Cardiac size and performance during pregnancy estimated with echocardiography

Cardiac Size and Performance During Pregnancy Estimated With Echocardiography

SHIRLEY RUBLER, MD, FACC PRABODHKUMAR M . DAMANI, MD . EDWARD R . PINTO, MD

Philadelphia, Pennsylvania

From the Cardiology Department, University of Pennsylvania Division, Philadelphia General Hospital, Center Boulevard, Philadelphia, Pennsylvania- Manuscript received January 31, 1977 ; revised manuscript received April 28, 1977, accepted May 5, 1977 . Address for reprints : Shirley Rubler, MD, Department of Cardiology, New York Veterans Administration Hospital, New York University School of Medicine, First Avenue at 24th Street, New York, NY 10010 .

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Echocardiography was performed In 55 women in the following groups : Group I, 15 normal nonpregnant control subjects ; Group 11, 13 normal women In the 13th to 23rd weeks of gestation; Group III, 15 normal women In the 24th to 32nd weeks of gestation ; and Group IV, 12 women at term pregnancy . The heart rate was 20 percent greater In pregnant women than In normal control subjects, and left ventricular dimensions and volumes were significantly larger during gestation . The right ventricular dimension was significantly Increased in women in Group 111 (P <0 .001) . Stroke volume increased by 32 percent in the 13th to 23rd weeks (Group 11, P <0 .005) and remained increased later (Group III) . There was a parallel rise in ejection fraction . Cardiac output, 3 .93 ± 0 .53 (mean f 1 standard deviation) liters/min in normal nonpregnant women, increased to 6 .05 ± 1 .58 in the second trimester (P <0 .001) and to 6 .15 4 1 .5 liters/min later in gestation (P <0 .001) . When women at term pregnancy were studied in the left lateral position they had a higher cardiac output (5 .88 ± 1 .69 liters/min) (P <0 .001) than normal control subjects (Group I), but when they were studied supine their cardiac output was almost as low as that in Group I although they had a higher heart rate . The velocity of circumferential shortening and posterior wall slope both increased to a significant extent in all pregnant women . In Group III, the velocity of circumferential shortening increased to 1 .35 ± 0 .19 circumferences/sec compared with 1 .13 f 0 .12 circumferences/sec in control subjects (P <0 .005), and the slope of posterior wall motion increased to 61 .1 ± 8.7 mm/sec compared with 50 .5 ± 4 .9 in control subjects . Cardiac output increased early in pregnancy because of an increase in both stroke volume and heart rate. Enhanced myocardial contractility may have contributed to the observed increase .

A study of pregnant women affords an excellent opportunity to observe the hemodynamic alterations in cardiac function that occur when a physiologic stress is imposed on a normal myocardium . Previous investigators' demonstrated an increase in cardiac output in the first trimester of pregnancy that persists throughout gestation until the time of delivery . However, the precise period of maximal increase is disputed . Some authors' reported that the peak occurred between 28 and 32 weeks, others 3 between 24 and 28 weeks ; recently, Metcalfe and Ueland 4 found it to occur between 20 and 24 weeks, Furthermore, cardiac output in some series' remained elevated throughout the last trimester, but in others 2ss it declined to control levels at 38 to 40 weeks . Because most prior studies 3 .5-s used invasive methods that can elicit stimulation of the sympathetic nervous system, they may not have been performed under truly basal conditions . Other studies performed in animals'' 10 demonstrated that enhanced cardiac output during pregnancy could be partially attributed to an increase in myocardial contractility ; this hypothesis has not been systematically studied in man .

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FIGURE 1 . Echocardiogam of a normal control subject demonstrating method of measurement of right and left ventricle- cai = carotid pulse tracing ; EKG = electrocardiogram; IVS = interventricular septum ; Ivldd = left ventricular dimension in diastole ; Ivids = left ventricular dimension in systole ; pw = posterior wall of left ventricle ; Rv = right ventricular dimension in diastole .

