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Gender Differences in Coronary Artery Disease

Eastwood, Jo-Ann PhD, RN, CCNS, CCRN; Doering, Lynn V. DNSc, RN, FAAN

The Journal of Cardiovascular Nursing: September-October 2005 - Volume 20 - Issue 5 - p 340–351

Coronary artery disease in women is associated with higher morbidity and mortality than in men. The purpose of this article is to summarize recent literature concerning gender-based differences. Specific differences in pathophysiology, traditional and psychosocial risk factors, symptom presentation, treatments, and outcomes between women and men will be reviewed.

Jo-Ann Eastwood, PhD, RN, CCNS, CCRN Director, Clinical Programs, UCLA School of Nursing. Postdoctoral Fellow, Greater Los Angels, VA Healthcare.

Lynn V. Doering, DNSc, RN, FAAN Associate Professor, UCLA School of Nursing.

Corresponding author Jo-Ann Eastwood, PhD, RN, CCNS, CCRN, 1712 Faymont Ave, Manhattan Beach, CA 90266 (e-mail:

Authors have no conflict of interest.

Coronary artery disease (CAD) is the leading cause of death and disability among adult women in the United States.1 It is the number 1 cause of death in women older than 50 years.2 As many as 1 in 8 women aged 45 to 54 has clinical evidence of CAD, with the prevalence increasing to 1 in 3 in women older than 65.1 Among CAD patients, the death rate has declined less for women than for men.3 Additionally, CAD outcomes are less favorable in women than in men. Data from the Myocardial Infarction Triage and Intervention Registry reveal that hospital mortality rates for acute myocardial infarction (AMI) are 16% for women and 11% for men.4,5 Clinical manifestations of CAD in women lag by approximately 10 years when compared with men. Coronary events such as acute coronary syndromes (ACS) and sudden cardiac death may lag as much as 20 years. As the US population ages, US women are outnumbering men since 1984 and more women than men have died of cardiovascular disease. There are distinct gender differences in terms of pathophysiology, presentation of symptoms, validity of diagnostic tests, and response to therapies. Despite the fact that 1 of every 2.4 deaths in women is due to cardiovascular disease, women perceive breast cancer, which accounts for only 1 of every 29 female deaths, as their greatest threat.6

Current programs in disease management of CAD are based on information obtained primarily from research on men. To tailor interventions specifically to the needs of women, researchers and clinicians need to be aware of their differences in pathophysiology, presentation, and outcomes of treatment. The following provides an overview of the physiological, emotional, and psychosocial differences between men and women with CAD and a look at the differences in health outcomes for women.

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Physiologic Differences

Several investigators have considered gender-mediated differences in underlying mechanisms of atherosclerosis, including anatomic and pathophysiolgic differences. Regarding gender-mediated anatomic differences, smaller epicardial vessels in women have long been assumed to negatively influence treatment outcomes, particularly those related to revascularization. When revascularization is performed, whether by percutaneous coronary intervention (PCI) or by coronary artery bypass graft (CABG) surgery, the degree of technical difficulty increases when the arteries are smaller. Size and gender differences in prognosis have been supported by angiography and autopsy studies showing that the left main and left anterior descending arteries are smaller in women, independent of their body size.7 This finding suggests an intrinsic gender effect on coronary dimensions and provides a plausible explanation for gender differences related to anatomy in coronary outcomes.7 Therefore, simply by virtue of their smaller diameter vessels, women may be more prone to coronary occlusion than men. Recently, Sheifer and colleagues confirmed that women had smaller left main and proximal left anterior descending arterial and luminal areas than men by intravascular ultrasound.7

