The increase in pulse pressure (PP) may be transmitted to the glomerulus and thus impair renal blood flow autoregulation. This subtle change could predispose patients to the detrimental effect of contrast media. We sought to determine whether elevated central PP is associated with increased contrast-induced nephropathy (CIN) and future cardiovascular events in patients undergoing percutaneous coronary intervention (PCI).
In total, 448 consecutive patients receiving PCI were enrolled. In each patient, central and peripheral blood pressures were measured before PCI. The occurrence of CIN was identified and defined as a rise in serum creatinine of 0.5 mg/dl or a 25% increase from the baseline value within 48 h after the procedure. All patients were then followed up for at least 3 years or until the occurrence of a major adverse cardiovascular event (MACE) including death, nonfatal myocardial infarction, and ischemic stroke after coronary intervention.
Overall, CIN occurred in 52 (11.6%) patients. Patients developing CIN had higher baseline central PP (P = 0.004). Patients were then stratified into three groups (low/intermediate/high) according to baseline central PP. Compared to that with the lowest tertile of central PP, patients with the highest tertile of central PP had a significantly increased incidence of CIN after PCI (odds ratio, 2.94; 95% confidence interval, CI 1.02–8.51). By Cox regression analysis, elevated central PP was an independent predictor of future MACE in all patients undergoing PCI (hazard ratio, 2.07; 95% CI 1.04–4.12).
Elevated baseline central PP was associated with an increased risk of CIN and future cardiovascular events in patients with PCI. Further clinical study may be indicated to determine whether pharmacological modulation on baseline central PP could prevent CIN and future MACE after PCI.