categorical variables were calculated with the chi-square test. Continuous variables were compared using the independent sample t test. The identification of the independent predictors of AKI was assessed using logistic regression model at the enter mode. We adjusted for age, gender, hypertension, diabetes mellitus, LVEF, E/e′ ratio, e′ velocity, and admission eGFR. 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
A total of 386 patients with STEMI treated by primary PCI were enrolled in the study, 34 (9.7%) of whom developed AKI in accordance with the AKI network criteria. The baseline clinical characteristics of patients with and without AKI are listed in Table 1 . Patients with AKI were more likely to be older, to have more co-morbidities, longer time to reperfusion, and lower baseline eGFR. No significant difference in contrast volume was found between patients with and without AKI. Median time to echocardiography was 1.4 days (interquartile range 1 to 2) for both groups. Table 2 presents the echocardiographic findings according to the occurrence of AKI. Patients having AKI had lower LVEF (41.3% ± 9.9 vs 47.7% ± 7.5, p <0.001), lower e’ septal (p = 0.001), e′ lateral (p = 0.01), and higher E/average e′ ratio (p = 0.006; Table 2 ).In addition, systemic pulmonary artery pressure was higher in patients with AKI (39 ± 13 vs 29 ± 8 mm Hg, p <0.001) as was a right atrial pressure (8 ± 5 vs 6 ± 3 mm Hg, p = 0.001). Patients having LVEF <45% had significantly higher rate of AKI compared with those with LVEF ≥45% (14.4% vs 5.7%, p = 0.02).
Variable | Acute kidney injury | p value | |
|---|---|---|---|
| No (n=352) | Yes (n=34) | ||
| Age (years) | 59 ± 11 | 66 ± 11 | <0.001 |
| Men | 286 (81%) | 29 (85%) | 0.527 |
| Diabetes mellitus | 57 (16%) | 13 (38%) | 0.004 |
| Dyslipidemia | 154 (44%) | 16 (47%) | 0.864 |
| Hypertension | 138 (39%) | 20 (59%) | 0.05 |
| Smoker | 201(57%) | 14 (41%) | 0.097 |
| Family history of CAD | 72 (20%) | 7(7%) | 0.013 |
| Prior myocardial infarction | 33 (9%) | 3(11 %) | 0.678 |
| No. of narrowed coronary arteries: | |||
| 1 | 173 (49%) | 14 (41%) | 0.219 |
| 2 | 90 (26%) | 11 (32%) | |
| 3 | 89 (25%) | 9 (27%) | |
| Anterior MI location | 186 (53%) | 16 (47%) | 0.430 |
| Heart failure | 13 (3%) | 7 (20%) | <0.001 |
| Time to reperfusion (minutes) | 224 ± 312 | 384 ± 410 | 0.002 |
| Admission eGFR (ml/minute/1.73m 2 ) | 75 ± 19 | 60 ± 21 | <0.001 |
| Admission creatinine, (mg/dl ) | 1.14 ± 0.22 | 1.32 ±0.45 | <0.001 |
| Peak creatinine ( mg/dl) | 1.11 ± 0.21 | 2.06 ± 1.04 | <0.001 |
| sCr change in hospital( mg/dl) | -0.03 ± 0.14 | 0.74 ± 0.75 | <0.001 |
| Creatinine at discharge ( mg/dl) | 1.09 ± 0.4 | 1.6 ± 0.78 | <0.001 |
| Contrast volume (ml) | 148 ± 39 | 139 ± 65 | 0.302 |
| Peak CPK (Units/L) | 1354 ± 1684 | 1560 ±2020 | 0.314 |
| Variable | Acute kidney injury | p value | |
|---|---|---|---|
| No (n=352) | Yes(34) | ||
| Biplane LV ejection fraction (mean ± SD) | 47.7 ± 7.5 | 41.3 ± 9.9 | <0.001 |
| Wall motion index (mean ± SD) | 1.56 ± 0.40 | 1.97 ± 0.4 | <0.001 |
| Heart rate (beats/min) (mean ± SD) | 75 ± 12 | 74 ± 14 | 0.764 |
| Systolic blood pressure( mm/Hg) (mean ± SD) | 136 ± 19 | 133 ± 28 | 0.204 |
| Diastolic blood pressure ( mm/Hg) (mean ± SD) | 81 ± 13 | 79 ± 14 | 0.596 |
| Cardiac output(L/min) (mean ± SD) | 5.2 ± 1.13 | 4.6 ± 1.27 | 0.01 |
| Left atrial volume( ml 3 ) (mean ± SD) | 61.7 ± 18.6 | 66.4 ± 20.2 | 0.181 |
| Left atrial volume index (ml/ m 2 ) (mean ± SD) | 32.3 ± 9.6 | 36.9 ± 10.8 | 0.02 |
| Mitral inflow E wave( cm/s) (mean ± SD) | 75 ± 19 | 79 ± 28 | 0.528 |
| Mitral inflow E/A ratio (mean ± SD) | 1.13 ± 0.48 | 1.23 ± 0.64 | 0.508 |
| Septal e′ ( cm/s) (mean ± SD) | 6.64 ± 1.86 | 5.57 ± 1.43 | 0.001 |
| E wave velocity/ septal e′ (mean ± SD) | 12.1 ± 4.6 | 15.0 ± 6.2 | 0.008 |
| Lateral e′ (cm/s) (mean ± SD) | 8.67± 2.71 | 7.3 ± 2.28 | 0.01 |
| E wave velocity/ lateral e′ (mean ± SD) | 9.5 ± 4.6 | 11.2 ± 3.9 | 0.005 |
| E wave velocity/ average e′ (mean ± SD) | 10.3 ± 3.8 | 12.4 ± 4.4 | 0.006 |
| Mitral E deceleration time (ms) (mean ± SD) | 183 ± 46 | 182 ± 49 | 0.952 |
| LV end diastolic dimension(mm) (mean ± SD) | 48 ± 10 | 51 ± 11 | 0.07 |
| LV end systolic dimension(mm) (mean ± SD) | 31 ± 9 | 35± 12 | 0.02 |
| Ventricular septal thickness (mm) (mean ± SD) | 10± 2 | 10± 2 | 0.74 |
| Posterior LV wall thickness (mm) (mean ± SD) | 10± 3 | 9 ± 4 | 0.41 |
| Peak systolic PA pressure (mm/Hg) (mean ± SD) | 29 ± 8 | 39 ± 13 | < 0.001 |
| Right atrial pressure | 6 ± 3 | 8 ± 5 | 0.001 |
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