There is evidence to link smaller artery dimension to an increase in adverse cardiac events. For example, after a PCI, the resultant luminal diameter is a strong predictor of restenosis.7 In CABG the size of the target vessel correlates with the long-term patency of the graft. When an atherosclerotic plaque ruptures in a vessel with a smaller luminal area, there is an increase in the risk of total occlusion and myocardial infarction (MI). The Coronary Artery Surgery Study showed that the operative mortality for women was 4.5%, compared with 1.9% for men.8 The discrepancy was attributed to smaller vessel size in women. In more recent comparisons using data from the National Heart Lung and Blood Institute (NHLBI) Dynamic Registry, Suwaidi and colleagues compared outcomes of patients with large coronary artery lesions (>3 mm), and those with smaller coronary artery lesions (<3 mm) outcomes.9 Patients with lesions in small coronary arteries were more often insulin-dependent diabetic women, who had had prior CABG surgery. Between July 1997 and February 1998, conventional angioplasty was performed more often, and angioplasty with stents was performed less often in this group. At 1-year follow-up, major adverse events including death, MI, and CABG were relatively low in both groups. However, patients with small coronary arteries were more likely to be diabetic women and were more likely to undergo repeat revascularization (17.4% vs 13.6%, P < .05).9

Despite having smaller vessels, women are less likely to experience acute events associated with total occlusion (ie, ST elevation), and are more likely to have partial occlusions manifested by unstable angina10 and to present with signs and symptoms more difficult to diagnose.11–13 Women present more frequently with unstable angina and non–ST-elevation myocardial infarction, whereas men have ACS with ST elevation myocardial infarction (STEMI). Mortality is higher in women with STEMI than in men.10,14 Women are less likely to receive appropriate treatment and less likely to be considered for thrombolytic therapy and PCI even when it would be appropriate for their clinical presentation.15 Therefore, they may experience significant myocardial damage. In addition, women are known to have reduced collateral blood flow, which may lead to higher rates of complications when STEMIs occur.16

There is initial intriguing epidemiological evidence that the inflammatory process associated with plaque development may differ in women and men. High levels of C-reactive protein (CRP) have been shown to have similarly strong prognostic values in women and men.17,18 However, median levels of high-sensitivity CRP in women were slightly higher than those in men, and the absolute risk associated with elevated CRP was greater than that seen in earlier studies of men.19 Interestingly, CRP appears to be increased in the presence of increased estrogen levels, as evidenced by recent clinical trials of hormone replacement therapy (HRT).20,21 Together, these findings suggest that estrogen may be involved in altering plaque stability via inflammatory mechanisms. This inference is consistent with reports that female victims of sudden cardiac death demonstrate greater incidence of plaque erosion than do male victims.16 This may also shed light on findings from the Heart and Estrogen/Progestin Replacement Study (HERS) and Estrogen Replacement and Atherosclerosis trials, in which lipid reduction was not accompanied by reduction in cardiac events. It is possible that proinflammatory effects of HRT may cause plaque instability that offsets its benefits on lipids.22

In addition to gender differences in plaque development, there may also be gender differences in thrombosis and plaque composition. This hypothesis stems from data that show greater incidence of plaque erosion, rather than plaque rupture, in women, than in men, who experience sudden cardiac death.16 Currently, it is believed that plaque rupture, associated with interruption of a thin fibrous cap and continuity of the intraluminal thrombus with the necrotic core of the plaque, is the primary culprit in ACS. In women, acute events may be initiated not by this classic rupture, but rather by plaque erosion, which is characterized by direct contact of the thrombus with the fibrointimal plaque itself, rather than the necrotic core of the plaque. Some studies have suggested that there are gender differences in plaque composition, with women having “younger” less dense and less calcified plaque than men. However, potential links between plaque composition, thrombosis formation, and clinical outcomes have not been elucidated.

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Risk Factors

Because of the fact that CAD is a major cause of death in women, a comprehensive risk-factor profile is needed in relationship to gender.23 There has been limited information regarding female risk factor profiles and the prediction of CAD mainly because this type of information has been investigated in men and applied to women. For example, in the Framingham study, women between 60 and 64 years and at highest risk (in the top 10% of the risk factor distribution) had only a 12% probability of acquiring CAD during a 6-year follow-up.24,25 This low probability of CAD in high-risk women indicates that traditional cardiac risk factors lack specificity for women. These risk factors were adopted from information gathered on men and incorporated into the equations in the Framingham analysis. Therefore, the traditional risk factor profiles explain only a limited portion of the variance in risk among women.23 The role of less well-established variables, such as psychological, social, and behavioral factors, have also been studied less frequently in women than in men.26

