Marked reductions in coronary heart disease (CHD) mortality in women have been achieved over the past decade.1 These improvements have been driven by an increase in awareness, increased focus on women and their cardiovascular risk, and use of evidence-based primary and secondary CHD prevention therapies.2,3 Despite these advancements, CHD remains the leading cause of morbidity and mortality affecting millions of American women.1 It is disconcerting to say the least that CHD remains understudied, underdiagnosed, and undertreated in women. However, 2 recent scientific statements from the American Heart Association examined acute myocardial infarction (AMI)2 and ischemic heart disease3 in women. Mehta et al2 provided a comprehensive review of the current evidence of the clinical presentation, pathophysiology, treatment, and outcomes of women with AMI.

Since 1984, the annual heart disease mortality rate has remained greater for women than for men.2 The prevalence of CHD is 6.6 million among US women.1 Of these, 2.7 million have had an myocardial infarction (MI), more than 53 000 died of an MI, and an estimated 262 000 women were hospitalized for an acute coronary syndrome (AMI and unstable angina).1 Regardless of age, within a year of a first AMI, more women than men will die (26% of women and 19% of men); within 5 years of a first AMI, more women than men will die (47% of women and 36% of men), have heart failure, or experience a stroke.1 Reasons for the disparate AMI outcomes among women are multifactorial and related to disease prevalence and the influence of age, race, and ethnicity.2

Women are often older when they present with their first AMI, at an average age of 71.8 years, compared with 65 years for men.1 The older age at CHD onset in women compared with men is thought to be because of the protective role of circulating estrogens on the vascular endothelium. Data suggest, however, a need to focus on AMI among younger women as well. Of particular concern, the substantial decline in AMI event and AMI mortality rates in the United States in the past decade is absent in young women.2 Moreover, there are troubling trends of worsening risk factor profiles and higher mortality among younger compared with older women.2 Mehta et al2 concluded that the mechanisms contributing to excess risk and inferior outcomes among young women are likely multifactorial and may include unique sex-specific biology and disease manifestations and distinctive psychosocial stressors that interfere with health behaviors and interact with biology.2

Racially and ethnically diverse women with AMI have distinct experiences in terms of clinical presentation, risk factor burden, guideline-based care, and outcomes.2 Ethnically diverse women present at a younger age with their incident MI compared with white women.4 The prevalence of MI is higher in black women than in all other racial and ethnic groups of women.1 Black and Hispanic women, compared with non-Hispanic white women, have more comorbidities (eg, diabetes, hypertension, heart failure, and obesity) at time of presentation with AMI.5-7 Older (60%) and younger (54%) black women have high prevalence of clustering of 3 or more risk factors at time of presentation with AMI.8 Blacks, Hispanics, and American Indians as a whole have greater delay in presenting to the hospital after AMI symptoms.9 Despite greater cardiac risk factor burden, black and Hispanic women are less likely to receive secondary prevention therapies.2 For example, rates of lipid-lowering medication use and counseling for smoking cessation are lower among nonwhite women.10 Evidence suggests that multilevel strategies to increase adherence to guidelines may reduce these disparities for black and Hispanic women.11,12

Mehta et al2 determined that the underlying causes of differences between women and men with AMI are multifactorial and related to the pathophysiological sex differences in CHD.2 Coronary pathology interacts with the biological sex characteristics of women to produce differences in plaque characteristics (rupture versus erosion) as well.2 Furthermore, although men and women share similar risk factors for CHD, certain risk factors, including tobacco abuse, diabetes, depression, and other psychosocial risk factors, are more potent in women.2

Sex differences in clinical presentation and symptom experience may impact timely identification of ischemic symptoms and appropriate triage, diagnostic testing, and management.2 Although most patients with AMI present with typical chest pain or chest discomfort, women often present with atypical chest pain and angina-equivalent symptoms such as dyspnea, weakness, fatigue, and indigestion.2 The detrimental consequences of this "atypical" clinical presentation for women include misdiagnosis, delayed therapy including revascularization, and higher AMI mortality rates.2 Finally, despite mortality benefits of therapy, women are less likely to receive appropriate referral for treatment during an AMI and cardiac rehabilitation after AMI compared with men.2

Despite success over the past decade in reducing CHD-related morbidity and mortality, significant disparities in treatment and outcomes of AMI among women remain. Women receive suboptimal treatment with guideline-based recommendations and experience higher mortality and worse outcomes in the first year after MI. Women from ethnically or racially diverse backgrounds experience even greater disparities in care and outcomes. Reducing CHD-related morbidity and mortality and closing the knowledge and practice gaps on AMI clinical presentation and treatment for all women must be public health priorities. Recommended strategies to improve outcomes in women with AMI2 included the following:

1. Increase awareness among women, healthcare providers, the public, and policymakers of AMI risk and sex-specific symptoms and clinical presentation;

2. Examine genetic-environment interactions in the prediction of early-onset CHD in women;

3. Evaluate the mechanisms by which psychosocial risk factors (eg, depression, perceived stress, marital conflict, anxiety, poor social support) influence the development and progression of CHD;

4. Improve methods to diagnose and treat CHD in women;

5. Implement effective approaches to increase adherence to guideline-based secondary prevention therapies among healthcare providers and patients;

6. Develop and test effective, culturally appropriate primary and secondary prevention behavioral interventions for women across the life span and in a variety of clinical and community settings;

7. Develop and test tailored secondary prevention strategies for women after AMI as an alternative to center-based cardiac rehabilitation programs using mobile technology, peer support, health coaches, community health workers, and telehealth; and

8. Develop strategies to increase the inclusion of women of all ages in cardiovascular clinical research.

REFERENCES