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it is well known that the maternal cardiovascular system undergoes significant circulatory changes , including increases in cardiac output ( co ) and blood volume and reductions in systemic vascular resistance and arterial pressure.1,2 although these physiological adaptations are well tolerated by healthy woman , they might result in heart failure and even death in those with heart disease.3   maternal heart disease occurs in approximately 0.54% of all pregnancies and it is the most important indirect cause of maternal mortality .
the prevalence of cardiac disease depends on the studied population . in developing countries , the most common cardiac disease is rheumatic heart disease , mainly mitral stenosis and/or regurgitation.4   little information is available about cardiac alterations and the association between pregnancy and mitral regurgitation ( mr ) , which probably results from the concept that mr is usually well tolerated during pregnancy because of the physiological decrease in systemic vascular resistance and afterload.3   chronic mr causes volume overload that can lead to eccentric hypertrophy .
most patients with mr remain asymptomatic for many years until decompensated hypertrophy occurs , leading to cardiac dysfunction and overt heart failure . in contrast
, pregnancyinduced hypertrophy is known to be physiological , being reversible after pregnancy without harmful effects on cardiac function .
therefore , it is possible to hypothesize that women with mr present unfavorable structural and functional cardiac adaptation during pregnancy and the puerperal period .
the aim of this study was to evaluate the structural and functional heart abnormalities in women with mr during pregnancy and early puerperium .
this is a case  control , prospective , longitudinal study performed in a university general hospital .
the study protocol was approved by the institutional review board of the school of medicine of botucatu  unesp  brazil and all participants gave informed consent .
eighteen consecutive women with singleton pregnancy and isolated mr or with mr as the predominant lesion were included in the study .
an assessment of functional class was made according to the criteria of the new york heart association ( nyha ) at the time of examination .
women with moderate or severe mitral stenosis , atrial fibrillation or any other cardiovascular disease , or pregnancyinduced hypertension were excluded .
all participants received routine prenatal care and were followed at the antenatal and cardiologic clinics in the university teaching hospital .
echocardiographic studies were performed in both groups at the 12th ( t1 ) and 36th ( t2 ) weeks of pregnancy and on the 45th day post partum ( t3 ) .
all measurements were obtained with the subjects in the left lateral recumbent position and allowed to rest for about 15  min .
all studies were performed with a hewllet packard sonos 2000 system , with a multifrequency phasedarray transducer ( 2.53.5  mhz ) .
blood pressure was measured from the brachial left artery with a manual cuff and with the subject in the left lateral decubitus position .
systolic blood pressure ( sbp ) was taken at the first korotkoff sound and diastolic blood pressure ( dbp ) was taken at the fourth korotkoff sound .
mean arterial pressure ( map ) was calculated from the equation map ( mmhg )  =   sbp + 2dbp/3 .
stroke volume ( sv ) was the product of the crosssectional area of the left ventricle ( lv ) outflow tract and the velocity time integral of the pulsed doppler subaortic waveform measured in the fivechamber view . cardiac output ( co )
ejection time was obtained from the aorticpulsed doppler waveform , the sample volume being placed a few millimeters below the valve . left ventricular and atrial dimensions were calculated according to the recommendations of the american society of echocardiography5 from the parasternal longaxis view .
the following indexes were calculated : 1 ) ejection fraction ( ef )  =   [ ( lvdd  lvsd ) / lvdd ] ; 2 ) fractional shortening ( fs )  =   ( lvdd  lvsd ) / lvdd  100 ; 3 ) relative wall thickness ( rwt )  =   [ ( swt + pwt ) / 2 ] / lvdd , where swt is septal wall thickness , pwt is posterior wall thickness , lvdd is left ventricular diastolic diameter and lvsd is left ventricular systolic diameter . left ventricular mass ( lvm ) was calculated using the mmode measurements by the formula of devereux and reichek6 : lvm  =  { [ ( swt + pwt + lvdd )  lvdd ]  1.04 }  13.6 .
total peripheral resistance ( tpr ) and peak systolic stress ( pss ) were calculated from the formulas : tpr ( dyn / s / cm )  =   map  80/co ; pss ( g / cm )  =   { [ ( sbp  lvdd)/4dwt ( 1 + dwt / lvdd ) ] }  1.36 . where dwt is mean dystolic wall thickness .
the results were statistically analyzed according to a splitplot design over time by considering the collection moments as plots and the groups as subplots .
multiple comparisons were performed using a test analogous to the tukey test using the pdiff option of sas proc glm , version 9.1 .
