This is the story of a 37-year-old woman in her own words. She had no other cardiovascular risk factors than a history of smoking and being 3 months in the postpartum period.
I woke up with severe chest pain, my left arm was weak and heavy. I went to my general practitioner at the Primary Care Center. There, a nurse registered my ECG and a doctor came and asked me about my symptoms. I told him carefully about my severe chest pain and that my left arm felt weak. I told him that the pain prevented me from taking care of my 3-month-old baby. He told me that if you have a heart attack it would induce pain in my arm, not weakness and besides “you are too young to have a myocardial infarction.” He sent me home with antacids for my stomach. Two days later I called my doctor and described a feeling of general chest discom- fort and when walking rapidly chest pain was provoked.
He told me not to worry but if the pain came back he recommended me to seek the Emergency Care Unit at the hospital. I stayed at home.
Two days later the same chest pain came back, now even worse than before and I went to the hospital. After two hours of waiting in the corridor an ECG was per- formed and the doctor told me that the ECG was normal.
I got a paper bag to breathe in without any explanations (panic disorder?) or perhaps, as I was breastfeeding, it could be something with my breasts. I was sent to the gynecologist but he told me that this had nothing to do with gynecology and I was sent back to the emergency care unit. I still had my chest pain. Again I was sent home with antacids. The same day at home the chest pain was even worse. I went back to the emergency ward and a new ECG again revealed no changes. This time the pain radiated to my back and the doctor asked me to take a deep breath and did the pain increase? Perhaps.
The doctor said, we are going to send you home with something for the pain. After a while the doctor told me
that there was something wrong with my blood samples and I was sent immediately to the CCU. A coronary angiogram showed three-vessel disease and two days later CABG was performed. I felt ignored by the doctors and nurses and their little knowledge of female heart disease.
Introduction
One important aim with cardiac rehabilitation is to reduce cardiovascular risk factors after a cardiac event. However, the risk factors are differ- ent and have a different impact in men than in women. Still, little is known about the needs and experiences of women with regard to cardiac rehabilitation. For example, lack of social support may be a more important risk factor in women for coronary heart disease (CHD) and for the reha- bilitation process. Therefore, we might need spe- cially designed programs for the female patients.
There are obvious benefits of structured cardiac rehabilitation programs. However, so far, there are few or no trials of adequate size (especially not in women) to answer the question if and which type of cardiac rehabilitation programs are effective in reducing mortality or cardiac events and achiev- ing a better quality of life. There is convincing evidence that physical activity reduces CHD morbidity and mortality among men but few studies have been carried out in women. There- fore, we might need specially designed programs for female patients. Questions emerge, like when after the cardiac event is the optimal time to start rehabilitation and for how long will the program
46
Gender Issues in Rehabilitation
Karin Schenck-Gustafsson and Agneta Andersson
376
last? We know that it is impossible to try to reha- bilitate a patient with a deep depression, you have to treat the depression first. We also know that a standard 6–8-week training program with bicycle exercise twice a week after the myocardial infarc- tion is not enough and does not cover the psy- chological part of the recovery process. Other questions: do certain patients need cardiac reha- bilitation more than others do or could it be dangerous to expose some patients to cardiac rehabilitation? How to involve patients with a low quality of life, suffering from depression, anxiety, and negative stress?
Gender Differences in Coronary Heart Disease
Coronary heart disease is the leading cause of death and disability among men and women in Western countries. Of the 4 million people in Europe dying every year of cardiovascular disease, 53% are women. In recent decades CHD mortality rates have declined across all age groups among middle-aged and older persons, in a majority of Western countries; however, the overall decline rate has been slower in women than in men. The gender difference in CHD mortality has conse- quently been reduced. Women have a longer life expectancy than men and suffer from clinical manifestations of CHD about 10 years later than men. Younger women have a lower incidence of CHD compared with men the same age, but by age 70 the incidence of CHD is comparable for men and women. This gender differential in CHD inci- dence is not fully understood. A cardioprotective effect of endogenous estrogens has been hypoth- esized as the main pathophysiological explana- tion. In addition, a gender bias among physicians in recognizing CHD in women has been claimed.