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Traditional Risk Factors

Traditional risk factors differ between men and women. Although in the past the difference has been attributed to the presence of estrogen in the premenopausal period, the most significant difference is diabetes mellitus, which is associated with a 3- to 7-fold increased CAD risk in women compared to a 2- to 3-fold elevation in CAD risk in men. The reason for this gender difference is not known.27 In women older than 65 years, dyslipidemia may also put women at a greater risk than men. High levels of triglycerides and low levels of high-density lipoproteins (HDLs) are strongly correlated with CAD in women.13 Coronary risk factors are highly prevalent among US women aged 20 to 74. More than one third have hypertension, more than a quarter have elevated cholesterol levels, more than a quarter are cigarette smokers, more than a quarter are overweight, and more than a quarter have a sedentary lifestyle.1

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Cardiovascular health in women is greatly influenced by abnormalities in carbohydrate metabolism. Women who are obese or have diabetes are at an increased risk for CAD. Having diabetes negates the presumed gender-protective effect of estrogen in premenopausal women.28,29 The prevalence of diabetes is 2% to 6% in the United States, with impaired glucose tolerance in as many as 20% of women. The risk of cardiovascular death among women with diabetes is more than 3-fold greater than that of nondiabetic women. In addition, there may be an interactive effect between smoking and diabetes. The risk of death among diabetic patients who smoke is twice that of nonsmoking diabetic patients. Smoking confers greater health risks in diabetic women than in men with diabetes.30–32

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Hypertension has been recognized as a risk factor for cardiovascular disease and mortality since the 1920s. Hypertension is more prevalent in women than in men after 65 years of age. According to the National Health and Nutrition Examination Surveys (NHANES III) study, hypertension is present in 51% of white women and 79% of black women in the United States.4,33 During adolescence, gender differences in blood pressure levels emerge. Through middle age, men tend to have higher mean systolic and diastolic blood pressures by 6 to 7 mm Hg and 3 to 5 mm Hg, respectively, than women. In women, there is an age-associated rise in systolic blood pressure after age 59 and in advanced ages hypertension prevalence is higher in women than in men.4

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According to the National Health Interview Survey conducted by the Centers for Disease Control and Prevention, 22% of women smoke versus 26% of men in the United States.31 Smoking rates are declining less in women than in men.27,34 This disturbing fact was validated globally in the World Health Organization MONICA project, whose goal was to determine how trends in event rates for coronary heart disease (CHD) were related to trends in classic coronary risk factors over 10 years across 38 populations from 21 countries on 4 continents.34 Certain characteristics in combination with cigarette smoking place women at higher risk of CAD than men. In women who smoke over the age of 35, there is a strong recommendation that they are not prescribed oral contraceptives.35,36 Smoking, resistance to smoking cessation, and smoking relapse are linked to depression, which increases CAD risk and worsens the response to ACS and MI.37 According to the NHANES I Epidemiologic Follow-up Study, cigarette smoking is associated with a 45% higher risk of congestive heart failure (CHF) in men and an 88% higher risk of CHF in women.38 Weight control is the most frequently cited reason for smoking among adult women.31,32

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Throughout the life span, HDL levels are 5 to 10 mg/dL higher in women than in men.39 Low-density lipoproteins (LDLs) and triglycerides rise after menopause and exceed those of men after 65 years of age.4 High triglycerides can indirectly promote atherosclerosis by lowering HDL and promoting small dense LDLs,40,41 which may explain in part why LDL levels increase in women after menopause. The power of cholesterol substrates in predicting coronary events varies in women in comparison with men. An elevated level of LDL is less predictive of CAD in women than in men.39 The reverse is true in the case of triglycerides, which are more predictive in women than in men. Elevations of serum HDL are a more powerful predictor of lower coronary risk in women than in men.41 Even though LDLs are less useful in predicting cardiac risk in women, interventions to lower LDL levels are highly effective in preventing major coronary events in women.40

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Obesity and Physical Inactivity

Obesity and physical inactivity are highly correlated.42 While obesity has been increasing, a significant number of adult women, up to 25%, admit to getting no regular physical activity.43 Both of these factors may contribute to rising rates of insulin resistance and, consequently, type II diabetes in both women and men.44 Cardiac risk factors especially predictive in women, such as hypertrigylceridemia and hypertension, are also associated with type II diabetes.42,44 Women with abdominal fat accumulation are also at risk for type II diabetes.36,42 According to the NHANES III, women have a lower prevalence of being overweight (body mass index [BMI], 25–29.9) than men, 25% versus 40%, but a higher prevalence of obesity (BMI > 30), 25% versus 20%.28,45,46

