Introduction: Acute kidney injury (AKI) is a common and serious complication in critically ill patients, particularly those with ST-elevation myocardial infarction (STEMI). Mechanical ventilation (MV) is often needed when respiratory deterioration occurs and is continuously associated with higher risk for AKI. Whether MV is an independent predictor for AKI in STEMI patients has not been evaluated before. We aimed to determine a potential association between MV and the occurrence of AKI in STEMI patients. Methods: A single-center retrospective cohort in a tertiary referral hospital. We evaluated consecutive patients that were admitted to the cardiac intensive care unit with acute STEMI between 2008 and 2019. Patients were divided into groups based on their need for MV upon admission. To minimize baseline differences between the two groups, propensity matching was performed. The primary outcome was the occurrence of AKI after intubation and secondary outcomes included severe AKI (>2 times the baseline creatinine) and renal recovery. Results: 2,929 patients were included and of them, 143 (5%) were intubated. After using the propensity matching, 138 pairs were available for analysis with similar demographic and clinical characteristics. MV was a predictor for AKI (Table 2, odds ratio [OR]: 3.3, 95% confidence interval [CI]: 1.9–5.6) and severe AKI (OR: 6.3, 95% CI: 2.5–16). These results remained significant after adjusting for the occurrence of a new heart failure and bleeding. Early or partial renal recovery was similar between the groups. Conclusion: MV is independently associated with the occurrence of AKI and severe AKI. The possible mechanism might be temporary, reflected by similar rates of renal recovery.

In the critically ill subset of patients, acute kidney injury (AKI) is a common and serious complication of intensive care unit (ICU) patients in general, and of ST-elevation myocardial infarction (STEMI) in particular, that cause higher rates of adverse outcomes and mortality [1‒6]. As a result, great efforts are undertaken to identify patients who are at increased risk for AKI in order to prevent or minimize adverse effects [6‒10].

Mechanical ventilation (MV) is commonly used for life support in various critical care settings [11]. However, positive pressure ventilation was associated with numerous end-organ damages and specifically renal injury [12]. AKI was recognized and associated with MV as early as 1947, with current studies still attempting to measure and evaluate this connection [1, 2, 13, 14].

STEMI patients were found to be more prone to AKI for numerous reasons, including baseline comorbidities, contrast-induced nephropathy following cardiac catheterization, microvascular injury, hemodynamic changes, and drug exposure [9, 10]. However, whether MV is an independent predictor for renal injury in STEMI patients and its effect on renal recovery once AKI has been established were not evaluated before. In the current study, we aimed to determine a potential association between MV and the occurrence of AKI in STEMI patients.

Study Population

This is a single-center retrospective cohort that was performed in a single tertiary referral hospital (Tel Aviv Sourasky Medical Center) with a 24/7 primary percutaneous coronary interventions. The inclusion and analysis process appears in Figure 1. We evaluated 2,929 consecutive patients that were admitted to the cardiac intensive care unit (CICU) with the diagnosis of acute STEMI between January 2008 and December 2019. We then stratified patients based on their need for invasive MV prior to admission. The mechanically ventilated patients (MVP) group included all patients that underwent MV during their emergency department stay or upon their admission to the CICU. Reasons for MV included the treatment for malignant arrhythmias, cardiogenic shock, or acute decompensated heart failure. Ventilation parameters were determined by the physician in charge and in adherence to the CICU protocol. In order to address the difference in baseline characteristics, we then performed propensity matching between the two groups (as discussed below). In addition, to account for changes in practice and guidelines overtime as a confounding factor, we divided all participants into 4 groups (2008–2010, 2011–2013, 2014–2016, 2017–2019) based upon admission date prior to statistical analysis.

Fig. 1.

Study design – Study protocol illustrated by flowchart. MV, mechanical ventilation; STEMI, ST elevation myocardial infarction.

Fig. 1.

Study design – Study protocol illustrated by flowchart. MV, mechanical ventilation; STEMI, ST elevation myocardial infarction.

