Open access peer-reviewed chapter

Non-Dipping Patten of Blood Pressure and Gestational Hypertension

Written By

Aleksandra Ilic, Djordje Ilic, Jelena Papović, Snezana Stojsic, Aleksandra Milovancev, Dragana Grkovic, Anastazija Stojsic- Milosavljevic, Tatjana Redzek-Mudrinic, Artur Bjelica, Olivera Rankov and Lazar Velicki

Submitted: October 23rd, 2017 Reviewed: April 5th, 2018 Published: November 5th, 2018

DOI: 10.5772/intechopen.77018

Chapter metrics overview

956 Chapter Downloads

View Full Metrics


Gestational hypertension (GH) is one of the entities of the hypertensive disorders in pregnancy (HDP), a major cause of maternal, fetal, and neonatal morbidity and mortality. Also, the HDP have been recognized as an important risk factor for cardiovascular diseases. Thus, women who develop GH or preeclampsia (PE) are at increased risk of hypertension, ischemic heart disease and stroke in later life. An ambulatory blood pressure monitoring (ABPM) takes an important role in diagnosing of hypertension in pregnancy. Also, it has been shown that ABPM had higher accuracy in the prediction of GH, premature childbirth and low birth weight, compared with the conventional blood pressure (BP) measurements. In addition, we have found that non-dipping pattern of BP is very highly related with worse pregnancy outcome in a term of preterm delivery and intrauterine growth restriction. Also, it is associated with worse maternal hemodynamics, more impaired systolic function and more pronounced cardiac remodeling compared to women with GH and dipping pattern of BP. This review aimed to explore the (a) current classifications of the HDP; (b) pathogenesis of GH and PE; (c) physiological changes of BP and maternal hemodynamics in pregnancy; and (d) pathophysiological changes of BP and maternal cardiac function, especially in a term on BP pattern.


  • echocardiography
  • fetal growth restriction
  • hemodynamics
  • pregnancy
  • blood pressure
  • cardiac function

1. Introduction

The hypertensive disoders in pregnancy (HDP) have a great clinical significance both for mother and for fetus, complicating up to 15% of pregnancies. Approximately 15–33% of the total maternal mortality and quarter of all antenatal admissions during pregnancy is due to HDP [1]. Hypertensive pregnant women are at higher risk of intracranial bleeding, severe organ failure and disseminated intravascular coagulopathy. Hypertension is associated with placental abruption, intrauterine growth restriction (IUGR) and fetal death. Fetal mortality is 4% higher if mother has hypertension during pregnancy, and even 7% more if preeclampsia (PE) develops [2, 3, 4]. In addition, preeclampsia is one of the most common causes of preterm delivery and 25% cases of very low birth weight (<1500 g) is due to PE. Also, it has been found that mothers’ deaths due to HDP in developing countries, are taking epidemic proportions, and that mortality rates in these countries are 100–200 times higher than in Europe and North America [5].


2. Hypertensive disoders in pregnancy, definition and classification

2.1. Definition of hypertension in pregnancy

The definition of hypertension in pregnancy is based on absolute blood pressure (BP) values according to the JNC 8 classification and is defined as systolic blood pressure (SBP) value ≥140 mmHg and/or diastolic blood pressure (DBP) ≥ 90 mmHg [1, 6]. In contrast to the gradation of hypertension of the European Association for Hypertension for a general (non-pregnant) population there are two stages of hypertension in the pregnancy: mild (140–159/90–109 mmHg) and severe (≥160/110 mmHg) hypertension [7, 8].

2.2. Classification of hypertensive disoders in pregnancy

There are several classifications of the hypertensive disoders in pregnancy (HDP) in contemporary literature.

We consider that the classification of the International Society for the Study of Hypertension in Pregnancy (ISSHP) is the most appropriate and least confusing: chronic hypertension, gestational hypertension (GH), preeclampsia (PE)—de novo or superimposed on chronic hypertension and white coat hypertension (WCH) [9].

2.2.1. Chronic hypertension

Chronic hypertension exists before pregnancy or develops before 20 weeks of gestation (GW) and persists 42 days post-partum. It complicates 1–5% of pregnancies and may be associated with proteinuria.

2.2.2. Gestational hypertension

Gestational hypertension (GH) is pregnancy-induced hypertension with occurrence after 20 GW and resolves within 42 days post-partum. This means that after 42 days post-partum, re-assessment to be sure that it is not chronic hypertension, is necessary. It is characterized by poor organ perfusion. It complicates 6–7% of pregnancies. [8].

2.2.3. Preeclampsia: de novo or superimposed on chronic hypertension

If GH is associated with clinically significant proteinuria (≥0.3 g/day in a 24 h urine collection) then it is known as preeclampsia (PE). It is a pregnancy-specific syndrome that occurs after mid-gestation, defined by de novo appearance of hypertension, accompanied by new-onset of significant proteinuria. It is a systemic disorder with both maternal and fetal manifestations. Edema is no longer considered part of the diagnostic criteria, as it occurs in up to 60% of normal pregnancies. Overall, PE complicates 5–7% of pregnancies, but increases to 25% in women with chronic hypertension. It is associated with placental insufficiency, often resulting in IUGR [8, 10]. ISSHP consider that PE is diagnosed when de novo hypertension is accompanied by (a) proteinuria, or (b) evidence of other maternal organ system dysfunction such as impaired GFR, neurological problems, thrombocytopenia, abnormal liver function or (c) fetal growth restriction. Severe PE includes blood pressure ≥ 160 mmHg systolic or ≥110 mmHg diastolic but is not based upon the degree of proteinuria. This is recommended for use in research but in clinical practice all cases of preeclampsia should be considered potentially severe. Early onset preeclampsia is apparent before 34 GW. It is important to note that PE occurs in about 50% of pregnant women in whom GH appeared between 24 and 35 GW [8].

Symptoms and signs of severe preeclampsia include (Figure 1): pain in the upper abdomen (due to liver edema/hepatic hemorrhage), headache—visual disturbance (cerebral edema), hyperreflexia—clonus—convulsions (cerebral edema), HELLP syndrome: hemolysis, elevated liver enzymes, low platelet count.

Figure 1.

Signs and symptoms of severe preeclampsia (HELLP: hemolysis, elevated liver enzymes, low platelet count).

Since proteinuria may appear later, pregnant woman with de novo hypertension accompanied by headache, visual disturbances, abdominal pain, or abnormal laboratory tests, specifically low platelet count and abnormal liver enzymes should be treated as PE [9, 11].

The relatively new term is non-proteinuric PE. Recent study highlighted differences between non-proteinuric PE and GH and suggested that the subclassification of “non-proteinuric preeclampsia” should be added to existing classification of HDP. It is worth mentioning that non-proteinuric PE presents significant risk to the mother but less risk to the baby than proteinuric PE [12]. ISSHP recommends a diagnosis of preeclampsia that may not necessarily include proteinuria [9].

