Coronary Artery Disease in Women: A Review
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Cardiovascular disease (CVD) is the leading cause of death in women and men in the United States. Coronary artery disease (CAD), heart failure, and stroke cause around 500,000 deaths in U.S. women every year, with the most deaths caused by CAD.1 While CAD is the leading cause of death in both sexes, the etiology, recognition, management, and outcomes of CAD differ between men and women. Many of the common risk factors associated with CAD also have different clinical presentations and chronology in women. Additionally, women may have pregnancy-, ovarian-, and estrogen-related complications that increase their risk for developing CAD.2
On average, CAD and other CVDs will present in women 10 years later than in men. This may be due to the potential benefits of estrogen in premenopausal women.3 While the incidence of CAD in women is initially lower than in men, it rises steadily after the fifth decade. Because CAD risk factors vary between men and women across age ranges, underestimating these differences is a reason why women with CAD are treated later in their events and have poorer outcomes than men.4 This is most evident during acute coronary syndrome (ACS) scenarios where women’s clinical presentations are under-recognized, under-studied, under-diagnosed, and under-treated.5-7 While women’s cardiac health screening and care has greatly improved, it is important to understand female-specific CAD risks, clinical presentations, treatment options, and outcomes.8,9 Despite updated CVD prevention guidelines that emphasize women’s unique risk factors and clinical manifestations, treatment gaps in women’s heart health continue to be a challenge.10
This review will discuss CVD risk factors and special considerations for women, including unique issues related to estrogen, menopause, and pregnancy. CVD in women, such as microvascular disease (MVD), spontaneous coronary artery dissection (SCAD), and takotsubo cardiomyopathy (TCM) will also be discussed. Because of sex and gender differences, clinical management and recognition of these differences is essential in the diagnosis, management, and improved outcomes for women with CVD.5
The Role of Estrogen in CVD Prevention
Estrogen provides many health benefits to women, including higher high-density lipoprotein (HDL) cholesterol levels, promotion of normal blood clot formation, the dilation and relaxation of blood vessels to improve blood flow, blood pressure control, and reduced rates of CVD in comparison to men. Estrogen is largely responsible for the average 10-year gap in the onset of CAD between men and women. When women go through menopause, estradiol levels decrease by 75%.10-12 The reduction in estrogen is associated with increased rates of CVD and cardiovascular risk factors. In women who use tobacco or have diabetes, the benefits of estrogen are significantly reduced, to the point where no discernable benefits from estrogen are evident.3-5
Risk Factors
While CVD risk factors are often similar for men and women, there are important considerations that are specific to women. Smoking, for instance is a major CVD risk factor for both sexes. However, smoking is more detrimental to women, with the risk of CAD and myocardial infarction (MI) for women twice as high as for men.3,11 There is also a compounded CAD risk between smoking and the use of hormonal treatment, which may be due to prothrombotic effects.12 Smoking more than a pack a day of cigarettes may increase a women’s risk of myocardial infarction by 12-fold, and this risk is more than doubled in women using oral contraception.12 Furthermore, smoking is known to reduce the concentration of HDL in both men and women, but is more significant in women.3 Smoking also has anti-estrogenic effects in women and has been linked to premature menopause.3 Due to these effects, smoking quadruples a premenopausal woman’s risk for CAD.4
Dyslipidemia is common in women and changes in their lipid profiles are associated with menopausal changes.13 The Study of Women’s Health Across the Nation (SWAN) study found that during menopause, women have substantial increases in total cholesterol, triglycerides, and low-density lipoprotein (LDL) cholesterol. On average, women over the age of 50 have higher total cholesterol levels than men over 50.14,15 An increase in HDL levels, which has major health benefits such as atheroprotective properties in the premenopausal phase, has been found to be paradoxically associated with increased atherosclerosis progression after menopause.14 This may be due to changes in HDL function resulting from hormonal changes.15 Elevated triglyceride levels also increase CAD risks in postmenopausal women. During menopause, the concentration of LDL cholesterol in women can also significantly increase.
Hypertension (HTN) is the most common modifiable risk factor for CVD, and occurs in over 80 million adults in the United States.16 HTN is associated with shorter life expectancy, a shorter life expectancy free of CVD, and more years lived with CVD.16-18 Women tend to have lower rates of hypertension than men under the age of 65, but women over 65 are more likely to have hypertension than men over 65 (Figure 1).
