Serum complement C1q level is associated with left ventricular hypertrophy induced by coarctation of the aorta: A

Li Chen1, Hong-Zhou Duan2, Chen Zhang1

  • 1Department of Pediatric Cardiology, Beijing Anzhen Hospital, Capital Medical University, Beijing, China.

Insights

Serum complement C1q levels are lower in children with coarctation of the aorta (CoA), suggesting an inhibitory role in left ventricular hypertrophy. C1q may offer protection against myocardial injury during cardiac surgery.

Area of Science:

  • Cardiovascular Science
  • Immunology
  • Pediatric Cardiology

Background:

  • The complement system is implicated in left ventricular hypertrophy (LVH).
  • Complement C1q, a key component of the classical complement pathway, is linked to inflammatory conditions.
  • The relationship between serum C1q and LVH in coarctation of the aorta (CoA) requires investigation.

Purpose of the Study:

  • To investigate the association between serum complement C1q levels and LVH in pediatric patients with CoA.
  • To compare C1q levels in patients with simple CoA, complex CoA, and healthy controls.

Main Methods:

  • Serum C1q levels were measured using immune transmission turbidity.
  • Patients were categorized into simple CoA, complex CoA (with VSD or PDA), large VSD, and normal control groups.
  • Correlations between C1q levels, cardiac structure, and surgical parameters were analyzed.

Main Results:

  • Preoperative C1q levels were significantly lower in simple CoA patients compared to complex CoA and normal groups.
  • A negative correlation was observed between preoperative C1q and interventricular septal thickness and left ventricular posterior wall thickness.
  • Postoperative C1q decrease correlated positively with cardiopulmonary bypass and aortic cross-clamp times in CoA patients.

Conclusions:

  • Complement C1q appears to inhibit the development of LVH in CoA, potentially independent of lipid metabolism.
  • C1q may exert a protective effect against myocardial injury during cardiac surgery for CoA.
Abstract

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