Obesity has a substantial impact on circulatory function. Increases in cardiac preload, marked increases in cardiac output, and an expansion of the plasma volume have all been associated with obesity.47 There is a substantial increase in stroke volume and left ventricular filling pressures as demands on cardiac output rise. These changes can lead to peripheral edema even though no right-sided heart failure is present.42 Obesity increases hypertension.36,46 An increase in 10% of body weight increases systolic blood pressure 6.5 mm Hg, according to the Framingham study.48 These circulatory derangements explain how obesity alters the risk-benefit ratio unfavorably for all patients undergoing revascularization procedures. There is continuing evidence of the increase in the prevalence of obesity according to estimates from NHANES 1999–2002 in women and children.49 Since obesity is more prevalent in women, researchers have suggested that it may explain why women have significantly more operative complications and a higher 30-day mortality rate after both PCI and CABG than men.47

A constellation of 5 risk factors (high triglycerides, low HDL cholesterol, high blood pressure, hyperglycemia, and abdominal obesity) comprises the “metabolic syndrome.”50 Results from the Women's Ischemia Syndrome Evaluation (WISE) shed some light on the independent risk of future cardiovascular events associated with metabolic syndrome in women. In WISE, obesity measured by BMI (reflecting total body obesity) was not a valuable risk predictor.51,52 In contrast to overall obesity, visceral fat in combination with other components of metabolic syndrome is a more important predictor of cardiovascular risk. The WISE investigators recommend that physicians pay more attention to abnormal metabolism than to obesity when assessing a woman's cardiovascular risk.51,52

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Psychosocial Risk Factors

A growing body of clinical and scientific information links heart disease to the emotions. Women's psychological and behavioral characteristics are now being recognized as likely risk factors for the development of CAD. The expanding body of evidence confirms that psychosocial and socioeconomic factors are associated with heart disease risk and outcomes in women. Many researchers have speculated that social relationships and an individual's framework of social interactions have an effect on the etiology of CAD.23 High rates of heart disease in women have been shown to be inversely related to income, educational attainment, and socioeconomic status.23

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Social Isolation

During the first year after a cardiac event, women are less physically, sexually, and socially active than men.53 During the recovery period following a cardiac event or CABG surgery, women return to work less often, experience more cardiac symptoms, and report lower levels of satisfaction with social support than men do.26,53,54 It is important to note that women experience higher levels of depression and anxiety and lower levels of perceived control than men following the diagnosis of heart disease.55 Women tend to be older and more socially isolated then men. Compared to men, a greater percentage of women living alone experience recurrent cardiac events.56

Age alone does not account for the effect of social isolation on CAD outcomes in women. Three studies have investigated network or support characteristics in relation to total mortality among women. In the Alameda County study, investigators found a consistent and significant pattern of increased mortality rates in women with decreased social connections. Compared to women scoring high on social ties, women lacking social ties were more than 3 times as likely to die of CAD. It was found that nonmembership in groups was significantly associated with ischemic heart disease mortality among women aged 40 years and older.57

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Another major psychological influence associated with an increase in cardiac events is depression. Kaplan first noted this association in the 1980s. However, it was ignored as others focused on coronary-prone behavior.23,58 In a meta-analysis about psychosocial predictors of CAD published by Booth-Kewley and Friedman,59 depression had the strongest association with CAD. Compelling new evidence of the importance of depression in CAD risk has been gathered in more recent years. Depressed patients were found to have a 5-fold greater risk of mortality 6 months after MI than nondepressed patients. Depression was identified as an independent predictor of mortality and recurrence of clinical cardiac events in the Recurrent Coronary Prevention Project.60 There is a 2-fold greater prevalence of depression in women than in men.61

