The role of the Syndrome X in the pathophysiology of sleep-apnea syndrome

Yıl 2010, Cilt: 37 Sayı: 4, 358 - 362, 01.12.2010

Zuhal Arıtürk Abdurrahman Abakay Ebru Tekbaş Habib Çil Gökhan Kırbaş Sait Alan Mehmet Yazıcı

Öz

Objective: Syndrome X or microvascular angina pectoris is defined as angina pectoris due to coronary microvas­cular dysfunction in patients with non-stenotik epicardial arteries. The aim of his study was to investigate the re­lationship between obstructive sleep apnea syndrome (OSAS) and syndrome X. Materials and methods: Twenty patients (11 male, 9 fe­male) with the complaint of chest pain who referred to Cardiology Clinics of Dicle University were enrolled in the study as Group 1. All of the patients\' exercise tests were positive, epicardial coronary arteries were normal and coronary flows were slow in Group 1. Thirty healthy person were enrolled in the study as group 2. Polysom­nography (PSG) and echocardiography (ECHO) was per­formed in all patients. Results: In Group 1, 11 (55%) patients had obstructive sleep apnea. In Group 2, three patients (10%) had OSAS. There were significant differences in terms of OSAS fre­quency among groups. There were no significant differ­ences in terms of left ventricular ejection fraction (LVEF), left ventricular end-systolic diameter (LVESD), left ven­tricular end diastolic diameter (LVEDD), stroke volume, deceleration time (DT) , ejection time (ET) and the left atrium (LA) diameter between Syndrome X and control groups according to echocardiographic examination (p>0.05). However, IVRT, RA diameter, the myocardial performance index (MPI), PAP, and MEV / mav rates were significantly different (p

Anahtar Kelimeler

Syndrome X, Obstructive sleep apnea syn­drome, Echocardiography.

Sendrom X fizyopatolojisinde uyku-apne sendromu\'nun rolü

Öz

Amaç: Sendrom X veya mikrovasküler anjina pektoris, koroner anjiyografide, nonstenotik epikardiyal arterle­ri olan hastalarda, koroner mikrovasküler disfonksiyona bağlı gelişen anjina pektoris olarak tanımlanır. Bu ça­lışmada sendrom X ile obstüktif uyku apnesi sendromu (OSAS) arasındaki ilişki araştırılmıştır. Gereç ve yöntem: Bu çalışmaya Dicle Üniversitesi Tıp Fakültesi Kardiyoloji polikliniğine göğüs ağrısı nedeniyle başvuran ve efor testi pozitif olup koroner anjiyografisinde epikardiyal koroner arterleri normal veya yavaş koroner akım saptanan 20 hasta (11 erkek, 9 kadın) ile (Grup I) yapılan tetkiklerinde herhangi bir hastalık tespit edilme­miş 30 kişi (Grup II) dahil edildi. Hastalara polisomnografi (PSG) ve ekokardiyografi (EKO) uygulandı. Bulgular: Çalışmaya alınan hastalar iki ayrı gruba alındı. Grup 1; Kardiyak sendrom X tanılı 20 hasta, Grup 2; 30 sağlıklı birey. Her iki grubun kardiyak yapı ve fonksiyonla­rı ekokardiyografik olarak değerlendirildi. Grup I hastala­rın 11\'inde (%55) OSAS saptandı. Grup II hastalarda ise 3 olguda (%10) OSAS tespit edildi. Her iki grup arasın­da OSAS sıklığı bakımından anlamlı fark bulunmakta idi (p

Anahtar Kelimeler

Sendrom X, obstruktif uyku apne sendromu, ekokardiyografi.

Kaynakça

• Michaelides A, Ryan JM, VanFossen D, Pozderac R, Bou- doulas H. Exercise-induced QRS prolongation in patients with coronary artery disease: A marker of myocardial isch- emia. Am Heart J 1993; 126: 1320–5.
• Kemp HG, Kronmall RA, Vlıetstra RE, Frye RL. Seven year survival of patients wıth normal or near normal coronary arteriograms. A CASS registry study. J Am Coll Cardiol 1986; 7: 479–83.
• Baim DS, Harrison DC. Nonatherosclerotic coronary heart disease (including coronary artery spasm In: Hurst JW, eds. The Heart, 5th ed. New York: McGraw-Hill, 1982: 1158– 70.
• Masseri M, Yaram R, Gotsman MS, Hasin Y. Histologic evi- dence for small vessel coronary artery disease in patients with angina pectoris and patent large coronary arteries. Cir- culation 1986; 74: 964-72.
• Vrints C, Herman AG. Role of the endothelium in the regula- tion of coronary artery tone. Acta Cardiol 1991; 46: 399– 418.
• Bertolet BD, Pepine CJ. The vascular endothelium as a key to understanding coronary spasm and syndrome X. Curr Opiın Cardiol 1991; 6: 496–502.
• Goel PK, Gupta SK, Aggarwal A, Kapoor A. Slow coronary flow: a distinct angiographic subgroup in Syndrome X. An- giology 2001; 52: 507–14.
• Beltrame JF, Limaye SB, Horowitz JD. The coronary slow flow phenomenon - a new coronary microvascular disorder. Cardiology 2002; 97: 197–202.
• Rosen SD, Uren NG, Kaski JC, Tousoulis D, Davies GJ, Camici PG. Coronary vasodilator reserve, pain perception, and sex in patients with syndrome X. Circulation 1994; 90: 50–60.
• Chauhan A, Mullins PA, Taylor G, Petch MC, Schofield PM. Both endothelium-dependent and endothelium independent function is impaired in patients with angina pectoris and normal coronary angiograms. Eur Heart J 1997; 18: 60–4.
• Koren W, Koldanov R, Peleg E, Rabınowitz B, Rosenthal T. Enhanced red cell sodium-hydrogen exchange in microvas- cular angina. Eur Heart J 1997; 18: 1296–9.
• Yazıcı M, Balcı B, Demircan S, et al. Yavaş koroner akım- lı hastalarda plazma ET-1 düzeylerı ve düzeltılmış TİMİ kare sayısı ıle ılışkısı. Türk Kardıyol Dern Arş 2002; 30: 466–72.
• Zimmet PZ. The pathogenesis and prevention of diabetes in adults. Genes, autoimmunity, and demography. Diabetes Care 2000; 8: 1050–64.
• Rosana GM, Kaski JC, Arie S, et al. Failure to demonstrate myocardial ischemia in patients with angina and normal coronary arteries. Evaluation by continuous coronary sinus pH monitoring and lactate metabolism. Eur Heart J 1996; 17: 1175–80.
• Norris JW, Hachinski VC, Myers MG, et al. Serum cardiac enzymes in stroke. Stroke. 1979; 10:548–53.
• Kolin A, Norris JW. Myocardial damage from acute cere- bral lesions. Stroke 1984;15:990–3
• Cechetto DF, Wilson JX, Smith KE, Wolski D, Silver MD, Hachinski VC. Autonomic and myocardial changes in mid- dle cerebral artery occlusion: stroke models in the rat. Brain Res 1989; 502: 296-305.
• Silverberg DS, Oksenberg A, Laina A. Sleep related breath- ing disorders are common contributing factors to the pro- duction of essential hypertension but are neglected, under diagnosed and undertreated. Am J Hypertens 1997; 10: 1319-25.