Arterial injury mechanism of homocysteine after PCI in patients with premature coronary heart disease

Background: One cause of mortality among young people in modern societies is coronary heart disease (CHD). Numerous studies have demonstrated an association between major adverse cardiac events (MACEs) and percutaneous coronary intervention (PCI) in patients with premature CHD, but the risk factors for MACEs after PCI are poorly understood. This study investigated the risk factors for premature CHD after PCI and compared the long-term prognosis of patients with premature CHD with or without MACEs after PCI. Homocysteine was found to be an independent risk factor for patients with early CHD. Previous animal studies have demonstrated that atorvastatin inhibits homocysteine-induced inflammation and that atorvastatin has preventive and therapeutic effects in patients with early CHD.Methods: A total of 1408 patients who underwent PCI were enrolled and divided into a MACE group and a non-MACE group according to the recurrence of cardiovascular events. Basic information and follow-up data of the patients were recorded, and risk factors affecting prognosis were analysed. Western blotting and reverse transcription polymerase chain reaction were used to identify that atorvastatin inhibited the expression of NF-κB, IL-1β, IL-6, and CRP inflammatory factors induced by homocysteine, thereby inhibiting the occurrence and development of atherosclerosis.Results: Univariate Cox proportional risk models showed that the homocysteine level is a risk factor for recurrent MACEs. Multivariate Cox regression analysis also suggested that homocysteine is an independent risk factor for MACEs. The receiver operating characteristic curve showed that Hcy was a strong factor for predicting the occurrence of MACEs in patients with premature CHD. Atorvastatin was found to inhibit the expression of NF-κB, IL-1β, IL-6, and CRP inflammatory factors induced by homocysteine and delay the occurrence of reactive oxygen species.Conclusions: Homocysteine is an independent risk factor for MACEs in patients with premature CHD after PCI. Atorvastatin can effectively antagonize the expression of NF-κB, IL-1β, IL-6, CRP and other inflammatory factors induced by homocysteine.