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Does mild preeclampsia cause arterial stiffness and ventricular remodeling through inflammation?

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(1)Ginekol Pol. 2014, 85, 900-907. P R A C E O R Y G I N A L N E ginekolog i a. Does mild preeclampsia cause arterial stiffness and ventricular remodeling through inflammation? Czy łagodny stan przedrzucawkowy powoduje sztywność tętnic i przebudowę komory serca poprzez zapalenie? Faika Ceylan Ciftci1, Ozgur Ciftci2, Hakan Gullu2, Mustafa Caliskan2, Ayla Uckuyu1, Ebru Emel Ozcimen1 1 2. Department of Obstetrics and Gynecology, Baskent University Ankara, Turkey Department of Cardiology, Baskent University Ankara, Turkey. Abstract Background: A link between preeclampsia (PE) and excessive maternal morbidity and mortality is a commonly recognized fact. Moreover, it has been suggested that chronic inflammatory state connected with PE contributes to accelerated atherosclerosis. There is also an association between PE and maternal cardiac remodeling and biventricular diastolic dysfunction. The aim of the study was to investigate the presence of impaired myocardial performance and increased arterial stiffness in patients who experienced a mild case of PE five years previously. Methods: The study included forty PE patients (40 women; mean age 33.75±7.95) and 27 healthy volunteers (27 women; mean age 36.44±10.45)Transthoracic echocardiography, including Doppler echocardiography combined with tissue Doppler imaging (TDI), and aortic stiffness index (AoSI), aortic distensibility (AoD), and aortic elastic modulus (AoEM) values were measured in each study participant. Results: There was a statistically significant increase in hsCRP, aortic stiffness index, and aortic elastic modulus in PE patients as compared to controls (2.43±1.91 vs. 3.80±2.06, p=0.007; 3.09±2.41 vs. 7.32±6.89, p=0.001; 2.89±2.11 vs. 7.00± 6.83, p=0.001), while a significant decrease was observed in the aortic strain and distensibility (respectively, 22.35±15.99 vs. 12.24±9.22, p=0.005; 11.17±9.68 vs. 6.13±4.99, p=0.018). No differences between the two groups were observed with regard to the left ventricular myocardial performance index (MPI) (0.55± 0.16 vs. 0.53± 0.19, p= 0.630). Conclusions: To the best of our knowledge, this has been the first study to demonstrate impaired aortic elasticity and unaffected myocardial performance index in patients with mild PE. Moreover, these effects turned out to be significantly correlated with inflammation.. Key words: preeclampsia / arterial stiffness / ventricular dysfunction /. Address for correspondence: Faika Ceylan Ciftci Baskent University, Konya Application and Research Center, Department of Obstetrics and Gynecology, Hoca Cihan Mah., Saray Cad., No:1, 42080, Selcuklu, Konya, TURKEY Tel: +90 332 2570606-3300 Fax: +90 332 2570637 E-mail: faikaceylanciftci@gmail.com. 900. © Polskie Towarzystwo Ginekologiczne. Otrzymano: 17.11.2013 Zaakceptowano do druku: 14.05.2014. Nr 12/2014.

(2) Ginekol Pol. 2014, 85, 900-907. P R A C E. O R Y G I N A L N E g i n e kol og i a. Faika Ceylan Ciftci et al. Does mild preeclampsia cause arterial stiffness and ventricular remodeling through inflammation?. Streszczenie Wstęp: Istnieje powiązanie pomiędzy stanem przedrzucawkowym (PE) a nadmierną zachorowalnością i śmiertelnością. Ponadto, sugeruje się, że przewlekły stan zapalny udzielający się w PE przyczynia się do przyspieszenia miażdżycy. Istnieje również związek między PE przebudowy mięśnia sercowego ze strony matki i dwukomorową dysfunkcją rozkurczową. Zaplanowaliśmy ocenić w tym badaniu, czy nie została osłabiona wydolność mięśnia sercowego oraz zwiększenie sztywności tętnic u pacjentek, które pięć lat wcześniej miały łagodny przypadek PE. Metody: W badanie włączonych zostało czterdzieści pacjentek (40 kobiet; średnia wieku 33,75±7,95) oraz 27 zdrowych ochotniczek (27 kobiet: średnia wieku: 36,44±10,45). Każda z pacjentek została zbadana za pomocą echokardiografii przezklatkowej, w tym echokardiografii dopplerowskiej w połączeniu z tkankową echokardiografią dopplerowską (TDI). Zostały również zmierzone takie wartości, jak wskaźnik sztywności aorty (AoSI), rozciągliwość aorty, a także moduł sprężystości aorty (AoEM). Wyniki: Stwierdzono statystycznie istotny wzrost hsCRP, wskaźnika sztywności aorty i modułu sprężystości aorty u pacjentów z PE w porównaniu z grupą kontrolną (2,43±1,91vs. 3,80±2,06, p=0.007; 3,09±2,41 vs. 7,32±6,89, p=0,001; 2,89±2,11 vs. 7,00± 6,83, p=0,001), natomiast znaczne zmniejszenie zaobserwowano w odkształceniu aorty i jej rozciągliwości (odpowiednio 22,35±15,99 vs. 12,24±9,22, p= 0,005; 11,17±9,68 vs. 6,13±4,99, p=0.018). Nie wystąpiły różnice pomiędzy tymi dwoma grupami w odniesieniu do wskaźnika wydolności mięśnia sercowego lewej komory (0,55± 0,16 vs 0,53± 0,19, p=0,630). Wnioski: Stwierdziliśmy po raz pierwszy w tym badaniu, że wystąpiły osłabiona elastyczność aorty i niezmieniony wskaźnik wydolność mięśnia sercowego (MPI) u pacjentek z łagodnym PE, ponadto, efekty te były znacząco skorelowane ze stanem zapalnym.. Słowa kluczowe:  

