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Year : 2021  |  Volume : 1  |  Issue : 2  |  Page : 46-50

Maternal pulse waveform in second trimester and risk of preeclampsia

Department of Obstetrics and Gynaecology, Saveetha Institute of Medical and Technical Sciences, Chennai, Tamil Nadu, India

Date of Submission05-Jul-2021
Date of Acceptance21-Dec-2021
Date of Web Publication28-Feb-2022

Correspondence Address:
Nidhi Sharma
Department of Obstetrics and Gynaecology, Saveeetha Medical College, Saveetha Institute of Medical and Technical Sciences, No 5 Jayanthi Street, Dr Seethapathi Nagar Velachery, Chennai 600042, Tamil Nadu.
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/JCDM.JCDM_13_21

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Background: Preeclampsia is a multisystem heterogeneous disorder occurring in 4%–7% of all pregnancies. Objectives: This study was conducted to define the relation between arterial stiffness and perinatal outcome in a tertiary care center. The relationship between maternal pulse wave augmentation index and adverse perinatal outcome is explored in this study. Materials and Methods: Peripheral pulse waveform of the brachial artery and mean arterial pressure measurement was performed in the second trimester in women with singleton pregnancy. Preeclampsia was recorded in (7%) of all pregnancies. Results: Abnormal peripheral pulse wave augmentation in the second trimester is a good tool for the prediction of preeclampsia (sensitivity 91.23% and specificity 99.06%, P < 0.05). Conclusion: Increased peripheral augmentation index (>2 SD) and mean arterial pressure measurement in combination have better detection rates for early-onset preeclampsia and fetal growth restriction (FGR).

Keywords: Hypertension, mean arterial pressure, preeclampsia pregnancy, pulse waveform

How to cite this article:
SharanR, Rasendrakumar N, Sharma N. Maternal pulse waveform in second trimester and risk of preeclampsia. J Cardio Diabetes Metab Disord 2021;1:46-50

How to cite this URL:
SharanR, Rasendrakumar N, Sharma N. Maternal pulse waveform in second trimester and risk of preeclampsia. J Cardio Diabetes Metab Disord [serial online] 2021 [cited 2023 Sep 22];1:46-50. Available from: http://www.cardiodiabetic.org/text.asp?2021/1/2/46/338609

  Introduction Top

The augmentation index (AI) is a measure of arterial stiffness and is calculated as a ratio in the blood pressure (BP) waveform. When arteries are stiff, a reflected wave is formed where arteries split. This reflected wave moves back to the heart and the heart pumps against a higher pressure after receiving this impact. The AI is calculated from the arterial pulse. AI depends on the relationship between augmentation pressure and pulse pressure.[1] The arterial pulse comprises a forward wave generated by left ventricular ejection and a backward wave that depends on elastic properties of the arterial tree, the wave transmission velocity, and the distance from the reflection sites.[1] There are two types of AI based on the reflection site: the central AI and peripheral AI. The peripheral AI is defined as the difference between the second and the first systolic peak and is expressed as a percentage of the central pulse pressure (PP). The AI percentage is calculated as pAI% = [(P2–P1)/PP] × 100.

Preeclampsia can result in high BP and/proteinuria or manifest itself as eclampsia (Greek word eklampsis meaning lightening). These complications are associated with severe complications such as cerebral hemorrhage, lung edema or liver hemorrhage, and rupture.[2

Pregnancy has a superadded fetoplacental circulation. The maternal increase in blood volume and cardiac output is 40% after the first 20 weeks of pregnancy.[3],[4] These changes will result in increased afterload and severe hypertension in nonpregnant women and yet BP falls in pregnancy. This change has been attributed to the decrease in stiffness of blood vessels due to relaxed smooth muscle cells in tunica media under the influence of progesterone secreted by placenta. BP decreases until around 18 weeks of pregnancy and progressively increases toward term. Systolic and diastolic BP both decline early in the first trimester, reaching a nadir by 24–28 weeks; then they gradually rise toward term but never return quite to prepregnancy baseline. Diastolic falls more than systolic, as much as 15 mm Hg. Arterial BP is never normally elevated in pregnancy.[5] This is possible by a steep reduction in systemic vascular arterial resistance and an increase in venous capacitance. The heart rate increases by 20% to compensate for the drop in systemic vascular resistance.[6] Normal pregnancy, therefore, has warm skin, prominent veins, and orthostatic hypotension.