2.2.4. White-coat hypertension

White-coat hypertension (WCH) has been recognized in one quarter of patients with elevated office blood pressure (OBP) in the general population [13]. If a diagnosis of WCH is confirmed in the first half of pregnancy, that means normal BP using 24 h ambulatory BP monitoring (ABPM), pregnant women can be managed with regular home blood pressure (HBP) assessments. Antihypertensives can be avoided, at least up to BP levels of 160–170/110 mmHg. It is considered that near half women with WCH will develop true GH or PE [14].

ISSHP recommends that the criterion for defining hypertension in pregnancy depends on the method of measuring BP. If OBP measurement is ≥140/90 mmHg before 20 GW, it is necessary to preform ABPM. If values are:

  • awake BP ≥ 130 /80 mmHg

  • sleep BP ≥ 115/70 mmHg,

it is a diagnose of chronic hypertension and risk of PE is 25%. There is a need to monitor with HBP measurement if a white-coat effect is apparent on ABPM.

If values are:

  • awake BP ≤ 130 /80 mmHg

  • sleep BP ≤ 115/70 mmHg,

it is a diagnose of WCH, risk of GH is 50% and risk of PE is 8%.

For HBP measurement ≥135 /85 mmHg after 20 GW, hypertension is diagnosed [15].


3. Pathogenesis in gestational hypertension and preeclampsia

It is still common to consider GH and PE as “diseases of many theories” [16].

The most consistent findings indicate that an inadequate function of trophoblast, plays an important role in their origin. Actually, in normotensive pregnancies trophoblasts invade the wall of the spiral arteries and this process takes place in two phases. The first one is during the first trimester when there is a significant transformation of the decidual parts of the spiral arteries. There is a degeneration of an inner, elastic layer, and consequently the destruction of a middle, muscular, and external layer. Destroyed structures of the arterial wall are replaced by hyaline and fibrin.

The second phase coincides with the second trimester. At that time, the endovascular invasion of trophoblast involves the segment of the arcuate arteries, belonging to the myometrium. Unlike the first phase, the invasion takes place only to the muscular layer. Process is the most intense between 16 and 20 GW, and at the same time there is the largest drop in resistance of uteroplacental circulation. These morphological changes allow maximum blood flow with the least resistance through dilated blood vessels to the fetus. On the other hand, morphologically altered blood vessels become relatively insensitive to vasoconstrictor substances because they have very few smooth muscles.

The lack of endothelin 1 (ET1) in trophoblast cells during the first trimester causes inadequate proliferation and invasion of trophoblast cells, causing the absence of physiological changes in the spiral arteries of the uterus, the musculoelastic layer of spiral arteries remains unchanged, and the arteries remain narrowed throughout the pregnancy and sensitive to vasoconstrictor substances. As a consequence, there is a reduced blood supply of the placenta and hypoxia of the placenta and the fetus. This causes increased secretion of ET1 with an increase in its concentration in the bloodstream and consequent vasoconstriction. The pathophysiological mechanism itself further leads to so-called “vicious cycle” (Figure 2) because vasoconstriction provokes insufficiency of the placenta. This is an oxidative stress that causes an endothelial dysfunction, leads to reduced secretion of vasodilatory substances (nitric oxide—NO, prostacyclin, thromboxane A2), with simultaneous increased secretion of vasoconstrictor substances (ET1, serotonin, neuropeptide Y). Another, not less important reason for provocation and maintenance GH, is an increased reactivity of blood vessels to angiotensin II in women with this type of hypertension (in normotensive pregnant women, reactivity to this most powerful vasoconstrictor is physiologically reduced) [16, 17, 18, 19, 20].

Figure 2.

Pathophysiology of gestational hypertension and preeclampsia—“vicious cycle”.


4. Physiology changes in arterial blood pressure in pregnancy

There are numerous changes in the body of the pregnant woman as a result on an adaptation to the newborn condition. In the first trimester of pregnancy, due to a development of a new vascular network, relaxation of the blood vessels and increased influence of mediators such as NO, prostacyclin, thromboxane A2, peripheral vascular resistance decreases, causing a systemic vasodilatation which results in a physiological fall in arterial BP in that period. Systolic BP drops during the first two trimesters, with an increase in the third. Due to declining tonus of blood vessels, the decrease of diastolic BP is more prominent than systolic.

This may mask the chronic hypertension and, when hypertension is recorded later in pregnancy, it may be interpreted as gestational.

Although there is an increase in plasma renin activity during pregnancy, blood vessels of pregnant women are refractory to the vasoconstrictor effect of angiotensin II. In the further course of gravidity, there is an increase of BP, but always in the reference values ​​ [21, 22, 23, 24, 25]. Mean arterial pressure (MAP), as well as peripheral vascular resistance, are also decreased during the first two trimesters, and elevated in the third trimester [26]​​.


5. Changes of blood pressure in gestational hypertension

As it has been already mentioned, in contrast to normotensive pregnancy characterized by systemic vasodilatation, there is systemic vasoconstriction that caused the increase in the total vascular resistance (TVR) in GH [27, 28]. More frequent absence of dipping profile of BP in women who develop hypertension in pregnancy was registered by performing ABPM [29, 30, 31].

5.1. 24-h arterial blood pressure pattern

5.1.1. Classification

There is a predictable pattern of BP in healthy individuals—BP is normally lower during the night-time and higher during the daytime. A dipping pattern represents a drop of nocturnal BP for >10%, of the daytime BP—their ratio is between 0.8 and 0.9 [32]. Absence of the night-time BP drop (<10% of the daytime BP, i.e., their ratio is between 0.9 and 1—non-dipping pattern) is a crucial risk factor for the cardiac and cerebrovascular events, also for the remodeling of the left ventricle (LV) in general population [33]. An increase in the prevalence of dipping profile by 10% reduces cardiovascular morbidity for 25% [34].

It is necessary to know that there are so-called extreme dippers—when a nocturnal drop of BP is >20%, (average nightly and average daily BP ratio is less than 0.8) and inverse dippers—there is no drop in BP during the night, on the contrary, there is an increase over the daily BP values (the ratio of average nightly and average daily BP is greater than 1) [32, 35].

5.1.2. The causes of the non-dipping pattern of blood pressure

There are several causes of the non-dipping pattern of BP: endocrinological disorders, renal dysfunction, disorder of the autonomic nervous system, salt-sensitivity hypertension, preeclampsia, malignant hypertension, heart transplantation, menopause, ethnicity, sex, metabolic syndrome, obesity, age, and smoking.