Two recent investigations' 1,12 using noninvasive techniques demonstrated abbreviation of the preejection period during pregnancy and raised the possibility that such increased contractility might indeed exist. The use of echocardiography permits one to estimate myocardial performance in the basal state and to assess chamber size without subjecting the pregnant patient to cardiac catheterization or angiography or exposing her to x-irradiation . It is the only technique that can be employed with complete safety, can be repeated at frequent intervals and is entirely without discomfort to the subject. Material and Methods Subjects : Fifty-five women were studied after giving informed consent . They were distributed as follows : Group I, 15 normal control subjects aged 20 to 35 years (mean age 24 .4 ± 4 .3 [mean ± 1 standard deviation] years) ; Group II, 13 normal women aged 16 to 32 years (mean 23 .5 f 4 .8 years) in the 13th to 23rd weeks of gestation (approximately the second trimester) ; Group III, 15 normal women aged 18 to 26 years (mean 21 .7 ± 2 .8 years) in the 24th to 32nd weeks of pregnancy (approximately the third trimester) (this period of pregnancy included the period of gestation during which most authors have observed the maximal cardiac output) ; and Group IV, 12 normal women aged 20 to 29 years (mean 23 .8 ± 3 .6 years) at term pregnancy . All but one of these women in Group IV were studied in both the left lateral and supine positions to evaluate the effect upon cardiac output . Left atria) and right ventricular size were not assessed in this group . All pregnan-

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ties were uncomplicated, and there were no twin gestations. Echocardiographic measurements : Echocardiograms were obtained primarily with a Smith-Kline Ekoline 20A ultrasonoscope utilizing an Irex 150-120 recorder and a 2 .25 megahertz focused transducer 0 .5 inches (1.27 cm) in diameter with a repetition rate of 1,000 impulses/sec . Some of the earlier studies were performed with a Unirad ultrasonoscope and a DR-8 Electronics for Medicine recorder . Paper speed was carefully calibrated at 100 mm/sec . Carotid arterial pulse tracings were simultaneously obtained with a funnel-shaped pickup attached to a Sanborn pulse wave transducer (21050B) . Echocardiograms were performed with the subjects in the left lateral position . Women at term underwent additional recordings in the supine position with the transducer maintained at the same anatomic site and with care given to maintaining the same echocardiographic landmarks . Left ventricular minor axis dimensions were obtained as follows : The transducer was positioned at the third to fourth

left intercostal spaces and directed posteriorly, scanning from apex to base . Recordings of the left posterior ventricular wall and septum were made according to the method of Feigenbaumr3 at the position where elements of the anterior and posterior mitral valve leaflet structures were just visible. Only high fidelity tracings with clearly delineated echoes from the endocardium of both the septum and posterior wall were included . (Approximately 60 percent of our studies were successful .) End-diastolic dimension was measured at the onset of the QRS complex, and end-systolic dimension was measured from the peak anterior motion of the endocardial echo of the left ventricular posterior wall to the left side of the interventricular septal echo (Fig. 1) . The left ventricular end-

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diastolic dimension was then divided by body surface area to derive the left ventricular dimension index . The right ventricular dimension ( Fig. 1) was derived by measuring the distance between the anterior right ventricular wall and the right side of the septum at the onset of the QRS complex . This dimension was obtained in 14 subjects in Group I, 13 in Group II and 14 in Group III ; it was not obtained in women in Group IV (at term pregnancy) because these patients were uncomfortable and we chose to limit the variables studied . Right ventricular end-diastolic dimension was divided by the body surface area to obtain the right ventricular dimension index . 14 Body surface area was determined from the weight of the subjects before pregnancy . Left atrial size was measured at end-systole from the posterior aortic wall to the posterior left atrial wall.' 1 Aortic root motion was measured in echocardiographic tracings that included elements of the aortic leaflet as the transducer was directed superiorly and medially to define the aortic root. The amplitude of the anterior motion of both walls of the aortic root during systole was measured from initial to peak anterior motion'-' (Fig . 2) . Ventricular volumes at end-diastole and end-systole were calculated from the cube of each dimension in end-diastole and end-systole, respectively. 1 s The geometry of the ventricle was assumed to be normal . The mean velocity of circumferential fiber shortening was calculated from the formula : LVDD - I VD,' LVD0 X LVET where LVDD and LVD s are left ventricular dimensions

measured at end-diastole and end-systole, respectively, and LET is left. ventricular ejection time as measured simultaneously from the carotid pulse tracing.18 The slope of posterior wall motion was obtained from the endocardial echo of the posterior wall from a tangent drawn from the onset of anterior motion at the initiation of systole to the point of maximal anterior motion at the peak of systole . 19 All measurements were obtained by two independent observers from the mean of five consecutive cardiac cycles . Statistical studies were performed with a TDP 10 computer . Student's t test was utilized to assess statistical significance . Results

