Left ventricular end diastolic pressure and contrast-induced acute kidney injury in patients with acute coronary syndrome undergoing percutaneous coronary intervention.Cardiovasc Revasc Med. 2018 09; 19(6S):16-20.CR
Left ventricular end-diastolic pressure (LVEDP) reflects ventricular performance and volume status. We sought to analyze the relationship between LVEDP and the incidence of contrast-induced acute kidney injury (AKI) in patients with acute coronary syndrome undergoing percutaneous coronary intervention (PCI).
Between January 2006 and December 2008, a total of 254 patients presenting with an acute coronary syndrome had the LVEDP assessed prior to the intervention. Contrast-induced AKI was defined as an increase in serum creatinine ≥25% from baseline or an absolute increase of >0.5 mg/dL from baseline. Patients were divided into three groups according to baseline LVEDP (<12 mmHg, 12-20 mmHg and > 20 mmHg). Baseline clinical, angiographic and procedural characteristics, as well as serum creatinine and estimated glomerular filtration rate (eGFR) at baseline and at 24, 48 and 72 h were retrospectively collected.
Baseline clinical characteristics were similar in all three groups with the exception of lower left ventricular ejection fraction in patients with elevated LVEDP (p = 0.02). Among the 17 patients with an LVEDP < 12 mmHg, only one (5.9%) developed AKI; among the 82 patients with an LVEDP = 12-20 mmHg, 15 (18.3%) developed AKI; and among the 155 patients with an LVEDP > 20 mmHg, only 22 developed AKI (13.6%). There was no correlation between LVEDP and the change in GFR at 24 h and at 48 h. Further comparison between the group of patients that developed contrast induced AKI versus those that did not, showed a that there was a significantly lower baseline left ventricular ejection fraction (LVEF) among patients that developed contrast induced AKI compared to those that did not (41.4% vs. 48.3%, p = 0.045, respectively).
In patients with acute coronary syndrome undergoing PCI, baseline LVEDP was not associated with contrast-induced AKI. However patients with reduced ejection fraction seemed to be at a higher risk of developing AKI. More studies are needed to assess the relationship between LVEDP, LVEF and the risk of developing contrast induced AKI.