Cardiovascular disease risk factors for women . A life course-events perspective

Cardiovascular disease (CVD) in women is the most common cause of death and in 2009 accounted for one third of all deaths. The purpose of this paper is to present what conditions during pregnancy and during the pre-menopause period lead to a greater risk of CVD. The early recognition and the application of interventions may decrease this risk. To emphasize this point we have taken a «Life course-events perspective». Current data suggests that genetic predisposition to disease in conjunction with behavior and environmental factors during fetal life is related to permanent changes in fetalplacental-maternal physiology and function, resulting in fetal programming characterizing the phenotype of the child which may persist into adulthood. Longitudinal studies have identified biological, behavioral and environmental factors related to childhood diseases such as hypertension, insulin resistance and mental health disorders. Gender differences have been identified and animal studies have suggested that estrogens in women are protective and when the risk of CVD in men is considered, the risk in women is delayed by 10 years. Thus, a normal pregnancy may be protective and reduce the risk of CVD in women. However, hypertension developing in women before or during pregnancy is a significant risk factor for women and diabetes further increases this risk of CVD, as does smoking. It is very clear that an «intervention action plan» must be developed. It is the current opinion of the authors that this action plan must be implemented early in life to decrease the risk for the development of CVS in women.

Introduction.When does the risk for cardiovascular disease (CVD) begin?Why wait for the disease to develop?Is it time to begin interventions early in life if the risk for this disease has been determined?The purpose of this paper is to link two important concepts; first, the «fetal origin of diseases that occur later in life» such as hypertension, diabetes and atherosclerosis, based upon the Barker hypothesis which proposes that these diseases have their origin during fetal life [1].Second, that «behavioral practices and environmental exposures associated with inherited and acquired genetic changes increases the risk of disease during fetal life», prior to pregnancy for the woman, during pregnancy for the fetus and mother, infancy and adolescence (Figure, Phase I) [2,3].
Back ground.Matched for age white women are at lower risk of cor o nary heart dis ease rel a tive to white men; how ever, there are re cent pub li ca tions to sug gest that cer tain fe male chil dren and ad o les cents are at risk for hy per ten sion and in su lin re sis tance [4,5]; some women with a his tory of prior preg nan cies are at increased risk dur ing the in ter val be tween preg nan cies and within the next 15 years sug gest ing that cer tain con di tions dur ing preg nancy in creases their risk of hyper ten sion, di a be tes and ath ero scle ro sis, and fi nally women dur ing the premenopausal pe riod with hypoestrogenemia of hy po tha lamic or i gin have a greater risk of cor o nary ar tery dis ease than those with nor mal men strual cy cles [6,7], thus iden ti fy ing a group of women at an ear lier age that are at risk (Figure, Phase II).
It is well know as women en ter the post meno pause pe riod the in ci dence of cor o nary heart dis ease al most equals that in men [8].This sub ject is im por tant for three rea sons.First, CVD is the lead ing cause of death for both men and women and the sec ond rea son is that the pro por tion of life lost is higher (18 %) in de vel oped coun tries and ap prox i mately 10 % in de vel op ing countries and in the later the rates are in creas ing.These data sug gest that there is some thing unique in de vel oped coun tries that place women at risk which could have a be hav ioral, nu tri tional, en vi ron men tal or epigenetic ba sis.Third, CVD in women is the most com mon cause of death and ac counts for one third of all deaths [9].More women than men have died from CVD causes on a yearly ba sis since the mid 1980's.One rea son for this dis par ity was the fail ure to in clude women in clin i cal tri als which ap peared to be pri mar ily de signed for men, which lead the Na tional In sti tutes of Health to im plement a pol icy in 1986 to in clude more women in clin ical tri als (Fig ure , Phase III).Thus, the pur pose of this pa per is to take a «life course-events per spec tive» and re view the lit er a ture to iden tify what con di tions prior to preg nancy, dur ing preg nancy and prior to meno pause lead to a greater risk of CVD whereby the early recognition of risk and the ap pli ca tion of in ter ven tions could de crease the risk of cor o nary ar tery dis ease [10][11][12][13].
