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Impaired endothelium-dependent vascular reactivity in patients with familial combined hyperlipidaemia
  1. M De Michele1,
  2. A Iannuzzi2,
  3. A Salvato3,
  4. P Pauciullo3,
  5. M Gentile3,
  6. G Iannuzzo3,
  7. S Panico3,
  8. A Pujia4,
  9. G M Bond5,
  10. P Rubba3
  1. 1Division of Cardiology, Moscati Hospital, Aversa, Italy
  2. 2Division of Internal Medicine, Cardarelli Hospital, Naples, Italy
  3. 3Department of Clinical and Experimental Medicine, Federico II University, Naples, Italy
  4. 4Department of Clinical and Experimental Medicine “G Salvatore”, University of Catanzaro Magna Graecia, Catanzaro, Italy
  5. 5Division of Vascular Ultrasound Research, Wake Forest University, Winston Salem, North Carolina, USA
  1. Correspondence to:
    P Rubba
    Department of Clinical and Experimental Medicine, Federico II University, Via Pansini 5, Naples 80145, Italy; rubba{at}unina.it

Abstract

Background: Familial combined hyperlipidaemia (FCHL) is associated with a markedly increased risk of premature coronary artery disease. This study was designed to evaluate whether preclinical atherosclerotic functional abnormalities are detectable in the arteries of patients with FCHL.

Methods: 60 subjects were recruited for the study: 30 probands of families with FCHL (mean (standard deviation (SD)) age 48 (10) years, 77% men), defined by fasting total plasma cholesterol or triglyceride concentration >250 mg/dl (>6.5 mmol/l cholesterol, >2.8 mmol/l triglyceride) and by the occurrence of multiple lipoprotein phenotypes within a family, and 30 age-matched and sex-matched healthy controls. All subjects underwent high-resolution B-mode ultrasound examination and the brachial arterial reactivity, a marker of endothelial function, was measured by a semiautomated computerised program. Lipid profile, resting blood pressure, body mass index (BMI), smoking status, insulin and homocysteine levels were also determined.

Results: Compared with controls, patients with FCHL had significantly higher BMI, diastolic blood pressure and insulin levels. No difference was observed in baseline brachial diameter between the two groups (mean (SD) 3.45 (0.51) mm for FCHL v 3.60 (0.63) mm for controls; p = 0.17). In response to flow increase, the arteries of the controls dilated (mean (SD) 8.9% (4.9%), range 2.3–20.8%), whereas in the patients with FCHL, brachial arterial reactivity was significantly impaired (5.5% (2.5%), range 0–10.1%; p = 0.002). In multivariate linear regression analysis, apolipoprotein B and BMI were independent determinants of brachial artery response to reactive hyperaemia.

Conclusions: The findings of our study suggest that vascular reactivity is impaired in the arteries of patients with FCHL.

  • apo, apolipoprotein
  • BMI, body mass index
  • FCHL, familial combined hyperlipidaemia
  • LDL, low-density lipoprotein

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Footnotes

  • Published Online First 3 July 2006

  • This study was supported by funds from MIUR 2001—no 068937 and 2004—no 065985.

  • Competing interests: None declared.

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