Some of the listed reasons can be of importance for developing GH. Disorder of the autonomic nervous system

It is known that excessive sympathetic activity or decreased parasympathetic activity has an inadequate drop in BP during the night [36]. There is the greatest sympathetic activity overnight in inverse dippers [37], i.e., there is a significant negative correlation between sympathetic activity and a fall of BP during the night. Non-dippers have a lower drop in catecholamine levels in the urine overnight compared with dippers, and a higher activity of an α1-adrenergic receptors. [38]. Sensitivity to NaCl

Hypertensive patients, sensitive to NaCl intake do not have an adequate fall in night-time BP, while they are eating a food rich in salt. If they reduce the NaCl intake, they become dippers. The opposite, people who are resistant to NaCl intake, has no significant change in BP overnight regardless of salt intake [39, 40]. Obesity

The body mass index is inversely proportional to the drop in the night-time BP, and the prevalence of the non-dipping pattern is greater among obese people [41]. The possible cause is an increase in the concentration of catecholamines in the blood of obese people [42]. Gender

Hypertensive women with non-dipping profile have a significantly higher risk of cardiovascular events in the future than women with dipping pattern. There is no such difference in men [43]. Preeclampsia

It has been shown that there is a connection between non-dipping profile in the first trimester of pregnancy in normotensive pregnant women with a subsequent onset of hypertension and PE, but also with IUGR [44, 45]. Eight of hypertensive pregnant women whose pregnancy were complicated with PE, had an increased activity of the sympathetic autonomic nervous system [46].

5.2. Role of 24-h ambulatory blood pressure monitoring

ABPM provides the most accurate and reliable determination of the BP pattern. The results obtained by ABPM significantly more correlated with target organ damage, as well as with the prognosis of cardiovascular events, than the results obtained during an OBP measurements [33, 47, 48, 49, 50]. In addition, ABPM is also recommended for the detection of the WCH [13].

It has been shown that ABPM is superior to OBP in the prognosis of premature termination of pregnancy, low birth weight and onset of proteinuria later in pregnancy [51, 52, 53]. A prospective double-blind study, revealed that differences in the daily-night BP pattern in hypertensive pregnant women can be helpful in determining the severity of PE and that the increase in night-time BP predominantly occurs in PE [54].

It is well known that nocturnal hypertension is associated with an exacerbation of endothelial damage in PE [55]. On the other hand, recent study has shown that the non-dipping pattern of BP in GH is associated with IUGR, preterm delivery and with the deterioration of maternal hemodynamics [56].


6. Physiology changes in cardiac function and geometry in pregnancy

Due to so-called systemic vasodilatation, characteristic of the first and the second trimester of pregnancy and decreased resistance of peripheral arteries, activation of the compensatory homeostatic mechanisms of blood flow—sympathetic nervous system, renin-angiotensin-aldosterone system, and non-osmotic secretion of vasopressin occurs. It leads to retention of sodium and water, and consequently to a purposefully increase of intravascular fluid to provide sufficient uteroplacental circulation in order to assure development and growth of the fetus [57]. This expansion of the intravascular volume leads to an increase in stroke volume (SV), which reaches the highest values ​​between 30 and 36 GW. Due to this increase, but also because of the rise in heart rate, the cardiac output also (CO) increases. Compared with the period before pregnancy, the heart rate is 16–35% higher during pregnancy [58, 59, 60, 61], as a compensatory mechanism due to vasorelaxation, to provide an adequate CO [23].

All mentioned leads to changes in cardiac morphology and systolic and diastolic function during pregnancy. Myocardial contractility increases, resulting in a shortening of the pre-ejection time with the prolongation of the left ventricular (LV) ejection time (ET), which is consequence of an increased SV. Most studies have shown that the parameters of systolic function, such as an ejection fraction (EF), end-diastolic volume of the LV (LVEDV), SV, ET, the systolic velocity of the mitral-septal and lateral anulus (s’), progressively increase during pregnancy, with a slightly lower value in the third trimester [62, 63, 64]. There is an increase in the volume of the left and right atrium, the left and right chambers, and the thickening of the walls of the LV, which with an increased preload in the first half of the pregnancy and an increased afterload in the last trimester of pregnancy, leads to physiological cardiac hypertrophy and to increase of myocardial mass. The LV hypertrophy becomes visible in the second trimester, while maximum values are reached toward the end of the pregnancy [23, 25, 61, 62, 64]. Myocardial mass is 12–30% higher than before pregnancy [23, 25, 61]. Due to increased preload, and therefore increased LVEDV, according to Frank Starling’s law, there is an increase in the strength of muscle contraction during the systole. Also, due to the increase in LVEDV and end-diastolic left ventricular diameter, there is an increase of the pressure on the walls of the LV, that leads to increased CO and oxygen demands. According to Laplace’s law, wall stress is directly proportional to the pressure on the wall of the LV and the radius of the chamber, and inversely proportional to the thickness of the walls. In order to reduce wall stress, the walls of the left ventricle become thicker [65, 66, 67].

An increased preload in the first and the second trimester of pregnancy also affects changes in diastolic function, and there is an increase of the velocity of an early filling of the LV (E), but also an increase of the velocity of a late filling of the LV (A). Thus, during this period, the ratio E/A remains unchanged. In the last trimester of pregnancy, when there is an increase of MAP and peripheral vascular resistance, and consequently increase of afterload, the early stage of diastolic filling slows down. It is reflected in the reduction of E wave velocity and the deceleration time of E wave (DTE). As a consequence, there is a greater retention of blood in the left atrium (LA) at the end of the diastole, and consequently increase of LA work that leads to an increase of A wave velocity. The increase of A wave is also affected by an increase of heart rate. During this period there is a decrease of E/A ratio [63, 64, 65, 66, 67, 68, 69]. While some authors suggested that there is prolongation of the isovolumetric relaxation time of the LV (IVRT), others did not show significant changes in it during pregnancy [70].


7. Changes in cardiac function in gestational hypertension/preeclampsia

There are two hemodynamic disorders, characteristic for GH and PE, both the consequences of the endothelial dysfunction: reduction of CO and increasing of TVR. The first one is a result of the reduction of the total plasma volume [71, 72, 73]. The second one occurs because of vasoconstriction, increased sensitivity of blood vessels to angiotensin II and increased peripheral vascular resistance. It is interesting to note that the transition from a hypervolume state with increased CO ​​and decreased TVR into a condition characterized by low CO and high TVR coincides with the clinical manifestation of symptoms and signs in women whose pregnancies are complicated by hypertension and preeclampsia [26, 28, 74, 75].

7.1. Systolic function in gestational hypertension/preeclampsia

Mentioned hemodynamic changes affect the function and morphology of the LV. According to the literature data, which are unfortunately, due to the specificity of the problem, still scarce and done in a small number of cases, there is mainly a change of the diastolic function of LV in GH, while the data on the change of the systolic function are fewer and more controversial [76, 77, 78, 79].

The systolic function is determined by the ability of the heart muscle to make contraction and to pump the blood (stroke volume) into the arterial system. One of the reasons for an inconsistent data about systolic function of the LV in GH is that in most studies the systolic function was evaluated using standard parameters such as EF and SV, which are dependent, besides the contractility of the heart, on volume and heart rate. Besides, the heart loses its classical ellipsoid shape during the pregnancy [23, 80]. In order to avoid the influence of geometric remodeling, but also the influence of preload, the longitudinal systolic function of the LV has to be evaluated (Figure 3). Myofibrils of the LV are arranged mainly longitudinally and oblique in the subendocardial and subepicardial layers, and circumferently in the middle layers. LV subendocardial fibers are more susceptible than the circumferential fibers to the effects of ischemia or pressure-load. First, there is a contraction of the longitudinal and the oblique myofibrils at the onset of the systole, causing a spherical LV shape, and then contraction of the circumferential myofibrils, which are responsible for the ejection [81].