Data obtained from https://www.cdc.gov/nchs/data/databriefs/db289.pdf
Systolic blood pressure (SBP) increases in women as they age. After menopause, there is an increase in SBP that has been theorized to be secondary to factors such as the withdrawal of vasodilator effects of endogenous estrogen, increased arterial stiffness, reduced vascular compliance, and decreased endothelial nitric oxide production.19 The increase in both SBP and pulse pressure in postmenopausal women is greater than in men in the same age group, while diastolic blood pressure shows little difference between the sexes.17-19 Isolated systolic hypertension (ISH) significantly increases the risk for CVD, such as stroke, left ventricular hypertrophy and CAD. ISH continues to increase disproportionately in women until the age of 80, is closely linked to obesity, and is 6 times higher in women with a body mass index (BMI) >30.17,18
Diabetes mellitus (DM) and obesity are also common risk factors contributing to CAD in both men and women. In women, type 2 DM is associated with a higher CAD risk than in men, and a higher mortality rate from MI.3,19 A BMI >30 increases CAD risks in women by 64% and men by 46%.3 Compared with men with the same condition, women with diabetes have higher rates of cardiovascular death and overall morality than men.20 While men typically develop CVD about a decade before women, in diabetic women, CVD risk occurs around the same age as men. It is theorized that diabetes eliminates much of the protection premenopausal women would normally get from estrogen. DM increases the risk of cardiovascular disease by three to four times in women and two to three times in men, after adjusting for other risk factors.21 Diabetes and obesity are also linked to pregnancy-related hypertension risks such as preeclampsia and gestational hypertension.
For women, a family history of heart disease or sudden death from MI is a significant risk factor for the development of CAD or an MI. The risk increases based on which family member is involved. For example, if a parent has history of MI or sudden death, the risk increases 3-fold. If the family member is a brother, the risk increases 6-fold, and in a sister, the risk increases 12-fold.4
Risks Specific to Women
There are also multiple risk factors for CVD that are specific to women, including menopausal and pregnancy-related issues. The largest increase of CVD-related deaths in women occurs in the menopausal and postmenopausal periods.22,23 A reduction in estrogen is related to a higher incidence of hypertension, diabetes, dyslipidemia, and obesity.24-26 In the peripartum setting, CVD presentations include:
• Chronic hypertension (CHTN);
• Peripartum cardiomyopathy (PPCM);
• Gestational hypertension (GHTN);
• Preeclampsia.
These pregnancy-related complications have been shown to substantially increase the risk for CVD in the short and long term.22,23 Additionally, PPCM, GHTN, and preeclampsia are also causes for preterm delivery. HTN and PPCM are associated with vascular dysfunction, and pregnancy may cause the manifestation of a vascular dysfunction or a preexisting medical condition.23,24 PPCM can develop in late pregnancy or shortly postpartum, and is characterized by significant left ventricular dysfunction with a low ejection fraction and heart failure. PPCM can also cause the development of thromboembolism, arrhythmias, and progressive heart failure.26
Preeclampsia is a pregnancy-related hypertensive disorder, defined by a new onset of HTN after 20 weeks of gestation, and accompanied by proteinuria or systemic disease.27 Evidence shows the effects and damage of eclampsia may continue postpartum, and in some cases, preeclampsia may develop postpartum. It is believed that the underlying cause of preeclampsia is endothelial dysfunction that corresponds to higher levels of coronary calcium. The damage from preeclampsia may not resolve postpartum, doubling women’s long-term risk for CVD, particularly stroke, cardiac ischemia, and venous thrombosis (Table 1). 2,27,28 Preeclampsia may also progress and cause eclampsia or hemolysis, elevated liver enzymes, and low platelet count, in a syndrome known as (HELLP).27-29
Women and Coronary Artery Disease
While CAD is the most common type of heart disease and the leading cause of death in both sexes, there are other coronary and cardiac syndromes that affect women at much higher rates than men. This includes coronary microvascular disease (CMD), spontaneous coronary artery dissection (SCAD), and takotsubo syndrome. CMD is characterized by ischemia and/or angina with no obstructive CAD. CMD is an increasingly recognized cause of angina and is much more common in women. CMD is associated with abnormal dilation and constriction of the small vessels of the heart, and is a major cause of ischemia and nonobstructive coronary artery disease (INOCA) in as many as 50% of women with ischemia and angina symptoms.30,31 Low levels of estrogen before menopause raise a woman’s risk for developing CMD and it is a major source of angina in younger women.29-31
In the January 2023 edition of Cath Lab Digest, Dr. Jennifer Tremmel explains that while CMD, either structural or functional, may be independently responsible for the development of angina with nonobstructive coronary arteries (ANOCA), there are several other possible causes.32 These etiologies include endothelial dysfunction, epicardial vasospasm, and myocardial bridging.32 If a patient presents with ANOCA, it is important to determine the underlying cause. Typical stress testing may not find any abnormality in these patients. Instead, patients presenting with ANOCA may need further invasive testing in the cardiac catheterization lab that includes the use of acetylcholine, fractional flow reserve, and coronary flow reserve.32
Spontaneous coronary artery dissection (SCAD) is a nonatherosclerotic etiology of ACS, including sudden cardiac death, which frequently affects younger women.8-10 Among women, SCAD is the cause of ACS in as many as 35% of cases8,10 and the most common etiology of MI associated with pregnancy.31,33 SCAD can occur in men and at any age, but is most common in women in their fourth and fifth decades.33-35 Most people with SCAD do not have other risk factors like hypertension or dyslipidemia. However, women who have experienced childbirth, fibromuscular dysplasia, and hormone use are at increased risk of SCAD.34,35 While SCAD has been linked to childbirth, most often occurring in the first few weeks postpartum, it can also occur during pregnancy.34,35 Oral contraceptives, hormone replacement therapy, and infertility treatments have also been linked to SCAD.35,36
Figure 2 illustrates two cases of SCAD diagnosed in women with ST-elevation MI symptoms. In the first case, the patient was treated with medical therapy because the dissection was located too distal in the left anterior descending coronary artery to deploy a stent. The second patient was treated with a drug-eluting stent. Both patients had successful outcomes, and are also being managed with medications and regular cardiology follow-up care.
