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Volume 122, Issue 1, Pages 56-60 (31 October 2007)


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Relationship of thyroid stimulating hormone with coronary atherosclerosis in angina patients

Kyeong Ho Yuna, Myung Ho JeongbCorresponding Author Informationemail address, Seok Kyu Oha, Eun Mi Leea, Je Leea, Sang Jae Rheea, Nam Jin Yooa, Nam-Ho Kima, Young Keun Ahnb, Jin-Won Jeonga

Received 11 August 2006; received in revised form 22 October 2006; accepted 2 November 2006. published online 15 January 2007.

Abstract 

Background

In the previous recent reports, subclinical hypothyroidism is an independent risk factor for acute myocardial infarction in elderly women. It was not established whether a normal range of thyroid stimulating hormone (TSH) influences the presence of coronary atherosclerosis. We postulated that the level of TSH is risk factor of coronary atherosclerosis in angina patients who have normal thyroid function.

Methods

We studied 344 angina patients (62.5±9.72 years, male 50%) who underwent elective coronary angiography. TSH, free thyroxine, serum lipid levels and high-sensitivity C-reactive protein levels were measured and compared to the severity of coronary artery disease.

Results

In patients with high level of TSH (≥2.1 μIU/mL), age (p=0.016), the levels of serum creatinine (p=0.004) and Gensini's score (p=0.016) were significantly higher than those in patients with low TSH levels. The incidence of multi-vessel disease was higher in patients with high TSH level (p=0.026). TSH level showed a significant correlation with age (r=0.109, p=0.044) and Gensini's score (r=0.117, p=0.045). The multivariate analysis revealed that age (OR 2.39, p=0.001), diabetes (OR 3.74, p=0.001), creatinine (OR 2.06, p=0.008), and smoking (OR 1.85, p=0.045) were independent predictors for significant coronary artery disease, but TSH level did not predict coronary artery stenosis.

Conclusions

Although the high level of serum TSH is associated with multi-vessel disease, it was not the determinant of coronary artery disease in patients with normal range of thyroid function.

a Department of Cardiovascular Medicine, Wonkwang University Hospital, Iksan, South Korea

b Department of Cardiovascular Medicine, Chonnam National University Hospital, Gwangju, South Korea

Corresponding Author InformationCorresponding author. The Heart Center of Chonnam National University Hospital, Hakdong 8, Dongku, Gwangju, South Korea 501–757. Tel.: +82 62 220 6243; fax: +82 62 228 7174.

PII: S0167-5273(06)01447-1

doi:10.1016/j.ijcard.2006.11.039


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