The subjects in Groups I, II and IV were of comparable age ; those in Group III were slightly younger (P <0.05) . Heart rate: The heart rate was significantly higher in all pregnant subjects than in the normal control group . The rise occurred in the earliest gestational period studied (Group II) (19 percent) and remained similarly elevated later and at term (19 percent and 20 percent, respectively, in Groups III and IV) (Table I, Fig. 3) . Blood pressure: Although the patients in Groups III and IV had a somewhat higher systolic blood pressure than the normal control subjects, none had hypertension (mean systolic pressure was 118.4 ± 5.9 mm Hg in Group III and 118 .0 ± 8 .3 mm Hg in Group IV) . Diastolic pressures in all four groups were comparable (Table I) .

FIGURE 2. Echocardiogram demonstrating method of determining amplitude of excursion for anterior aortic root (AAR) and posterior aortic root (PAR) motion . EKG = electrocardiogram; LA = left atrium .

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TABLE I Comparison of Chamber Size, Heart Rate and Blood Pressure in Pregnant and Nonpregnant Subjects (mean ± 1 standard deviation)'

Subjects (no .) Age (yr) Heart rate (beats/min) Blood pressure (mm hg) Systolic Diastolic RVDD (mm)

Nonpregnant Women (Group I)

Group II (13 to 23 weeks' gestation)

15 24 .4 ± 4 .3 71 .1 ± 8 .9

13 23 .5 ± 4.8 84 .5 ± 8.2 P<0 .001 111 .8 ± 11 .3 NS 73 .0±8 .3 16 .9 ± 3 .7

110 .0 ± 7 .3 73 .0 ± 6.0 15 .2+ 2.3

LVD0 (mm)

(14 subjects) 43 .1 ± 2.5

LVD 5 (mm)

29 .1 ± 2 .2

LA (mm)

27 .1 ± 3 .9

(13 subjects) 45.5 ± 3 .1 P<0 .05 28.8±2 .5 NS 28.9 ± 5 .0 NS

Pregnant Women Group III (24 to 32 weeks' gestation) 15 21 .7 ± 2.8 84 .9 ± 8.5 P<0 .001 118 .4±5 .9 P <0 .001 73 .3±9 .1 19 .0 ± 2 .8 P <0 .001 (14 subjects) 46 .0±2 .6 P<0 .01 29 .4±2 .9 NS 29 .3 ± 3 .8 NS

Group IV (term) 12 23 .8±3 .6 85 .1 ± 12 .5 P<0.001 118 .0 ± 8 .3 P <0.025 68 .5 ± 12 .8

45 .2±3 .2 NS 28 .7±3.0 NS

P (probability) values indicate significant difference from values in Group I (NS = not significant) . LA = left atrium ; LVDD = left ventricular end-diastolic dimension ; LVD s = left ventricular end-systolic dimension ; RVD 0 = right ventricular enddiastolic dimension ; . . . = not studied .

Left ventricular dimensions: End-diastolic dimensions were somewhat larger in Groups II and III than in the normal control group (P <0 .05 and P <0 .01, respectively), but the end-systolic dimensions in Groups 11, III and IV were similar to those in the control group (Table I) . The largest end-diastolic dimension recorded in the 15 nonpregnant normal subjects in Group I was 47 mm. Septal and posterior wall thickness: The thickness of the septum (mm) in the control group (Group I) ranged from 7 .2 to 9 .0 (mean 7 .7 ± 0.6) . In Group II the range was 7 .3 to 10.0 (mean 8 .0 ± 0.9) ; in Group III, 6 .6 to 9 .5 (mean 7 .9 ± 0.9) ; and in Group IV, 6.5 to 8 .8 (mean 7.8 ± 0.7) . The posterior wall thickness (mm) for each

of the groups was as follows : Group 1, 7 .2 to 9 .4 (mean 8.0 ± 0.7); Group II, 7 .0 to 9 .5 (mean 8 .3 ± 0.8) ; Group III, 7.0 to 10 (mean 8.3 ± 1.0) ; Group IV, 7 .5 to 9 .7 (mean 8.6 ± 0.6) . No significant differences were found among groups. Ventricular volumes at end-diastole and endsystole : The end-diastolic volumes in Groups II, III and IV were statistically higher than in Group I, but the end-systolic volumes were similar (Table II) . Stroke volume: Throughout the gestational period, stroke volume was significantly greater than in normal control subjects (32 percent increase in Group II and 29 percent increase in Group III) . Groups II and III had comparable stroke volume, and, although stroke volume

f Cordioc Output Stroke Volume Heart

Role

FIGURE 3. Cardiac output, stroke volume and heart rate for four subject groups including determinations in lateral and supine positions for Group IV . Group I = normal control subjects ; Group II = women in the 13 to 23rd weeks of pregnancy ; Group III, women in the 24th to 32nd weeks of pregnancy : Group IV, women of term pregnancy . L = liter ; Vol . = volume .