Figure 3.

The longitudinal systolic function of the LV evaluated by tissue Doppler measurement—s′—longitudinal systolic velocity at mitral valve annulus.

The longitudinal systolic velocity—s′ and end-systolic elasticity of the left ventricle (Ees), parameters independent of the volume, are more precise measure of contractility of the heart than EF and SV [64, 82, 83, 84, 85, 86]. More recently, the relationship between effective arterial elasticity (Ea), which is the measure of afterload, and the elasticity of the LV at the end of the systole—Ea/Ees, has been used. The elasticity of the LV at the end of the systole shows how much the end-systolic volume of the LV increases, and the SV decreases in response to an increase of end-systolic pressure [86]. The velocity of the contraction of circumferential myofibrils (Vcf) is also a parameter that indicates the condition of the left ventricular systolic function. Similarly as the longitudinal systolic function, Vcf also decreases towards the end of the pregnancy, but never below the reference values. On the other hand, the pressure-load parameter—end-systolic wall stress (ESS) increases, especially in the third trimester, so the ratio between Vcf and ESS decreases [64, 87].

More precise data on the myocardial contractility are obtained using these parameters in patients who have a preserved EF (i.e., a preserved pump function of the heart), as the subendocardial layers of the LV are more sensitive to ischemia.

Most of the authors consider that there is depression of systolic function either as decrease of EF, SV and CO, either as decrease of longitudinal systolic velocity s′ [69, 78, 85].

It has been shown that regional longitudinal systolic function is markedly reduced in preeclamptic women, without regional systolic abnormalities in GH (had not observed an impact of the non-dipping pattern) [88]. Similarly, we have revealed that longitudinal systolic function is significantly reduced in women with GH and non-dipping pattern of BP, compared with both, normotensive pregnant women and those who developed GH with dipping pattern of BP, without the difference between normotensive and dippers in GH, as well as Vcf. Also, CO index was the most reduced, while Ees was the most increased in non-dippers [56].

7.2. Diastolic function in gestational hypertension/preeclampsia

The diastolic function is the ability of the LV to fill up to the normal end-diastolic volume, both at rest and in effort, with the mean pressure in LA ≤ 12 mmHg. The optimal function of the left ventricle depends on two cycles: its ability to relax and its compliance. Ability of the LV to relax, allows filling of the LV chamber from the LA in diastole. An increase in the chamber’s compliance due to a sudden increase in pressure in the LV, enables the ejection of the SV into the arterial system in the systole. Since the LV relaxation process is more dependent on energy than the contraction of the heart muscle, it is logical that abnormalities of the diastolic function occur before systolic dysfunction in all situations in which myocardial circulation is compromised (ischemia, increased myocardial mass, hypertrophy) [89, 90].

If there is an increased need, for example during physical effort, pregnancy, the SV is increased without a significant increase in pressure in the LA [91]. This optimal situation is possible due to the cyclic interaction of myofilaments and the competence of the mitral and aortic valve [92]. Increased afterload will lead to decreased relaxation, especially if there is an increased preload, and this will contribute to increase of the LV filling pressure. This increase in pressure is the main consequence of the diastolic dysfunction [92, 93].

As it is mentioned, during pregnancy there is an increase in preload and myocardial mass. In hypertensive pregnancies, due to increased after-load and peripheral vascular resistance, hemodynamics is further complicated. There is a more pronounced decrease in the E/A ratio, prolongation of IVRT and DTE, changes of volume and dimensions of the LA [77, 78, 79, 80, 81]. In normotensive pregnant women, increased preload and decreased afterload lead to improved discharge of the LV during systole and reduction of end-systolic pressure. This results in a decrease of the pressure gradient between the LA and the LV, that reduces the required time for the drop of the pressure in the LV below the values of the pressure in the LA. As a result, filling of the LV in the diastole is done under the best conditions [25, 94]. In GH, increased afterload and TVR are followed by reduction in the LV discharge, leading to increased end-systolic volume and then to increased end-systolic pressure. This explains the prolonged IVRT because it takes longer time for the drop of the LV pressure below the LA pressure values. The delayed opening of the mitral valve and reduced LV compliance lead to reduced filling of the LV in the diastole.

It was revealed that diastolic function is more impaired in non-dippers with GH, compared to dippers, as well as global cardiac function and cardiac remodeling [56].


8. Conclusions

Recent studies have shown that the determination of the non-dipping pattern of BP, and therefore the role of ABPM, is of a great importance in women with GH.

Being an important risk factor for the remodeling of the LV in general population, the non-dipping profile of BP is also associated with a deterioration of maternal hemodynamics in GH. It is revealed that a depression of systolic function, an impaired diastolic function and remodeling of the LV are more pronounced in non-proteinuric women with non-dipping pattern of BP then in women with GH and dipping profile of BP. Besides, the non-dipping pattern was related with IUGR and preterm delivery.

According to the fact that, until nowadays, there are no data about the reversibility of these changes after delivery in the term on BP pattern, further research is needed to reveal that.138728


Conflicts of interest

None declared.


Apeak velocity of the A wave
ABPMambulatory blood pressure monitoring
BPblood pressure
DBPdiastolic blood pressure
DTEdeceleration time of the E wave
Epeak velocity of the E wave
Eaeffective arterial elastance
E/e′index of the left ventricular filling pressure
Eesleft ventricular end-systolic elastance
EFejection fraction of the left ventricle
ESSend-systolic wall stress
ETejection time of the left ventricle
ET1endothelin 1
GHgestational hypertension
HDPhypertensive disoders in pregnancy
ISSHPInternational Society for the Study of Hypertension in Pregnancy
IVRTisovolumetric relaxation time of the LV
COcardiac output
GWgestational week
HBPhome blood pressure
HRheart rate
IUGRintrauterine growth restriction
LAleft atrium
LVleft ventricle
LVEDVleft ventricle end-diastolic volume
MAPmean blood pressure
massleft ventricle myocardial mass
NOnitric oxide
OBPoffice blood pressure
SBPsystolic blood pressure
s′longitudinal systolic velocity at mitral valve annulus
SVstroke volume
TVRtotal vascular resistance
Vcfcircumferential systolic velocity
WCHwhite coat hypertension