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Anxiety and tension predict coronary-related deaths and MI in women.62 A rise in blood pressure, cardiac irritability, and increases in basal metabolic rate and bronchodilation are the cardiovascular results of an increase in anxiety.63 Influences on catecholamines, myocardial oxygen demand, and platelet aggregation have also been well documented. Contributing factors for increases in anxiety in women may be age, developmental changes, social roles, and life circumstances such as cardiac disease.64 Women appear to be at a higher risk than men for anxiety after cardiac revascularization procedures and AMI.65,66 Higher anxiety levels may be a partial contributor to the poorer prognosis of women.67

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Differences in Clinical Presentation

Between the ages of 45 and 64, 1 in 9 women will be diagnosed with some form of cardiovascular disease. The incidence rises to 1 in 3 in women after age 65.3 In women, the clinical signs and symptoms of CAD develop an average of 8 to 10 years later than in men. Women tend to be older, present later after symptom onset, have different symptoms, and have higher prevalence of diabetes, systemic hypertension, CHF, smoking, and family history of CAD.66 Coronary artery disease progresses more rapidly in women, which may explain why they have fewer collateral vessels, as confirmed by angiographic studies.68

Epigastric pain, chest pain, or unusual fatigue is prodromal symptoms to ACS that are often repeatedly ignored by women and their healthcare professionals.11,12 Research shows that even when women experience ACS symptoms, they delay seeking treatment.10,15,69,70 Increased delay in seeking treatment by women may reflect several factors. First, female symptoms differ from the commonly recognized pattern of crushing chest pain attributed to men, so that women may fail to recognize their symptoms as “classic heart attack” or “typical” symptoms.71,72 “Typical” symptoms are based on the experience of white, middle-aged men with any deviations labeled “atypical.”12 Second, few women, less than 7% of those participating in a national survey, recognize heart disease as a major health threat for women.73 Therefore, women may fail to appreciate their own risk for ACS and so may not consider their symptoms to be serious.

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The Framingham cohort of women was the first to report important differences in the presentation of women with CAD compared to men.10 In women, the most common initial presentation of ischemia is angina, whereas in men it is STEMI.10,55,74 When women do experience ACS, they call later for professional help and present more frequently with atypical symptoms,10,11,72,75 with 95% of women reporting having had prodromal symptoms in the month preceding the ACS.11 When complaining of “chest pain,” women describe “burning, squeezing, or upper abdominal fullness” rather than discomfort centralized over the sternum.24 Other descriptors that women frequently report in an acute cardiac event are dyspnea, nausea, weakness, cold sweat, dizziness, and fatigue.11,12 In a recent study of more than 500 women with AMI, prodromal symptoms of fatigue (71%), sleep disturbance (48%), and shortness of breath (42%) were reported.11

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During the first year following a cardiac event, women experience greater risks of death, cardiac distress, and reinfarction than men.3 Postmenopausal women have a 31% lifetime mortality risk from CAD in contrast to a 3% risk from hip fracture and a 4% risk for breast cancer.30 Women have poorer outcomes than men after AMI and PCI.76 Hospital mortality rates for AMI are higher in women at 16% than in men at 11%.3

During the past decade, CABG surgery and PCIs on women have had a 3-fold increase. The mortality for CABG surgery in women is twice that for men. Women have lower rates of graft patency, less postoperative symptomatic relief, and more frequent perioperative infarction than men.77 They experience more heart failure and are more likely to require reoperation within 5 years following CABG surgery.78,79

In contrast, mortality associated with PCIs is comparable in women and men initially, but there is less favorable long-term survival and less late symptomatic relief in women.80–82

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Gender Differences in Treatment