Group 8 Supine

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TABLE II Comparison of Cardiac Output and Wall Motion In Pregnant and Nonpregnant Subjects (mean ± 1 standard deviation)* Nonpregnant Women (Group I) Subjects (no .) EDV

15 81 .0 ± 2.6

ESV SV

27 .1 ± 3.9 56 .0 ± 10 .4

EF

0 .69 ± 0.05

CO

3 .93 ± 0.53

CI

2 .46±0.41

PWS

50 .5±4.9

VCF

1 .13 ± 012

Group II

Pregnant Women Group III

13 95 .4 ± 19 .1 P = 0 .025 24.4 ± 6 .4 74.1±14 .2 P <0 .005 0 .75 ± 0 .04 P <0 .005 6 .05 ± 1 .58 P <0 .001 3 .1 ± 0 .95 P <0 .001 54.8 ± 5 .6 P <0 .05 1 .30 ± 0 .12 P <0 .005

15 98 .4 ± 18.8 P<0.01 26 .1 ± 7 .7 72 .3 ± 12 .7 P <0 .001 0.75 ± 0 .04 P <0 .01 6.15 ± 1 .27 P<0 .001 3.62±0 .67 P <0 .001 61 .1 ± 8 .7 P <0 .001 1 .35±0 .19 P <0 .001

Group IV 12 94 .0±19 .0 P<0 .05 24 .3±7 .5 69 .7±8 .4 P <0 .025 0 .74 ± 0 .08 5 .88±1 .69 P<0 .001 3 .51 ± 1 .0 P <0 .005

1 .29 ± 0 .27

NS

P (probability) values indicate significant difference from values in Group I (NS = not significant) . CI = cardiac index (liters/min per m2); CO = cardiac output (Itters/min) ; EDV = end-diastolic volume (ml) ; EF = ejection fraction ; ESV = end-systolic volume (ml); PWS = posterior wall slope (mm/sec) ; SV = stroke volume (ml); VCF = velocity of circumferential shortening (circumferences/

sec) .

decreased in women at term, it remained 24 percent higher than in normal control subjects (Table II) . The ejection fraction was also increased to a similar degree in Groups II, III and IV (Table II, Fig . 3) . Cardiac output : The increase in cardiac output was readily observed in women in the second trimester (6 .05 ± 1 .58 liters/min versus 3 .93 ± 0.53 liters/min in the normal control subjects) . This increase was present to the same degree in Group III, and the cardiac output for Groups II and III was almost identical (Table II) . At term (Group IV), although output was significantly greater than in Group I (P <0.001), a distinct decrease was noted (Table II, Fig. 1). It was apparent throughout gestation that there were large intragroup deviations . Such differences in cardiac output might represent inherent variability in individual responses to pregnancy because Roy et al . 2 found that cardiac output determinations obtained with the dye-dilution method ranged from 6 to 10 liters/min at 28 weeks of gestation . The cardiac index in all stages of gestation was significantly increased above that of nonpregnant normal control subjects (Table II) . The validity of deriving body surface area from the body weight before pregnancy can be questioned . However, correction for the weight at the time of study can introduce a greater error because the contribution of a real increase in maternal weight as opposed to that contributed by the products of conception would be variable and difficult to assess . Left and right ventricular dimensional indexes were therefore found to be of questionable accuracy although they also increased during pregnancy . Velocity of circumferential shortening and the slope of posterior wall motion : The velocity of circumferential shortening was significantly greater in all study groups than in the normal control subjects (Group 1) . The slope of posterior wall motion was also distinctly

