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Table of Contents
ORIGINAL ARTICLE
Year : 2019  |  Volume : 9  |  Issue : 1  |  Page : 24-27

Relationship between angiographic outcomes and occurrence of acute kidney injury in st-segment elevation myocardial infarction patients treated by primary percutaneous coronary intervention


Department of Cardiology, Ainshams University, Cairo, Egypt

Date of Web Publication10-May-2019

Correspondence Address:
Dr. Mohamed Zahran
Doctor Mohamed Zahran's Cardiology Clinic, 3 Abdelazeem Awadallah Street, Higaz Square, Heliopolis, 11786 Cairo
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/JICC.JICC_3_19

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  Abstract 


Introduction: Acute kidney injury (AKI) complicates 7%–10% of the cases of critically ill patients; several studies found a similar incidence among ST-segment elevation myocardial infarction (STEMI) patients, especially those complicated by cardiogenic shock. Primary percutaneous coronary intervention (PPCI) is the gold standard treatment for STEMI patients, and using contrast during the procedure is mandatory and inevitably increases the risk of development of AKI. AKI complicating STEMI is associated with poor long-term clinical outcomes with mortality reaching nearly one-third of the affected patients. Patients and Methods: This study included 110 STEMI patients treated by PPCI presented to our Cath lab at Ainshams university hospitals (a 24/7 Tertiary Referral Center for PPCI) during the period between February 2014 and May 2015. The patients with impaired kidney functions, chronic kidney disease, and those on hemodialysis were excluded from the study. Results: AKI was defi ned as an increase of ≥0.3 mg/dL in serum creatinine within 48 h after admission. Eleven patients (10%) developed AKI. The presenting hemodynamics were worse in the patients complicated by AKI (systolic blood pressure 80 ± 35 mmHg vs. 105 ± 60 mmHg, P < 0.001). The pain-to-door time was signifi cantly higher in the patients that developed AKI (156 ± 68 min vs. 114 ± 53, P < 0.001). The volume of contrast was signifi cantly higher in the patients that developed AKI (192 ± 54 ml vs. 128 ± 63 ml, P < 0.001). The patients that developed AKI were signifi cantly more likely to have multivessel affection during their PPCI (5/11 [45.5%] vs. 16/99 [16.2%], P < 0.001), anterior wall location of the infarction (7/11 [63.6%] vs. 40/99 [40.4%], P < 0.001), and no-refl ow phenomenon (5/11 [45.5%] vs. 21/99 [21.2%], P < 0.001). Conclusions: Multivessel affection in PPCI patients, anterior wall location of the infarction and no-reflow phenomenon were significantly associated with occurrence of acute kidney injury in STEMI patients undergoing PPCI.

Keywords: Acute kidney injury, primary percutaneous coronary intervention, ST-segment elevation myocardial infarction


How to cite this article:
Zahran M. Relationship between angiographic outcomes and occurrence of acute kidney injury in st-segment elevation myocardial infarction patients treated by primary percutaneous coronary intervention. J Indian coll cardiol 2019;9:24-7

How to cite this URL:
Zahran M. Relationship between angiographic outcomes and occurrence of acute kidney injury in st-segment elevation myocardial infarction patients treated by primary percutaneous coronary intervention. J Indian coll cardiol [serial online] 2019 [cited 2019 Jul 22];9:24-7. Available from: http://www.joicc.org/text.asp?2019/9/1/24/257958




  Introduction Top


Among primary percutaneous coronary intervention (PPCI) patients treated for ST-segment elevation myocardial infarction (STEMI), worsening of renal function resulting in acute kidney injury (AKI) is not uncommon and is known to be associated with increased morbidity and mortality.[1],[2],[3] Although contrast-induced (CI) nephropathy is considered a major determinant for this complication,[4],[5] other important factors among this specific patient population includes an adverse hemodynamic state resulting in reduced renal perfusion, as well as other metabolic factors.[6],[7] Previous reports have demonstrated that chronic congestive heart failure, especially NYHA class III and IV are at an added risk due to systolic dysfunction and low-stroke volume.[8],[9]


  Methods Top


We performed a prospective, single-center observational study at Ain Shams University Hospital, a Tertiary Referral Hospital with a 24/7 PPCI service offered to all incoming STEMI patients. One hundred and ten consecutive patients admitted from February 2014 to December 2015 from the Emergency Department with the diagnosis of acute STEMI were included in the study. We did not include patients with chronic kidney disease (CKD) or on hemo/peritoneal dialysis. Patient's baseline demographics, cardiovascular history, clinical risk factors, treatment characteristics, and laboratory results were all recorded. 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.[10] The study protocol was approved by the local Institutional Ethics Committee. PPCI was offered to patients presenting with symptoms <12 h in duration and in patients with symptoms lasting 12–24 h in duration if the symptoms persisted at the time of admission. After coronary interventional procedures, isotonic (0.9%) saline solution was given intravenously at a rate of 1 ml/kg/h for 12 h after contrast exposure. In patients with overt heart failure, the hydration rate was reduced on patient by the patient basis. The contrast medium used in procedures was iodixanol (Visipaque; GE healthcare, Ireland) or iohexol (Omnipaque; GE health care, Ireland). The serum creatinine (sCr) level was determined on hospital admission, and once a day during the CCU stay. The estimated glomerular filtration rate (eGFR) was estimated using the abbreviated Modification of Diet in Renal Disease equation.[11] Baseline renal insufficiency was categorized as admission eGFR of 60 ml/min/1.73 m2.[12] AKI was determined using the AKI network criteria[13] and defined as a sCr increase of >0.3 mg/dL compared with admission sCr.