The life course-events per spec tive and the or igin of adult dis eases.Fe tal pro gram ming.To day it is well rec og nized that changes in the en vi ron ment dur ing the pe riod of fe tal de vel op ment, is as so ci ated with perma nent changes in phys i ol ogy and func tion [2].Some of the changes are the re sult of gene al ter ations by epige netic fac tors such as DNA methylation and histone changes [3].Sev eral stud ies by the ep i de mi ol o gist, David Barker in the United King dom doc u mented the influ ences of pre na tal fac tors on the risk of de vel op ing hy per ten sion, di a be tes mellitus and ath ero scle ro sis [14,15].The fac tors as so ci ated with this risk of dis ease was de ter mined to be re lated to those con di tions re lated This figure divides the Life Events-Course into three phases.Phase I is the period beginning before pregnancy and extended through out the gestational period into infancy and childhood.Phase II begins during the reproductive years and extends to the peri-menopausal period where reproductive performance is near zero.Phase III begins during the pre-menopausal period and the end is a terminal event to poor fe tal nu tri tion and re duced size at birth [16].
The tim ing of these as so ci ated events has been de termined to be im por tant.Early first tri mes ter un der nu trition was pri mar ily re lated to the de vel op ment of hy perten sion later in adult hood, while poor fe tal nu tri tion dur ing the sec ond tri mes ter was as so ci ated with a greater risk of de vel op ing di a be tes, while poor nu trition dur ing the third tri mes ter was as so ci ated with hyper ten sion and stroke [1] (Fig ure , Phase I).Thus, small size at birth sec ond ary to poor nu tri tion and de creased nu tri ent sup ply to the fe tus in creases the risk for the de vel op ment of CVD; how ever, poor fe tal growth also plays an im por tant role in mak ing an in divid ual per ma nently «thrifty» (thrifty phe no type) by being small and in su lin re sis tant and pre pared at birth to live un der ad verse con di tion which has been re ferred by James Jones as «The Best of a Bad Start» [17] (Figure, Phase II).Un for tu nately all too of ten the child is born into an en vi ron ment of plenty (ad e quate or exces sive food sup ply) and its phe no type is al tered.This pro cess is re ferred to as the «Thrifty ge no type» a hypoth e sis sug gested by Neel who pro posed that the thrifty as pects of the con tem po rary in di vid ual who arose from genes se lected over a long pe riod of time to sur vive in an en vi ron ment in which nu tri ent sup plies were lim ited but found it self in an en vi ron ment of plenty and de vel oped obe sity and a greater risk of disease [18].A third ex am ple is the «nat u ral short term exper i ment» such as the Dutch Fam ine dur ing the Sec ond World War when the Ger mans formed a block ade of Hol land ar gues against a purely ge netic ba sis.Only hun ger dur ing the last part of preg nancy for Dutch women did the hun ger ef fect fe tal growth and the risk of dis ease in later life [19].The ef fect of short term nutri tion de pri va tion (ad verse event) could oc cur be cause of epigenetic changes that oc cur within the fe tus re sulting in ge netic changes which in crease the risk of a subse quent dis ease.Cu mu la tive path way dur ing in fancy, child hood and ad o les cence.Sev eral lon gi tu di nal stud ies have been car ried out which have iden ti fied bi o log i cal, behav ioral and en vi ron men tal fac tors re lated to childhood dis eases such as hy per ten sion, in su lin re sis tance and men tal health dis or ders which could con trib ute to the de vel op ment of adult dis eases [20].The clas sic study by Rutter et al. on the long term ef fects of se vere de -pri va tion of Ro ma nian or phans af ter adop tion [21].Two the o ries were con sid ered.First, one was based on the idea of phys i o log i cal plas tic ity due to bi o log i cal pro gram ming sim i lar to that which oc curs in intra uterine pro gram ming.Sec ond, was based upon en vi ronmen tal ex po sures that dis rupted nor mal de vel op ment such as ma ter nal smok ing, al co hol con sump tion and tox ins, all or which can cause min i mal brain pa thol ogy and/or ad verse be hav ioral con se quences.At this point it is some times dif fi cult to sort out what are changes in plas tic ity (adap tive changes) and what is the re sult of patho log i cal changes lead ing to min i mal brain dysfunc tion.