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elevated in Group III (P <0 .001) . In Group II, although the slope of posterior wall motion was higher (54 .8 15 .6 compared with 50 .5 ± 4 .9 mm/sec in Group 1), the differences were less significant (P <0 .05) (Table II) . Aortic root motion : The anterior aortic root motion in 13 normal control subjects (Group I) was 11 .3 ± 0 .6 mm compared with 12 .0 ± 1 .6 mm in 10 subjects in Group II and 13 .8 ± 0.4 mm in 10 subjects in Group III . The increase in Groups IT and III compared with the value in Group I was highly significant (Table III, Fig . 2) . The posterior aortic root motion was increased to a similar degree in Groups II and III (Table III, Fig . 2) . Effect of positional changes at term: In 11 subjects at the end of pregnancy, the heart rate did not vary when they shifted from the lateral to the supine position . The stroke volume was higher when the subjects lay on their left side than when they were supine 69 .7 ± 18 .4 and 54 .6 ± 15 .1 ml, respectively) . The cardiac output was 5 .88 ± 1 .69 liters/min with the patients in

TABLE III Comparison of Anterior and Posterior Aortic Root Motion in Pregnant and Nonpregnant Subjects (mean ± 1 standard deviation)* Nonpregnant Women (Group I) Subjects (no .) Aortic root motion (mm) Anterior Posterior

Pregnant Women Group II

Grout III

13

10

10

11 .3 ± 0 .6'

12 .0 ± 1 .6 (P <0 .001) 10 .1 ± 1 .3 (P <0 .025)

13 .8 ± 0 .4 (P <0.005) 10 .5 ± 0 .3 (P <0.001)

8 .9 ± 0 .7

P (probability) values indicate significant difference from values in Group I.

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TABLE IV Comparison of Values for Cardiac Size and Cardiac Output in Lateral and Supine Positions in Patients in Group IV (at term) (mean ± 1 standard deviation)

Lateral (12) Supine (11) P values*

HR

LVD D

LVDs

EDV

ESV

SV

Co

EF

85.1 ± 12 .4

45 .3 ± 3 .2

28 .7 ± 3 .0

94 .3 ± 19 .0

24.3 ± 7 .5

69 .7 ± 18 .4

5 .88 ± 1 .69

0 .74 ± 0 .09

86 .3±12 .5

42 .6 ± 3 .2

28 .5 ± 3.2

78 .7 ± 17 .3

24 .0 ± 8 .1

54 .6±15 .1

4 .63 ± 1 .24

0 .69±0 .10

NS

NS

NS

NS

NS

P <0 .025

NS

NS

P (probability) values indicate significant difference between values In the lateral and supine positions (NS = not significant) . CO = cardiac output (liters/min); EDV = end-diastolic volume (ml) ; EF = ejection fraction : ESV = end-systolic volume (ml) ; HR = heart rate (beats/min) ; LVD D = left ventricular end-diastolic dimension ; LVDs = left ventricular end-systolic dimension ; SV = stroke volume .

the lateral position and 4 .63 ± 1 .24 liters/min when they were supine (Table IV) . Discussion The physiologic changes of pregnancy afford an excellent opportunity to examine the effects of an increased metabolic demand, a decreased vascular resistance with its resultant diminution in afterload and an expanded blood volume with the consequent increase in preload upon the performance of the normal myocardium. Previous studies derived much valuable information concerning the cardiac responses to gestation from cardiac catheterization data 3' 5--8 and from animal studies . 9,10 However, except for two recent studies utilizing systolic time intervals, 11,12 few investigations were performed in the noninvasive laboratory . The advent of echocardiography presented us with an unusual opportunity to assess both cardiac chamber size and myocardial function in healthy pregnant women using a safe, accurate and noninvasive technique . To establish a baseline for the pregnant woman, we determined the chamber size in the normal nonpregnant subject and found that the largest left ventricular dimensions was 47 mm . Although other investigators 13 have considered dimensions as great as 55 mm within the normal range, it appears that these values may be too high for young women and that the early stage of left ventricular enlargement may be overlooked in this group. The right and left ventricular dimensions were slightly greater in the pregnant than in the nonpregnant state probably because of increased blood volume and venous return . Cardiac output in pregnancy : Prior studies 13,2o established a close correlation between the values for left ventricular dimensions and derived volumes obtained with echocardiography and those obtained with angiocardiography . Indeed, our echocardiographic estimates of cardiac output closely parallel those previously documented by Palmer and Walker 7 utilizing cardiac catheterization . Their estimated output for nonpregnant women was 4 .6 liters/min . However, our data indicate that a significant elevation in stroke volume is already apparent in women in the 13th to 23rd weeks of gestation (Group II) as well as those in the 24th to 32nd weeks (Group III) . The early group showed a 32