All data were summarized and displayed as mean ± standard deviation 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. A two-tailed P < 0.05 was considered statistically significant for all analyses. All analyses were performed using the SPSS software (SPSS Inc., Chicago, Illinois, USA).


  Results Top


A total of 110 patients with STEMI treated by PPCI were enrolled in the study, 11 (10%) 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 males, presenting with a lower systolic blood pressure at the time of presentation to the ER, with lower admission (eGFR) and higher sCr on admission.
Table 1: Baseline characteristics

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The angiographic parameters of the PPCI procedure are presented in [Table 2]. The Patients who developed AKI had a significantly longer pain-to-door time (156 ± 68 min vs. 114 ± 53, P < 0.001), significantly more likely to have an anterior STEMI (40/99 [40.4% of the patients with no AKI] vs. 7/11 [63.6% of the patients with AKI], P < 0.001), significantly more complex coronary anatomy with multivessel disease affection in (16/99 [16.1% of the patients with no AKI] vs. 5/11 [45.5% of the patients with AKI, P < 0.001]), significantly higher incidence of no reflow phenomenon (21/99 [21.2% of the patients with no AKI] vs. 5/11 [45.5% of the patients with AKI, P < 0.001]), and more contrast volume was used in the PPCI procedures (128 ± 63 mL in the no AKI group vs. 192 ± 54 mL in the AKI, P < 0.001).
Table 2: Angiographic parameters of primary percutaneous coronary intervention

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  Discussion Top


This prospective, single-center, observational study at Ainshams University Hospitals included a cohort of 110 patients presented by STEMI who underwent PPCI for revascularization as per guidelines; we were interested to identify the factors relating the angiographic outcomes with the occurrence of AKI in those patients.

We found that the older age, male gender, and worse hemodynamics on presentation are significant predictors of AKI complicating the STEMI patients treated by PPCI, despite that the patients are presenting to a PPCI tertiary center within a door-to-balloon time matching with the concurrent guidelines.

The acute myocardial insult in STEMI leading to stunning of the myocardium results in an acute reduction of cardiac output, and this early hemodynamic deterioration leads to reduced effective renal blood flow that causes hypoxic changes on the renal cellular level and the production of reactive oxygen species. Moreover, the increased sympathetic tone, renin–angiotensin–aldosterone system activation, associated with the increased production of many humoral factors such as catecholamines, endothelin, vasopressin, proinflammatory cytokines, superadded by the effect of reduced nitric oxide levels can cause vascular, endothelial cell damage, initiating the viscous circle/cascade of events ultimately leading to making the kidney more susceptible to AKI.[14]

More delayed presentation of the patient with a longer pain-to-door time, increased complexity of the procedure with >1 vessel as a culprit in STEMI, anterior location of the STEMI and higher incidence of no-reflow phenomenon all of which translate to more myocardial muscle at Jeopardy were found to be also significant predictors of AKI, this can be explained by their deleterious effects on the myocardial pumping function, the more seriously it is affected, the more is the hemodynamic compromise, and hence, the more reduction in the renal perfusion that initiates the cascade of events leading to the viscous circle of renal hypoperfusion in the context of cardiogenic shock.[15]

The baseline kidney function parameters on presentation were also measured in this study. eGFR on presentation and baseline sCr were found to be significant predictors of AKI developing in STEMI patients treated by PPCI. These findings suggest that preexisting CKD plays an important role in increasing the risk of AKI in patients with STEMI, beyond possible kidney hypoperfusion secondary to acute left ventricular failure, and supporting the implementation of dedicated renal protection protocols in patients known to have chronic renal failure.[16]

Contrast volume is still considered the major reason for AKI development in patients with STEMI after PCI. CI-AKI is a prevalent and deleterious complication of coronary angiography and reported to be the third most common cause of hospital-acquired renal failure.[16] We found that the volume of contrast used in the patients that developed AKI was significantly higher than those who did not develop AKI, as mentioned previously, those patients were presented by more complex clinical and angiographic presentations with longer door-to-balloon times, and probably longer procedures with more steps and more coronary injections to reach a TIMI three flow in the culprit vessel.