Noninvasive Treatment

Clinical trials have demonstrated that lowering cholesterol decreases CAD morbidity and mortality and slows lesion progression in men, but most studies have included few women.22 Only 4 primary prevention trials and 2 secondary prevention studies have focused on women (Table 1). In general, both diet and pharmacological lipid lowering decreased first and subsequent cardiac events in women. With lovastatin, the effect of treatment on the reduction of first events was greater in women than in men.88 For recurrent cardiac events, women had twice the rate of risk reduction as men when given equivalent doses of pravastatin.89 Diet and lifestyle changes can have a profound effect on morbidity and mortality from CAD in women. There is strong evidence that CAD in women is largely preventable through diet and lifestyle modifications. Stampfer and colleagues estimate that “82% of coronary events in the study cohort of the Nurses' Health Study could be potentially prevented by adhering to lifestyle guidelines involving diet, exercise, body weight, and abstinence from smoking.”36 In the study, CAD incidence declined by almost one third from the early 1980s to the early 1990s. This decline in CAD has been attributed to an increase in physical activity and more emphasis on better nutrition by the nurses in this study.90,91 A higher intake of trans fatty acids was strongly associated with increased risk of CAD, and saturated fat intake was associated with a weaker and nonsignificantly increased risk.90 A higher intake of unsaturated fats, especially polyunsaturated fat, was associated with a lower risk of CHD using 14-year follow-up data from the Nurses' Health Study.90



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Invasive Treatments

A report of the NHLBI on gender-related differences regarding percutaneous transluminal coronary angioplasty (PTCA) revealed women were older, had a higher prevalence of severe and unstable angina, and had a higher incidence of hypertension than men. Men had more multivessel disease, previous CABG surgery, and an ejection fraction less than 50% at baseline. Despite these differences of more advanced disease in men, women had a lower clinical success rate (56% vs 62%), lower angiographic success rate (60% vs 66%), and higher in-hospital mortality rate (2% vs 1%). There was a higher incidence of intimal tear and coronary dissection in women than in men. Female gender was an independent correlate of reduced success with angioplasty.92

In 1985, the NHLBI PTCA Registry reported that even though men had a higher prevalence of multivessel disease and worse ventricular function, women undergoing PTCA had lower success rates and a higher number of complications and in-hospital deaths.76 Women were more likely to experience coronary dissection, had a 6 times higher rate of procedure-related deaths, and a 5 times higher mortality rate with emergency bypass surgery. Multivariate analysis showed that female gender was an independent predictor of a lower success rate and early mortality.93 However, women had better late outcomes that were confirmed by the Thrombolysis in Myocardial Infarction (TIMI III) Registry.94 These include fewer infarctions, repeat angioplasties, bypass surgical interventions, and deaths.94

Several studies have shown that women have a higher in-hospital event rate, higher numbers of repeat PCIs, myocardial reinfarctions, and in-hospital and short-term mortality. The Primary Coronary Angioplasty for Acute Myocardial Infarction (PAMI) Registry showed a 3.3 times greater in-hospital mortality in women than in men.95 Women have a worse prognosis despite the fact they have less severe CAD than men. This suggests that the worse prognosis is probably due to unknown risk factors and anatomically different profiles.93

There is little understanding of the role of hormones on the responses to the treatment of CAD by PCI procedures to date. Small animal models have shown the benefits of estrogen in the amelioration of the restenosis process after balloon vessel injury. In 1997, O'Keefe and colleagues reported on the PTCA database of the Mid-America Heart Institute covering the years 1983–1993.96 Of 337 women who underwent PTCA, 137 were on estrogen replacement therapy (ERT), at the time of the PCI and during 6 years of follow-up. Repeat revascularization was equal at 50% for the groups with and without ERT. The risk of cardiovascular event was 16% in the ERT-treated women versus 27% in the non-ERT group. The total mortality was significantly lower in the ERT group (9%) compared to the non-ERT group (17%). In this study, estrogen did not change the need for repeat angioplasty, but improved the long-term and event-free survival following PCI in postmenopausal women.96 Studies by Herrington and colleagues as well as the HERS showed that HRT was not effective as secondary preventive measures and did indeed increase the risk of cardiovascular events. Hormone replacement therapy was initiated late, an average of 23 years after the cessation of menses in women approximately 65 years of age.41,97 Attention has been directed toward results from animal studies and the role that estrogen may play in the primary prevention of atherosclerosis. In monkeys, estrogen has beneficial effects in the early stages of atherogenesis, but little or no effect on the final stages of plaque complications, instability, and CHD events.98 Promising results of inhibition of atherosclerosis progression were found in those animals given contraceptive steroids premenopausally and administered estrogen replacement postmenopausally.41,98 In humans, HRT may alter the biology of the vessel wall, providing protection through vasodilatory, anti-inflammatory, and antiproliferative mechanisms if started at, or around, age 54.99 Studies are in progress testing this hypothesis. In regards to outcomes from interventional procedures other than balloon angioplasty, the effects of hormones on distal blood flow on atherectomy, rotoblator, and stenting have yet to be investigated.100