  1. 1. James PR, Nelson-Piercy C. Management of hypertension before, during, and after pregnancy. Heart. 2004;90:1499-1504. DOI: 10.1136/hrt.2004.035444
  2. 2. Magee LA, Helewa M, Moutquin J-M, et al. Diagnosis, evaluation, and management of the hypertensive disorders of pregnancy. Journal of Obstetrics and Gynaecology Canada. 2008;30:S1-S48. DOI: 10.1016/S1701-2163(16)32776-1
  3. 3. ACOG. Practice bulletin no. 125: Chronic hypertension in pregnancy. Obstetrics and Gynecology. 2012;119(2 Pt 1):396-407. DOI: 10.1097/AOG.0b013e318249ff06
  4. 4. Working Group Report on High Blood Pressure in Pregnancy. Journal of Clinical Hypertension. 2001;3:75-88. DOI: 10.1111/j.1524-6175.2001.00458.x
  5. 5. Mackay AP, Berg CJ, Atrash HK. Pregnancy-related mortality from preeclampsia and eclampsia. Obstetrics and Gynecology. 2001;97:533-538. DOI: 10.1016/S0029-7844(00)01223-0
  6. 6. James PA, Oparil S, Carter BL, et al. Evidence-based guideline for the management of high blood pressure in adults. Report from the panel members appointed to the eighth joint national committee (JNC 8). Journal of the American Medical Association. 2014;311(5):507-520. DOI: 10.1001/jama.2013.284427
  7. 7. Chobanian AV, Bakris GL, Black HR, Cushman WC, Green LA, Izzo JL Jr, Jones DW, Materson BJ, Oparil S, Wright JT Jr, Roccella EJ. Seventh report of the joint national committee on prevention, detection, evaluation, and treatment of high blood pressure. Hypertension. 2003;42:1206-1252. DOI: 10.1161/01.HYP.0000107251.49515.c2
  8. 8. The Task Force on the Management of Cardiovascular Diseases during Pregnancy of the European Society of Cardiology (ESC). ESC Guidelines on the management of cardiovascular diseases during pregnancy. European Heart Journal. 2011;32:3147-3197. DOI: 10.1093/eurheartj/ehr218
  9. 9. Tranquilli AL, Dekker G, Magee L, Roberts J, Sibai BM, Steyn W, Zeeman G, Brown MA. The classification, diagnosis and management of the hypertensive disorders of pregnancy: A revised statement from the ISSHP. Pregnancy Hypertension: An International Journal of Women's Cardiovascular Health, DOI. 2014;4:97-104. DOI: 10.1016/j.preghy.2014.02.001
  10. 10. Steegers EA, von Dadelszen P, Duvekot JJ, Pijnenborg R. Pre-eclampsia. Lancet. 2010;376:631-644. DOI: 10.1016/S0140-6736(10)60279-6
  11. 11. Holston AM, Qian C, Yu KF, Epstein FH, Karumanchi SA, Levine RJ. Circulating angiogenic factors in gestational proteinuria without hypertension. American Journal of Obstetrics and Gynecology. 2009;200(4):392e1-10. DOI: 10.1016/j.ajog.2008.10.033
  12. 12. Homer CS, Brown MA, Mangos G, Davis GK. Non-proteinuric pre-eclampsia: A novel risk indicator in women with gestational hypertension. Journal of Hypertension. 2008;26(2):295-302. DOI: 10.1097/HJH.0b013e3282f1a953
  13. 13. Franklin SS, Thijs L, Hansen TW, O’Brien E, Staessen JA. White-coat hypertension: New insights from recent studies. Hypertension. 2013;62(6):982-987. DOI: 10.1161/HYPERTENSIONAHA.113.01275
  14. 14. Brown MA, Mangos G, Davis G, Homer C. The natural history of white coat hypertension during pregnancy. BJOG : An International Journal of Obstetrics and Gynaecology. 2005;112(5):601-606. DOI: 10.1111/j.1471-0528.2004.00516.x
  15. 15. Brown M. Is there a role for ambulatory blood pressure monitoring in pregnancy? Clinical and Experimental Pharmacology & Physiology. 2014;41(1):16-21. DOI: 10.1111/1440-1681.12106
  16. 16. Broughton Pipkin F, Rubin PC. Pre-eclampsia—“the disease of theories”. British Medical Bulletin. 1994;(2):381-96. DOI: /10.1093/oxfordjournals.bmb.a072898
  17. 17. Granger JP, Alexander BT, Bennett WA, Khalil RA. Pathophysiology of pregnancy-induced hypertension. American Journal of Hypertension. 2001;14(3):S178-S185. DOI: 10.1016/S0895-7061(01)02086-6
  18. 18. Lyall F, Bulmer JN, Duffie E, Cousins F, Theriault A, Robson SC. Human trophoblast invasion and spiral artery transformation. The role of PECAM-1 in normal pregnancy, preeclampsia, and fetal growth restriction. The American Journal of Pathology. 2001;158(5):1713-1721. DOI: 10.1016/S0002-9440(10)64127-2
  19. 19. Pijnenborg R, Luyten P, Vercrusysse L, Van Assche FA. Attachement and differentation in vitro of trophoblast from normal and preeclamptic human placentas. American Journal of Obstetrics and Gynecology. 1996;175:30-36. DOI: 10.1016/S0002-9378(96)70246-6
  20. 20. Many A, Hubel CA, Fisher SJ, Roberts JM, Zhou Y. Invasive cytotrophoblasts manifest evidence of oxidative stress in preexlampsia. The American Journal of Pathology. 2000;156:321-331. DOI: 10.1016/S0002-9440(10)64733-5
  21. 21. Robertson WB, Manning PJ. Elastic tissue in uterine blood vessels. The Journal of Pathology. 1974;112:237-243. DOI: 10.1002/path.1711120408
  22. 22. Peters RM, Flack JM. Hypertensive disorders of pregnancy. Journal of Obstetric, Gynecologic, and Neonatal Nursing. 2004;33:209-220. DOI: 10.1177/0884217504262970
  23. 23. Duvekot JJ, Cheriex EC, Pieters FA, Menheere PP, Peeters LH. Early pregnancy changes in hemodynamics and volume homeostasis are consecutive ajustments triggered by a primary fall in systemic vascular tone. American Journal of Obstetrics and Gynecology. 1993;169:1382-1392. DOI: 10.1016/0002-9378(93)90405-8
  24. 24. Carbillon L, Uzan M, Uzan S. Pregnancy, vascular tone, and maternal hemodynamics: A crucial adaptation. Obstetrical & Gynecological Survey. 2000;55:574-581. DOI: 10.1097/00006254-200009000-00023
  25. 25. Poppas A, Shroff SG, Korcarz CE, Hibbard JU, Berger DS, Lindheimer MD, Lang RM. Serial assessment of the cardiovascular system in normal pregnancy. Role of arterial compliance and pulsatile arterial load. Circulation. 1997;95:2407-2415. DOI: 10.1161/01.CIR.95.10.2407
  26. 26. Hall ME, George EM, Granger JP. The heart during pregnancy. Revista Española de Cardiología. 2011;64:1045-1050. DOI: 10.1016/j.recesp.2011.07.009