In preeclampsia due to arterial stiffness, two stages of vascular dysfunction exist. In the first stage, there is a hemodynamic maladaptation to the increased cardiac output and blood volume in pregnancy and suboptimal development of placenta [Figure 1]. This leads to the second stage of placental vascular hypoperfusion and defective placentation. There is acute atherosis and spiral arteries are occluded by fibrinoid material and surrounded by foam cells. Acute atherosis and placental thrombi are also seen in low-birth-weight babies. The functional biochemical changes in placenta are decreased ratio of prostacyclin I2 to thromboxane A2. Furthermore, in preeclampsia, there is impaired vasodilator response to endothelium-dependent agonists such as acetylcholine and bradykinen. Various adaptive mechanisms are employed at the feto-maternal interphase and subsequently after 20 weeks a clinically evident maternal syndrome hypertension, edema, and proteinuria develop. The development of the second stage of systemic and placental inflammation can also happen independently of the first stage. In preeclampsia, there is a latent preclinical stage with impaired vascular resilience, hyperdynamic circulation, and a decreased cardiac output as clinical disease develops. This decreased cardiac output leads to renal and uteroplacental insufficiency. There may also be leaky capillaries leading to pulmonary and cerebral edema. Severe and early-onset preeclampsia has abnormal brachial artery waveform in the preclinical stage and hypertension in the clinical stage. Thus, increased augmentation of the brachial artery may be considered as a local noninvasive imaging of a more generalized systemic vasculopathy. This may mediate further future cardiovascular risks. Women with preeclampsia are also two and a half times likely to die from ischemic heart disease in later life.[7],[8],[9] This study was conducted to identify the fetomaternal outcome in high peripheral AI of the brachial artery.
Figure 1: (A) Conceptual framework of the central augmentation index.

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Figure 1: (B) Conceptual framework of the peripheral augmentation index pAI% = [(P2–P1)/PP] ×100

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Raised brachial artery impedance is a marker of early endothelial dysfunction. It is associated with an increased aortic pulse wave index and AI in the first trimester of pregnancy. Increased aortic pulse wave index and AI are also a marker of future cardiovascular risk.[10],[11],[12] The faster the pulse wave returns from the periphery, the stiffer the arteries are and the higher the AI. Increased homocysteine levels have also been implicated in both cardiovascular risks and preeclampsia.[13] Brachial artery impedance is also associated with adverse perinatal outcomes such as preterm labor, fetal growth restriction (FGR), and abruption placenta.[14],[15] Preterm labor was defined as onset of true labor pains with dilatation of cervix before 37 weeks of pregnancy.[16] FGR was defined as fetal biometry less than 2 SD below that of average of that gestational age.[17] Abruption placenta was defined as premature separation of a normally situated placenta.[18]

The predominant physiological stimulus for endothelial nitric oxide synthesis is flow-induced shear stress.[19],[20] The clinical presentation of preeclampsia, FGR, preterm birth, and abruption placenta are associated with vessel wall stiffness and late endothelial dysfunction. This prospective study was conducted to evaluate the association of increased AI of brachial artery with various disorders of fetomaternal interphase resulting from endothelial dysfunction in the placental insufficiency.

  Materials and Methods Top

Waveform analysis of the brachial arteries was performed at 20–23 weeks gestation in 141 women with singleton/multiple pregnancies attending a routine target scan. All women with no major fetal anomaly are offered the option of brachial artery evaluation. Written consent was obtained in all cases. Ultrasound was done in all cases in first trimester for correct estimation of gestational age of pregnancy.

Arteriography, popularly known as sphygmocor test, was carried out in the Department of Obstetrics and Gynecology after getting written informed consent from participants in local language. Multiple pregnancies and pregnancies with congenital anomalies are especial considerations and were excluded. Detailed maternal factors like age, gestational age, parity, prepregnancy body mass index, previous low birth weight, hemoglobin levels, chronic hypertension, gestational diabetes, and previous preeclampsia are recorded. Placental problems such as low-lying placenta, infarcts, retro placental calcifications, small placenta, and premature separation are noted. The pregnant women are asked to rest in left lateral position for 10 min. The brachial artery pulse waveforms were recorded with a pressure tonometer. Tonometer machines used for the study were SphygmoCor System; Atcor Medical, Sydney, NSW, Australia (http://www.atcormedical.com/sphygmocor.html). A measurement was considered adequate only the operator index was >80 (as per manufacturer’s instructions, the range of 0–100 was depicted as increasing quality).

