The American Heart Association Statistics Committee1 estimates the annual prevalence of myocardial infarction (MI) in the United States to be 3 million cases in women and 5 million cases in men. These latest statistics from 2013 reveal that 370 000 women experience either an incident or recurrent MI with annual mortality, resulting in about 74 000 annual deaths in women. Despite significant development in primary and secondary prevention therapies for cardiovascular disease (CVD), reductions in CVD mortality rates among women are not occurring at the same rate as in men.2 In fact, US deaths from coronary heart disease in women between the ages of 35 and 54 years have increased over the past 40 years because of the obesity epidemic.3 Obesity has been shown to be an independent risk factor for the development of CVD in both sexes.4,5 The prevalence of obesity in the United States has increased dramatically over the past 30 years, more than doubling in women (from 17% to 36%). The age-adjusted prevalence of being overweight (25.0–29.9 kg/m2) increased from 56% to 65% during that time, obesity (30.0–39.9 kg/m2) from 23% to 31%, and extreme obesity (≥40 kg/m2) from 3% to 5%.6 Waist circumference (WC) has also increased; approximately 55% of women can be categorized as “high risk,” exceeding the World Health Organization (WHO) cutoff of less than 88 cm (Figure).6 Cardiovascular disease, in particular, is intensified by the presence of obesity as a risk factor, contributing to a higher percentage of women than men who develop hypertension7,8 or diabetes mellitus or who experience a stroke.3 While non- Hispanic black women appear to have the highest overweight/obesity prevalence, it has been estimated that, overall, 2 of 3 women older than 20 years are either overweight or obese.
Adiposity has been shown in a variety of studies to have a direct relationship with the risk factors of CVD. Regional distribution of adipose tissue has been shown to be an important indicator of CVD and metabolic dysfunction in both animal and human subjects. Adipose tissue appears to be responsible for perpetuating a mild chronic inflammatory state in the body as well as being a mediator of atherosclerosis.9 Body mass index (BMI) continues to be the most frequently applied anthropometric measure in most studies even though it offers no information regarding overall fat distribution, especially visceral fat. Findings regarding differences in gender and ethnicity with the current cutoff points for BMI levels have raised questions regarding BMI’s accuracy as a risk indicator. Over the past 3 decades, various anthropometric measures have been studied to assess their individual association with CVD risk factors, CVD morbidity and mortality, and their predictive nature for incident and recurrent cardiac events. Waist circumference, waist-to-hip ratio, sagittal abdominal diameter (SAD), and thigh circumference have all been evaluated to determine their precision and predictive ability, independent of BMI.
Few studies have examined the impact of body weight/BMI on recurrent cardiovascular events or whether fat distribution influences morbidity/mortality beyond known CVD risk factors. Although visceral fat is an established risk factor for incident coronary heart disease, little is known about its association with recurrent events or mortality within MI survivors. Results indicate a similar association seen in healthy populations, but these studies have been limited by small sample sizes, cross-sectional designs, inconsistent cut-points of the anthropometric measures used, or focus on 1 or race/ethnic group.10–13 Even fewer studies have assessed this association while controlling for the evidence-based secondary prevention interventions that dominate an MI survivor’s postevent management.14,15
The objective of this prospective study, therefore, was to examine the association between fat distribution and recurrent fatal and nonfatal cardiovascular events in women, independent of relative weight (measured as BMI) and secondary prevention interventions, in a large, population-based cohort of female incident MI survivors. The research question to be answered was as follows: Will central fat distribution be an independent predictor of recurrent CVD outcomes after incident MI in women, independent of BMI and after adjustment for secondary prevention influences?
This study used a prospective design, with an average length of follow-up of 3.5 years (minimum to maximum range, 0.01–8.7 years), beginning on March 19, 1996, and ending on December 31, 2004. Between 1996 and 2004, 1496 individuals who were discharged alive from 12 of 14 hospitals located in Erie and Niagara (New York) counties with a diagnosis of acute incident MI (International Classification of Diseases, Ninth Revision: 410.0–410.9; International Statistical Classification of Diseases, 10th Revision: I00–I78) were originally collected as part of the Western New York Health Study, a series of case-control studies coordinated by Maurizio Trevisan, MD, MS, and colleagues in the Department of Social and Preventive Medicine at the University at Buffalo. The cases from this group of Western New York participants became the focus of the present study and included 356 women between the ages of 35 and 70 years. The study protocol was approved by the University at Buffalo Institutional Review Board.