Gen der dif fer ences in the risk of car dio vas cu lar dis ease.De vel op ing within the past 10 years there has been ev i dence that ar te rial dis ease in both sexes' be gins early in life (Barker Hy poth e sis); how ever, over time the pro gres sion of CVD in women com pared with men is de layed and/or in creased by ap prox i mately 10 years.What is the pri mary pro tec tive mech a nism?
Im por tant an i mal pri mate stud ies.The re search car ried out by Thomas Clark son in the non hu man primate model (Cynomolgus ma caque) has been help ful to un der stand the in flu ence of estrogens on the de velop ment of ath ero scle ro sis.This re search group has shown that the ma caque mon key like premenopausal white women are pro tected against cor o nary ar tery athero scle ro sis [22][23][24].In these stud ies these in ves ti gators showed that ovariectomy and the rel a tive es tro gen de fi ciency that ac com pa nies low so cial sta tus in fe male monkeys are both as so ci ated with a loss of «fe male pro tec tion» against cor o nary ar tery dis ease.In 1987 these in ves ti ga tors showed that re peated preg nancy (in creased win dow of es tro gen ex po sure) is also as soci ated with a marked re duc tion in the ex tent of diet-induced cor o nary ar tery ath ero scle ro sis and pro vided evi dence that en dog e nous es tro gen has an in hib i tory ef fect on the atherosclerotic pro cess [25].These stud ies formed the ba sis for stud ies in the hu man.
Im por tant hu man stud ies.Stim u lated by the higher gen der spe cific cor o nary mor tal ity ob served in women, Bairey Merz et al. tested the hy poth e sis that hypoestrogenemia of hy po tha lamic or i gin is as so ci ated with cor o nary ar tery dis ease in young women who were stud ied in the Women's Ischemia Syn drome Eval u a tion (WISE) [26][27][28].Bairey Merz showed that premenopausal women with angiographic cor o nary ar tery dis ease had sig nif i cantly lower estradiol and fol li cle-stim u lat ing hor mone lev els than women without angiographic find ings, even af ter con trol ling for age [7].This study was the first time that hypoestrogenemia of hy po tha lamic or i gin was found to be as so ci ated with cor o nary ar tery dis ease in premenopausal women.Her find ings sup ported the con cept that fe male pro tec tion is lost when ovar ian func tion is dis rupted and that this find ing is con sis tent with previ ous pri mate work noted above ini ti ated by Clark son et al.
Is hor mone re place ment ther apy ef fec tive?Exogenous hor mone ther apy (HT) may have antiatheroscle rotic ef fects [29,30].How ever, re cent clin i cal trials have failed to show pro tec tive car dio vas cu lar effects in postmenopausal women [31][32][33].Re cently Bairey Merz et al. as sessed the re la tion ships be tween de tailed mea sure ments of en dog e nous and ex og e nous es tro gen ex po sure time with angiographic cor o nary ar tery dis ease and ma jor ad verse car dio vas cu lar events [34].These in ves ti ga tors found no in de pendent re la tion of es tro gen ex po sure time to angiographic cor o nary ar tery dis ease or ma jor ad verse car dio vas cular events in women be ing eval u ated for sus pected ischemia.These re sults sug gest that the con cept of estro gen pro tec tion for this dis ease in women is more com plex than es tro gen ex po sure du ra tion alone.