Arteriography of brachial artery in longitudinal scan was used to obtain 10 similar consecutive waveforms. A corresponding central aortic waveform is projected with the help of a validated computerized inbuilt mathematical function. The same is repeated for the contralateral brachial artery and the mean of the two vessels is calculated. Recordings for measurements are obtained in the absence of fetal breathing movement and maternal heart rate between 70 and 80 and fetal heart rate between 120 and 160 beats per minute. The arteriography cuff covered more than three-fourths circumference of the arm. Patients were called for antenatal visits every 2 weeks till 36 weeks and weekly thereafter. BP was measured in the right arm in the sitting posture and koratkoff 5 sound as taken as the diastolic BP. Urine albumin was measured at each visit.

If hypertension and/or proteinuria developed before 34 weeks, the gestation was classified as early-onset preeclampsia. If hypertension and/or proteinuria developed after 34 weeks, the pregnancy was diagnosed as late-onset preeclampsia.

Preeclampsia was defined according to the guidelines of the International Society for the Study of Hypertension in Pregnancy. This requires two recordings of diastolic BP of ≥90 mm Hg at least 4 h apart in previously normotensive women after 20 weeks of pregnancy, and proteinuria of 300 mg or more in 24 h, or two readings of at least + + on dipstick analysis of midstream or catheter urine specimens if no 24-h collection is available. FGR was defined as a fetal weight below the expected weight in the customized population fetal growth charts. Preterm Labor is defined as a regular uterine activity before 37 completed weeks of gestation associated with dilatation of cervix. Abruption of placenta is identified as presence of retro placental clots in ultrasound or placental examination after delivery. Descriptive and inferential statistics were used to analyze the data. Differences were considered significant when P < 0.05. Logistic regression was used to obtain the odds ratio (OR) and 95% confidence interval (CI).

  Results Top

After waveform examination of brachial arteries, satisfactory waveforms were obtained in 99% (138) of all pregnancies. All the recruited pregnancies were followed up during the antenatal and postnatal period. Brachial artery AI is not normally distributed but is found skewed to the right. [Table 1] summarizes the maternal history variables and demographic characteristics of mothers associated with preeclampsia.
Table 1: Maternal demographic variables associated with high pulse wave augmentation index in first trimester

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[Table 2] brings up the fact that the presence of high pulsatility is a significant risk factor for early-onset preeclampsia as compared to late-onset preeclampsia. Approximately 8.18% pregnancies resulted in preeclampsia. There were no intrauterine deaths in this study. Out of hypertensive pregnancies, approximately 30% were early onset (<34 weeks) and 70% were late onset (>34 weeks).
Table 2: High pulse wave augmentation index (>2 SD) of brachial artery in second trimester and prediction of preeclampsia, fetal growth restriction (FGR), preterm labor and Abruption placenta

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Gestational age rather than weight was a predictor of neonatal mortality, as all FGR babies beyond 34 weeks had no neonatal mortality. In few neonates, sometimes no maternal cause of FGR can be identified. [Table 2] brings up the fact that the presence of high pulse wave AI as compared to low pulsatility confers a significant risk (31.58% vs. 2.19%) for FGR (P < 0.05).

It also brings up the fact that the presence of high peripheral pulse wave AI as compared to low peripheral pulse wave AI is a significant risk factor for preterm labor and abruption placenta. There were cases of grade one abruption, grade 2 abruption, and grade three abruption. There can also be grade 0 abruption. Out of FGR newborns, almost all survived beyond four weeks of life, as there is a catch-up growth after delivery.

[Table 2] also tells us the sensitivity, specificity, positive predictive value, negative predictive value, likelihood ratio positive and likelihood ratio negative of early- and late-onset preeclampsia, FGR, preterm birth, and abruption placenta when there is a high peripheral pulse AI percentage.