The diagnosis of acute incident MI, or a “definite” MI, was based on the WHO definition as the presence of 2 or more of the following criteria: an abnormal electrocardiogram result (diagnostic Q waves in serial records +/or S-T elevation lasting longer than 1 day and T-wave progression on ≥3 records), clinical symptoms of chest pain (lasting longer than 20 minutes and no other definite noncardiac/cardiac nonatherosclerotic cause), and abnormal cardiac enzymes (an elevation of any cardiac enzyme more than twice the upper limit of the normal range of the local laboratory).
The women were interviewed within 12 weeks of discharge, chosen to minimize both biological and behavioral influences of the acute clinical event. At baseline, participants completed a comprehensive interviewer-assisted survey and underwent a complete physical examination. Extensive information was collected by both paper and computer questionnaires regarding sociodemographics, including age, marital status, education level, and annual household income. Women were asked about their smoking status and lifetime alcohol consumption, and current physical activity was determined using the 7-Day Physical Activity Recall Questionnaire.16 A self-reported medical history was used to document provider-diagnosed illnesses as hypertension, dyslipidemia, diabetes mellitus, cancers, and chronic lung diseases. Participants were asked to detail their menstrual history and menopausal status (natural or surgical) as well as current or past hormone use. All women were asked to bring their current prescription and over-the-counter medications, which were recorded, including dosage, frequency, and duration of use.
Physical examination included measurement of height, weight, WC, and SAD. Height was measured with the participant without shoes on a permanently mounted vertical board and measured in feet and inches. Weight was measured to the nearest 10th of a pound on a calibrated beam scale. Body mass index was calculated as weight (kg) divided by height squared (m2). Waist circumference was determined with subjects standing erect; the tape was placed horizontally around the smallest circumference between the bottom of the rib cage and the top of the iliac crest, measured to the nearest 0.1 cm. Sagittal abdominal diameter was measured using the Holtain-Kahn abdominal caliper.17
The women were instructed to fast for at least 8 hours before the interview appointment. Blood count, biochemical and lipid profiles, and serum glucose were obtained.
Follow-up questionnaires were sent in 1998, 1999, 2003, and 2004. The women were asked to detail any hospital admission for any reason, any emergency department visit or hospital stay of less than 24 hours, and any new provider-diagnosed illnesses, all since the previous survey. Those who did not return the last survey were phoned and asked to answer the questions with a trained interviewer over the telephone. Data from the National Death Index (NDI) Plus of the Centers for Disease Control and Prevention’s National Center for Health Statistics were obtained to verify the vital status of all participants and to determine a Uniform Code of Death for all deceased participants. The NDI records included all deaths as of December 31, 2004.
The study outcomes were measured in years and were defined as (a) time to first recurrent cardiovascular event after incident MI or as (b) time to death from all causes (all-cause mortality). A “recurrent cardiovascular event” was defined as any nonfatal or fatal event, International Classification of Diseases, Ninth Revision–coded diagnosis between 390 and 450 (or International Statistical Classification of Diseases, 10th Revision: I00–I78). All-cause mortality included any death that occurred during the study period (1996–2004).
All statistical analyses were conducted using the Statistical Package for the Social Sciences for Windows, version 17.0 (release date 2008, SPSS, Inc, Chicago, Illinois). Each anthropometric measure was used in its continuous form unless the analyses required a categorical form, in which case each variable was then divided into quartiles. The first and lowest quartiles for each measure were used in all analyses as the referent category.
Descriptive statistics were examined and differences between event statuses were compared using Student t tests for continuous variables and χ2 for categorical variables. All tests were 2 sided, and a P value of <.05 was considered statistically significant. Pearson product-moment correlations were examined for the anthropometric variables for all 356 incident MI female survivors at baseline.