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The diagnosis of STEMI was made if a typical history of chest pain occurred, with diagnostic electrocardiographic changes, and serial elevation of serum cardiac biomarkers [15]. The diagnosis was verified for each patient before inclusion to the cohort. Primary percutaneous coronary intervention was carried out in all patients with symptoms under 12 h in duration and in patients with 12–24 h if pain consisted upon admission. Treatment with statins, renin/angiotensin blockers, and β-blockers were started in all patients unless contraindicated. Following PCI, 0.9% saline was given for 12 h at a rate of 1 mL/kg/h or lower if patients had an overt heart failure.

We retrieved the baseline demographic and medical history, treatment characteristics, and laboratory results of all included patients. Left ventricular ejection fraction was measured within the first 48 h by a bedside echocardiography for all patients.

The study was conducted according to the Declaration of Helsinki and approved by the Tel Aviv Sourasky Medical Center Review Board (TLV-16-0224). Informed consent was obtained from all subjects involved in the study.

Study Outcomes

The primary outcome of our study was the occurrence of AKI after intubation. The baseline serum creatinine level was evaluated upon admission and prior to intubation. Creatinine levels were then assessed on a daily basis until 72 h from intubation. AKI was defined as peak creatinine equals or above 1.5 times/0.3 mg/dL the baseline creatinine [16]. The secondary outcomes included the occurrence of severe AKI and the recovery of kidney functions. We defined severe AKI as peak creatinine higher than twice the baseline creatinine level, which is correlated to stages 2 and 3 of the KDIGO AKI staging. Patients with a return of creatinine level to under 0.3 mg/dL from baseline in 72 h were regarded has having an early recovery [17]. Improvement in creatinine levels to above 0.3 mg/dL from baseline in 72 h was termed partial recovery.

Statistical Analysis

Normally distributed continuous variables were presented as mean ± standard deviation and compared using independent t tests. Non-normally distributed variables were presented as median (interquartile range) and compared using the Mann-Whitney U test. Normality was assessed with the Kolmogorov-Smirnov test. Categorical variables were presented as number (percentage) and compared with the χ2 test. All reported p values are considered to be statistically significant when p < 0.05.

A propensity score matching (PSM) was used to reduce confounding variables between MVPs and non-MVPs [18]. The relationship between the clinical variables of patients with STEMI and AKI was previously evaluated [4, 5, 19, 20]. Based on these analyses, the covariates were selected for the PSM, all without missing data, and included: age, sex, hyperlipidemia, hypertension, diabetes, past MI, atrial fibrillation, chronic kidney disease, admission left ventricular ejection fraction, extant of coronary artery disease, baseline creatinine, and inotrope medications use. Matching was performed using the nearest neighbor algorithm with a 1:1 ratio between intubated and non-intubated patients. Matching was restricted by a caliper distance of 0.05 without replacement. To assess the association between intubation and AKI, a univariate analysis was performed between the matched cohorts with odds ratio (OR) and 95% confidence interval (CI). An additional multivariate logistic regression analyses were performed for outcomes with significant associations in univariate analysis, accounting for a new heart failure, malignant, arrhythmia, the year of the event (divided into groups of 3 consecutive years), and bleeding complications, as they were not included in the matching. All analyses were performed with the SPSS software (SPSS Inc., Chicago, IL, USA).

Study Cohort and Matching

The study cohort included 2,929 patients that were admitted with STEMI and of them, 143 (5%) were intubated. After using the PSM with the definitions above, 138 pairs were matched (97% of the MVPs). Table 1 presents the characteristics of MV patients and non-MV groups in our initial cohort and after matching. Before matching, most baseline and clinical characteristics were different between the groups. MVPs were older males with higher rates of hypertension and chronic kidney disease, extensive coronary artery disease, higher baseline creatinine level, and needed more ionotropic treatment.

Table 1.

