Key result
High day 7 CDC42 levels predict ~85% lower TLF risk after DCB in small-vessel CAD.
Why the study?
Cell division control 42 regulates atherosclerosis, lipids, and inflammation, but its utility in drug-coated balloon-treated small-vessel coronary artery disease patients is unclear.
Does circulating CDC42 level predict target lesion failure and major adverse cardiovascular events in patients with small-vessel coronary artery disease undergoing drug-coated balloon treatment?
Observational (n=261)
None
No
Does circulating CDC42 level predict target lesion failure and major adverse cardiovascular events in patients with small-vessel coronary artery disease undergoing drug-coated balloon treatment?
Higher circulating CDC42 levels at day 7 post-procedure independently predict lower risks of target lesion failure and MACE in patients with small-vessel CAD treated with drug-coated balloons.
Answers are grounded in this paper and cite their sources.
May aid post-DCB risk stratification in small-vessel CAD; hypothesis-generating and requires prospective validation before clinical use.
BACKGROUND: Cell division control 42 (CDC42) regulates atherosclerosis, blood lipids, and inflammation and thus affects coronary artery disease (CAD), but its utility in drug-coated balloon (DCB)-treated small-vessel CAD (SV-CAD) patients is unclear. This study intended to evaluate the change and prognostic role of CDC42 in SV-CAD patients underwent DCB. METHODS: Serum CDC42 was measured by enzyme-linked immunosorbent assay in 211 SV-CAD patients underwent DCB at baseline, day (D) 1, D3, and D7, as well as in 50 healthy controls (HCs). RESULTS: CDC42 was decreased in SV-CAD patients compared to HCs (P < 0.001), and it was negatively associated with total cholesterol (P = 0.015), low-density lipoprotein cholesterol (P = 0.003), C-reactive protein (P = 0.001), multivessel disease (P = 0.020), and American college of cardiology/American heart association type B2/C lesions (P = 0.039) in SV-CAD patients. Longitudinally, CDC42 decreased from baseline to D1 and then gradually increased to D7 (P < 0.001) in SV-CAD patients after DCB. Interestingly, high CDC42 (cut-off value = 500 pg/mL) at baseline (P = 0.047), D3 (P = 0.046), and D7 (P = 0.008) was associated with a lower accumulating target lesion failure (TLF) rate; high CDC42 at D3 (P = 0.037) and D7 (P = 0.041) was related to a lower accumulating major adverse cardiovascular event (MACE) rate in SV-CAD patients underwent DCB. Importantly, CDC42 at D7 (high vs. low) independently predicted lower accumulating TLF (hazard ratio (HR) = 0.145, P = 0.021) and MACE (HR = 0.295, P = 0.023) risks in SV-CAD patients underwent DCB. CONCLUSIONS: Circulating CDC42 level relates to milder disease conditions and independently estimates lower risks of TLF and MACE in SV-CAD patients underwent DCB, but further validation is still needed.
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Wu et al. (2023) conducted an observational in Small-vessel coronary artery disease (SV-CAD) (n=261). High circulating cell division control 42 (CDC42) level at day 7 vs. Low CDC42 level at day 7 was evaluated on Target lesion failure (TLF) (HR 0.145, 95% CI 0.028-0.744, p=0.021). High circulating CDC42 levels at day 7 independently predicted a lower risk of target lesion failure (HR 0.145) and major adverse cardiovascular events (HR 0.295) in patients with small-vessel coronary artery disease undergoing drug-coated balloon treatment.
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