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Angiotensin converting enzyme in patients with sleep apnoea syndrome: plasma activity and gene polymorphisms

¹ International University of Health and Welfare, Sanno Hospital, Akasaka, Minato-ku, ² Dept of Pulmonary Medicine, Yokohama City University Medical Centre, and ³ Dept of Psychiatry, Juntendo University School of Medicine, Tokyo, Japan

To the Editor:

In a recent issue of the European Respiratory Journal, Barcelo et al. 1 reported results on the plasma angiotensin converting enzyme (ACE) activity and the distribution of an insertion (I)/deletion (D) polymorphism of the ACE gene both in obstructive sleep apnoea syndrome (OSAS) patients and in healthy controls. They found that ACE activity was higher in OSAS patients (53.9±2.5 international units (IU)·L^–1) than in healthy controls (42.4±3.1 IU·L^–1, p<0.01). However, the frequency distribution of the DD, II and ID genotypes in OSAS patients (30%, 16%, 54%, respectively) was not significantly different from that seen in healthy subjects (31%, 28%, 41%, respectively, p=0.356). They speculated that the increased ACE plasma activity contributed to the pathogenesis of the cardiovascular disease in these patients. The authors also described that "this is the first study investigating ACE in patients with OSAS". This is true, but the current study was not the first study examining the association of ACE gene polymorphism with OSAS.

Xiao et al. 2 firstly reported that the distribution of the DD, ID, and II ACE genotypes was 16%, 52%, and 32% in the control subjects and 0%, 56%, and 44% in OSAS patients, respectively. Although they did not measure ACE activity in the patients, they suggested that the II genotype and I allele might be a risk factor for OSAS in Chinese subjects. Following the first study, other investigators have examined the association of ACE gene polymorphism with OSAS using a larger sample of Chinese subjects 3. The frequency of I allele and II genotype were significantly higher in the moderate to severe OSAS group than in the other groups. Further, the higher frequency of ACE gene I allele and II genotype was closely associated with the hypertensive patients with OSAS. They indicated that the inherited factors including ACE II genotype played an important role in the pathogenesis of hypertensive patients with OSAS.

However, it has been suggested that ACE DD genotype is associated with heart weight and hypertension in Japanese and Caucasian subjects 4, 5. Further comparative studies concerning the association of ACE gene polymorphism with cardiovascular complications of OSAS between Asians and Caucasians are needed.

Because cardiovascular disorders are known to increase among patients with OSAS 6–8, the genetic susceptibility to hypertension and cardiac hypertrophy may exist in a population with OSAS. As the predictors of cardiovascular complications in patients with OSAS are not yet conclusively determined, another screening strategy is necessary to determine the high-risk group for cardiovascular disorders among OSAS patients. The risk of future cardiovascular diseases may be associated with the genetic susceptibility to cardiovascular disorders in OSAS patients. Thus, it is important to know whether the genetic background of OSAS patients with or without cardiovascular diseases exists. It has recently been reported that a significant portion of sleep-disordered breathing is associated with apolipoprotein (Apo)E epsilon4 in the general population 9. Because sleep-disordered breathing occurs in Alzheimer-disease patients and increases the risk for cardiovascular disease, complex interactions among sleep, brain pathology, and cardiovascular disease may occur in ApoE epsilon4 carriers. However, the other candidate gene polymorphisms associated with OSAS and OSAS related cardiovascular diseases are not extensively examined.

Because ethnic differences in the prevalence of obstructive sleep apnoea syndrome exist, further confirmation of the candidate gene polymorphisms and the association with obstructive sleep apnoea syndrome is needed, in both Caucasians and Asians using a large sample size 10.

References

1. Barcelo A, Elorza MA, Barbe F, Santos C, Mayoralas LR, Agusti AG. Angiotensin converting enzyme in patients with sleep apnoea syndrome: plasma activity and gene polymorphisms. Eur Respir J 2001;17:728–732.[Abstract/Free Full Text]
2. Xiao Y, Huang X, Qiu C. Angiotension I converting enzyme gene polymorphism in Chinese patients with obstructive sleep apnea syndrome. Zhonghua Jie He He Hu Xi Za Zhi 1998;21:489–491.[Medline] [Order article via Infotrieve]
3. Zhang J, Zhao B, Gesongluobu SY, et al. Angiotensin-converting enzyme gene insertion/deletion (I/D) polymorphism in hypertensive patients with different degrees of obstructive sleep apnea. Hypertens Res 2000;;23:407–411.[Medline] [Order article via Infotrieve]
4. Nakahara K, Matsushita S, Matsuoka H, et al. Insertion/deletion polymorphism in the Angiotensin-Converting enzyme gene affects heart weight. Circulation 2000;101:148–151.[Abstract/Free Full Text]
5. Hamon M, Amant C, Bauters C, et al. Association of angiotensin converting enzyme and angiotensin II type I receptor genotypes with left ventricular function and mass in patients with angigraphically normal coronary arteries. Heart 1997;77:502–505.[Abstract/Free Full Text]
6. Teramoto S, Kume H, Matsuse T, Fukuchi Y. The risk of future cardiovascular diseases in the patients with OSAS is dependently or independently associated with obstructive sleep apnoea. Eur Respir J 2001;17:573–574.[Free Full Text]
7. Teramoto S, Ohga E, Ouchi Y. Obstructive sleep apnoea. Lancet 2000;355:1213–1214.
8. Barcelo A, Elorza MA, Barbe F, Vila M, Pons S, Agusti AG. Abnormal lipid peroxidation in patients with sleep apnoea. Eur Respir J 2001;16:644–647.
9. Kadotani H, Kadotani T, Young T, et al. Association between apolipoprotein E epsilon4 and sleep-disordered breathing in adults. JAMA 2001;285:2888–2890.[Abstract/Free Full Text]
10. Teramoto S, Ishii T. No association of tumor necrosis factor-alpha gene polymorphism and COPD in Caucasian smokers and Japanese smokers. Chest 2001;;119:315–316.[Free Full Text]

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