There are several important limitations of this study. This was a single-center, prospective, and nonrandomized observational study and may have been subject to bias, although we included consecutive patients. The true incidence of AKI described in this study may have been underestimated because the definition of AKI network criteria refers to sCr change within a time frame of 48 h.[13] The change in sCr can lag beyond this period because of delayed effects of contrast material and drugs, worsening of renal function might have occurred after hospital discharge in some patients, and this has not been recorded in this study.


  Conclusion Top


Multivessel affection in PPCI patients, anterior wall location of the infarction and no-reflow phenomenon were significantly associated with occurrence of acute kidney injury in STEMI patients undergoing PPCI.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Goldberg A, Hammerman H, Petcherski S, Zdorovyak A, Yalonetsky S, Kapeliovich M, et al. Inhospital and 1-year mortality of patients who develop worsening renal function following acute ST-elevation myocardial infarction. Am Heart J 2005;150:330-7.  Back to cited text no. 1
    
2.
Parikh CR, Coca SG, Wang Y, Masoudi FA, Krumholz HM. Long-term prognosis of acute kidney injury after acute myocardial infarction. Arch Intern Med 2008;168:987-95.  Back to cited text no. 2
    
3.
Amin AP, Spertus JA, Reid KJ, Lan X, Buchanan DM, Decker C, et al. The prognostic importance of worsening renal function during an acute myocardial infarction on long-term mortality. Am Heart J 2010;160:1065-71.  Back to cited text no. 3
    
4.
James MT, Samuel SM, Manning MA, Tonelli M, Ghali WA, Faris P, et al. Contrast-induced acute kidney injury and risk of adverse clinical outcomes after coronary angiography: A systematic review and meta-analysis. Circ Cardiovasc Interv 2013;6:37-43.  Back to cited text no. 4
    
5.
Seeliger E, Sendeski M, Rihal CS, Persson PB. Contrast-induced kidney injury: Mechanisms, risk factors, and prevention. Eur Heart J 2012;33:2007-15.  Back to cited text no. 5
    
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Ebina T, Kosuge M, Kimura K. Acute kidney injury and acute myocardial infarction. Circ J 2014;78:1329-30.  Back to cited text no. 6
    
7.
Marenzi G, Assanelli E, Campodonico J, Lauri G, Marana I, De Metrio M, et al. Contrast volume during primary percutaneous coronary intervention and subsequent contrast-induced nephropathy and mortality. Ann Intern Med 2009;150:170-7.  Back to cited text no. 7
    
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Rosenstock JL, Gilles E, Geller AB, Panagopoulos G, Mathew S, Malieckal D, et al. Impact of heart failure on the incidence of contrast-induced nephropathy in patients with chronic kidney disease. Int Urol Nephrol 2010;42:1049-54.  Back to cited text no. 8
    
9.
Nikolsky E, Mehran R, Turcot D, Aymong ED, Mintz GS, Lasic Z, et al. Impact of chronic kidney disease on prognosis of patients with diabetes mellitus treated with percutaneous coronary intervention. Am J Cardiol 2004;94:300-5.  Back to cited text no. 9
    
10.
Ibanez B, James S, Agewall S, Antunes MJ, Bucciarelli-Ducci C, Bueno H, et al. 2017 ESC guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation: The task force for the management of acute myocardial infarction in patients presenting with ST-segment elevation of the European Society of Cardiology (ESC). Eur Heart J 2018;39:119-77.  Back to cited text no. 10
    
11.
Levey AS, Bosch JP, Lewis JB, Greene T, Rogers N, Roth D, et al. A more accurate method to estimate glomerular filtration rate from serum creatinine: A new prediction equation. Modification of diet in renal disease study group. Ann Intern Med 1999;130:461-70.  Back to cited text no. 11
    
12.
National Kidney Foundation. K/DOQI clinical practice guidelines for chronic kidney disease: Evaluation, classification, and stratification. Am J Kidney Dis 2002;39:S1-266.  Back to cited text no. 12
    
13.
Levin A, Warnock DG, Mehta RL, Kellum JA, Shah SV, Molitoris BA, et al. Improving outcomes from acute kidney injury: Report of an initiative. Am J Kidney Dis 2007;50:1-4.  Back to cited text no. 13
    
14.
Mehran R, Aymong ED, Nikolsky E, Lasic Z, Iakovou I, Fahy M, et al. A simple risk score for prediction of contrast-induced nephropathy after percutaneous coronary intervention: Development and initial validation. J Am Coll Cardiol 2004;44:1393-9.  Back to cited text no. 14
    
15.
Shacham Y, Leshem-Rubinow E, Gal-Oz A, Arbel Y, Keren G, Roth A, et al. Relation of time to coronary reperfusion and the development of acute kidney injury after ST-segment elevation myocardial infarction. Am J Cardiol 2014;114:1131-5.  Back to cited text no. 15
    
16.
Tumlin J, Stacul F, Adam A, Becker CR, Davidson C, Lameire N, et al. Pathophysiology of contrast-induced nephropathy. Am J Cardiol 2006;98:14K-20K.  Back to cited text no. 16
    



 
 
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