for all tests , a p value of < 0.05 was considered statistically significant . using the mean of the left atrium diameter in the first and third trimester of normal pregnancies obtained from a previous study,2
it was calculated that 11 subjects would be necessary , with a 5% level of significance ( p  =  0.05 ) and power of 80% (   =   0.20 ) .
this is a case  control , prospective , longitudinal study performed in a university general hospital .
the study protocol was approved by the institutional review board of the school of medicine of botucatu  unesp  brazil and all participants gave informed consent .
eighteen consecutive women with singleton pregnancy and isolated mr or with mr as the predominant lesion were included in the study .
an assessment of functional class was made according to the criteria of the new york heart association ( nyha ) at the time of examination .
women with moderate or severe mitral stenosis , atrial fibrillation or any other cardiovascular disease , or pregnancyinduced hypertension were excluded .
all participants received routine prenatal care and were followed at the antenatal and cardiologic clinics in the university teaching hospital .
echocardiographic studies were performed in both groups at the 12th ( t1 ) and 36th ( t2 ) weeks of pregnancy and on the 45th day post partum ( t3 ) .
all measurements were obtained with the subjects in the left lateral recumbent position and allowed to rest for about 15  min .
all studies were performed with a hewllet packard sonos 2000 system , with a multifrequency phasedarray transducer ( 2.53.5  mhz ) .
blood pressure was measured from the brachial left artery with a manual cuff and with the subject in the left lateral decubitus position .
systolic blood pressure ( sbp ) was taken at the first korotkoff sound and diastolic blood pressure ( dbp ) was taken at the fourth korotkoff sound .
mean arterial pressure ( map ) was calculated from the equation map ( mmhg )  =   sbp + 2dbp/3 .
stroke volume ( sv ) was the product of the crosssectional area of the left ventricle ( lv ) outflow tract and the velocity time integral of the pulsed doppler subaortic waveform measured in the fivechamber view . cardiac output ( co )
ejection time was obtained from the aorticpulsed doppler waveform , the sample volume being placed a few millimeters below the valve . left ventricular and atrial dimensions were calculated according to the recommendations of the american society of echocardiography5 from the parasternal longaxis view .
the following indexes were calculated : 1 ) ejection fraction ( ef )  =   [ ( lvdd  lvsd ) / lvdd ] ; 2 ) fractional shortening ( fs )  =   ( lvdd  lvsd ) / lvdd  100 ; 3 ) relative wall thickness ( rwt )  =   [ ( swt + pwt ) / 2 ] / lvdd , where swt is septal wall thickness , pwt is posterior wall thickness , lvdd is left ventricular diastolic diameter and lvsd is left ventricular systolic diameter . left ventricular mass ( lvm ) was calculated using the mmode measurements by the formula of devereux and reichek6 : lvm  =  { [ ( swt + pwt + lvdd )  lvdd ]  1.04 }  13.6 .
total peripheral resistance ( tpr ) and peak systolic stress ( pss ) were calculated from the formulas : tpr ( dyn / s / cm )  =   map  80/co ; pss ( g / cm )  =   { [ ( sbp  lvdd)/4dwt ( 1 + dwt / lvdd ) ] }  1.36 . where dwt is mean dystolic wall thickness .
the results were statistically analyzed according to a splitplot design over time by considering the collection moments as plots and the groups as subplots .
multiple comparisons were performed using a test analogous to the tukey test using the pdiff option of sas proc glm , version 9.1 .
for all tests , a p value of < 0.05 was considered statistically significant . using the mean of the left atrium diameter in the first and third trimester of normal pregnancies obtained from a previous study,2 it was calculated that 11 subjects would be necessary , with a 5% level of significance ( p  =  0.05 ) and power of 80% (   =   0.20 ) .
at the time of the study 1 patient presented as nyha class iii , 6 were class ii and the remaining patients were nyha class i. the predominant etiology of mitral insufficiency was rheumatic fever ; only 2 patients had congenital disease .
the left atrium diameter ( lad ) , lvdd and lv mass were higher in the mr group in all evaluations .
however , compared with controls , the mr group presented a decreased relative wall thickness during the puerperium , suggesting ventricular dilation ( figure 1 ) .
there were no changes in the heart rate ( hr ) , map and total peripheral resistance ( tpr ) in the mr group during pregnancy . during the puerperium
the results of this study have demonstrated that pregnancy represents an additional overload to the heart of women with mr , worsening cardiac remodeling .
