Clinical Research in Cardiology https://doi.org/10.1007/s00392-018-1266-7

ORIGINAL PAPER

Association between central venous pressure as assessed by echocardiography, left ventricular function and acute cardio-renal syndrome in patients with ST segment elevation myocardial infarction Shafik Khoury1 · Arie Steinvil1 · Amir Gal‑Oz2 · Gilad Margolis1 · Aviram Hochstatd1 · Yan Topilsky1 · Gad Keren1 · Yacov Shacham1 Received: 11 February 2018 / Accepted: 30 April 2018 © Springer-Verlag GmbH Germany, part of Springer Nature 2018

Abstract Background  Recent reports have demonstrated the adverse effects of venous congestion on renal function in patients with heart failure. None of these trials, however, has evaluated the effect of acute myocardial ischemia on the occurrence of acute kidney injury (AKI). Methods  We conducted a retrospective study of 1336 ST segment elevation myocardial infarction (STEMI) patients undergoing primary percutaneous coronary intervention (PCI) between June 2012 and June 2016. Comprehensive echocardiographic examination was performed within 72 h of hospital admission. Non-invasive evaluation of central venous pressure (CVP) was estimated from measurements of inferior vena cava diameter and its collapsibility. Intermediate-high CVP was defined as ≥ 8 mm/Hg. Patients were stratified according to left ventricular ejection fraction (LVEF) and CVP and assessed for AKI. Results  Intermediate-high CVP was associated with AKI both in patients with LVEF greater than 45% and those with 45% or lower. Patients having LVEF ≤ 45% and intermediate-high CVP had a 10-fold increase in the incidence of AKI compared to patients with LVEF > 45% and normal CVP (39 vs. 4%). In a multivariable logistic regression model, intermediate-high CVP was independently associated with AKI (OR = 2.73, 95% CI 1.54–4.87; p = 0.001). Other variables associated with AKI included LVEF ≤ 45% (OR = 2.37, 95%CI 1.25–4.51; p = 0.008), time to reperfusion, mechanical ventilation and chronic kidney disease. Conclusions  Among STEMI patients undergoing PCI, the utilization of simple echocardiographic measurements (LVEF and CVP) may be useful for early identification of those at high risk for AKI. Keywords  Acute kidney injury · ST elevation myocardial infarction · Central venous pressure · Cardiorenal syndrome

Introduction The occurrence of acute kidney injury (AKI) following myocardial infarction has complex and multifactorial pathogenesis [1–5]. Among this specific patient population, AKI may Shafik Khoury and Arie Steinvil contributed equally to this paper. * Yacov Shacham [email protected] 1



Department of Cardiology, Tel-Aviv Sourasky Medical Center affiliated to the Sackler Faculty of Medicine, TelAviv University, Tel Aviv, Israel



Department of Intensive Care, Tel-Aviv Sourasky Medical Center affiliated to the Sackler Faculty of Medicine, Tel-Aviv University, Tel‑Aviv, Israel

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represent type I cardiorenal syndrome (CRS) [6, 7]. The acute reduction in left ventricular (LV) systolic function often results in decreased cardiac output leading to reduced renal perfusion [6, 8]. Recently published studies on heart failure patients suggested the role of venous congestion in renal dysfunction and pointed out the importance of elevated central venous pressure (CVP) rather than low cardiac output as the main predictor for worsening renal function [9, 10]. However, no data are currently available on the relation between CVP and the occurrence of CRS in patients with acute myocardial infarction. We aimed to evaluate the possible interactions between reduced LV systolic function, elevated CVP and the development of type I CRS in a large population of ST elevation myocardial infarction (STEMI) patients undergoing reperfusion with primary percutaneous coronary intervention (PCI).