percent the later group a 29 percent increase. Heart rate also increased (20 and 23 percent in Groups II and III, respectively) . This increase in both stroke volume and heart rate resulted in a substantial increase in cardiac output in the second trimester as well as later in pregnancy . No further increment occurred after the 23rd week of gestation . This finding is at variance with previous observations that cardiac output reached its highest levels between 24 and 28 weeks or between 28 and 32 weeks. Our data are more compatible with those who maintain that peak output is reached before 24 weeks of gestation .' In conjunction with this enhanced output, we observed an exaggerated aortic root motion . A correlation between increased flow and such motion was recently reported, 15 and we also noted this association . The level of cardiac output at term pregnancy has been a subject of controversy . Lees et al . 21 stated that the output was maintained at a high level to term although until 1966 it was commonly accepted that cardiac output returned to the levels before pregnancy. Our data are in agreement with the more recent observations that cardiac output near the end of gestation remains elevated when the patient assumes the left lateral position (5 .88 liters/min) . However, it was less high than in the earlier stages of gestation . In the supine position, it declined toward the levels of nonpregnant women because of a diminution in venous return induced by the enlarged uterus . This organ has demonstrably occluded vena caval flow in studies performed during cesarean section and could therefore be expected to reduce return of blood to the heart and decrease myocardial fiber stretch . Causes of increased cardiac output : The increased cardiac output could be attributed to several factors . 22 Blood volume has been demonstrated to increase by 30 to 100 percent, representing an increment in both plasma and red blood cells .23 This increase has been observed in the second trimester before fetal metabolic demands are fully in evidence and to a lesser degree in the third trimester . This is consistent with the slightly larger cardiac size and end-diastolic volume that we observed . Therefore, increased myocardial fiber stretch and larger stroke volume probably produced an increased cardiac output . However, considering that the temporal relation between blood volume and cardiac

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output has been found to be disparate (blood volume increases later in gestation) it . is unlikely that this is the only factor . Other elements may have been involved in this process because these variables do not operate in parallel . The higher heart rate could also be implicated in elevating the cardiac output . Enhanced myocardial contractility may have made a significant contribution . We observed not only a greater ejection fraction but also an increase in the slope of posterior wall motion and the velocity of circumferential fiber shortening . The latter increment was observed in the earlier stage of gestation as well as in the period between 24 and 32 weeks and was noted even at term pregnancy . Decreased peripheral vascular resistance and consequent diminished afterload may also have played a role because Bader et al . 3 found that systemic resistance decreased during pregnancy to 980 dynes-See-CM -5 . ( We did not investigate this variable .) The stability of the blood pressure despite an increased cardiac output in our subjects was consistent with a decreased resistance . An intriguing possibility remains that the enhanced contractility was due to the inotropic effect of estrogens . Oral contraceptive agents containing both estrogens and progesterone were reported to cause an increase in cardiac index in six healthy women . 24 Estradiol and Premarin* administered to ewes also increased cardiac output .lo ,26 Moreover, estrogens were found to alter actomyosin adenosine triphosphatase relations in the myocardium and thereby increase contractilityL 5 ; this enzyme was noted to be reduced after oophorectomy

and restored after administration of estrogens . 26 The observed increase in the velocity of circumferential shortening and the increment in the slope of posterior wall motion might have reflected the changes in hormonal status . Indeed, although such a mechanism was previously considered to exert a major influence in the cardiac hemodynamic changes of pregnancy and, although such effects were demonstrated in animals, such heightened myocardial performance has not been clearly delineated in human subjects . The recent observation of an abbreviated preejection period was consistent with such a concept but could have been attributed to the increased volume and greater myocardial fiber length ." However, velocity of circumferential shortening is a sensitive measure of such contractility and the observed increase suggests that an inotropic factor may be a significant element in the enhanced cardiac output of pregnancy although decreased afterload may again have exerted an influence on the velocity of contraction . Increased heart rate may also produce a heightened inotropic response . Implications: Our results seem to indicate that echocardiographic examination of the heart during pregnancy may expand understanding of the normal cardiac responses to an altered physiologic state . Moreover, the establishment of normal criteria for cardiac chamber size and function for healthy pregnant women could facilitate the early detection of abnormal cardiac states complicating pregnancy or arising as a result of gestation.