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(1056) Ginekol Pol. 2014, 85, 900-907. P R A C E. O R Y G I N A L N E g i n e kol og i a. Faika Ceylan Ciftci et al. Does mild preeclampsia cause arterial stiffness and ventricular remodeling through inflammation?. Table I. Demographic and baseline biochemical measurements of patient and control groups. Preeclampsia (n=40). Control (n=27). p. 33.75±7.95. 36.44±10.45. 0.262. Total cholesterol (mg/dl). 187.55±32.48. 182.77±30.77. 0.545. HDL cholesterol (mg/dl). 47.20±8.42. 49.96±11.02. 0.276. LDL cholesterol (mg/dl). 115.77±25.49. 108.03±22.35. 0.194. Triglyceride (mg/dl). 113.50±52.71. 125.29±62.44. 0.424. Age (year). hsCRP(mg/L). 3.80±2.06. 2.43±1.91. 0.007. Creatinin(mg/dl). 0.79±0.12. 0.78±0.08. 0.591. Fasting Glucose(mg/dl). 93.27±6.89. 95.18±7.40. 0.292. ALT. 21.20±11.84. 20.25±7.92. 0.698. Uric acid(mg/dl). 4.01±.77±. 3.65±.87. 0.099. Hemoglobin (g/dL). 13.59±3.81. 13.39±1.27. 0.762. A bbre v i a t io ns: HDL – high density lipoprotein cholesterol. LDL – low density lipoprotein cholesterol. hsCRP – high sensitive C-reactive protein. ALT – Serum Alanine Amino Transferase. Data was presented as mean ± standard deviation.. Table II. Left ventricular systolic and diastolic function measurements.. Emax (cm/s). Preeclampsia. Control. p. 83.52± 17.83. 82.22± 16.09. 0.757. Amax (cm/s). 70.45± 19.43. 63.55± 11.89. 0.077. E DT (ms). 209.20± 32.53. 223.43± 41.39. 0.219. Mitral IVRT(ms). 91.30± 15.34. 88.41± 15.26. 0.488. Emax/Amax ratio. 1.23± 0.29. 1.32± .28. 0.213. Sm (cm/s). 14.31± 2.71. 14.44± 2.93. 0.853. Em (cm/s). 20.35± 3.97. 18.70± 4.67. 0.138. Am (cm/s). 15.83± 3.31. 15.37± 3.31. 0.579. Em/Am ratio IVRT (ms). 1.32± 0.30. 1.28± .47. 0.741. 98.19± 26.71. 104.40± 38.16. 0.468. IVCT (ms). 53. 73± 12.06. 49.51± 11.46. 0.153. ET (ms). 282.74± 36.55. 299.88± 44.43. 0.103. MPI. 0.55± 0.16. EF. 69.02± 4.59. 67.03± 5.57. 0.53± 0.19. 0.630 0.133. E/e’. 4.22±1.23. 4.61±1.27. 0.214. A bbre v i a t io ns: Sm – systolic peak velocity; Em – early peak velocity; Am – atrial peak velocity; IVRT – isovolumic relaxation time; IVCT – isovolumic contraction time; ET – ejection time; MPI: myocardial performance index; EF – left ventricular ejection fraction.; EDT – Mitral Emax wave deceleration time. E/e’ – ratio of the mitral velocity to the early-diastolic velocity of the mitral annulus. Data was presented as mean ± standard deviation.. 

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