Cox proportional hazards regression models18 were used to conduct the survival analyses and calculate the hazard ratios (HRs) and 95% confidence intervals. These were also used to assess the independent contribution of central fat distribution to the risk of subsequent cardiovascular events and mortality after incident MI in this female cohort, taking into consideration secondary prevention interventions. Both outcomes shared the same time frame: from entrance into the study at initial examination until the end of the study period, December 31, 2004. The participants who were identified as “lost to follow-up” were censored by the receipt of the subject’s last follow-up survey and were considered to be event-free at the date of the last contact. Those participants who died of noncardiovascular causes (eg, cancer, acute trauma) were censored at the time of their death.
The baseline descriptive characteristics of the female participants according to recurrent cardiovascular event status are shown in Table 1. Eighty-five women who survived an incident MI experienced a recurrent CVD event, with 8 experiencing a fatal outcome. Women who had a recurrent event were slightly younger (mean ± SD, 53.5 ± 8.8 years) than those who did not (56.1 ± 8.4 years; P = .021) and had a shorter time to event of 2.6 ± 1.9 years versus 3.7 ± 2.7 years (P = .001). Socioeconomic variables of race and education revealed no statistical significance between the event/no event groups, except for those women who were currently married (P = .004). Smoking status descriptives revealed that 94 of the 356 women (26%) never smoked, even though 15 these of never-smokers experienced both an incident and a recurrent MI. Eighteen former smokers had a recurrent event, as did 52 (61%) of the 181 women who identified themselves as to be current smokers.
Women who experienced a recurrent event weighed, on average, only 2 kg more than those in the no event group, with mean BMIs in both groups also relatively similar (30.2 vs. 29.3 kg/m2, respectively; P = .374). Waist circumferences for the 2 groups were larger than the WHO recommendation of 88 cm or less, with measurements of 96.0 ± 12.9 cm and 92.5 ± 14.4 cm for the event and no event groups, respectively (P = .000). Women in the event group had a slightly higher SAD (22.7 cm) than did those in the no event group (21.9 cm), but this was not statistically significant (P = .86).
Women who had a recurrent event had a mean ± SD fasting serum cholesterol level of 208 ± 44.7 mg/dL and a mean ± SD serum glucose level of 125.7 ± 52.5 mg/dL. Those women who did not experience a CVD event had a lower mean fasting baseline cholesterol level (191.2 ± 38.6 mg/dL) and a mean serum glucose level (112.0 ± 44 mg/dL). Both had statistically significant P values of .002 and .035, respectively.
Of the 85 women who experienced a recurrent CVD event, 29% were on aspirin therapy (acetylsalicylic acid) compared with 38% on acetylsalicylic acid in the no event group. A similar percentage of women in the event group were on statins and β-blockers compared with those who had encountered no event (61% vs 62% and 58% vs 58%, respectively). There was no statistical significance identified among groups for any of the 3 secondary prevention medications.
Table 2 shows the distribution of the study participants according to the common anthropometric measures collected. Of the 85 MI survivors who experienced a recurrent CVD event, 45 (53%) had a BMI of 30.0 kg/m2 or greater (WHO classification: obese) compared with 133 (49%) no event participants classified as obese or greater. Fifty-seven women (67%) who had a recurrent CVD event had a WC of 88 cm or greater (∼35 in.) compared with 164 participants in the no event group (61%). Forty-nine women (58%) who had a recurrent CVD event had a SAD measurement of 21.89 cm or greater (∼8.6 in.) compared with 129 (48%) in the no event group.
Cox Proportional Hazard Statistics
Survival analyses expressed as HRs were obtained using the Cox proportional hazards method. Table 3 reflects the results according to the anthropometric measures for those women who experienced a recurrent CVD event after incident MI. With all anthropometric measures converted to quartiles and the lowest quartile selected as the referent category, a crude HR (model 1) was obtained. Adjusting for age, race, and education (model 2), plus smoking status, alcohol use, and diabetes history (model 3), plus statin use, aspirin use, and β-blocker use (model 4), HRs with confidence intervals were determined. Overall, no HR at any BMI quartile within any model was statistically significant. The crude model for BMI suggested that after incident MI, a woman had a 36% to 39% risk of a recurrent CVD event. However, after adjusting for the aforementioned variables, the risk was the same—a decrease of 25% to 27%—in all other models.