  Discussion Top

Brachial artery is a continuation of subclavian artery and the main artery entering the forearm and hand, whose anterior division gives of the radial artery. Endothelial dysfunction and arterial stiffness might show two varied aspects of vessel wall. The arterial stiffness is determined by elastin to collagen ratio in the vessel wall muscle. On the contrary, the endothelium responds to nitric oxide, and other cytokines and inflammatory mediators such as vascular endothelial growth factor (VEGF), transforming growth factor (TGF), placental growth factor (PLGF), and soluble endoglin (sENG).

Generalized vasodilatation starts during the luteal phase after conception and peripheral resistance falls substantially after 5 weeks gestation until reaching values 34% lower than the prepregnant state at 20 weeks gestation.[21],[22] Arterial pulse wave velocity and AI are consistent with vessel wall dysfunction in vivo[19] and in vitro[23] studies. The likely cause is deranged nitric oxide availability, although the precise underlying pathophysiology is unclear. Numerous clinical studies have shown the efficacy of nitric oxide donors to suppress hypertension and improve umbilical cord flow to fetus.[24],[25] Ischemic placenta may secrete sFLT (soluble fms like tyrosine kinase) and sENG. These decoy molecules trap the available growth factors. The decoy molecule sFLT binds to VEGF and PLGF, sENG binds to TGF-β and thus there is an imbalance of proangiogenic and antiangiogenic factors leading to preeclampsia and fetoplacental complications. The molecule sFLT is a free-floating variant of FLT-1. FLT-1 is a receptor––a docking point of VEGF and PLGF in the vessel wall. This binding process is necessary for vessels to remain healthy. sFLT-1 binds the available VEGF and PLGF and the vessel walls deprived of VEGF and PLGF remain stiff and inelastic and deteriorate. Endoglin receptor on the vessel wall is a docking point of TGF-β. The free circulating levels of sENG act as a decoy diverting TGF-β away from vessels. Deprived of TGF-β the vessel wall becomes less elastic. However, the effect of these molecules on vessel wall stiffness is still to be correlated.

The maternal increase in blood volume and cardiac output is 40% to supply an added fetoplacental circulation. These changes will result in severe hypertension in nonpregnant women but still BP falls in pregnancy. This adaptation to pregnancy is the result of a steep reduction in systemic vascular arterial resistance and an increase in venous capacitance. Normal pregnancy therefore has warm skin, prominent veins, and orthostatic hypotension. There is an increased flow to skin, kidneys, and uterine arteries. Severe and early-onset preeclampsia is characterized by hypertension and abnormal brachial artery waveform. Thus, pulse waveform analysis of brachial artery may be considered as a local noninvasive imaging of a more generalized systemic vasculopathy.[26],[27],[28] This may be a common factor of cardiovascular risks. Further studies to resolve the maternal cardiovascular maladaptation will involve the echocardiography of maternal heart and mediators of atherosclerosis and oxidative stress in preeclampsia.[29] The plausible explanation of early-onset preeclampsia is reduced nitric oxide from vascular endothelium as a result of shear stress that subsequently leads to noncompliant and stiff vessels.[30],[31] High brachial artery AI is an impaired ability of vasculature to respond to the profound changes required for normal pregnancy.[32] The decreased AI as happens in normal pregnancy has a protective role and will tend to dampen the increased pulse pressure.[33],[34] This will reduce the transmission of pulsatile energy to the delicate fetal tertiary stem villi floating in the intervillous space. Future research can identify how VEGF165-dependent mitogenic activity, tube formation, and receptor phosphorylation regulate the elasticity and augmentation pressure index in vessel wall.[35]

  Conclusion Top

Brachial artery AI identifies a subset of pregnant women with a nonresilient and nonelastic cardiovascular system that fails the hemodynamic stress imposed by the superadded fetoplacental circulation. The women manifest as increased peripheral BP, damage of fetal villi, and premature separation of the placenta. Vascular inelasticity and increased AI in pregnancy can be useful in identifying adverse perinatal outcomes. High peripheral pulses AI may be used in further long-term follow-up studies in pregnant women to predict future cardiovascular risk.