Recently the use of glycoprotein (GP) IIb/IIIa agents in the catheterization laboratory improved the survival of patients undergoing stenting and led to a decrease in acute complications in high-risk patients. In women, the risk reduction related to cardiac events, such as restenosis and angina, attributed to the use of GP IIb/IIIa is similar to that observed in men. However, women are generally at higher risk for major hemorrhages, regardless of GP IIb/IIIa treatment. Female gender is a significant predictor of major bleeding after PCI and it is thought to be related to differences between thrombotic substrates in women and men.101

In the 1980s and 1990s, gender disparities were reported regarding the use of CABG surgery as a treatment of ischemic heart disease.

Approximately 180,000 CABG surgeries are performed on women in the United States annually, which is approximately 28% of the total.1 Previous literature on gender differences in physical and psychological outcomes after CABG surgery have yielded conflicting results. Some studies show no significant differences in symptoms and functional outcomes during the first year in women and men.102–104 In contrast, some studies show poorer functioning and more symptoms in women than in men.77,79,81 In a recent study, Vaccarino and colleagues found important unfavorable outcomes in women in their hospital readmission rates, functional status, and worsening mental health that were higher than expected in the face of a low mortality rate of 2.2%.79

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Gender Bias

Despite the fact that women are at a higher risk for cardiovascular disorders than men, gender differences in the referral rate for coronary angiogram seem to reflect bias.105,106 A RAND Review rated indications for coronary angiography and found that women were less likely to be considered for this diagnostic procedure. When chest pain was of unclear etiology, women waited longer than men to go to cardiac angiography. In women younger than 49 years, angiography was considered necessary only if more than 1 stress test was consistent with ischemia. However, regardless of age, men were referred to angiography with a single positive stress test.107 The TIMI III study also found that women were treated less aggressively and received coronary angiography less frequently than men.94 More recent studies are showing less of a gender-related difference in referral patterns for coronary angiography than earlier studies reported.108

Women's complaints have been consistently attributed to mental rather than physical problems.101,106 An example of this is in the Survival and Ventricular Enlargement (SAVE) study, where women were only half as likely as men to undergo a coronary angiography before index infarction, despite greater symptomatology and functional disability from angina.105 The American College of Cardiology/American Heart Association has established gender independent guidelines for the use of coronary angiography for patients presenting with chest pain.

Upon coronary angiography, women are 5 times as likely as men to have normal coronary findings.16 This seems to suggest that upon the presentation of chest pain women are referred inappropriately for angiography. The fact that chest pain in women is not well understood complicates the picture. It has been suggested that atypical chest pain in women may be due to the higher prevalence of vasospastic or microvascular disease and mitral valve prolapse.16,105,109,110 Women whose coronary arteries appear smooth or have only mild plaque may have endothelial vasomotor dysfunction that modulates myocardial ischemia. This is due to coronary constriction or failure to dilate appropriately under conditions of increased demand. With the advances in new technology such as the Doppler-tipped flow-wire, this phenomenon was demonstrated by measuring coronary vasodilator reserve in patients with chest pain but angiographically normal coronary arteries. Greater intracoronary reserve was found in men than in women.111

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There has been an explosion in knowledge of risk factors for CAD in the past few decades. In response to this information, public health strategies for smoking cessation, control of blood pressure, and lipid lowering are now being mobilized. In 1998, the American Heart Association defined obesity as a major risk factor for CAD and added diabetes in 1999.112,113 Traditionally epidemiological studies of diet and CAD have focused on men. Despite this, there are data to support the importance of obesity, diabetes, smoking, physical inactivity, hypertension, and hypertrigylceridemia in women's risk for CAD. Recent results from the Nurses Health Study also indicate that CAD risk in women can be reduced by diet and lifestyle changes. Despite the proven benefits of physical activity and low-fat, fiber-rich diets for women, many women face challenges to improving diet and physical activity in their daily routines. More than 60% of women work and have family demands that limit time for physical activity, increase stress-related behaviors, like smoking, and regularly consume “fast foods” that are rich in fat and calories.73

Because of the limited amount of data on women, it is difficult to draw conclusions regarding the relationships of psychosocial variables and the development of CAD.114 Post-MI psychosocial adjustment seems to be worse in women than in men.115 Psychosocial and socioeconomic factors influence CAD in women to a greater degree than in men. After being diagnosed with CAD, women experience higher levels of depression and anxiety and lower levels of perceived control than men. Women lacking a social network and experiencing depression have higher rates of mortality after the diagnosis of CAD or during the recovery from a cardiac event or procedure than men.

