王文君 程秋實
[摘 要] 目的:分析甲狀腺功能亢進并發甲亢性心臟病的危險因素,總結防治對策。方法:80例甲亢性心臟病患者作為A組,65例單純甲狀腺功能亢進患者作為B組。比較兩組患者年齡、性別、病程、個人史、實驗室檢查結果等臨床資料,運用Logistic多因素回歸分析,總結影響甲狀腺功能亢進并發甲亢性心臟病的危險因素,探討高危患者判別依據及干預策略。結果:年齡≥60歲、病程≥6個月、FT4≥35 pmol/L是影響甲亢并發甲亢性心臟病的獨立危險因素(P<0.05)。結論:應重視高齡、病程較長及高水平血清FT4者甲亢病情的控制。
[關鍵詞] 甲狀腺功能亢進;甲亢性心臟病;危險因素
中圖分類號:R581 文獻標識碼:A 文章編號:2095-5200(2017)05-043-03
DOI:10.11876/mimt201705018
Analysis of risk factors of hyperthyroid heart disease complicated with hyperthyroidism WANG Wenjun, CHENG Qiushi. (Department of Endocrinology,Qingdao Municipal Hospital, Qingdao 266000, china)
[Abstract] Objective: The objective of this study was to analyze the risk factors of hyperthyroid heart disease complicated with hyperthyroidism and to summarize countermeasures of prevention and cure. Methods: A total sample of 145 patients were selected as objects of study including 80 patients with hyperthyroid heart disease as A group and 65 patients with simple hyperthyroidism as group B. The clinical data were compared between the two groups in age, gender, disease duration, personal history and laboratory examination results, and Logistic multivariate regression analysis was used, in order to summarize the risk factors of hyperthyroid heart disease complicated with hyperthyroidism and to explore the distinguish basis and intervention strategy of high-risk patients. Results: Age≥60, disease duration≥6 months and FT4≥35 pmol/L were independent risk factors of hyperthyroid heart disease complicated with hyperthyroidism (P<0.05). Conclusions: Attention should be paid to the control of hyperthyroidism patients with advanced age, longer course and high levels of serum FT4.
[Key words] hyperthyroidism; hyperthyroid heart disease; risk factors
甲亢患者常伴有心率加快、心肌收縮力增強、全血容量容量增加、外周血管阻力降低等病理生理改變[1],心血管系統處于高動力狀態,加之過量甲狀腺激素對心臟的直接毒性作用,均導致甲亢患者心臟疾病發生風險較高[2]。甲亢性心臟病約占甲亢患者的10%~20%,患者往往病程較長、年齡較大[3]。因此,在注重甲亢性心臟病早期診斷的前提下,進一步明確甲亢性心臟病的危險因素、預防甲亢向甲亢性心臟病進展,對于改善患者預后及生存質量均具有重要意義。為此,本研究選取145例患者進行了對照分析,現予報道。
1 對象與方法
我院2015年1月至2017年1月就診患者中發生甲亢性心臟病的80例患者作為A組,同期65例單純甲狀腺功能亢進[4]患者作為B組。A組患者合并心臟增大、心律失常、心肌缺血或心力衰竭等癥狀且甲亢控制后心臟異常癥狀緩解,明確甲亢性心臟病診斷[5],排除合并其他原因所致心臟疾病者、臨床及實驗室檢查資料不完整者以及合并惡性腫瘤患者。
整理兩組患者病歷資料并抽取其停藥7 d次日清晨空腹靜脈血,化學發光法檢測其血清游離三碘甲狀腺素原氨酸(FT3)、游離甲狀腺素(FT4)水平;正常參考范圍[6]:FT3:3~9 pmol/L;FT4:2.4~15.4 pmol/L。對所有數據采用SPSS 18.0進行分析,單因素分析對比兩組患者臨床資料,將存在統計學差異的資料納入Logistic多因素回歸分析,總結影響甲亢患者并發甲亢性心臟病的相關因素。
2 結果
兩組患者年齡、病程及FT3、FT4比較,差異有統計學意義(P<0.05)。
將存在統計學差異的單因素分析指標進行Logistic多因素回歸分析得出年齡≥60歲、病程≥6個月、FT4≥35 pmol/L是影響甲亢并發甲亢性心臟病的獨立危險因素(P<0.05)。endprint
3 討論
甲狀腺疾病尤其是甲亢的發病率近年呈上升趨勢[7]。隨著年齡的增長,機體功能的逐漸退化伴隨著心肌細胞纖維化的進展,此時心肌膠原含量上升,心肌細胞對甲狀腺激素的耐受度不足,故過量甲狀腺激素水平可造成心臟負荷加重、心肌損害加劇[8-10]。甲亢是一種消耗性疾病,故患者病程越長,機體整體狀態越差,加之長時間高濃度甲狀腺激素對心臟產生的不良影響[11-12],患者心臟受損風險更高、心功能不全發生風險顯著上升。因此,本組患者隨著年齡、病程的增加并發甲亢性心臟病的風險顯著上升。
甲亢發生后,心肌細胞Na+-K+-ATP酶活性增強,Na+外流、K+內流明顯,心肌細胞正常電生理平衡打破,此時心肌細胞對外周組織FT4的降解能力顯著下降,而過量的FT4可直接作用于傳導系統,引發心肌和傳導系統內淋巴細胞浸潤,嚴重時可導致灶性壞死或纖維化,造成各類傳導阻滯的發生[13-14]。此外,有學者發現,大量FT4還可使交感神經張力上升、心肌細胞膜β受體數量增加,此時心肌細胞對兒茶酚胺的敏感性急劇上升、心肌耗氧量大幅增加,心動過速發生風險也隨之上升[15]。
既往有學者就單純甲亢患者與甲亢性心臟病患者心臟結構和功能指標進行對比發現甲亢性心臟病患者處于明顯的收縮壓增高和脈壓差增大狀態[16]。也有研究指出,甲亢性心臟病患者血清總膽固醇、甘油三酯水平顯著下降,其原因可能與過量甲狀腺激素所致體脂動員、合成和分解加速有關[17]。因此,在甲亢性心臟病的治療中,可關注心肌細胞功能的改善以及血脂水平的調控。
對于尚未進展至甲亢性心臟病的患者,建議早期識別其高齡、長病程、高FT4濃度等危險因素,篩選高危患者并注重超聲心動圖檢查的定期開展、甲狀腺激素水平的調控,做到甲亢性心臟病的早預防、早發現、早治療,降低甲亢性心臟病發生風險。在甲亢的治療藥物中,碘劑(131I)不僅治療效果顯著優于β受體阻滯劑、利尿劑等抗甲狀腺藥物,而且在調節甲狀腺激素水平、降低甲狀腺激素對心臟毒性等方面也具有確切作用[18],值得作為甲亢以及甲亢性心臟病的首選治療藥物。
參 考 文 獻
[1] Grais I M, Sowers J R. Thyroid and the heart[J]. Am J Med, 2014, 127(8): 691-698.