Ethical policy and institutional review board statement

Institutional ethical committee approval is obtained and preserved by authors.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Townsend RR Arterial stiffness: Recommendations and standardization. Pulse (Basel) 2017;4:3-7.  Back to cited text no. 1
Shimizu M, Kario K Role of the augmentation index in hypertension. Ther Adv Cardiovasc Dis 2008;2:25-35.  Back to cited text no. 2
Roberts JM, Hubel CA The two-stage model of preeclampsia: Variations on the theme. Placenta 2009;30:S32-7.  Back to cited text no. 3
Van Wijka MJ, Kublickienec K, Boera K, Van Bavel E Vascular function in preeclampsia. Cardiovas Res 2000;47:38-48.  Back to cited text no. 4
Boutouyrie P, Achouba A, Trunet P, Laurent S; EXPLOR Trialist Group. Amlodipine-valsartan combination decreases central systolic blood pressure more effectively than the amlodipine-atenolol combination: The Explor study. Hypertension 2010;55:1314-22.  Back to cited text no. 5
McGrath BP, Liang YL, Kotsopoulos D, Cameron JD, Impact of physical and physiological factors on arterial function. Clin Exp Pharmacol Physiol 2001;28:1104-7.  Back to cited text no. 6
Enkhmaa D, Wall D, Mehta PK, Stuart JJ, Rich-Edwards JW, Merz CN, et al. Preeclampsia and vascular function: A window to future cardiovascular disease risk. J Womens Health (Larchmt)2016;25:284-91.  Back to cited text no. 7
Mac Donald-Wallis C, Lawler DA, Fraser A, May M, Nelson SM, Tilling K Blood pressure change in normotensive, gestational hypertensive, preeclamptic, and essential hypertensive pregnancies. Hypertension 2012;59:1241-8.  Back to cited text no. 8
Wilkinson IB, MacCallum H, Flint L, Cockcroft JR, Newby DE, Webb DJ The influence of heart rate on augmentation index and central arterial pressure in humans. J Physiol 2000;525:263-70.  Back to cited text no. 9
Duvekot JJ, Cheriex EC, Pieters FA, Menheere PP, Peeters LH Early pregnancy changes in hemodynamics and volume homeostasis are consecutive adjustments triggered by a primary fall in systemic vascular tone. Am J Obstet Gynecol 1993;169:1382-92.  Back to cited text no. 10
Rich-Edwards JW, Fraser A, Lawlor DA, Catov JM Pregnancy characteristics and women’s future cardiovascular health: An underused opportunity to improve women’s health? Epidemiol Rev 2014;36:57-70.  Back to cited text no. 11
Fraser A, Nelson SM, Macdonald-Wallis C, Cherry L, Butler E, Sattar N, et al. Associations of pregnancy complications with calculated cardiovascular disease risk and cardiovascular risk factors in middle age: The Avon longitudinal study of parents and children. Circulation 2012;125:1367-80.  Back to cited text no. 12
Brown MC, Best KE, Pearce MS, Waugh J, Robson SC, Bell R Cardiovascular disease risk in women with pre-eclampsia: Systematic review and meta-analysis. Eur J Epidemiol 2013;28:1-19.  Back to cited text no. 13
Wykretowicz A, Adamska K, Guzik P, Krauze T, Wysocki H Indices of vascular stiffness and wave reflection in relation to body mass index or body fat in healthy subjects. Clin Exp Pharmacol Physiol 2007;34:1005-9.  Back to cited text no. 14
Nürnberger J, Keflioglu-Scheiber A, Opazo Saez AM, Wenzel RR, Philipp T, Schäfers RF Augmentation index is associated with cardiovascular risk. J Hypertens 2002;20:2407-14.  Back to cited text no. 15
Muglia LJ, Katz M The enigma of spontaneous preterm birth. N Engl J Med 2010;362:529-35.  Back to cited text no. 16
Gordijn SJ, Beune IM, Thilaganathan B, Papageorghiou A, Baschat AA, Baker PN, et al. Consensus definition of fetal growth restriction: A Delphi procedure. Ultrasound Obstet Gynecol 2016;48:333-9.  Back to cited text no. 17
Tikkanen M, Luukkaala T, Gissler M, Ritvanen A, Ylikorkala O, Paavonen J, et al. Decreasing perinatal mortality in placental abruption. Acta Obstet Gynecol Scand 2013;92:298-305.  Back to cited text no. 18