Does preg nancy have an ef fect on the sub sequent de vel op ment of cardiovascuar dis ease?Begin ning in the early 60's and 70's in ves ti ga tors be gan to ad dress the re la tion ship be tween the num ber of preg nan cies and ath ero scle ro sis and the re sults were con tro ver sial; how ever, re cently it has been brought to our at ten tion that preg nancy can be a prodrome to vas cu lar dys func tion and car dio vas cu lar risk in some women [6,35].In 1964 a pa per pub lished by Win kelstein and Rakate showed that there were an ex cess of preg nan cies in women dy ing of cor o nary heart disease and then a pa per pub lished in 1974 by Berngtsson, Rybo and Westerberg showed sim i lar find ings [36,37].Three other stud ies pro vided no ev i dence for an as so ci a tion be tween cor o nary heart dis ease risk and the num ber of preg nan cies [38][39][40].Then years later in 1984 Beard, Fuster and Annegers, found that women whose first preg nancy was be fore the age of 25 were found to be at greater risk of cor o nary heart disease [41].The im por tance of this pa per was the fo cus toward con found ing vari ables such as lower socioeconomic sta tus, lower ed u ca tional lev els and psychoso cial vari ables in youn ger women that could con trib ute to the risk of cor o nary heart dis ease.The role of psy cho-so cial fac tors will be discussed below in the section titled stress and the risk of CVD.
Hy per ten sion and the risk of car dio vas cu lar disease.Be gin ning in 2001 sev eral large pop u la tion stud ies be gan to show that hy per ten sive dis or ders in preg nancy (preeclampsia and ges ta tional hy per ten sion) were makers of fu ture risk of CVD [42][43][44].In 2007 a meta anal ysis by Bellamy et al. showed an in ter re la tion ship between risk fac tors and that hy per ten sive dis or ders were clearly re lated to a great risk of CVD in later years [45].Most stud ies have shown that there are other com mon risk factors as so ci ated with hy per ten sive dis or ders in pregnancy, such as higher blood pres sure prior to clin i cal disease, obe sity, el e vated lipids and ges ta tional dia be tes.
It is im por tant to dis cuss the most re cent pa per published by Magnussen et al. in Nor way on the as so ci a tion between hy per ten sion in preg nancy and the risk of CVD.These in ves ti ga tors linked data from the Med i cal Birth Registry to a large pop u la tion based health sur vey (HUNT study) to as sess the as so ci a tion of hy per ten sive disorders in preg nancy with car dio vas cu lar risk fac tors as sessed ap prox i mately 28 years later (mean du ra tion of sub ject par tic i pa tion in this study was 23 years) [46].These in ves ti ga tors iden ti fied 13,623 sub jects with no hypertensive dis or ders and 1,433 with hy per ten sive disorders.Women who de vel oped preeclampsia or gestational hy per ten sion had sig nif i cantly higher body mass indices (BMI's) and ab nor mal lipid pro files.In ad di tion the anal y sis showed that as so ci ated risk fac tors be came stron ger with in creas ing ma ter nal age and par ity.Fi nally these in ves ti ga tors showed that women with hypertensive dis or der in preg nancy were also sig nif i cantly more likely to de velop di a be tes at fol low up sug gest ing that they may have had some de gree of in su lin re sis tance during preg nancy.
This study also clearly show that both preeclampsia and ges ta tional hy per ten sion most likely share a sim i lar patho log i cal mech a nism lead ing to a greater risk of CVD, but that the «con di tion of preg nancy» (normal group fol lowed) is not re lated to the risk of CVD.