[2] Pearce E N. Overt and subclinical hyperthyroidism are associated with increased mortality whereas subclinical hypothyroidism is associated with decreased mortality[J]. Clin Thyroidol, 2014, 26(5): 120-122.
[3] Erem C, Civan N, Coskun H, et al. Signal peptide-CUB-EGF domain-containing protein 1 (SCUBE1) levels in patients with overt and subclinical hyperthyroidism: effects of treatment[J]. Clin Endocrinol, 2016, 84(6): 919-924.
[4] Biondi B. Impact of Hyperthyroidism on the Cardiovascular and Musculoskeletal Systems and Management of Patients with Subclinical Graves Disease[M]//Graves Disease. Springer New York, 2015: 133-146.
[5] 王曙. 甲亢性心臟病[C]// 中華醫學會第十一次全國內分泌學學術會議論文匯編. 2012.
[6] 胡艷云,張冬迅,趙新翠.Graves病甲亢治療前后脂聯素水平變化[J].現代儀器與醫療,2016,22(6):106-107.
[7] Takeuchi D, Honda K, Shinohara T, et al. Incidence, clinical course, and risk factors of amiodarone-induced thyroid dysfunction in Japanese adults with congenital heart disease[J]. Circ J, 2015, 79(8): 1828-1834.
[8] 路方紅, 劉振東, 范存芳,等. 甲狀腺功能亢進癥患者Tei指數與左心室應變率的相關性[C]// 第十三次全國心血管病學術會議論文集. 2011.
[9] Danzi S, Klein I. Thyroid disease and the cardiovascular system[J]. Endocrinol Metab Clin North Am, 2014, 43(2): 517-528.
[10] Collet T H, Bauer D C, Cappola A R, et al. Thyroid antibody status, subclinical hypothyroidism, and the risk of coronary heart disease: an individual participant data analysis[J]. J Clin Endocrinol Metab, 2014, 99(9): 3353-3362.endprint
[11] 李超. 甲狀腺素對心肌Ca2+/鈣調蛋白依賴性蛋白激酶Ⅱ的影響[D]. 武漢:華中科技大學, 2011.
[12] Onat A, Ayd?n M, Can G, et al. Normal thyroid-stimulating hormone levels, autoimmune activation, and coronary heart disease risk[J]. Endocrine, 2015, 48(1): 218-226.
[13] Biondi B, Bartalena L, Cooper D S, et al. The 2015 European Thyroid Association guidelines on diagnosis and treatment of endogenous subclinical hyperthyroidism[J]. Eur Thyroid J, 2015, 4(3): 149-163.
[14] Klein I, Danzi S. Thyroid disease and the heart[J]. Curr Probl Cardiol, 2016, 41(2): 65-92.
[15] 蘇莉, 黃誠剛, 牛文強. 巨大甲狀腺腫伴甲亢性心臟病的~(131)I治療[C]// 中華醫學會第九次全國核醫學學術會議. 2011.
[16] Greene J P, Lefebvre S L, Wang M, et al. Risk factors associated with the development of chronic kidney disease in cats evaluated at primary care veterinary hospitals[J]. J Am Vet Med Assoc, 2014, 244(3): 320-327.
[17] Liao Z, Xiong Y, Luo L. Low-dose spinal-epidural anesthesia for Cesarean section in a parturient with uncontrolled hyperthyroidism and thyrotoxic heart disease[J]. J Anesth, 2016, 30(4): 731-734.
[18] Bijsmans E S, Jepson R E, Wheeler C, et al. Plasma N-Terminal Probrain Natriuretic Peptide, Vascular Endothelial Growth Factor, and Cardiac Troponin I as Novel Biomarkers of Hypertensive Disease and Target Organ Damage in Cats[J]. J Vet Intern Med, 2017, 31(3): 650-660.endprint