Effect of Carvedilol Versus Metoprolol on Contrast-Induced Nephropathy in Patients with Acute Coronary Syndrome Undergoing Percutaneous Intervention Therapy

Abstract

Carvedilol can inhibit inflammation, vasoconstriction, and oxidative stress, which play important roles in the development and progression of contrast-induced nephropathy (CIN). To the best of our knowledge, no studies have investigated the potential effect of carvedilol on the prevalence of CIN after percutaneous coronary intervention (PCI) for acute coronary syndrome (ACS). The present study aimed to determine whether carvedilol use is associated with the development of CIN. A total of 319 patients (mean age, 59.2 ± 12.4 years; 77.7% male) with ACS who underwent urgent PCI at our institution between May 2019 and May 2022 were included prospectively. Overall, 100 and 219 patients were assigned to the carvedilol and metoprolol groups, respectively. The prevalence of CIN was significantly lower in the carvedilol group (6.0%) than in the metoprolol group (18.3%; P = .003). Multivariate analysis revealed that carvedilol use (odds ratio [OR] .250, 95% confidence interval [CI] .092-.677, P = .006), amount of contrast agent (OR 1.004, 95% CI 1.000-1.008, P = .031), and admission estimated glomerular filtration rate (OR .978, 95% CI 0.960-.995, P = .014) were independently associated with the development of CIN. The use of carvedilol may be a promising option for the prevention of CIN in patients with ACS undergoing urgent PCI.

Association of red blood cell distribution width and hemoglobin‐to‐RDW ratio with contrast‐associated acute kidney injury in patients undergoing coronary angiography: A retrospective study

“…41,42 The use of carvediol in patients with ACS can reduce the prevalence of CIN after urgent PCI, because carvedilol can inhibit inflammation, vasoconstriction, and oxidative stress. 43 It is well-established that oxidative stress and inflammation are intertwined, promoting each other. 44 Both oxidative stress and inflammation can cause erythrocyte destruction and erythrocyte deformation, which can also be reflected through the change in RDW and HRR levels clinically.…”

“…The proposed possible mechanism of CA‐AKI indicates that the injection of contrast medium can change renal hemodynamics and lead to hypoxia and ischemia in renal vessels, further resulting in the production of a large number of reactive oxygen species and the formation of oxidative stress 41,42 . The use of carvediol in patients with ACS can reduce the prevalence of CIN after urgent PCI, because carvedilol can inhibit inflammation, vasoconstriction, and oxidative stress 43 . It is well‐established that oxidative stress and inflammation are intertwined, promoting each other 44 .…”