Thus, it ap pears that there is some form of en do thelial dys func tion that oc curs in sub jects who de velop hy per ten sive dis or ders of preg nancy.In ad di tion there ap pears to be three ad di tional risk fac tors that may contrib ute to this risk.First, is that re cur rent preg nancy (increased par ity) could be a prodrome or dose ef fect to increase the risk.Sec ond, is that the in crease in ci dence of obe sity could play a role in the de vel op ment of in su lin re sis tance and di a be tes later (at fol low up) which brings up the is sue as to whether or not women at risk for hy per ten sion may also have a co-mor bid risk for devel op ing in su lin re sis tance dur ing the preg nancy without hav ing made the di ag no sis of pre-di a be tes or ges tational di a be tes.This will be dis cussed be low.Third, psy cho log i cal fac tors are also thought to play an im portant role in the de vel op ment of hy per ten sion and it may also be an im por tant fac tor in the de vel op ment of the risk of CVD [47].This will also be dis cussed be low.Finally, ma ter nal age as so ci ated with in creas ing par ity could it self in crease the risk of ath ero scle ro sis.Ma ternal age has been shown to be an in de pend ent risk fac tor for CVD dis ease and the his tory of prior hy per ten sion and the re cur rent car dio vas cu lar stress as so ci ated with preg nancy and or ad verse life style may play an im portant role over time [48,49].
What is the as so ci a tion be tween dysglycemia and di a be tes and the risk of car dio vas cu lar dis ease?The Framingham Study ini ti ated be tween 1948 and 1952 in the United States stud ied 5070 men and women who were orig i nally free of CVD when first ex am ined and who later de vel oped var i ous man i fes ta tions of CVD be tween the ages of 35 and 64.In 1987 a re port on the Framingham Study by Stokes et al. on the rel a tive impor tance of se lected risk fac tors 30 years later on the risk of var i ous man i fes ta tions of CVD (stroke, con gestive hear fail ure, cor o nary heart dis ease and in ter mit ted at claudication) found that hy per ten sion con trib uted most con sis tently to short term risk of all man i fes tations of CVD [8].An im por tant part of this early re port was the ob ser va tion that there were sig nif i cant dif ferences be tween the sexes and age groups.One im por tant find ing was that di a be tes was re ported to be a sig nif icant risk fac tor for to tal CVD risk for both men and women.
At about this same time in 1987 in ves ti ga tors be gan to fo cus on the im por tance of fam ily his tory as an in de -pend ent risk fac tor for in ci dent cor o nary ar tery dis ease.A re port by Hopkins et al. showed that af ter con trol ling for age, sex, to tal cho les terol, higher den sity li po protein cho les terol, hy per ten sion, di a be tes, cig a rette smok ing and body mass in dex, fam ily his tory re mained a highly sig nif i cant pre dic tor for the de vel op ment of cor o nary ar tery dis ease [50].In ref er ence to di a be tes this study showed that the in ci dence of di a be tes in the pa tients who had in ci dent cor o nary ar tery dis ease (CAD) was 18.8 per cent com pared to 3.4 per cent in those without CAD.
