ABSTRACT
Patients with chronic kidney disease (CKD) suffer disproportionately from a high burden of cardiovascular disease, which, despite recent scientific advances, remains partly understood. Vascular calcification (VC) is the result of an ongoing process of misplaced calcium in the inner and medial layers of the arteries, which has emerged as a critical contributor to cardiovascular events in CKD. Beyond its established role in blood clotting and bone health, vitamin K appears crucial in regulating VC via vitamin K-dependent proteins (VKDPs). Among these, the matrix Gla protein (MGP) serves as both a potent inhibitor of VC and a valuable biomarker (in its inactive form) for reflecting circulating vitamin K levels. CKD patients, especially in advanced stages, often present with vitamin K deficiency due to dietary restrictions, medications, and impaired intestinal absorption in the uremic environment. Epidemiological studies confirm a strong association between vitamin K levels, inactive MGP, and increased CVD risk across CKD stages. Based on the promising results of pre-clinical data, an increasing number of clinical trials have investigated the potential benefits of vitamin K supplementation to prevent, delay, or even reverse VC, but the results have remained inconsistent.
Subject(s)
Extracellular Matrix Proteins , Matrix Gla Protein , Renal Insufficiency, Chronic , Vascular Calcification , Vitamin K Deficiency , Vitamin K , Humans , Vascular Calcification/etiology , Renal Insufficiency, Chronic/complications , Vitamin K Deficiency/complications , Extracellular Matrix Proteins/blood , Extracellular Matrix Proteins/metabolism , Calcium-Binding Proteins/blood , Dietary Supplements , Cardiovascular Diseases/etiology , Cardiovascular Diseases/prevention & control , Biomarkers/bloodABSTRACT
BACKGROUND: In patients treated with bare metal stents and first-generation drug-eluting stents (DES) smaller stent diameter (SD) has been associated with worse long term outcomes after percutaneous coronary intervention (PCI). Data on the impact of small SD on outcomes after PCI with second-generation DES is scarce. METHODS: Consecutive patients treated with second-generation DES between 2010 and 2016 were included in a single tertiary center. Patients were grouped according to SD: ≤2.50 mm, 2.75 ≤ 3.00 mm, 3.25 ≤ 3.50 mm, and >3.50 mm. One-year event rates were estimated using the Kaplan-Meier method and adjusted hazard ratios were generated using Cox regression analysis. The primary endpoint was major adverse cardiac events (MACE; death, myocardial infarction [MI], or target vessel revascularization [TVR]). RESULTS: Of the 17,607 patients who underwent PCI with second-generation DES, 32.6% (n = 5,741) had SD ≤2.5 mm, 39.1% (n = 6,890) had SD 2.75 ≤ 3.0 mm, 22.2% (n = 3,910) had SD 3.25 ≤ 3.5 mm, and 6.1% (n = 1,066) had SD >3.5 mm. At 1 year, MACE rates were 10.5%, 9.5%, 8.0%, and 8.0%, respectively, with increasing SD (p = .006). TVR rates decreased with increasing SD (7.2%, 5.8%, 4.7%, and 3.3%, respectively [p < .0001]) whereas rates of MI across SD groups were comparable (1.7%, 1.9%, 2.0%, and 1.5%, respectively [p = .60]). After multivariable adjustment, smaller SD remained associated with higher rates of MACE, TVR, and target lesion revascularization. CONCLUSION: In a large cohort of patients undergoing PCI with second-generation DES, smaller SD was associated with increased MACE, driven by higher rates of repeat revascularization. Further research into the optimal treatment of small coronary arteries is warranted.