Takotsubo cardiomyopathy (TCM), also known as takotsubo syndrome, stress-induced cardiomyopathy, transient apical ballooning, or broken heart syndrome, is a condition that is generally triggered by emotional or physical stress, and is characterized by transient regional left ventricular systolic dysfunction.36,37 Symptoms of TCM are often similar to ACS prior to clinical assessment and imaging, and may present as an apical, anterior STEMI or non STEMI. The onset of symptoms in most TCM cases is usually preceded by an identifiable acute emotional or physical stressor, or a combination of both.29 In the International Takotsubo Registry study, 36% of patients had experienced a physical trigger, 28% reported an emotional trigger, and 8% experienced both.35,36 It is estimated that >90% of TCM occurs in women.37,38 Fortunately, TCM will usually resolve within several months without complications and rarely causes other cardiovascular events.
In Figure 3, a 70-year-old woman, whose spouse had recently died presented with signs and electrocardiographic presentation of an anterior wall MI. Angiography revealed no obstructive coronary disease. Left ventriculography revealed a classic apical ballooning pattern associated with TCM. The patient was treated with medications and followed up with serial echocardiography. In less than 2 months, her left ventricular function had returned to normal.
ACS Presentation and Treatment
ACS symptoms may also differ between men and women. Women can present with different symptoms such as shortness of breath. Angina in women has a higher likelihood of being present during rest and mental stress, while in men, angina is most often caused by physical exertion.4,39 Women may also present with symptoms such as back pain, abdominal discomfort, fatigue, lightheadedness that have been traditionally classified as noncardiac, or atypical symptoms (Table 2). The Women’s Ischemia Syndrome Evaluation (WISE) study concluded 65% of women who had CAD were misdiagnosed because of disparity in symptoms compared to men.4
Studies also show that women present to the hospital later in the course of an MI than men. Some of the reasons for this may be because women’s symptoms develop more gradually, have longer ischemic times than men, and may be described as “atypical”.39-41 Women generally have a poorer prognosis and more severe outcomes than men after MI, PCI, and coronary artery bypass grafting (CABG) that include heart failure, re-infarction, recurrent ischemia, bleeding and stroke.38-40
Women are also more likely than men to die after a first MI, and for survivors, there is higher risk of recurrent MI, heart failure, or death.8 In the Framingham Heart Study, the one-year mortality rate following an MI was 44% in women versus 27% in men.41,42 Research has shown that women with ACS are less likely to be treated with guideline-directed medical therapy, less likely to undergo PCI, and more likely to have a time delay to reperfusion.38,39
In Figure 4, a 75-year-old female initially developed nausea and vomiting, and self-treated at home for gastrointestinal distress. The next day, she developed atypical chest pain. She went to her family physician and had 12-lead ECG performed that suggested an inferior wall STEMI. She was transported to an acute care facility for STEMI and had a right coronary artery infarct that was successfully treated with PCI. Patient follow-up will help determine the possible long-term effects of the delayed time to PCI.
Conclusion
The goal of this literature review is to promote awareness of the complexity of women’s cardiovascular health. While significant advancements have been made in women’s cardiovascular health due to increased awareness, there are still many disparities between men and women in terms of timely care received and treatment outcomes. These disparities are most apparent when treating women with suspected ACS. Risk factors are strongly influenced by menopause and estrogen levels in women, requiring skilled care providers to address the unique clinical challenges in women’s cardiovascular health. There are also unique presentations such as PPCM, GHTN, preeclampsia, MVD, SCAD, and TCM, further complicating diagnoses and treatment for women with cardiac disease.
The authors can be contacted via Richard J. Merschen, EdS, RT(R)(CV), RCIS, at richard.merschen@pennmedicine.upenn.edu.
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More from Richard J. Merschen, EdS, RT(R)(CV), RCIS:
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• Hemodynamic Knowledge: Part II
• Octogenarians and Issues in Cath Lab Care
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