Hazard ratios in the crude model for WC were more intense than those for BMI, showing that female MI survivors had more than double the risk of experiencing another cardiac event especially as the WC quartiles increased, with statistical significance (P = .010) noted at the fourth level. The risks in models 2 and 3 were attenuated with variable adjustment, but, although not statistically significant, all showed a higher risk of event recurrence at all quartile levels when compared with BMI.
The results for SAD revealed higher HRs than in either BMI or WC results. All HRs were higher in all quartiles in all models for this variable when compared with BMI and WC. The third SAD quartile, especially, not only was the highest HR in each model but also was statistically significant in each model (P = .015). For each anthropometric measure, the third quartile (irrespective of variable adjustment) was shown to have the greatest risk of CVD recurrence.
This study is one of the first to examine the influence of central fat distribution in a population-based prospective cohort of female incident MI survivors and 1 of very few studies where the association between visceral fat distribution and CVD has been explored.13,19,20 In this cohort, the risk of a recurrent CVD event increased by 2% for every 1-cm WC increase and by 7% for every 1-cm SAD increase. Sagittal abdominal diameter was found to be a better predictor of recurrent cardiovascular events than WC in women, even after multivariate adjustment. However, the results of this study show that the risk for postincident MI women was similar for both WC and SAD, especially in the top quartiles. Body mass index was the least predictive measure of recurrent CVD events and the only measure that suggested protective effects at various quartiles.
The findings in this study may be simply due to differences in the location of fat distribution. Central adiposity has been consistently shown to be positively associated with CVD risk factors and CVD outcomes.21–23 Sagittal abdominal diameter measures visceral abdominal tissue in a supine position, whereas WC includes all fat and organs located at the determined measurement line.24 Body mass index is essentially a measure of general adiposity because it cannot distinguish fat mass and lean body mass and can distort the relationship between obesity and event recurrence especially when a low BMI is the result of an underlying illness rather than the cause.13,25 Recent research by Guzzaloni et al20 described how, through computed tomography, the total amount of subcutaneous tissue could be further distinguished into 2 subcompartments: a superficial subcompartment and a deep subcompartment. The superficial subcompartment was the predominant subcompartment in women, whereas deep subcompartment was predominant in men.
There is little evidence in the literature of the association of fat distribution with recurrent cardiac events; most previous studies have focused solely on the influence of BMI.19,26–30 In the present study, 3 anthropometric measures were separately examined. Hazard ratios for all measures were much higher than those reported in previous analyses of both incident and recurrent MIs. It should also be noted that many studies have reported results on CVD-free cohorts. Participants who are CVD-free are different from those who have already sustained and survived an MI. Although CVD risk factors may be identical for both groups, the MI survivor has the added risk of irreversible heart muscle injury and changes in the electrophysiology of the heart secondary to oxygen decompensation. Survivors of a first MI may be different from those who do not survive, perhaps sustaining less myocardial damage or having less intense risk factors overall. Most studies that have looked at recurrent events and/or cardiac deaths were short-term prospective studies (6 months to 2 years), whereas a strength of this current study is a follow-up period of over 8 years.19,31–33
It has been well documented that women and men differ anatomically and physiologically cardiovascular-wise as well as in their distribution patterns of central fat.35,36 This study’s findings are similar to the conclusions of Larsson and colleagues34 that abdominal body fat distribution may be responsible for the sex differences seen in the incidence of MI due to genetic or hormonal factors. In a systematic review of the literature, Coutingo et al35 found that in men and women with coronary heart disease, measures of central obesity (WC and waist-to-hip ratio), but not BMI, were directly associated with mortality.