References 1 . Lees MM, Taylor SH, Scott DS : A study of cardiac output at rest throughout pregnancy . J Obs Gynec Brit Comm 74 :319-328, 1967 2. Roy SB, Malkani PK, Virik R : Circulatory effects of pregnancy . Am J Obstet Gynec 96 :221-225, 1966 3. Bader RA, Bader ME, Rose DJ, et al: Hemodynamics at rest and during exercise in normal pregnancy as studied by cardiac catheterization . J Clin invest 34:1524-1536, 1955 4 . Metcalfe J, Ueland K : Maternal cardiovascular adjustments to pregnancy . Prog Cardiovasc Dis 16 :368-374, 1974 5 . Hamilton HFH : Cardiac output in normal pregnancy as determined by Cournand right heart catheterlzation techniques . J Obstet Gynecol Br Emp 56 :548-552, 1949 6. Rovlnky JJ, Jallin H : Cardiovascular hemodynamics in pregnancy . Am J Obstet Gynecol 95 :781-786, 1966 7 . Palmer AJ, Walker AHC : Maternal circulation in normal pregnancy . J Obstet Gynecol Br Emp 56 :537-547, 1949 8 . Lagerlot H, Warlike L : Studies on the circulation in man . II . Normal values for cardiac output and pressure in the right auricle, right ventricle, and pulmonary artery. Acta Physiol Scand 16 :75-82, 1948 9 . Metcalfe J, Parer JT : Cardiovascular changes during pregnancy in ewes . Am J Physiol 210 :821-825, 1966 10 . Ueland K, Parer JT : Effects of estrogens on the cardiovascular system of the ewe . Am J Obstet Gynecol 96 :400-406, 1966 11 . Burg JR, Dodek A, Kloster FE, et al : Systolic time intervals during the third trimester of pregnancy (abstr) . Clin Res 20 :170, 1972 12 . Rubler S, Hammer N, Schneebaum R : Systolic time intervals in pregnancy and the postpartum period . Am Heart J 86 :182-188, 1973 13 . Felgenbaum H : Echocardiography, second edition . Philadelphia, Lea & Febiger, 1976, p 236, 316, 342-344, 464

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14. Radtke WE, Tajlk AJ, Gau GT, et al : Atrial septal defect . Echocardiographic observations . Ann Intern Med 84 :246-256, 1976 15. Pratt RC, Parlsl AF, Harrington JJ, et al : The influence of left ventricular stroke volume on aortic root motion . An echocardiographic study . Circulation 53:947-952, 1976 16 . Pombo JF, Russell RO Jr, Rackley CE : Comparison of stroke volume and cardiac output determination by ultrasound and dye dilution in acute myocardial infarction . Am J Cardiol 27:630-635, 1971 17 . Fortuln NJ, Hood WP, Craige E: Evaluation of left ventricular function by echocardiography . Circulation 46 :26-35, 1972 18. Welssler AM, Harris WS, Schoenfeld CO: Bedside technics for the evaluation of ventricular function in man . Am J Cardiol 23 : 577-583,1969 19. Kraunz RF, Ryan TJ: Ultrasound measurements of ventricular wall motion following administration of vasoactive drugs . Am J Cardiol 27 :464-473, 1971 20. Felgenbaum H, Popp RL, Wolfe SB, at al : Ultrasound measurements of the left ventricle . Arch Intern Med 129 :461-467, 1972 21 . Lees MM, Scott OS, Kerr MG : The circulatory effects of recumbent postural change in late pregnancy . Clin Sci 32:453-465, 1967 22 . Kerr MG : Cardiovascular dynamics in pregnancy and labour . Br Med Bull 34:19-24, 1968 23. Pritchard JR: Changes in the blood volume during pregnancy and delivery . Anesthesiology 26 :393-399, 1965 24. Walters WA, Lim YL : Cardiovascular dynamics in women receiving oral contraceptive therapy . Lancet 2 :879-881, 1969 25. Csapo A: Actomyosin formation by estrogen action . Am J Physiol 162 :406-410, 1950 26 . King TM, Whltehorn WV, Reeves 8, et al : Effects of estrogen on composition and function of cardiac muscle . Am J Physiol 196 : 1282-1285,1959

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