Protective Efficacy of Phentolamine in Patients at High Risk of Contrast-Associated Acute Kidney Injury After Complex Percutaneous Coronary Intervention

Coronary angiography is accepted as the gold standard diagnostic procedure in the management of coronary artery disease (CAD). It involves the visualization of the coronary arteries using contrast dye and dynamic X-ray imaging and allows for the identification of suitable lesions for percutaneous coronary intervention (PCI). PCI has more importance when performed as an emergency procedure during acute coronary syndromes (ACS) providing immediate relief of symptoms, preventing myocardial damage and reducing mortality rates despite its potential complications. These complications varies in its incidence including arrhythmias, coronary dissection, bleeding at the access site, allergy to contrast agent and kidney injury with varying risk on patient condition.

Contrast-associate acute kidney injury (CA-AKI), formerly termed contrast-induced nephropathy (CIN), is a significant complication of PCI and the third most common cause of renal failure in hospitalized patients. It is defined as a rise in creatinine of ≥ 50% of baseline or 0.3 mg/dL from the pre-contrast value within 48-72 hours of intravascular administration of a contrast medium, which is usually reversible acute kidney injury. The development of CA-AKI despite successful percutaneous coronary procedures is associated with prolonged hospitalization, an increase in health expenditure, and increased short and long-term mortality for most patients. Therefore, early risk prediction and management is crucial.

Over the past few decades, a number of risk scores have been introduced to predict contrast-associated acute kidney injury after PCI. The most commonly used is Mehran score that was introduced in 2004 for its simplicity and availability but it excluded patients with acute myocardial infarction. However, it recently updated with larger population and more emphasis on patient's ACS presentation and procedural features and reintroduced in 2021 as Mehran 2 CA-AKI Risk Score.

Exact pathophysiological mechanism of CA-AKI is not known and includes complex cascades of events. The most important elements of pathophysiological mechanism of CA-AKI seem to be the medullary hypoxia due to contrast-induced medullary vasoconstriction and direct renal tubular cytotoxicity, in addition to oxidative stress and the increase in blood and renal tubular viscosity which are complementary events that further exacerbates CA-AKI.

Several clinical interventions aimed to reduce the incidence of CA-AKI targeting various aspects of the pathophysiology including volume expansion with intravenous fluid, administration of N-acetylcysteine, sodium bicarbonate, vitamin E, statins and vasodilator agents with different protective efficacy but only few of them had been approved for clinical practice.