various studies evaluated the lv response to a volume overload in normal pregnancies;7,8 however , no studies were found comparing healthy and mr women . from the beginning of pregnancy , the heart size was increased in the mr group compared with control group , suggesting significant heart disease at that time .
none of patients presented with previous history of overt heart failure , indicating aha / acc stage b,9 although 2 patients presented criteria for diagnosis of decompensate heart failure at the time of inclusion in the study . during the follow up protocol 6 patients presented with decompensated cardiac history of overt heart failure indicating aha / acc stage b.9   physiologically , the lad gradually increases during pregnancy , returning to normal in the puerperium.7,8 in the present study ,
the lad was increased in the mr group , regardless of the time of evaluation .
in addition , these patients presented with an additional enlargement that was irreversible during the study period .
this is an important finding since the size of the left atrium is related to the severity of valve damage .
as this chamber increases , the risk of atrial fibrillation also increases , worsening the prognosis of these patients.10   the absence of additional enlargement in the lv chamber in both groups was an interesting finding . considering that both pregnancy and mr are conditions of volume overload , an increase in ventricular size
robson et al12 only observed enlargement of the left ventricle in pregnancy when comparisons were made with prepregnancy values .
therefore , it is reasonable to assume that mr women presented a physiological response to pregnancy as far as the lv chamber is concerned , although they presented increased lv size and mass during the study protocol period .
the most remarkable finding in the present study was the demonstration that at the puerperium , mr women showed a reduction in the relative thickness of the ventricular wall compared with controls , suggesting a persistent chamber dilation .
in chronic volume overload , cardiac dilation is associated with a worse prognosis , with a higher risk of overt cardiac failure .
this is an important finding and might explain the increased afterload demonstrated in the mr group compared with the control group in the puerperium , resembling decompensated hypertrophy .
it was concluded that pregnancy causes unfavorable structural alterations in women with mr that are associated with an aggravation of the hemodynamic overload .
the impact of such alterations in late clinical outcomes must be further evaluated in future studies .
prepregnancy assessment of the left chamber was not possible because patients were already pregnant when included in the study .
echocardiography evaluation did not include current indexes , such as left atrial volume or simpson 's biplane , which are more accurate for detection of cardiac changes .
however , we were able to show remarkable differences between the groups , indicating a need for more studies focusing on this issue .
prepregnancy assessment of the left chamber was not possible because patients were already pregnant when included in the study . however , the control group allowed comparisons between healthy and heart disease .
echocardiography evaluation did not include current indexes , such as left atrial volume or simpson 's biplane , which are more accurate for detection of cardiac changes .
however , we were able to show remarkable differences between the groups , indicating a need for more studies focusing on this issue .
prepregnancy assessment of the left chamber was not possible because patients were already pregnant when included in the study . however , the control group allowed comparisons between healthy and heart disease .
echocardiography evaluation did not include current indexes , such as left atrial volume or simpson 's biplane , which are more accurate for detection of cardiac changes .
however , we were able to show remarkable differences between the groups , indicating a need for more studies focusing on this issue .
this study was supported by fundao de amparo  pesquisa do estado de so paulo ( fapesp ) and conselho nacional de desenvolvimento cientfico e tecnolgico ( cnpq ) .
objectives : to evaluate the structural and functional heart abnormalities in women with mitral regurgitation during pregnancy.introduction:women with mitral regurgitation progress well during pregnancy 
 . however , the effects on the heart of the association between pregnancy and mitral regurgitation are not well established.methods:this is a case  control , longitudinal prospective study . 
 echocardiograms were performed in 18 women with mitral regurgitation at the 12th and 36th week of pregnancy and on the 45th day of the puerperium . 
 twelve agematched healthy and pregnant women were included as controls and underwent the same evaluation as the study group.results:compared with controls , women with mitral regurgitation presented increased left cardiac chambers in all evaluations . 
 increasing left atrium during pregnancy occurred only in the mitral regurgitation group . at the end of the puerperium , women with mitral regurgitation showed persistent enlargement of the left atrium compared with the beginning of pregnancy ( 5.0  1.1  cm vs 4.6  0.9  cm ; p<0.05 ) . reduced left ventricular relative wall thickness ( 0.13  0.02 vs 0.16  0.02 ; p<0.05 ) and an increased peak of afterload ( 278  55  g / cm2 vs 207  28  g / cm2 ; p<0.05 ) was still observed on the 45th day after delivery in the mitral regurgitation group compared with controls.conclusions:pregnancy causes unfavorable structural alterations in women with mitral regurgitation that are associated with an aggravation of the hemodynamic overload .