Dysglycemia and the risk of car dio vas cu lar disease.Dysglycemia was listed above in the sec tion on the risk of CVD.For the pur pose of this dis cus sion the defi ni tion of this term is «an el e va tion of glu cose val ues that do not meet the cri te ria used for the di ag no sis of dia be tes».The rea son for us ing this term is that it suggests that el e vated glu cose lev els are a con tin u ous variable and that at some point in ones life course-events the val ues will be come ab nor mal and the sub ject can be de fined as di a betic.One of the most in ter est ing pa pers pub lished this year was a pa per by Retnakaran and Shah who as sessed glu cose in tol er ance in preg nancy and the risk of CVD in a pop u la tion-based co hort study in On tario Can ada [51].In North Amer ica preg nant women com monly re ceive screen ing for ges ta tional dia be tes mellitus us ing a 50 gram glu cose screen ing test (GST) and if pos i tive is fol lowed by a glu cose tol er ance test (GTT) where two ab nor mal val ues are re quired for the di ag no sis of ges ta tional di a be tes.Thus, women with a pos i tive screen but a neg a tive GTT (which may in clude one ab nor mal value) are con sid ered dysglycemic (po ten tially at risk for di a be tes).This study by Retnakaran and Shah strat i fied their pop u la tion into 3 co horts of women: 1) Those with ges ta tional di a be tes (13,888); 2) women who re ceived a antepartum oral glu cose tol er ance test be cause they had a pos i tive screening test (71,831) and 3) those who did not have a GTT pre sum ably be cause their screen was neg a tive (349,977).Dur ing the in ter ven ing 12.3 years the women who had ges ta tional di a be tes had the high est risk for CVD with an ad justed haz ard ra tio of 1.66 (1.30-2.13)and next were those with a pos i tive screen but neg a tive GTT with an ad justed haz ard ra tio of 1.19 (1.02-1.39),when com pared to the group with a neg ative screen.This study was the first to iden tify a group of women most of ten con sid ered nor mal (pos i tive screen and neg a tive GTT) yet con sid ered dysglycemic and to be at risk for car dio vas cu lar dis ease within 12 + years af ter the as sess ment dur ing preg nancy.What is im por tant is that this study sug gests that in ad di tion to women with ges ta tional di a be tes a sub set of women with a lesser de gree of antepartum dysglycemia may also ben e fit from closer car dio vas cu lar sur veil lance.
Obe sity and the risk of car dio vas cu lar dis ease.Overweight and obe sity are as so ci ated with the de velop ment of hyperlipidemia, hy per ten sion, CVD, in su lin re sis tance, type 2 di a be tes and a shorter life span [52,53].Gunderson et al. as sessed the risk for the de vel opment of be com ing over weight with child bear ing by utiliz ing the CARDIA study data base [54].The CARDIA study be gan in 1986 and con tin ued up to 1996 and exam ined the par tic i pants at base line and again at 2, 5, 7, and 10 years and in cluded black and white nulliparous women who were not over weight at base line.These inves ti ga tors found an in ter est ing in ter ac tion be tween the risk fac tors smok ing and par ity.Women with 1 and 2 + births had a sig nif i cantly in creased risk for the de vel opment of be ing over weight if they never smoked compared to a de creased risk for those who were smok ers.Thus, smok ing de creased the risk of be com ing overweight; how ever, it is well known that smok ing is a signif i cant risk fac tor for CVD.This study also determined that race, fre quent weight cy cling, less ed u ca tion and less phys i cal ac tiv ity was also sig nif i cant risk factors.
Stress and the risk of car dio vas cu lar dis ease.Our re search group has fo cused con sid er able time and effort to un der stand the role of stress and preg nancy outcome [55,56].Hy per ten sion has long been shown to be a strong, in de pend ent, and eti o log i cally sig nif i cant risk fac tor for de vel op ing CVD [47].Yan L. L. et al. (2003) used the CARDIA study to ex am ine the role of psy choso cial fac tors such as time ur gency/im pa tience (TUI), achieve ment striv ing/com pet i tive ness (ASC), hos til ity, de pres sion, and anx i ety on the long-term risk of hy perten sion [57].As noted above the CARDIA study was a multi-cen ter, lon gi tu di nal study of the de vel op ment of cor o nary ar tery dis ease risk fac tors in young adults.This study showed a dose-re sponse in crease in the risk of de vel op ing hy per ten sion for those who had a higher ten dency of ur gency/im pa tience and hos til ity but not ASC, de pres sion or anx i ety in this young adult co hort.These in ves ti ga tors also rec og nized that the risk of hyper ten sion ap pears to dif fer across dif fer ent age, race and sex groups which re quire con tin ued re search.The bi o log i cally and plau si ble mech a nism of how psy choso cial fac tors in crease the risk of hy per ten sion is via the sym pa thetic ner vous sys tem stim u la tion from acute stress, lead ing to in creased car diac out put, vasoconstriction, ar te rial pres sure el e va tion and im paired en dothe lial dysregulation [58].Re cently, Denollet J. et al. as sessed the role of anx i ety in a 10 year fol low-up of mid dle-aged women who par tic i pated in the «Eindhoven Perimenopausal Os teo po ro sis Study in the Neth er lands» [10].These in ves ti ga tors used a threeitem anx i ety scale to as sess pri mary out comes of an allcause mor tal ity at 10-year fol low-up and sec ond ary out comes re lated to car dio vas cu lar and lung/breast can cer death [59].Smok ing, liv ing alone and lower edu ca tion were re lated to mor tal ity, but de pres sion was not.Ad just ing for these vari ables, anx i ety was as so ciated with a 77 % in crease in mor tal ity risk and it was related to car dio vas cu lar death.The au thors sum ma rized their find ings by stat ing that anx i ety ap pears to be related to un healthy life styles such as smok ing, obe sity, in ac tiv ity, hy per ten sion and di a be tes and that these factors may me di ate the anx i ety-mor tal ity re la tion ship.