Enhanced quality of life and psychological wellness has been linked to improved functional status, decreased cardiac symptoms, and reduced psychological distress after successful PTCA.16,66,100,116,117 Little is known about adjustment after other types of PCIs, such as stenting.

An increased incidence of CAD in women suggests worse outcomes even in the age of new devices and adjunctive therapy. There are many issues relevant to the diagnosis and management of women with CAD. Women experience symptoms that are different from those of men, which may account for their delay in seeking treatment and increase the difficulty in diagnosing ischemic syndromes in women.10

The use of coronary angiography as a diagnostic tool for obstructive CAD in women has steadily increased and is now well recognized as an appropriate treatment plan for women despite earlier gender-based differences in referral patterns. The literature indicates that women are referred less than men to coronary angiography, and that treatment is initiated much later in the course of their disease. Researchers have identified causes of poorer outcomes including anatomy, physiology, bleeding tendencies, gender bias in the selection, and referral to treatment despite the increased awareness of CAD in women.88,94,118

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Implications for Practice and More Research

Current management of CAD is based primarily on knowledge gained from the study of men. More research on women is needed so that we do not miss the effects of the interaction of gender and pathology on clinical presentation, symptoms, treatments, and outcomes in all patients with CAD. Using treatment plans specifically on the basis of knowledge of men limits our effectiveness to address areas that might have positive health outcomes for women. Learning more about the differences between men and women with CAD will help patients and families develop realistic expectations about their recovery from a cardiac event.

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      The 14th Annual Cardiovascular Nurse and Technologist Symposium

      The 14th Annual Cardiovascular Nurse and Technologist Symposium will be held during the Cardiovascular Research Foundation's Annual Transcatheter Cardiovascular Therapeutics (TCT 2005) symposium on Thursday, October 20th, at the Washington Convention Center, in Washington, DC. This symposium, designed for nurses and nurse practitioners, technologists, clinical research specialists, and physician assistants, will offer an exciting new format this year, with greater emphasis on interactive case presentations using a multidisciplinary panel of nurses, technologists, physicians, and physician assistants, led by interventional experts in the field including Michael Guiry, RPA-C, of New York-Presbyterian Hospital, Alexandra Lansky, MD, of NewYork-Presbyterian/Columbia University Medical Center and Cardiovascular Research Foundation, Thomas H. Maloney, MS, RCIS, of Memorial Regional Medical Center, and Hilary Nierenberg, MS, ANP, of NewYork-Presbyterian Hospital.

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      Best-selling author, Dr Mehmet Oz, Professor of Surgery at Columbia University College of Physicians & Surgeons, and Director, Cardiovascular Institute, Columbia University Medical Center in New York City, will be the keynote speaker. This renowned heart surgeon and accomplished author of award-winning books will provide insight into his unique approach to medical care and his use of complementary medicine, using his witty way of explaining medical topics, issues, and procedures through tangible, down-to-earth analogies. Dr Oz has appeared on numerous television programs, is a regular on Discovery's Second Opinion, and currently has a best-seller on Oprah's Book Selection list.

      This year's 14th Annual Cardiovascular Nurse and Technologist Symposium is expected to be more informative and interactive than ever. Registration is currently open. To obtain further information on this dynamic educational forum, or to register online, please visit

      118. Jenkins C, Stanton B. Quality of life as assessed in the recovery study. In: Wenger N, Matson M, Furberg C, eds. Assessment of Quality of Life in Clinical Trials of Cardiovascular Therapies. New York: Lejacq; 1984: 266–280.

      coronary artery disease; gender; percutaneous coronary intervention; women

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