Cohort characteristics with comparison between mechanical ventilation status and propensity matching

VariableUnmatchedMatched
ventilated (n = 143)non-ventilated (n = 2,786)SMDp valueventilated (n = 138)non-ventilated (n = 138)SMDp value
Age, yearsa 68 + 14 61 + 13 0.51 <0.01 68 + 14 65 + 14 0.18 0.17 
Female, sexa 40 (28) 502 (18) 0.11 <0.01 40 (29) 33 (24) 0.11 0.34 
Admission period 
 2008–2010 30 (21) 603 (22)   30 (22) 53 (38)   
 2011–2013 25 (18) 690 (25) 0.06 0.08 25 (18) 21 (15) 0.22 0.02 
 2014–2016 53 (37) 783 (28)   53 (38) 44 (32)   
 2017–2019 35 (25) 710 (25)   30 (22) 20 (15)   
Hyperlipidemiaa 66 (46) 1,384 (50) 0.02 0.62 65 (47) 58 (42) 0.10 0.40 
Hypertensiona 79 (56) 1,247 (45) 0.10 <0.01 77 (56) 67 (49) 0.17 0.22 
Diabetesa 45 (32) 659 (24) 0.08 0.03 44 (32) 35 (25) 0.14 0.23 
Past MIa 22 (15) 439 (16) 0.01 0.91 21 (15) 16 (12) 0.11 0.38 
Atrial fibrillationa 18 (13) 124 (4) 0.16 <0.01 17 (12) 13 (8) 0.14 0.23 
CKDa 69 (48) 534 (19) 0.31 <0.01 67 (49) 55 (40) 0.18 0.15 
Ejection fraction, %a 41 + 10 48 + 8 0.49 <0.01 38 + 14 40 + 11 0.19 0.11 
Time to reperfusion, min 152 (105–510) 180 (110–480) 0.01 0.95 160 (105–510) 180 (120–600) 0.07 0.55 
Coronary artery vessel diseasea 
 1 55 (39) 1,184 (43) 0.12 <0.01 54 (39) 56 (41) 0.18 0.23 
 2 32 (22) 853 (31) 30 (22) 40 (29) 
 3 56 (39) 749 (27) 54 (39) 42 (30) 
Creatinine, admissiona 1.4 + 1.1 1.1 + 0.3 0.80 <0.01 1.42 + 1.1 1.27 + 0.8 0.15 0.19 
HF exacerbation 62 (43) 231 (8) 0.25 <0.01 60 (44) 40 (29) 0.15 0.01 
VT/VF 66 (46) 159 (6) 0.33 <0.01 65 (47) 24 (17) 0.32 <0.01 
Bleedingb 41 (29) 126 (5) 0.22 <0.01 41 (30) 22 (16) 0.16 0.01 
Cardiogenic shocka, c 62 (43) 63 (2) 1.17 <0.01 59 (43) 56 (41) 0.04 0.71 
VariableUnmatchedMatched
ventilated (n = 143)non-ventilated (n = 2,786)SMDp valueventilated (n = 138)non-ventilated (n = 138)SMDp value
Age, yearsa 68 + 14 61 + 13 0.51 <0.01 68 + 14 65 + 14 0.18 0.17 
Female, sexa 40 (28) 502 (18) 0.11 <0.01 40 (29) 33 (24) 0.11 0.34 
Admission period 
 2008–2010 30 (21) 603 (22)   30 (22) 53 (38)   
 2011–2013 25 (18) 690 (25) 0.06 0.08 25 (18) 21 (15) 0.22 0.02 
 2014–2016 53 (37) 783 (28)   53 (38) 44 (32)   
 2017–2019 35 (25) 710 (25)   30 (22) 20 (15)   
Hyperlipidemiaa 66 (46) 1,384 (50) 0.02 0.62 65 (47) 58 (42) 0.10 0.40 
Hypertensiona 79 (56) 1,247 (45) 0.10 <0.01 77 (56) 67 (49) 0.17 0.22 
Diabetesa 45 (32) 659 (24) 0.08 0.03 44 (32) 35 (25) 0.14 0.23 
Past MIa 22 (15) 439 (16) 0.01 0.91 21 (15) 16 (12) 0.11 0.38 
Atrial fibrillationa 18 (13) 124 (4) 0.16 <0.01 17 (12) 13 (8) 0.14 0.23 
CKDa 69 (48) 534 (19) 0.31 <0.01 67 (49) 55 (40) 0.18 0.15 
Ejection fraction, %a 41 + 10 48 + 8 0.49 <0.01 38 + 14 40 + 11 0.19 0.11 
Time to reperfusion, min 152 (105–510) 180 (110–480) 0.01 0.95 160 (105–510) 180 (120–600) 0.07 0.55 
Coronary artery vessel diseasea 
 1 55 (39) 1,184 (43) 0.12 <0.01 54 (39) 56 (41) 0.18 0.23 
 2 32 (22) 853 (31) 30 (22) 40 (29) 
 3 56 (39) 749 (27) 54 (39) 42 (30) 
Creatinine, admissiona 1.4 + 1.1 1.1 + 0.3 0.80 <0.01 1.42 + 1.1 1.27 + 0.8 0.15 0.19 
HF exacerbation 62 (43) 231 (8) 0.25 <0.01 60 (44) 40 (29) 0.15 0.01 
VT/VF 66 (46) 159 (6) 0.33 <0.01 65 (47) 24 (17) 0.32 <0.01 
Bleedingb 41 (29) 126 (5) 0.22 <0.01 41 (30) 22 (16) 0.16 0.01 
Cardiogenic shocka, c 62 (43) 63 (2) 1.17 <0.01 59 (43) 56 (41) 0.04 0.71 