Smok ing and the risk of car dio vas cu lar dis ease.All of the stud ies that we re viewed for the as sess ment of risk fac tors and CVD iden ti fied smok ing as a sig nif icant risk fac tor.Camp bell et al. re cently re viewed the met a bolic ef fects of cig a rette smok ing and in di vid u als who smoke ex pe ri ence a wide range of phys i o logic side ef fects that in crease the risk of CVD, in clud ing insu lin re sis tance, el e vated catecholamine lev els which con trib ute to an el e vated heart rate and blood pres sure, and hy per cho les ter ol emia [60].How ever, as noted above the study by Gunderson showed that smok ing during preg nancy was pro tec tive and pre vented women from gain ing ex ces sive weight dur ing preg nancy and it is also well known that women who smoke dur ing preg nancy are less likely to de velop preeclampsia which like obe sity in creases the risk of de vel op ing CVD.The in ter est ing pa per by Ness et al. as sessed the in ter ac tion be tween weight gain dur ing preg nancy and its as so ci a tion with the pro tec tive ef fect of smok ing on the de vel op ment of preeclampsia [61].
Among un der weight and nor mal weight women, smok ing de creased the risk of preeclampsia af ter adjust ment for ma ter nal age, race and so cio eco nomic status.How ever, among over weight/obese women this trend was not ap par ent and among both un der weight and over weight women, smok ing sig nif i cantly increases the risk of de liv er ing a small for ges ta tional aged fe tus (SGA).Obe sity elim i nated the in verse as soci a tion be tween smok ing and preeclampsia.
Action for the prevention of cardiovascular diseases in women.Both American Heart Association and the World Health Organization have developed specific recommendations.Because CVD is the single leading cause of death and a significant cause of morbidity in the United States and Globally and an «Action Plan» must be implemented early in the life eventcourse of women because the risk factors for CVD are and finally the treatment.The ultimate and primary well documented and there is compelling data from epidemiological studies and randomized clinical trials to show that this disease is largely preventable.A «Guide to Preventive Cardiology for Women» was approved by the American College of Cardiology in 1999 and by the American heart Association in 1998 and published in 1999 [13].This guide to risk reduction for women addresses the goals, screening methods and recommendations for smoking cessation, physical activity, nutrition, weight management, psychosocial factors, blood pressure, lipids and lipoproteins, diabetes, hormone replacement therapy, oral contraceptive, and cardiovascular drugs.
The World Health Organization provides a structured life course-events perspective [12].First, WHO begins by focusing on the risk factors that begin in childhood and youth and then focus on the role of hypertension, lipids, tobacco, physical activity, obesity, diabetes and socioeconomic status as they consider women to be a «special case» when considering risk assessment.The «Action plan» proposed by WHO includes the importance of research, the role of regional organizations and prevention as guided by personal choices, population and system approaches, health education, policies and legislation goal is to prevent death and suffering, but there are also economic implications.