Ultraschall Med 2012; 33(7): E126-E131
DOI: 10.1055/s-0031-1273488
Original Article

© Georg Thieme Verlag KG Stuttgart · New York

Maternale Endothelfunktion in Schwangerschaft und Wochenbett – ultraschallgestützte longitudinale Erfassung mittels Flow Mediated Dilatation (FMD)

Maternal Endothelial Function in the Course of Pregnancy and Postpartum – Ultrasound-Based Longitudinal Assessment Using Flow-Mediated Dilatation (FMD)C. Seeliger1 , A. Brueckmann1 , E. Schleußner1
  • 1Abteilung Geburtshilfe, Universitätsfrauenklinik, Jena
Weitere Informationen

Publikationsverlauf

eingereicht: 20.12.2010

angenommen: 20.5.2011

Publikationsdatum:
29. August 2011 (online)

Zusammenfassung

Ziel: Die Verminderung des peripheren Gefäßwiderstands in der Schwangerschaft wird durch eine NO-getriggerte Gefäßdilatation vermittelt. Diese physiologische Änderung der Endothelfunktion während des Schwangerschaftsverlaufs und im Wochenbett wurde mittels der noninvasiven Erfassung der flussabhängigen Gefäßdilatation durch hochauflösende Ultraschallmessung ermittelt. Material und Methoden: In einer prospektiven Beobachtungsstudie wurde longitudinal an 16 schwangeren Frauen im 1. Trimenon (T1) < 14. Schwangerschaftswochen (SSW), 2. Trimenon (T2) ≥ 14. – 27. SSW, 3. Trimenon (T3) ≥ 28. SSW und > 6 Wochen postpartal (pp) sonografisch die FMD der A. brachialis ermittelt. 19 nicht schwangere Frauen (NS) wurden als Vergleichsgruppe in die Studie eingeschlossen. Ergebnisse: Die FMD (%) stieg vom 1. zum 2. Trimenon (T1 8,0 ± 5,58 vs. T 2 15,2 ± 5,19, p < 0,003) signifikant an und erreichte ihr Maximum in der Mitte der Schwangerschaft. Zum 3. Trimenon fiel die FMD wieder signifikant ab (T2 vs. T 3 9,15 ± 3,61, p < 0,004). Die Mittelwerte der FMD waren im 2. und 3. Trimenon verglichen mit den nicht schwangeren Kontrollen signifikant erhöht (T2 vs. NS 6,17 ± 4,39, p < 0,0001; T 3 vs. NS, p < 0,047). Postpartal fiel die FMD auf das Niveau der in der Frühschwangerschaft bestimmten Werte zurück. Schlussfolgerung: Im Schwangerschaftsverlauf ändert sich die maternale Endothelfunktion mit einer Zunahme der flussabhängigen Gefäßerweiterung, die im Wochenbett wieder verschwindet. Mittels der FMD-Messung lassen sich diese physiologischen Veränderungen im Schwangerschaftsverlauf zuverlässig erfassen.

Abstract

Purpose: NO-triggered vasodilatation decreases peripheral vascular resistance in pregnancy. Using a noninvasive ultrasound technique, flow-mediated vasodilatation can be quantified. We used this technique to detect changes in endothelial function during pregnancy and postpartum. Materials and Methods: In a prospective longitudinal study 16 healthy pregnant women were assessed for flow-mediated dilatation of the brachial artery during pregnancy (first trimester T 1 < 14th gestational week, second trimester T 2 ≥ 14th – 27th gestational week, third trimester T 3 ≥  28th gestational week) and postpartum (> 6 weeks postpartum). As a control group, flow-mediated dilatation was determined in 19 healthy non-pregnant women. Results: Flow-mediated dilatation (%) increased significantly in normal human pregnancy from the first trimester (T1 8.0 ± 5.58 vs. T 2 15.2 ± 5.19, p < 0.003) to the second trimester and reached its maximum in mid-trimester. Towards the end of pregnancy, flow-mediated dilatation decreased significantly (T2 vs. T 3 9.15 ± 3.61, p < 0.004). Mean values of flow-mediated dilatation are significantly higher during the second and third trimester of pregnancy compared to non-pregnant controls (T2 vs. NP 6.17 ± 4.39, p < 0.001; T 3 vs. NP, p < 0.047). Postpartum flow-mediated dilatation decreased to values of early pregnancy. Conclusion: During pregnancy maternal endothelial function shows an increase in flow-mediated dilatation and then reverts postpartum. Using ultrasound-based measurement of flow-mediated dilatation, these physiological changes in pregnancy can be reliably detected.