SMD, standardized mean difference; MI, myocardial infraction; CKD, chronic kidney disease; HF, heart failure; VT, ventricular tachycardia; VF, ventricular fibrillation.

aVariables that were included in the propensity matching analysis.

bIncluding any bleeding that required withholding antiplatelet or anticoagulation therapy.

cNeed for ionotropic support or intra-aortic balloon pump.

After PSM, all included variables were balanced in both groups and did not longer predict group membership in the matched patients. Baseline creatinine in the matched groups was 1.42 ± 1.1 mg/dL in MVPs and 1.27 ± 0.8 mg/dL in the non-MVPs. There was also no change in median time to reperfusion (160 vs. 180 min, p = 0.55), mean ejection fraction (38% vs. 40%, p = 0.11), or ionotropic use (43% vs. 41%, p = 0.71).

Primary and Secondary Outcomes

After matching, MV was still associated with AKI (Table 2, OR: 3.3, 95% CI: 1.9–5.6) and severe AKI (OR: 6.3, 95% CI: 2.5–16). On the contrary, there was a difference in the renal recovery before and after matching. Before matching, MVPs had a trend toward lower rates of early recovery (OR: 0.56, 95% CI: 0.3–1, p = 0.05) and higher rates of partial recovery (OR: 1.99, 95% CI: 1.1–3.8, p = 0.04). However, after matching, there was no difference between the groups in early or partial recovery. Peak creatinine levels were higher among MVPs compared with non-MVPs in the original cohorts (mean 1.86 vs. 1.04 mg/dL, p < 0.01) and matched cohorts (mean 1.87 vs. 1.3 mg/dL, p < 0.01, Fig. 2).

Table 2.