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Materials and 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 as previously described [11, 12]. All 1524 patients admitted between June 2012 and June 2016 to the Cardiac Intensive Care Unit (CICU) with the diagnosis of acute STEMI were included. We excluded patients who were treated either conservatively or by thrombolysis (n = 11) and those who were discharged with a diagnosis other than STEMI (e.g., myocarditis, Takotsubo cardiomyopathy; n = 34). We also excluded patients on chronic peritoneal dialysis or hemodialysis treatment (n = 4) and those who died within 24 h of admission (n = 26), since we presumed there was insufficient time for AKI to occur. Finally, patients whose echocardiographic assessment failed to demonstrate adequate imaging of the inferior vena cava flow (n = 113) were also excluded. In those patients, demonstration of the inferior vena cava was technically difficult and inadequate so that any assessment of pressure could not have been performed. Few cases contained only “frozen” images or very short video clips (< 2 s) that failed to demonstrate respiratory changes in diameter. The final study population included 1336 patients whose baseline demographics, cardiovascular history, clinical risk factors, treatment characteristics, echocardiographic and laboratory results were all retrieved from the hospital electronic medical records. Diagnosis of STEMI was established in accordance with the published guidelines including a typical chest pain history, diagnostic electrocardiographic changes, and serial elevation of cardiac biomarkers [13]. Data collection and assessment of co-morbidities were taken from discharge letters. Data were collected by S.K, G. M and Y. S. Quality control was available by comparing the co-morbidities list from the letters’ chronic problem list and thorough review of the discharge letters free text for verification and was performed for all patients included. The study protocol was approved by the local institutional ethics committee. Primary PCI was performed on patients with symptoms ≤ 12 h in duration as well as in patients with symptoms lasting 12–24 h in duration if the symptoms persisted at the time of admission. Time to coronary reperfusion was defined as the time from symptom onset (usually chest pain or discomfort), recorded upon admission, to the restoration of thrombolysis in myocardial infarction (TIMI) grade 3 flow in the infarct artery, as reported in the catheterization laboratory report. Following coronary interventional procedures, physiologic (0.9%) saline was given intravenously at a rate of 1 ml/ kg/h for 12 h after contrast exposure. In patients with overt

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Clinical Research in Cardiology

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 level was determined upon hospital admission, prior to primary PCI, and at least once a day during the CICU and/or step down unit stay until hospital discharge, and was available for all analyzed patients. The estimated glomerular filtration rate (eGFR) was estimated using the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equation and chronic kidney disease (CKD) was categorized as admission eGFR of ≤ 60 ml/ min/1.73 m2 [14]. AKI was determined using the KDIGO criteria [15] and was defined as an increase in serum creatinine ≥ 0.3 mg/dl within 48 h of admission or an increase in serum creatinine ≥ 1.5 times baseline, which was known or presumed to have occurred within the prior 7 days. Mortality was assessed over a median period of 1271 ± 405 days up to December 1st, 2017. Assessment of survival following hospital discharge was determined from computerized records of the population registry bureau.

Echocardiography All patients underwent a screening echocardiographic examination within 3 days of admission. Relevant data were collected from the clinical echocardiographic exam reports. Echocardiography was performed by Philips IE-33 equipped with S5-1 transducers (Philips Healthcare, Andover, MA, USA), and GE Vivid 7 model equipped with M4S transducer. LV ejection fraction was calculated by the Biplane method of disks (modified Simpson’s rule). Central venous pressure was estimated by the inferior vena cava (IVC) diameter as well as its response to inspiration [16]. The performance of this technique is reviewed and presented annually during routine training sessions to all the echocardiographic technicians and physicians performing the exams in our institution. Briefly, expiratory and inspiratory IVC diameters and percentage collapse were measured using 2D images in subcostal views, with the patient in the supine position at 1–2 cm from the junction with the right atrium, using the long axis view. IVC diameter < 2.1 cm that collapsed > 50% with a sniff suggested normal CVP pressure of 3 mm Hg (range 0–5 mm Hg), whereas an IVC diameter > 2.1 cm that collapsed < 50% with a sniff suggested high CVP pressure of 15 mm Hg (range 10–20 mm Hg). In scenarios in which IVC diameter and collapse did not fit this paradigm, hepatic flow patterns were used to assess CVP [17]. Systolic predominance in hepatic vein flow (i.e., velocity of the systolic wave greater than the velocity of the diastolic wave) was suggestive of normal CVP (3 mm Hg, range 0–5). If systolic predominance was lost, such that the hepatic vein systolic filling fraction (velocity of the systolic