Secondary prevention of a recurrent event calls for aggressive modification of those contributing cardiovascular risk factors, including smoking cessation, exercise training, and nutrition counseling with weight loss goals if required. Current evidence-based guidelines for medical management include the use of β-blockers, aspirin, and statin therapy.3 In this study, these evidence-based standards of secondary prevention were assessed in the models, and the findings suggested no attenuation of the cardiovascular risk. An explanation for this observed lack of protection by the secondary prevention interventions may include the possibility that those participants taking these medications were already maximally treated upon entrance into the study, and that despite these interventions, the role of central fat distribution may override any further protection from a recurrent cardiovascular event. The positive effects of the treatment of high cholesterols with statins and inflammation with aspirin may be mitigated by the prevalence of obesity as described by Kim et al.35 Their results are similar to these findings, whereas the use of medications appears to have minimal impact between the relation of anthropometric measures and recurrent CVD events.
This study does have some limitations. First, most of the data collected were by self-report, relying on each participant’s recall of medical histories and lifestyle habits going back days to years. With all subjects being recent incident MI survivors, recall could be also influenced by the clinical event itself or an awareness of personal lifestyle behaviors. The results may also be biased by the individual’s survival and, thus, a motivation to participate. Furthermore, anthropometric and blood measurements were taken at the baseline interview only; no repeat measures were available from date of study entry. This does not account for subjects who may have changed their body weight and/or changed other lifestyle factors (as quitting smoking) over the 8-year study period.
There is no universal cutoff for SAD as there is for BMI and WC. Being able to assess and predict the cardiovascular risk of a person with a “normal” BMI but an “abnormal” WC or SAD may lead to the development of better primary and secondary prevention interventions. Lastly, the presence of unknown confounders that were unable to be controlled for in the analyses cannot be ruled out.
The strengths of this study lie in its prospective design and comprehensive data collection. A significant strength is the implementation of a standardized methodology for interviewing and obtaining clinical measurements and the detailed information that was collected. Follow-up of the participants was intense. Whether by mail or by telephone, this allowed updated information collection on event recurrence, new medical diagnoses, and current medication lists. Event details were verified by obtaining local medical records and vital status was confirmed through NDI Plus.
Women appear to have a high risk of recurrent cardiovascular events for the anthropometric measures of central fat distribution. The underlying mechanisms for the observed results warrant further investigation, as does comparison of results with those of men.
It also appears that measures of central fat distribution are better predictors of recurrent cardiovascular events in a sample of female MI survivors than BMI is. The findings also support the use of central fat measurements, as WC or SAD rather than BMI, to identify, assess, and treat those individuals at risk for cardiovascular events. However, SAD is not necessarily “user friendly” for use in a day-to-day patient setting and is usually reserved for research purposes because it requires special calipers, training, and a concentrated time factor. Measurement of WC requires only a tape measure and a fraction of provider time but also has its own pitfalls, such as consistent placement of the tool. Body mass index is a matter of measuring height and weight; its calculation can be as simple as entering the numbers into an electronic device but reveals little about the body’s physiology.
The present study also suggests that use of evidence-based secondary prevention management—physical activity, statins, aspirin, and β blockers—may not reduce the risk of recurrent CVD events at any quartile level. The benefits of therapy may be reduced by the presence of adiposity, especially that of central fat distribution. Visceral fat may contribute more toward CVD risk and adverse outcomes than the positive impact of physical activity and CVD-directed medications. More research is needed to determine if an increase or decrease in visceral fat actually affects the pharmacodynamics and pharmacokinetics of medications for CVD.
What’s New and Important
- Central fat distribution, not BMI, is associated with an increase in a woman’s risk of developing a recurrent cardiovascular event after a first MI.
- Despite secondary prevention management, such as the use of statins, β-blockers, and aspirin, the risk of a recurrent cardiovascular event remains elevated.
- Nurses should include central fat measurement at every physical assessment opportunity. Further investigation is warranted to determine the impact of abdominal fat redistribution on cardiovascular recurrences in both genders.
The author thanks Joan P. Dorn for her patience and support of this project.
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