Everett TR, Mahendru AA, McEniery CM, Wilkinson IB, Lees CC Raised uterine artery impedance is associated with increased maternal arterial stiffness in the late second trimester. Placenta 2012;33:572-7.  Back to cited text no. 19
Savvidou MD, Kaihura C, Anderson JM, Nicolaides KH Maternal arterial stiffness in women who subsequently develop pre-eclampsia. PLoS One 2011;6:e18703.  Back to cited text no. 20
Macedo ML, Luminoso D, Savvidou MD, McEniery CM, Nicolaides KH Maternal wave reflections and arterial stiffness in normal pregnancy as assessed by applanation tonometry. Hypertension 2008;51:1047-51.  Back to cited text no. 21
Yu CK, Lakasing L, Papageorghiou AT, Spencer K, Nicolaides KH Uterine artery Doppler and mid-trimester maternal plasma homocysteine in subsequent pre-eclampsia. J Matern Fetal Neonatal Med 2004;16:134-9.  Back to cited text no. 22
Khan F, Mires G, Macleod M, Belch JJ Relationship between maternal arterial wave reflection, microvascular function and fetal growth in normal pregnancy. Microcirculation 2010;17:608-14.  Back to cited text no. 23
Wilkinson IB, Prasad K, Hall IR, Thomas A, MacCallum H, Webb DJ, et al. Increased central pulse pressure and augmentation index in subjects with hypercholesterolemia. J Am Coll Cardiol 2002;39:1005-11.  Back to cited text no. 24
Noris M, Morigi M, Donadelli R, Aiello S, Foppolo M, Todeschini M, et al. Nitric oxide synthesis by cultured endothelial cells is modulated by flow conditions. Circ Res 1995;76:536-43.  Back to cited text no. 25
Kublickiene KR, Cockell AP, Nisell H, Poston L Role of nitric oxide in the regulation of vascular tone in pressurized and perfused resistance myometrial arteries from term pregnant women. Am J Obstet Gynecol 1997;177:1263-9.  Back to cited text no. 26
Duvekot JJ, Peeters LL Maternal cardiovascular hemodynamic adaptation to pregnancy. Obstet Gynecol Surv 1994;49:S1-14.  Back to cited text no. 27
Robson SC, Hunter S, Boys RJ, Dunlop W Serial study of factors influencing changes in cardiac output during human pregnancy. Am J Physiol 1989;256:H1060-5.  Back to cited text no. 28
Savvidou MD, Hingorani AD, Tsikas D, Frölich JC, Vallance P, Nicolaides KH Endothelial dysfunction and raised plasma concentrations of asymmetric dimethylarginine in pregnant women who subsequently develop pre-eclampsia. Lancet 2003;361:1511-7.  Back to cited text no. 29
McCarthy AL, Woolfson RG, Raju SK, Poston L Abnormal endothelial cell function of resistance arteries from women with preeclampsia. Am J Obstet Gynecol 1993;168:1323-30.  Back to cited text no. 30
Grunewald C, Kublickas M, Carlström K, Lunell NO, Nisell H Effects of nitroglycerin on the uterine and umbilical circulation in severe preeclampsia. Obstet Gynecol 1995;86:600-4.  Back to cited text no. 31
Giles W, O’Callaghan S, Boura A, Walters W Reduction in human fetal umbilical-placental vascular resistance by glyceryl trinitrate. Lancet 1992;340:856.  Back to cited text no. 32
Mitchell GF, van Buchem MA, Sigurdsson S, Gotal JD, Jonsdottir MK, Kjartansson Ó, et al. Arterial stiffness, pressure and flow pulsatility and brain structure and function: The age, gene/environment susceptibility–reykjavik study. Brain 2011;134:3398-407.  Back to cited text no. 33
Tihtonen KM, Kööbi T, Uotila JT Arterial stiffness in preeclamptic and chronic hypertensive pregnancies. Eur J Obstet Gynecol Reprod Biol 2006;128:180-6.  Back to cited text no. 34
Ashikari-Hada S, Habuchi H, Kariya Y, Kimata K Heparin regulates vascular endothelial growth factor165-dependent mitogenic activity, tube formation, and its receptor phosphorylation of human endothelial cells: Comparison of the effects of heparin and modified heparins. J Biol Chem 2005;280:31508-15.  Back to cited text no. 35


  [Figure 1], [Figure 2]

  [Table 1], [Table 2]


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