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wave/ velocity of the diastolic wave) was lower than 55%, high CVP was assumed (15 mm Hg, range 10–20) [17]. If uncertainty remained, CVP pressure was left as intermediate value of 8 mm Hg (range, 6–10). Forward stroke volume was calculated by multiplying the LV outflow tract area at rest by the LV outflow tract velocity–time integral measured by pulsed wave with subsequent calculation of cardiac output and index. LV outflow tract area was calculated based on the formula: LVOT outflow ­diameter2 × 0.785. To ascertain the accuracy of the Doppler-echocardiographic measurements of stroke volume we used the clearest on-axis image of the LVOT providing the largest LVOT diameter and measured the LVOT diameter inner-edge-to-inner-edge from the base of the right coronary cusp anteriorly to the commissure posteriorly. Cardiac output (l/min) was determined by multiplication of the stroke volume by the pulse. Early transmitral flow velocity (E) was measured in the apical 4-chamber view to provide an estimate of LV diastolic function [18]. Early diastolic mitral annular velocity (e′) was measured using spectral tissue Doppler imaging in both septal and lateral positions. The ratio of peak E to peak e′ was calculated (E/e′ ratio) from the average of at least 3 cardiac cycles. In patients with atrial fibrillation, we have used the average measured from 5 to 7 cardiac cycles. Prior data demonstrated that an E/e′ ratio > 15 was independently associated with AKI in STEMI patients [19]. Accordingly, this cutoff was used for the analysis.

Statistical analysis All data were summarized and displayed as mean ± standard deviation for continuous variables and as number (percentage) 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 or the Mann–Whitney U test. A two-tailed p value of < 0.05 was considered significant for all analyses. The influence of intermediate-high CVP and LV ejection fraction on the risk for AKI was evaluated using multivariable binary logistic regression models at the enter mode, adjusted for age, gender, hypertension, diabetes mellitus, familial history of ischemic heart disease, smoking, coronary artery disease severity, admission Killip class ≥ 2, presence of chronic kidney disease, mechanical ventilation, time to reperfusion (1 h increment), peak CPK levels, admission C-reactive protein, E/e′ ratio ≥ 15, intermediate high CVP and LV ejection fraction ≤ 45%. To elucidate the effect of mechanical ventilation and chronic kidney disease, separate regression models were performed to patients not mechanically ventilated (model 2) and without chronic kidney disease (model 3). Inter-observer variability was assessed by independent blinded observers who reviewed the stored video clips of the echocardiographic exams in 190 randomly

selected patients and assessed CVP and LV ejection fraction from those stored clips. Inter-observer variability was assessed using a Pearson’s correlation test, a paired Wilcoxon test and a within-subject coefficient of variation. The within-subject coefficient of variation (calculated using the root mean square of the measurements delta/mean ratio) provides a scale-free, unit-less estimate of variation expressed as a percentage. We measured inter-observer reproducibility for CVP and LV ejection fraction and expressed it using the coefficient of variation. All analyses were performed with the SPSS software (SPSS Inc., Chicago, IL).

Results A total of 1336 patients were included in the study. The mean age of the study population was 61 ± 11 years and most of them, 657 (81%), were males. 152/1336 patients (11%) developed AKI. Patients with AKI were of older age, more likely to be females, and had multiple co-morbidities, greater extent of coronary artery disease, longer time to culprit vessel reperfusion, higher Killip class and higher levels of C-reactive protein on admission (Table 1). Patients with AKI demonstrated lower LV ejection fraction (42% ± 9 vs. 47% ± 7, p < 0.001), higher CVP (9.5 ± 5.4 vs. 6.1 ± 3.2 mm/hg, p < 0.001) and were more likely to have intermediate-high CVP and lower cardiac output (4.6 ± 1.1 vs. 5.1 ± 1.2 l/min, p = 0.002) (Table 2). A sub-analysis for non-ventilated patients (n = 1273) yielded similar results to those found in the entire cohort.

Interaction between LV systolic function, CVP and AKI Intermediate-high CVP was associated with AKI both in patients with LV ejection fraction greater than 45% and those with 45% or lower (Fig. 1). Patients having both LV ejection fraction ≤ 45% and intermediate-high CVP had a 10-fold higher incidence of AKI compared to patients with LV ejection fraction > 45% and normal CVP (39% vs. 4%). Intermediate-high CVP was also associated with higher maximal in-hospital serum creatinine change (Fig. 2). In multivariable binary logistic regression model for the entire cohort (model 1, Table  3), intermediate-high CVP was independently associated with AKI (OR = 2.73, 95% CI 1.54–4.87; p = 0.001). Other variables associated with AKI included LV ejection fraction ≤ 45% (OR = 2.37, 95%CI 1.25–4.51; p = 0.008), time to reperfusion, mechanical ventilation and chronic kidney disease. The effect of an intermediate-high CVP was maintained among non-ventilated patients (model 2, Table 3) and patients without CKD (model 3, Table 3).