Kidney outcomes with comparison between mechanical ventilation status and propensity matching

VariableUnmatchedMatched
MVPs (n = 143)non-MVPs (n = 2,786)OR (95% CI)p valueMVPs (n = 138)non-MVPs (n = 138)OR (95% CI)p value
AKI 63 (44) 191 (7) 10.7 (7.4–15) <0.01 61 (44) 27 (20) 3.26 (1.9–5.6) <0.01 
Severe AKIa 31 (22) 27 (1) 28.3 (16–49) <0.01 31 (22) 6 (4) 6.28 (2.5–16) <0.01 
Early recoveryb,c 23 (37) 97 (51) 0.56 (0.3–1.0) 0.05 21 (34) 11 (41) 0.76 (0.3–1.9) 0.57 
Partial recoveryb,d 19 (39) 34 (18) 1.99 (1.1–3.8) 0.04 19 (31) 9 (33) 0.90 (0.3–2.4) 0.84 
No recoveryb,e 21 (33) 60 (31) 1.09 (0.6–2.0) 0.78 21 (34) 7 (26) 1.50 (0.5–4.1) 0.52 
VariableUnmatchedMatched
MVPs (n = 143)non-MVPs (n = 2,786)OR (95% CI)p valueMVPs (n = 138)non-MVPs (n = 138)OR (95% CI)p value
AKI 63 (44) 191 (7) 10.7 (7.4–15) <0.01 61 (44) 27 (20) 3.26 (1.9–5.6) <0.01 
Severe AKIa 31 (22) 27 (1) 28.3 (16–49) <0.01 31 (22) 6 (4) 6.28 (2.5–16) <0.01 
Early recoveryb,c 23 (37) 97 (51) 0.56 (0.3–1.0) 0.05 21 (34) 11 (41) 0.76 (0.3–1.9) 0.57 
Partial recoveryb,d 19 (39) 34 (18) 1.99 (1.1–3.8) 0.04 19 (31) 9 (33) 0.90 (0.3–2.4) 0.84 
No recoveryb,e 21 (33) 60 (31) 1.09 (0.6–2.0) 0.78 21 (34) 7 (26) 1.50 (0.5–4.1) 0.52 

MVP, mechanical ventilated patients; AKI, acute kidney injury.

aDefined as peak creatinine higher than twice of the admission creatinine level.

bOnly patients with AKI were included in the analyses of these variables.

cDefined as recovery of creatinine to within 0.3 mg/dL of baseline level within 72 h.

dDefined as recovery of creatinine to more than 0.3 mg/dL of baseline level within 72 h.

eDefined as without improvement in creatinine within 72 h.

Fig. 2.

Creatinine level differences – Peak creatinine levels between mechanically ventilated (blue box) and non-ventilated patients (red box), before and after propensity matching.

Fig. 2.

Creatinine level differences – Peak creatinine levels between mechanically ventilated (blue box) and non-ventilated patients (red box), before and after propensity matching.

Close modal

In order to validate the association of MV as an independent predictor for AKI and severe AKI, we used a multivariate regression model (Tables 3, 4). Using our model (Table 3), MV remained an independent predictor for AKI (adjusted OR: 2.92, 95% CI: 1.61–5.12, p < 0.001), alongside the presence of a new heart failure exacerbation, which was also independently associated (AOR: 1.94, 95% CI: 1.06–3.52, p = 0.03). Similarly, MV was found to be independently associated with severe AKI (Table 4, AOR: 3.62, 95% CI: 1.22–11.8, p = 0.03). It is worth mentioning that admission date, as viewed by our 4 groups (see in methods), was not found independently associated with AKI in this multivariate regression.

Table 3.

Multivariate regression model for predicting AKI in the matched cohort

VariableAOR95% CIp value
Mechanical ventilation 2.92 1.61–5.12 <0.001 
Heart failure exacerbation 1.94 1.06–3.52 0.03 
VT/VF 0.74 0.41–1.34 0.32 
Admission perioda 0.83 0.64–1.09 0.18 
Bleedingb 1.47 0.77–2.81 0.25 
VariableAOR95% CIp value
Mechanical ventilation 2.92 1.61–5.12 <0.001 
Heart failure exacerbation 1.94 1.06–3.52 0.03 
VT/VF 0.74 0.41–1.34 0.32 
Admission perioda 0.83 0.64–1.09 0.18 
Bleedingb 1.47 0.77–2.81 0.25 

AOR, adjusted odds ratio; VT, ventricular tachycardia; VF, ventricular fibrillation.

aDivided into groups of three consecutive years.

bIncluding any bleeding that required withholding antiplatelet or anticoagulation therapy.