Literatur

  • 1 Williams D J, Vallance P J, Neild G H et al. Nitric oxide-mediated vasodilation in human pregnancy.  Am J Physiol. 1997;  272 H748-H752
  • 2 MacGillivray I, Rose G A, Rowe B. Blood pressure survey in pregnancy.  Clin Sci. 1969;  37 395-407
  • 3 Atkins A F, Watt J M, Milan P et al. A longitudinal study of cardiovascular dynamic changes throughout pregnancy.  Eur J Obstet Gynecol Reprod Biol. 1981;  12 215-224
  • 4 Page E W, Christianson R. The impact of mean arterial pressure in the middle trimester upon the outcome of pregnancy.  Am J Obstet Gynecol. 1976;  125 740-746
  • 5 Furchgott R F, Zawadzki J V. The obligatory role of endothelial cells in the relaxation of arterial smooth muscle by acetylcholine.  Nature. 1980;  288 373-376
  • 6 Pohl U, Holtz J, Busse R et al. Crucial role of endothelium in the vasodilator response to increased flow in vivo.  Hypertension. 1986;  8 37-44
  • 7 Nabel E G, Selwyn A P, Ganz P. Large coronary arteries in humans are responsive to changing blood flow: an endothelium-dependent mechanism that fails in patients with atherosclerosis.  J Am Coll Cardiol. 1990;  16 349-356
  • 8 Ludmer P L, Selwyn A P, Shook T L et al. Paradoxical vasoconstriction induced by acetylcholine in atherosclerotic coronary arteries.  N Engl J Med. 1986;  315 1046-1051
  • 9 Calver A, Collier J, Green D et al. Effect of acute plasma volume expansion on peripheral arteriolar tone in healthy subjects.  Clin Sci. 1992;  83 541-547
  • 10 Jäger K A, Staub D. Haben Sie die Intima-Media-Dicke gemessen?.  Ultraschall in Med. 2009;  30 434-437
  • 11 Schreuder F H, Graf M, Hameleers J M et al. Measurement of Common Carotid Artery Intima-Media Thickness in Clinical Practice: Comparison of B-Mode and RF-Based Technique.  Ultraschall in Med. 2009;  30 459-465
  • 12 Celermajer D S, Sorensen K E, Gooch V M et al. Non-invasive detection of endothelial dysfunction in children and adults at risk of atherosclerosis.  Lancet. 1992;  340 1111-1115
  • 13 Accini J L, Sotomayor A, Trujillo F et al. Colombian study to assess the use of noninvasive determination of endothelium-mediated vasodilatation (CANDEV). Normal values and factors associated.  Endothelium. 2001;  8 157-166
  • 14 Corretti M C, Anderson T J, Benjamin E J et al. Guidelines for the ultrasound assessment of endothelial-dependent flow-mediated vasodilation of the brachial artery: a report of the International Brachial Artery Reactivity Task Force.  J Am Coll Cardiol. 2002;  39 257-265
  • 15 Balletshofer B M, Goebbel S, Rittig K et al. Influence of experience on intra- and interindividual variability in assessing peripheral endothelial dysfunction with high resolution ultrasound.  Ultraschall in Med. 2001;  22 231-235
  • 16 Christianson R E. Studies on blood pressure during pregnancy. I. Influence of parity and age.  Am J Obstet Gynecol. 1976;  125 509-513
  • 17 Meredith I T, Currie K E, Anderson T J et al. Postischemic vasodilation in human forearm is dependent on endothelium-derived nitric oxide.  Am J Physiol. 1996;  270 H1435-H1440
  • 18 Dørup I, Skajaa K, Sørensen K E. Normal pregnancy is associated with enhanced endothelium-dependent flow-mediated vasodilation.  Am J Physiol. 1999;  276 H821-H825
  • 19 Faber-Swensson A P, O’Callaghan S P, Walters W A. Endothelial cell function enhancement in a late normal human pregnancy.  Aust N Z J Obstet Gynaecol. 2004;  44 525-529
  • 20 Quinton A E, Cook C M, Peek M J. A longitudinal study using ultrasound to assess flow-mediated dilatation in normal human pregnancy.  Hypertens Pregnancy. 2007;  26 273-281
  • 21 Noori M, Donald A E, Angelakopoulou A et al. Prospective study of placental angiogenic factors and maternal vascular function before and after preeclampsia and gestational hypertension.  Circulation. 2010;  122 478-487