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Table 1  Baseline characteristics

Clinical Research in Cardiology Variables

Acute kidney injury

Age (years) Male Systolic blood pressure (mm/Hg) Diastolic blood pressure (mm/Hg) Diabetes mellitus Dyslipidemia Hypertension Smoking history Family history of CAD Prior MI Time to reperfusiom (min) Admission Killip class ≥ 2 Mechanical ventilation Coronary artery disease severity: 1 2/3 Chronic kidney disease Peak CPK (Units/l) Contrast volume (ml) Admission C-reactive protein (mg/l) Duration of hospitalization (days)

No (n = 1184)

Yes (n = 152)

p value

60 ± 13 967 (82%) 136 ± 19 81 ± 13 268 (23%) 535 (45%) 489 (41%) 637 (54%) 285 (24%) 185 (16%) 379 ± 479 97 (8%) 28 (2%) 514 (43%) 670 (57%) 213 (18%) 1302 ± 1529 145 ± 56 11.5 ± 25.9 5.4 ± 2.8

70 ± 13 112 (74%) 133 ± 25 78 ± 14 51 (34%) 80 (53%) 99 (65%) 56 (37%) 18 (12%) 27 (18%) 599 ± 654 54 (35%) 35 (23%) 48 (31%) 104 (69%) 78 (52%) 1859 ± 1767 140 ± 51 23.8 ± 44.1 9.8 ± 8.2

< 0.001 0.01 0.214 0.584 < 0.01 0.08 < 0.001 < 0.001 < 0.001 0.49 < 0.001 < 0.001 < 0.001 < 0.001 < 0.001 < 0.001 < 0.001 0.328 < 0.001 < 0.001

CAD coronary artery disease, MI myocardial infarction, CPK creatine phosphokinase

Table 2  Key echocardiographic parameters according to acute kidney injury status

Variable

Acute kidney injury

Left ventricle ejection fraction (%) Left ventricle ejection fraction ≤ 45% E/e′ ratio E/e′ ratio ≥ 15 Central venous pressure (mm/Hg) Intermediate-high central venous pressure Cardiac output (l/min) Cardiac index (l/min/m2)

No (n = 1184)

Yes (n = 152)

p value

47 ± 7 640 (54%) 12.2 ± 5 213 (18%) 6.1 ± 3.2 151 (13%) 5.1 ± 1.2 2.7 ± 0.6

42 ± 9 121 (79%) 16.3 ± 7 68 (45%) 9.5 ± 5.4 78 (51%) 4.6 ± 1.1 2.3 ± 0.5

< 0.001 < 0.001 < 0.001 < 0.001 < 0.001 < 0.001 0.002 < 0.001

Long‑term outcomes

Discussion

Over a mean period of 3.5 ± 1.4 years, 115/1336 patients (8.6%) died. Mortality was significantly higher among those with AKI (44/152, 29%) following STEMI than those without AKI (71/1184, 6%; p < 0.001). The hazard ratio for all-cause mortality associated with AKI was 12.6 (95% CI 7.47–21.56, p < 0.001).

This is the first study to date suggesting the possible interaction between LV systolic function, CVP and the occurrence of AKI following STEMI. We have now demonstrated that among this patient population, the combination of reduced LV systolic function and elevated CVP was associated with a 10-fold increase in the incidence of AKI.

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Clinical Research in Cardiology Fig. 1  Incidence of AKI in patients with normal (blue boxes) and intermediate-high (red boxes) CVP according to left ventricular ejection fraction (EF) above and ≤ 45%

Fig. 2  Maximal in-hospital serum creatinine change in patients with normal and intermediate-high CVP

Acute (or type I) CRS described to date in patients with acutely decompensated heart failure is characterized by a rapid worsening of cardiac function leading to AKI [20]. Renal dysfunction in CRS type I is attributed to a combination of low cardiac output, which consequently causes reduction in blood flow and renal perfusion pressure, and/or venous congestion. Reduced LV systolic function is a known risk factor for the development of AKI following STEMI [8]. The sudden myocardial insult in STEMI results in an acute reduction of cardiac output and reduced effective renal blood flow leading to hypoxic changes and the synthesis of reactive oxygen species [21]. Following the resumption of coronary flow and the improvement of left ventricular function, as