  27. 27. Prefumo F, Sharma R, Brecker SJ, Gaze DC, Collinson PO, Thilaganathan B. Maternal cardiac function in early pregnancies with high uterine artery resistance. Ultrasound in Obstetrics & Gynecology. 2007;29:58-64. DOI: 10.1002/uog.3878
  28. 28. Bosio P, McKenna P, Conroy R. O’Herlihy. Maternal central hemodynamics in hypertensive disorders of pregnancy. Obstetrics and Gynecology. 1999;94:978-984. DOI: 10.1097/00006250-199912000-00014
  29. 29. Tranquilli AL, Giannubilo SR. Blood pressure is elevated in normotensive pregnant women with intrauterine growth restriction. European Journal of Obstetrics, Gynecology, and Reproductive Biology. 2005;122:45-48. DOI: 10.1016/j.ejogrb.2004.11.020
  30. 30. Ramon C, Hermida R, Ayala D, Mojon A, Fernandez J, Alonso I, Silva I, Uciede R, Iglesias M. Blood pressure patterns in normal pregnancy, gestational hypertension and preeclampsia. Hypertension. 2000;36:149-158. DOI: 10.1161/01.HYP.36.2.149
  31. 31. Thadhani R, Ecker J, Kettyle E, Sandler L, Frigolleto F. Pulse pressure and risk of preeclampsia: A prospective study. Obstetrics and Gynecology. 2001;97:515-520
  32. 32. Mancia G, Fagard R, Narkiewicz K, Redon J, Zanchetti A, Bohm M, Christiaens T, Cifkova R, De Backer G, Dominiczak A, Galderisi M, Grobbee DE, Jaarsma T, Kirchhof P, Kjeldsen SE, Laurent S, Manolis AJ, Nilsson PM, Ruilope LM, Schmieder RE, Sirnes PE, Sleight P, Viigimaa M, Waeber B, Zannad F. ESH/ESC guidelines for the management of arterial hypertension: The task force for the management of arterial hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC). European Heart Journal. 2013;34:2159-2219. DOI: 10.1093/eurheartj/eht151
  33. 33. Boggia J, Li Y, Thijs L, Hansen TW, Kikuya M, Bjorklund-Bodegard K, Richart T, Ohkubo T, Kuznetsova T, Torp-Pedersen C, Lind L, Ibsen H, Imai Y, Wang J, Sandoya E, O’Brien E, Staessen JA. Prognostic accuracy of day vs. night ambulatory blood pressure: A cohort study. Lancet. 2007;370:1219-1229. DOI: 10.1016/S0140-6736(07)61538-4
  34. 34. Hermida RC, Ayala DE, Mojón A, Fernández JR. Decreasing sleep-time blood pressure determined by ambulatory monitoring reduces cardiovascular risk. Journal of the American College of Cardiology. 2011;58:1165-1173. DOI: 10.1016/j.jacc.2011.04.043
  35. 35. O’Brien E, Sheridan J, O’Malley K. Dippers and non-dippers. Lancet. 1988;2:397. DOI: 10.1016/S0140-6736(88)92867-X
  36. 36. Kario K, Mitsuhashi T, Shimada K. Neurohumoral characteristics of older hypertensive patients with abnormal nocturnal blood pressure dipping. American Journal of Hypertension. 2002;15:531-537. DOI: 10.1016/S0895-7061(02)02266-5
  37. 37. Sherwood A, Steffen PR, Blumenthal JA, Kuhn C, Hinderliter AL. Nighttime blood pressure dipping: The role of the sympathetic nervous system. American Journal of Hypertension. 2002;15:111-118. DOI: 10.1016/S0895-7061(01)02251-8
  38. 38. Kohara K, Nishida W, Maguchi M, Hiwada K. Autonomic nervous function in non-dipper essential hypertensive subjects. Evaluation by power spectral analysis of heart rate variability. Hypertension. 1995;26:808-814. DOI: 10.1161/01.HYP.26.5.808
  39. 39. Damasceno A, Caupers P, Santos A, Esperanca S, Bicho M, Polónia J. F002: Influence of salt intake on the daytime-nighttime blood pressure variation in black normotensive and hypertensive subjects. American Journal of Hypertension. 2000;13(S2):169A. DOI: 10.1016/S0895-7061(00)01138-9
  40. 40. Kimura G. Sodium, kidney, and circadian rhythm of blood prresure. Clinical and Experimental Nephrology. 2001;5:13-18. DOI: 10.1007/PL00012172
  41. 41. Cuspidi C, Meani S, Valerio C, Negri F, Sala C, Maisaidi M, Giudici V, Zanchetti A, Mancia G. Body mass index, nocturnal fall in blood pressure and organ damage in untreated essential hypertensive patients. Blood Pressure Monitoring. 2008;13(6):318-324. DOI: 10.1097/MBP.0b013e32830d4bf8
  42. 42. Krieger DR, Landsberg L. Mechanisms in obesity-related hypertension: Role of insulin and catecholamines. American Journal of Hypertension. 1988;1:84-90
  43. 43. Schmieder RE, Rockstroh JK, Aepfelbacher F, Schulze B, Messerli FH. Gender-specific cardiovascular adaptation due to circadian blood pressure variations in essential hypertension. American Journal of Hypertension. 1995;8(12 Pt 1):1160-1166
  44. 44. Tranquilli AL, Giannubilo SR, Dell’Uomo B, Corradetti A. Prediction of gestational hypertension or intrauterine fetal growth restriction by mid-trimester 24-h ambulatory blood pressure monitoring. International Journal of Gynaecology and Obstetrics. 2004;85:126-131. DOI: 10.1016/j.ijgo.2003.10.003
  45. 45. Poon LC, Kametas NA, Maiz N, Akolekar R, Nicolaides KH. First-trimester prediction of hypertensive disorders in pregnancy. Hypertension. 2009;53(5):812-818. DOI: 10.1161/HYPERTENSIONAHA.108.127977
  46. 46. Rang S, Wolf H, van Montfrans GA, Karemaker JM. Serial assessment of cardiovascular control shows early signs of developing pre-eclampsia. Journal of Hypertension. 2004;22(2):369-376. DOI: 10.1097/00004872-200402000-00022
  47. 47. Conen D, Bamberg F. Noninvasive 24-h ambulatory blood pressure and cardiovascular disease: A systematic review and meta-analysis. Journal of Hypertension. 2008;26:1290-1299. DOI: 10.1097/HJH.0b013e3282f97854
  48. 48. Fagard RH, Celis H, Thijs L, Staessen JA, Clement DL, De Buyzere ML, DeBacquer DA. Daytime and night-time blood pressure as predictors of death and cause-specific cardiovascular events in hypertension. Hypertension. 2008;51(1):55-61. DOI: 10.1161/HYPERTENSIONAHA.107.100727
  49. 49. Fagard RH, Thijs L, Staessen JA, Clement DL, De Buyzere ML, De Bacquer DA. Prognostic significance of ambulatory blood pressure in hypertensive patients with history of cardiovascular disease. Blood Pressure Monitoring. 2008;13:325-332. DOI: 10.1097/MBP.0b013e32831054f5
  50. 50. De la Sierra A, Banegas JR, Segura J, Gorostidi M, Ruilope LM. Ambulatory blood pressure monitoring and development of cardiovascular events in high-risk patients included in the Spanish ABPM registry: The CARDIORISC event study. Journal of Hypertension. 2012;30:713-719. DOI: 10.1097/HJH.0b013e328350bb40
