İnsülin direncinin sol ventrikül diyastolik fonksiyonu üzerine etkisi

Abstract

Bnen bir sol ventrikul diyastolk disfonksiyonu nedeni olmayan hastalardansuln direncinin etyolojdeki yerini ara§trmayi amagladk.Arastrmaya 18-0 yas arasi ekokardiyografde erken yasta diyastolkdisfonksiyon saptanan 28 hasta dahil edidi. Dyabetes melus, gebelk, sol ventrikulkonsantrik hipertrofsi, koroner arter hastahgi, ciddi kapak hastahklan,kardiyomyopater, sistolk disfonksiyon ve hipertansiyon gibi relaksasyon kusurunuagiklayabiecek baska klnik durumu olan hastalar ?ahsma dsi brakid. Dyastolkonksiyonlar transtorasik ekokardiyografi cihazinn Doppler ve ssue Doppler magingmodu (TDI) kulanarak yapid. EKOda E ve A velosieler, izovolemk relaksasyonme (IVRT), izovolemk kontraksiyon me (ICT), ejeksiyon me (ET), E dalgasinndeselerasyon zamani (Edt) olguldu. Aynca doku doppler e myokardiyal velosielerolguldu. Ekokardiyografsi tamamen normal olan 24 olgu kontrol grubuna dahil edidi.HOMA nsuln rezistansi testi (HOMA-IR= glukoz (mmol/l) X nsuln (ull/mL) / 22.5) )ormulu e hesapland. Dyastolk disfonksiyonu olan ve olmayan olgulann HOMA-IRdegeri karsja§tndi. Boylece nsuln direncinin diyastolk disfonksiyon uzerine olanetkisi ara§tnd.Dyastolk disfonksiyonu olan 28 hastanin (45,64±5,47 yas) HOMA nsulnrezistansi degeri ortalama 22,64±1,37, kontrol gurubundaki 24 olgunun (41,60±9,7yas) HOMA nsuln rezistansi degeri 1.87±0,85 olarak bulundu. Student t esti ep:0.033 olarak hesapland. Sol ventrikul diyastolk disfonksiyonu bulunan hastalardakontrol grubundan anlamh oranda yuksek HOMA nsuln direnci seviyeleri saptand.Bu bulgu erken baslanggh diyastolk disfonksiyon gelsimnde nsuln direncininetyolojk rol oynadigini dusundurmektedir.

Our aim was o study he etological role of nsuln resistance n patentshaving eft ventricular diastolc dysfuncton whout any known cause.28 patents (age between 18-50) having diastolc dysfuncton diagnosed byelectrocardiagraphy at early age were ncluded n he study. Patents having clnicalcondions such as diabetes melus, pregnancy, eft ventricular concentrichypertrophy, coronary arter disease, severe valvular disease, cardiomyopathies,systolc dysfuncton and hypertension hat may contribute o relaxaton defect wereexcluded from the study.Dastolc unctons were measured using Doppler and ssue Doppler magingmode (TDI) of echocardiography equipment. In echocardiography, E and A velocies,sovolemc relaxaton me (IVRT), sovolemc contracton me (ICT, ejecton me(ET), deceleraton me of E wave (Edt) were measured. Moreover, ssue dopplerand myocardial velocies were measured. 24 patents w h otaly normalechocardiographies were ncluded n case control group. HOMA nsuln resistancewas calculated w h the formula: HOMA-IR= glukoz (mmol/l) X nsuln (ull/mL) / 225).HOMA-IR values of cases having and not having diastolc dysfuncton werecompared. Thus, he efect of nsuln resistance on diastolc dysfuncton wasevaluated.The average HOMA nsuln resistance value of 28 patents (age 45,64±5,47)having diastolc dysfuncton was ound as 2,26±1,37 whie HOMA nsuln resistanceof 24 patents n control group was 1.87±0,85. Sudent's t-test revealed p:0.03. Inpatents having eft ventricular dysfuncton, HOMA nsuln resistance evels wereound o be signicanty higher compared o control group. This suggest hat nsulnresistance has an etological role n development of early onset diastolc dysfuncton.