well as the resolution of arrhythmias, hemodynamic impairment often resolves while renal function may still remain impaired or lag in recovery. Recent studies on heart failure patients have highlighted the role of venous congestion on renal dysfunction and suggested that central venous pressure and right atrial pressure, rather than cardiac output, are the main predictors for worsening renal function [9, 10]. Recent sub-analysis of the ESCAPE trial has also suggested that renal impairment was related to CVP [9]. Venous congestion was the most important hemodynamic factor driving worsening of renal function in decompensated patients with advanced heart failure [22]. In a large cohort of patients with advanced heart failure, venous congestion was associated with decreased renal function. Moreover, the extent of congestion was also associated with the severity of renal impairment [23]. Venous congestion characterized by an increased right atrial pressure was also related to reduced renal blood flow and lower eGFR [24]. Increased venous congestion causes an increase in renal interstitial pressure and hypoxia to the renal parenchyma [25]. Increased oxidative stress and inflammation in the tubule-interstitium following venous congestion may also play a role in renal dysfunction [26]. Only limited data are present to date on the possible relation of echocardiographic parameters of elevated CVP and renal impairment among patients with acute ischemia. Tandon et al. evaluated the relation between right ventricular function and the development of CRS in patients presenting with inferior wall STEMI and right ventricular involvement [7]. They demonstrated that the presence of echocardiographic markers of reduced right ventricular function was associated with higher risk for the occurrence of type I CRS.

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Table 3  Multivariable binary logistic regression models for predicting acute kidney injury Correlates

Model 1 entire cohort adjusted OR (95% CI)

Age Male gender Hypertension Smoker Family history CAD severity Time to reperfusion (1 h increment) Killip class ≥ 2 Mechanical ventilation Peak CPK levels Diabetes mellitus C-reactive protein Chronic kidney disease LVEF ≤ 45% E/e′ ratio ≥ 15 Intermediate-high CVP

1.01 (0.98–1.04) 1.02 (0.52–2.02) 1.71 (0.97–3.03) 0.71 (0.4–1.24) 1.02 (0.49–2.12) 1.18 (0.85–1.63) 1.03 (1.00-1.05) 1.48 (0.74–2.93) 8.01 (3.11–20.06) 1.01 (1.00–1.01) 1.28 (0.72–2.31) 1.00 (0.97–1.01) 2.94 (1.49–5.78) 2.37 (1.25–4.51) 1.07 (0.56–2.03) 2.73 (1.53–4.87)

Model 2 non-ventilated patients adjusted OR (95% CI)

p value

Model 3 non-CKD patients p value adjusted OR (95% CI)

0.476 0.951 0.06 0.231 0.95 0.334 0.04

1.01 (0.97–1.03) 1.24 (0.61–2.56) 1.85 (1.01–3.38) 0.56 (0.31–1.01) 0.96 (0.44–2.11) 1.19 (0.84–1.69) 1.02 (0.99–1.05)

0.942 0.552 0.04 0.07 0.922 0.322 0.193

1.02 (0.98–1.05) 0.64 (0.22–1.85) 2.04 (0.91–4.59) 0.63 (0.29–1.37) 0.98 (0.41–2.37) 1.35 (0.85–2.16) 1.03 (1.00-1.07)

0.459 0.414 0.084 0.248 0.969 0.203 0.085

0.266 < 0.001 0.151 0.411 0.229 0.002 0.008 0.831 0.001

1.79 (0.87–3.66) – 1.01 (1.00–1.01) 1.14 (0.61–2.12) 1.00 (0.98–1.02) 3.19 (1.51–6.71) 2.15 (1.07–4.33) 1.22 (0.62–2.4) 3.11 (1.69–5.72)

0.113 – 0.07 0.684 0.215 0.002 0.03 0.551 < 0.001

1.63 (0.58–4.68) 12.2 (3.01–49.6) 1.01 (1.00-1.01) 0.76 (0.29–1.96) 1.00 (0.97–1.01) – 1.64 (0.69–3.91) 1.06 (0.38–2.93) 3.61 (1.62–8.08)

0.360 < 0.001 0.829 0.569 0.763 – 0.260 0.909 0.002

p value

CKD chronic kidney disease, CAD coronary artery disease, LVEF left ventricle ejection fraction, CVP central venous pressure, OR odds ratio