  51. 51. Halligan A, Shennan A, Thurston H, de Swiet M, Taylor D. Ambulatory blood pressure measurement in pregnancy: The current state of the art. Hypertension in Pregnancy. 2009;13:1-16. DOI: 10.3109/10641959509058046
  52. 52. Bergel E, Carroli G, Althabe F. Ambulatory versus conventional methods for monitoring 15 blood pressure during pregnancy. Cochrane Database of Systematic Reviews. 2002;(2):16. CD001231.3537. DOI: 10.1002/14651858.CD001231
  53. 53. Waugh J, Perry IJ, Halligan AW, De Swiet M, Lambert PC, Penny JA, Taylor DJ, Jones DR, Shennan A. Birth weight and 24-hour ambulatory blood pressure in nonproteinuric hypertensive pregnancy. American Journal of Obstetrics and Gynecology. 2000;183(3):633-637. DOI: 10.1067/mob.2000.106448
  54. 54. Brown MA, Davis GK, McHugh L. The prevalence and clinical significance of nocturnal hypertension in pregnancy. Journal of Hypertension. 2001;19(8):1437-1444. DOI: 10.1097/00004872-200108000-00012
  55. 55. Bouchlariotou S, Liakopoulos V, Dovas S, Giannopoulou M, Kiropoulos T, Zarogiannis S, Gatselos G, Zachopoulos T, Kyriakou DS, Kallitsaris A, Messinis I, Stefanidis I. Nocturnal hypertension is associated with an exacerbation of the endothelial damage in preeclampsia. American Journal of Nephrology. 2008;28(3):424-430. DOI: 10.1159/000112807
  56. 56. Ilic A, Ilic DJ, Tadic S, Stefanovic M, Stojsic-Milosavljevic A, Pavlovic K, Redzek A, Velicki L. Influence of non-dipping pattern of blood pressure in gestational hypertension on maternal cardiac function, hemodynamics and intrauterine growth restriction. Pregnancy Hypertension: An International Journal of Women's Cardiovascular Health. 2017;10:37-41. DOI:
  57. 57. Duvekort J, Peeters L. Renal hemodynamics and volume homeostasis in pregnancy. Obstetrical & Gynecological Survey. 1994;49:830-839. DOI: 10.1097/00006254-199412000-00007
  58. 58. Robson SC, Dunlop W, Moore M, Hunter S. Combined Doppler and echocardiographic measurement of cardiac output: Theory and application in pregnancy. British Journal of Obstetrics and Gynaecology. 1987;94:1014-1027. DOI: 10.1111/j.1471-0528.1987.tb02285.x
  59. 59. Clapp JF 3rd. Maternal heart rate in pregnancy. American Journal of Obstetrics and Gynecology. 1985;152:659-660. DOI: 10.1016/S0002-9378(85)80040-5
  60. 60. Clapp JF 3rd, Capeless E. Cardiovascular function before, during and after the first and subsequent pregnancies. The American Journal of Cardiology. 1997;80:1469-1473. DOI: 10.1016/S0002-9149(97)00738-8
  61. 61. Mabie V, DiSessa T, Crocker L, Sibai B, Arheart K. A longitudinal study of cardiac output in normal human pregnancy. American Journal of Obstetrics and Gynecology. 1994;170(3):849-856
  62. 62. Shannwell C, Zimmermann T, Schneppenheim M, Plehn G, Marx R, Strauer B. Left ventricular hypertrophy and diastolic dysfunction in healthy pregnant women. Cardiology. 2002;97(2):73-78. DOI: 10.1159/000057675
  63. 63. Bamfo JEAK, Kametas NA, Nicolaides KH, Chambers JB. Reference ranges for tissue Doppler measures of maternal systolic and diastolic left ventricular function. Ultrasound in Obstetrics & Gynecology. 2007;29:414-420. DOI: 10.1002/uog.3966
  64. 64. Estensen ME, Beitnes JO, Grindheim G, Aaberge L, Smiseth OA, Henriksen T, Aakhus S. Altered maternal left ventricular contractility and function during normal pregnancy. Ultrasound in Obstetrics & Gynecology. 2013;41(6):659-666. DOI: 10.1002/uog.12296
  65. 65. Ommen S, Nishimura R. A clinical approach to the assessment of left ventricular diastolic function by Doppler echocardiography. Heart. 2003;89:8-23. DOI: 10.1136/heart.89.suppl_3.iii18
  66. 66. Kametas N, McAuliffe F, Hancock J, Chambers J, Nicolaides K. Maternall left ventricular mass and diastolic function during pregnancy. Ultrasound in Obstetrics and Gynecology. 2001;18:460-466. DOI: 10.1046/j.0960-7692.2001.00573.x
  67. 67. Fok WY, Chan LY, Wong JT, Yu CM, Lau TK. Left ventricular diastolic function during normal pregnancy: Assessment by spectral tissue Doppler imaging. Ultrasound in Obstetrics and Gynecology. 2006;28:789-793. DOI: 10.1002/uog.3849
  68. 68. Mesa A, Jessurun C, Hernandez A, Adam K, Brown D, Vaughn WK, Wilansky S. Left ventricular diastolic function in normal human pregnancy. Circulation. 1999;99:511-517. DOI: 10.1161/01.CIR.99.4.511
  69. 69. Borghi C, Esposti D, Immoridino V, Cassani A, Boschi S, Bovicelli L, Ambrosioni E. Relationship of systemic hemodynamics, left ventricle structure and function, and plasma natriuretic peptide concentracions during pregnancy comlicated by preeclampsia. American Journal of Obstetrics and Gynecology. 2000;183:140-147. DOI: 10.1067/mob.2000.105684
  70. 70. Bosio PM, Wheeler BT, Anthony F, Conroy R, O’herlihy C, McKenna P. Maternal plasma vascular endothelial growth factor concentrations in normal and hypertensive pregnancies and their relationship to peripheral vascular resistence. American Journal of Obstetrics and Gynecology. 2001;184:146-152. DOI: 10.1067/mob.2001.108342
  71. 71. Fievet P, Pleskov L, Desailly I, et al. Plasma raenin activity, blood uric acid and plasma volume in pregnancy-induced hypertension. Nephron. 1985;40:429-432. DOI: 10.1159/000183513
  72. 72. Levario-Carrillo M, Avitia A, Tufiño-Olivares E, Trevizo E, Corral-Terrazas MMD, Reza-López S. Body composition of patients with hypertensive complications during pregnancy. Hypertension in Pregnancy. 2009:259-269. DOI: 10.1080/10641950600913032
  73. 73. Zondervan HA, Oosting J, Smorenberg-Schoorl ME, Treffers PE. Maternal whole blood viscosity in pregnancy hypertension. Gynecologic and Obstetric Investigation. 1988;25:83-88. DOI: 10.1159/000293751
  74. 74. Craici I, Khalil A, Jauniaux E, Harrington K. Antihypertensive therapy and central hemodynamics in women with hypertensive disorders in pregnancy. Obstetrics and Gynecology. 2009;113(3):646-654. DOI: 10.1097/AOG.0b013e318197c392