Table 4.

Multivariate regression model for predicting severe AKI in the matched cohort

VariableAOR95% CIp value
Mechanical ventilation 3.62 1.22–11.8 0.03 
Heart failure exacerbation 0.83 0.28–2.45 0.74 
VT/VF 0.85 0.33–2.18 0.74 
Admission perioda 0.74 0.45–1.20 0.22 
Bleedingb 1.72 0.61–4.86 0.30 
VariableAOR95% CIp value
Mechanical ventilation 3.62 1.22–11.8 0.03 
Heart failure exacerbation 0.83 0.28–2.45 0.74 
VT/VF 0.85 0.33–2.18 0.74 
Admission perioda 0.74 0.45–1.20 0.22 
Bleedingb 1.72 0.61–4.86 0.30 

AOR, adjusted odds ratio; VT, ventricular tachycardia; VF, ventricular fibrillation.

aDivided into groups of three consecutive years.

bIncluding any bleeding that required withholding antiplatelet or anticoagulation therapy.

To our knowledge, this is the first study attempting to evaluate the association of mechanically ventilated STEMI patients and renal injury. In our study, by using PSM and multivariate analysis to account for the many differences between ventilated and non-ventilated patients, we found that MV was independently associated with AKI. In addition, MV patients had similar rates of early or partial renal recovery compared with non-MV patients.

AKI is common in patients admitted to the ICU for various reasons, including sepsis, burns, organ failures, and acute coronary syndrome [3, 21]. Parallel studies investigated the relationships between MV, AKI, and the connection between STEMI and AKI. AKI is far more common in patients admitted for NSTEMI or STEMI than in elective PCI patients [22]. Previous analysis of a large cohort performed by Schmucker et al. [23] aimed to investigate the predictors for AKI in STEMI patients. In their analysis, contrast media exposure was unrelated to renal injury and they hypothesized that hemodynamic changes as a result of extensive infraction or failure of revascularization are responsible for the additive AKI risk in STEMI patients. Later attempts to identify the risk factors for AKI in STEMI patients found that acute heart failure upon admission, as classified by Killip score, was associated with higher rates of AKI [20]. STEMI patients who require early MV are Killip class 3 or above by definition and therefore represent early acute decompensated heart failure and significant impairment of coronary perfusion [24]. Hence, our findings support those above, by showing a strong and independent association between MV and AKI with possible strong emphasis on the initial insult that brought on this need for MV.

Previous studies also showed that there are common pathways which are responsible for renal injury and leading to the reduction of glomerular filtration rate. This reduction is attributed to the baseline characteristics, thrombosis, inflammation, reduced cardiac output, and relative hypoxia in STEMI patients [5, 19, 25]. Our results add an interesting aspect as we matched for baseline variables, extent of coronary disease, time to reperfusion, and inotropes. Yet, MV itself was found to be independently associated with AKI and severe AKI, suggesting other contributing factors associated with ventilation.

While multiple studies described the increased risk for AKI in ventilated patients, the exact mechanism of said risk remains unknown. Earlier works focused on compromised perfusion to the glomeruli as the main mechanism of insult while later studies attributed the injury to a more complex mechanism [26‒28]. In an article by Kuiper et al. [14], three possible mechanisms were proposed-atrial blood gas changes, reduced renal blood flow, and pulmonary-induced inflammatory mediators. Regarding our study group, in which all patients arrived with STEMI, an amount of forward failure can be assumed. Yet, ventilation was independently associated with renal injury even in the presence of STEMI as a marker of extensive cardiac damage. Therefore, our results further emphasis the complex mechanism in which ventilation causing AKI.