  • 22 Savvidou M D, Kametas N A, Donald A E et al. Non-invasive assessment of endothelial function in normal pregnancy.  Ultrasound Obstet Gynecol. 2000;  15 502-507
  • 23 Hunter S, Robson S C. Adaptation of the maternal heart in pregnancy.  Br Heart J. 1992;  68 540-543
  • 24 Pyke K E, Tschakovsky M E. The relationship between shear stress and flow-mediated dilatation: implications for the assessment of endothelial function.  J Physiol. 2005;  568 357-369
  • 25 Cooke J P, Stamler J, Andon N et al. Flow stimulates endothelial cells to release a nitrovasodilator that is potentiated by reduced thiol.  Am J Physiol. 1990;  259 H804-H812
  • 26 Joannides R, Haefeli W E, Linder L et al. Nitric oxide is responsible for flow-dependent dilatation of human peripheral conduit arteries in vivo.  Circulation. 1995;  91 1314-1319
  • 27 Palmer R M, Ashton D S, Moncada S. Vascular endothelial cells synthesize nitric oxide from L-arginine.  Nature. 1988;  333 664-666
  • 28 Collins P, Griffith T M, Henderson A H et al. Endothelium-derived relaxing factor alters calcium fluxes in rabbit aorta: a cyclic guanosine monophosphate-mediated effect.  J Physiol. 1986;  381 427-437
  • 29 Arnold W P, Mittal C K, Katsuki S et al. Nitric oxide activates guanylate cyclase and increases guanosine 3’:5’-cyclic monophosphate levels in various tissue preparations.  Proc Natl Acad Sci U S A. 1977;  74 3203-3207
  • 30 Vallance P, Collier J, Moncada S. Effects of endothelium-derived nitric oxide on peripheral arteriolar tone in man.  Lancet. 1989;  2 997-1000
  • 31 Ramsay B, Sooranna S R, Johnson M R. Nitric oxide synthase activities in human myometrium and villous trophoblast throughout pregnancy.  Obstet Gynecol. 1996;  87 249-253
  • 32 Sladek S M, Magness R R, Conrad K P. Nitric oxide and pregnancy.  Am J Physiol. 1997;  272 R441-R463
  • 33 Boccardo P, Soregaroli M, Aiello S et al. Systemic and fetal-maternal nitric oxide synthesis in normal pregnancy and pre-eclampsia.  Br J Obstet Gynaecol. 1996;  103 879-886
  • 34 Telfer J F, Itoh H, Thomson A J et al. Activity and expression of soluble and particulate guanylate cyclases in myometrium from nonpregnant and pregnant women: down-regulation of soluble guanylate cyclase at term.  J Clin Endocrinol Metab. 2001;  86 5934-5943
  • 35 Celermajer D S, Sorensen K E, Bull C et al. Endothelium-dependent dilation in the systemic arteries of asymptomatic subjects relates to coronary risk factors and their interaction.  J Am Coll Cardiol. 1994;  24 1468-1474
  • 36 Schiessl B, Kainer F, Oberhoffer R et al. Doppler sonography of the uterine and the cubital arteries in normal pregnancies, preeclampsia and intrauterine growth restriction: evidence for a systemic vessel involvement.  J Perinat Med. 2006;  34 139-144
  • 37 Adali E, Kurdoglu M, Adali F et al. The relationship between brachial artery flow-mediated dilatation, high sensitivity C-reactive protein, and uterine artery doppler velocimetry in women with pre-eclampsia.  J Clin Ultrasound. 2010;  . [Epub ahead of print]
  • 38 Filho E V, Mohr C, Filho B J et al. Flow-mediated dilatation in the differential diagnosis of preeclampsia syndrome.  Arq Bras Cardiol. 2010;  94 182-186, 195 – 200, 185 – 189
  • 39 Matsubara K, Matsubara Y, Hyodo S et al. Role of nitric oxide and reactive oxygen species in the pathogenesis of preeclampsia.  J Obstet Gynaecol Res. 2010;  36 239-247
  • 40 Savvidou M D, Noori M, Anderson J M et al. Maternal endothelial function and serum concentrations of placental growth factor and soluble endoglin in women with abnormal placentation.  Ultrasound Obstet Gynecol. 2008;  32 871-876

Christin Seeliger

Abteilung Geburtshilfe, Universitätsfrauenklinik

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07743 Jena

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eMail: christin.seeliger@med.uni-jena.de