This report, however, included a small number of patients and only 10% of them underwent primary PCI. In our cohort, the combination of reduced LV systolic function and elevated CVP was associated with the highest risk for AKI. The finding that patients with AKI had both reduced LV ejection fraction and elevated CVP may point out the importance of combined systolic and diastolic dysfunction resulting in elevated right heart and central venous pressures. This finding may support a plausible explanation for a pathomechanism in which the worsening of renal function in STEMI patients is related to a combination of pump failure and reduced perfusion as well as venous congestion, thus fulfilling the criteria for type I CRS. Contrast material is still considered the major reason for AKI development in STEMI patients undergoing primary PCI. Contrast-induced AKI is a prevalent and deleterious complication of coronary angiography and reported to be the third most common cause of hospital acquired renal failure [27]. Unlike previous reports in which the risk of contrastinduced AKI in patients undergoing PCI was directly associated with increasing contrast media volume, we did not find in our study a significant difference in contrast media volume between patients with and without AKI. Furthermore, we have previously demonstrated that contrast media volume did not predict AKI in this patient population [6, 8, 12]. This finding suggests that factors other than contrast media volume may contribute to AKI development in the setting of STEMI. These include mainly hemodynamic

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parameters which make the kidneys more susceptible to contrast-induced AKI. Our findings may bear some clinical implications. While various clinical factors and biomarkers have been studied in STEMI patients who develop AKI, only few studies focused on the relation between echocardiographic parameters and the occurrence of AKI [7, 8, 28]. As the treatment of AKI in STEMI patients following primary PCI is rather limited, the main strategy is early identification of those at risk for developing this complication and thus offering a better opportunity to apply appropriate preventive measures. The addition of simple and early echocardiographic measurements (LV ejection fraction and CVP) to other established clinical risk factors may be useful for early identification of those at high risk for post-PCI AKI. In these patients, physicians may consider daily assessment of serum creatinine. In addition, novel biomarkers offer the opportunity to diagnose early tubular injury and may help in early detection of cellular injury in response to various renal toxins, including contrast-induced nephropathy [29, 30].

Limitations We acknowledge several important limitations of our study. This is a single center retrospective and non-randomized observational study and, therefore, might have been subject to bias, although we included consecutive

Clinical Research in Cardiology

patients and attempted to adjust for confounding factors using the multivariate regression model. The data from echocardiographic reports were analyzed retrospectively. Echocardiography is highly operator dependent and our data were collected and recorded by different sonographers. We tried to adjust for this limitation by the assessment of inter-observer variability using independent blinded observers who reviewed the stored video clips of the echocardiographic exams and assessed CVP and LV ejection fraction. Comparison of inter-observer parameters showed good agreement, with statistically significant, yet clinically insignificant differences. No information was present on the concomitant medications patients were receiving (e.g., renin–angiotensin blockers, beta blockers and diuretics) upon hospital admission, throughout hospitalization and upon discharge; thus, their effect on the occurrence of AKI and long-term outcomes could not have been assessed. Patients having AKI were older, had greater coronary artery disease, longer time to culprit vessel reperfusion, more likely to have heart failure and had higher C-reactive protein levels on admission. In addition, they had larger infarct sizes. It is possible that the development of AKI in this group was not related to elevated CVP and may simply be reflective of a higher degree of underlying pathology. Patients with AKI were significantly more likely to be mechanically ventilated. Mechanical ventilation may result in decreased IVC collapsibility and increased pulmonary resistance and thus may lead to overestimation of CVP. We performed, however, a sub-analysis of data in non-ventilated patients yielding similar echocardiographic findings and adjusted the regression model also for non-ventilated patients. No information was present on patients with right ventricular dysfunction; thus, its relation to CVP could not have been assessed. Intravenous fluids have complex interaction effects on renal function. While fluids enhance forward flow and renal perfusion, with possible reduction of AKI, it may also cause venous congestion resulting in potential increase in AKI. No information was present regarding the amount of intravenous fluid administrated to patients throughout their CICU stay and, thus, their potential effect on renal function could not be assessed. The routine use of pulmonary artery catheter and/or pulse index continuous cardiac output is not a common practice in our CICU; thus, we could not correlate or confirm the CVP as assessed by echocardiography. Finally, worsening of renal function might have occurred following hospital discharge in some patients; thus, the true incidence of AKI described in our study might have been underestimated.

Conclusions Among STEMI patients undergoing primary PCI, the utilization of simple echocardiographic measurements (LV ejection fraction and CVP) may be useful for early identification of those at high risk for AKI.

Compliance with ethical standards  Conflict of interest  The authors declare that they have no conflict of interest.

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