It is worth mentioning that the presence of ongoing new heart failure was associated with AKI in our matched cohort with significant value (p = 0.03), although not with severe AKI. Heart failure has a proven association with renal injury, with either of them being a predictor for the other [29]. Still, it seems that in acute setting of intubated STEMI patients, with similar baseline characteristics, the added risk of heart failure does not have a major role in the pathogenesis of AKI, and especially severe AKI.

We hypothesize that there are a number of features in mechanically ventilated STEMI patients that are responsible for the higher occurrence of AKI. As mentioned above, all ventilated patients presented with acute decompensated heart failure causing significant reduction in systemic, and probably renal perfusion. This impairment to renal perfusion is enhanced by MV itself as previously described by Geri et al. [30] who found that high CVP and PEEP are associated with worse renal function in MV patients. MV is also accompanied by higher insensible loss, and together with the preference toward negative water balance in ICU settings, results in additional lowered renal perfusion and higher sensitivity to nephrotoxic drugs or contrast media. Moreover, ventilation itself causes hemodynamic changes, neurohormonal alterations, and systemic inflammation all can contribute to renal injury [14, 31].

Our cohort was gathered over a significant amount of time. As a result, changes in guidelines and practice could have confounded our results. To address this concern, we divided our patients into 4 groups according to their admission date. Although there was some difference in the rates of MV between the groups, this difference was not independently associated with AKI upon multivariate regression. This lack of temporal association enhances our thought that intubation itself poses higher risk for AKI regardless of changing practice as discussed above.

Interestingly, our results showed no significant difference in renal recovery in the matched cohorts (early recovery p = 0.57 or late recovery p = 0.84, Table 2). We attribute this fact to a number of reasons. First, as discussed above, the main initial insult that required intubation was STEMI and acute cardiac failure that most probably caused acute reduction in renal perfusion and tubular damage. Hence, after appropriate treatment, renal recovery should be expected. Second, all included patients were admitted to the intensive coronary care unit where there is a strict monitoring of renal functions, fluid balance, and nephrotoxic drugs. Finally, although exact intubation time was not available at the time of our analysis, the approach in the CICU is of early ventilation withdrawal once feasible, with a median extubation time of 48 h, resulting in a limited exposure time to the possible ventilatory insult.

Our study has several limitations, this was a single-center cohort, as such, the generalizability of our results is limited. In addition, ventilation parameters were determined by CICU protocol yet were not included in the dataset. Although a large meta-analysis found various ventilation parameters such as different tidal volumes or positive end expiratory pressure did not modify the risk for AKI [2], the lack of exact ventilation features limits our ability to learn about their contributing role. In addition, baseline values were determined by admission creatinine and thus may effect AKI definition. Furthermore, AKI was defined per creatinine only as urinary output was not a part of our dataset. Medications used during hospital admission were per protocol of our CICU and were not monitored, although they were the same for the two study groups. Creatinine levels were assessed only during hospitalization and it is possible that MV patients had different long-term renal-related outcomes after this period. Further studies with matched prospective cohorts are needed in order to fully understand the different mechanisms involved in the process of AKI among STEMI patients.

In conclusion, MV was found to be associated with AKI and severe AKI in STEMI patients. However, recovery of renal functions was not affected by the presence of MV. While the exact mechanism of injury remains obscure, a close follow-up of renal functions is needed in MV patients for early interventions and better results.

Study protocol was reviewed and approved by the Institutional Ethics Committee TLV-16-0224. Informed consent was obtained by writing from all participants.

All authors have no conflict of interest to declare.

No funding was received for this study; all authors have nothing to declare.

Shir Frydman: writing – original draft and data curation; Ophir Freund: statistical analysis and writing – original draft; Lior Zornitzky: data curation, formal analysis, and writing – review and editing; Shmuel Banai: methodology and writing – review and editing; Yacov Shacham: conceptualization, methodology, and writing – review and editing.

The data that support the findings of this study are not publicly available due to containing information that could compromise the privacy of research participants but are available from the corresponding author, S.F., upon reasonable request.

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