  75. 75. Valensise H, Vasapollo B, Novelli GP, Pasqualetti P, Galante A, Arduini D. Maternal total vascular resistance and concentric geometry: A key to identify uncomplicated gestational hypertension. BJOG: An International Journal of Obstetrics and Gynaecology. 2006;113:1044-1052. DOI: 10.1111/j.1471-0528.2006.01013.x
  76. 76. Vazquez BM, Roisinblit J, Grosso O, Rodriguez G, Robert S, Berensztein CS, Vega HR, Lerman J. Left ventricular function impairment in pregnancy-induced hypertension. American Journal of Hypertension. Journal of the American Society of Hypertension. 2001:271-275. DOI: 10.1016/S0895-7061(00)01264-4
  77. 77. Vazquez BM, Grosso O, Bellido CA, Iavicoli OR, Berensztein CS, Ruda VH, Lerman J. Dimensions of the left ventricle, atrium, and aortic root in pregnancy-induced hypertension. American Journal of Hypertension: Journal of the American Society of Hypertension. 2001;14:390-392. DOI: 10.1016/S0895-7061(00)01250-4
  78. 78. Valensise H, Novelli GP, Vasapollo B, Di Ruzza G, Romanini ME, Marchei M, Larciprete G, Manfellotto D, Romanini C, Galante A. Maternal diastolic dysfunction and left ventricular geometry in gestational hypertension. Hypertension. 2001;37:1209-1215. DOI: 10.1161/01.HYP.37.5.1209
  79. 79. Vazquez MB, Grosso O, Bellido CA, Iavicoli OR, Berensztein CS, Vega HR, Lerman J. Left ventricular geometry in pregnancy-induced hypertension. American Journal of Hypertension: Journal of the American Society of Hypertension. 2000;13:226-230
  80. 80. Kametas N, MCAuliffe F, Cook B, Nicolaides K, Chambers J. Maternal left ventricular transverse and long-axis systolic function during pregnancy. Ultrasound in Obstetrics & Gynecology. 2001;18:467-474. DOI: 10.1046/j.0960-7692.2001.00574.x
  81. 81. Waggoner AD, Bierig SM. Tissue Doppler imaging: A useful echocardiographic method for the cardiac sonographer to assess systolic and diastolic ventricular function. Journal of the American Society of Echocardiography. 2001;14:1143-1152. DOI: 10.1067/mje.2001.115391
  82. 82. Wang M, Yip GW, Wang AY, Zhang Y, Ho PY, Tse MK, Lam PK, Sanderson JE. Peak early diastolic mitral annulus velocity by tissue Doppler imaging adds independent and incremental prognostic value. Journal of the American College of Cardiology. 2003;41:820-826. DOI: 10.1016/S0735-1097(02)02921-2
  83. 83. Palmieri V, Russo C, Arezzi E, Pezzullo S, Sabatella M, Minichiello S, Celentano A. Relations of longitudinal left ventricular systolic function to left ventricular mass, load, and Doppler stroke volume. European Journal of Echocardiography. 2006;7:348-355. DOI: 10.1016/j.euje.2005.07.007
  84. 84. Ruan Q, Nagueh SF. Usefulness of isovolumic and systolic ejection signals by tissue Doppler for the assessment of left ventricular systolic function in ischemic or idiopathic dilated cardiomyopathy. The American Journal of Cardiology. 2006;97:872-875. DOI: 10.1016/j.amjcard.2005.10.024
  85. 85. Vlahović-Stipac A, Stankić V, Popović BZ, Putniković B, Nešković A. Left ventricular function in gestational hypertension: Serial echocardiographic study. American Journal of Hypertension. 2010;23(1):85-91. DOI: 10.1038/ajh.2009.168
  86. 86. Canterin FA, Poli S, Vriz O, Pavan D, Di Bello V, Nicolosi GL. The ventricular-arterial coupling: From basic pathophysiology to clinical application in the echocardiography laboratory. Journal of Cardiovascular Echography. 2013;23(4):91-95. DOI: 10.4103/2211-4122.127408
  87. 87. Mone SM, Sanders SP, Colan SD. Control mechanisms for physiological hypertrophy of pregnancy. Circulation. 1996;94:667-672. DOI: 10.1161/01.CIR.94.4.667
  88. 88. Melchiorre K, Sutherland GR, Baltabaeva A, Liberati M, Thilaganathan B. Maternal cardiac dysfunction and remodeling in women with preeclampsia at term. Journal of Hypertension. 2011;57:85-93. DOI: 10.1161/HYPERTENSIONAHA.110.162321
  89. 89. Nagueh S, Appleton C, Gillebert T, Marino P, Oh J, Smiseth O, Waggoner A, Flachskampf F, Pellikka P, Evangelisa A. Recommendations for the evaluation of left ventricular diastolic function by echocardiography. Journal of the American Society of Echocardiography. 2009;22(2):107-133. DOI: 10.1016/j.echo.2008.11.023
  90. 90. Brutsaert DL, Sys SU, Gillebert TC. Diastolic failure: Pathophysiology and therapeutic implications. Journal of the American College of Cardiology. 1993;22:318-325. DOI: 10.1016/0735-1097(93)90850-Z
  91. 91. Yip GW, Zhang Y, Tan PY, Wang M, Ho PY, Brodin LA, Sanderson LE. Left ventricular long-axis changes in early diastole and systole: Impact of systolic function on diastole. Clinical Science (London, England). 2002;102:515-522. DOI: 10.1042/cs1020515
  92. 92. Leite-Moreira AF, Correia-Pinto J, Gillebert TC. Afterload induced changes in myocardial relaxation: A mechanism for diastolic dysfunction. Cardiovascular Research. 1999;43:344-353. DOI: 10.1016/S0008-6363(99)00099-1
  93. 93. Paulus WJ, Tschope C, Sanderson JE, Rusconi C, Flachskampf FA, Rademakers FE, et al. How to diagnose diastolic heart failure: A consensus statement on the diagnosis of heart failure with normal left ventricular ejection fraction by the heart failure and echocardiography associations of the European Society of Cardiology. European Heart Journal. 2007;28:2539-2550. DOI: 10.1093/eurheartj/ehm037
  94. 94. Valensise H, Novelli GP, Vasapollo B, Borzi M, Arduini D, Galante A, Romanini C. Maternal cardiac systolic and diastolic function: Relationship with uteroplacental resistances: A Doppler and echocardiographic longitudinal study. Ultrasound in Obstetrics & Gynecology. 2000;15:487-497. DOI: 10.1046/j.1469-0705.2000.00135.x

Written By

Aleksandra Ilic, Djordje Ilic, Jelena Papović, Snezana Stojsic, Aleksandra Milovancev, Dragana Grkovic, Anastazija Stojsic- Milosavljevic, Tatjana Redzek-Mudrinic, Artur Bjelica, Olivera Rankov and Lazar Velicki

Submitted: October 23rd, 2017 Reviewed: April 5th, 2018 Published: November 5th, 2018