Until recently, knowledge about CHD regarding prevention, risk factors, clinical manifestations, therapy and prognosis was based on studies that involved predominantly or exclusively middle- aged men.1 Also, earlier reports from the Framingham cohort fostered the perception that angina pectoris is a benign problem in women.2 However, in the past several years the information about female CHD and the gender differential in CHD has expanded considerably.3
Although women and men share several conven- tional risk factors for CHD, both non-modifiable (age and genetic predisposition) and modifiable (cigarette smoking, hypertension, obesity, dyslipi- demia, diabetes mellitus, sedentary life style, and psychological stress), their impact may be different in women.4Recently nine major risk factors were found to be responsible for 90% of the myocardial infarctions.5Diabetes mellitus, lipid abnormalities, cigarette smoking, and possibly also psychosocial factors, seem to be of special importance in women.6 Diabetes mellitus seems to abolish the gender protection in women and is associated with a less favorable in-hospital and long-term progno- sis in subjects with MI, with a greater adverse impact for women than for men. Low HDL choles- terol and elevated triglyceride levels may be partic- ularly important in younger women and may better predict CHD in women than total and LDL choles- terol levels. Also the ApoB/ApoA1 ratio has been claimed to be of greater importance in women than in men.Cigarette smoking is one of the leading pre- ventable causes of CHD in women, and although the percentage of smokers in the population has decreased over the past three decades in Western countries, an alarming increase in smoking among young women has been reported. Among middle- aged women in the Nurses Health study more than 50% of MIs were attributable to tobacco. Also, a recent study showed that the smoking association with CHD was much stronger in women than men.7 The increased risk of CHD with smoking is dose- dependent, and smoking cessation decreased the risk within 3 to 5 years to the level of women who had never smoked.
It is also known that smoking women reach their menopause 2–3 years earlier probably because of the proposed lowering of endogenous estrogen levels induced by smoking.
A risk factor specific to women is ovarian hormone status, for example oral contracep- tives, pregnancy, and menopause and hormone replacement therapy. Polycystic ovarian syndrome, gestational diabetes or hypertension, pregnancy toxicosis and birth complications are also claimed to be important hormonal cardiovascular risk factors. Menopause, including premature menopause, is associated with negative changes in several cardiovascular risk factors. Meta-analyses of observational studies, mostly conducted in the
United States, showed a risk reduction of CHD events of 35–50% with hormone replacement therapy. The epidemiological evidence was sup- ported by clinical and experimental studies report- ing beneficial effects of estrogens on lipids and lipoproteins, carbohydrate metabolism, hemosta- sis, vasomotor effects, and atheroma formation.
However, there may be differential effects of estro- gens on components of the inflammatory response.
A major concern and criticism of the observational studies has been the selection bias. Recently, ran- domized, placebo-controlled trials (HERS) failed to show any beneficial effect of combined estro- gens/progestin therapy on coronary events.8,9 In 2002, the results of the first randomized primary prevention trial of HRT, the Women’s Health Initia- tive (WHI), were reported,10and the finding of an increased risk of CHD after initiation of combined estrogens/progestin therapy was similar to HERS, and the trial was stopped early. The part of the trial comparing estrogens alone with placebo was dis- continued because of the increased incidence of stroke and total cardiovascular disease, no effect on CHD incidence, and no overall benefit of estrogen use. Hence, to date, questions still remain regarding how estrogens and progestin modulate cardiovas- cular risk in women.
The symptoms of angina pectoris and MI are often not the same in men and women. Many women present with different ischemic symp- toms, and have chest pain triggered by emotional stress.11As women are usually about 10 years older than men when they present with acute MI, the difference may be more related to age than sex.
Some studies reported longer delay before seeking medical care and physician delay in recognizing signs of CHD in women. Fewer women were referred to a cardiologist, hospitalized and admit- ted to coronary care units. The initial MI was clin- ically unrecognized in a higher proportion of women than men in the Framingham cohort.
Women are older and have more co-morbidity, especially hypertension, diabetes mellitus and congestive heart failure, when they present with clinical manifestations of CHD. Some studies suggest that unstable angina and non-Q-wave infarction occurs more frequently in women. Also, women with chest pain have a greater likelihood of normal coronary arteries on angiograms in selected patient populations. Diagnosis of CHD
poses a particular problem in women as the accu- racy of many diagnostic techniques was validated in predominantly male populations. False-positive exercise tests are more prevalent in women than men, especially in younger women.6 Modern imaging techniques such as exercise and pharma- cological echocardiography can be useful for female CHD patients but have not solved the prob- lems encountered. Gender differences in the use of diagnostic tests and therapeutic measures have previously been reported from several studies.
Women were less likely than men to receive thrombolysis, to be referred to coronary artery angiography, to have revascularization proce- dures, to be prescribed aspirin, beta-blockers, ACE inhibitors. and lipid-lowering drugs,11and to be enrolled in cardiac rehabilitation.12In several, but not in all of these investigations, the sex differ- ences were diminished or abolished after control- ling for age and other baseline characteristics.
Although women have a lower mortality rate from CHD at a given age than men, this survival advantage is lost once CHD becomes clinically evident. The prognosis after MI in women is equal or even worse compared with men in several studies. Results from hospital-based studies have indicated that women have poorer short-term sur- vival both in the US and in Europe. In a 26-year follow-up of the Framingham population, women had an excess relative risk for death, over men, during a coronary event in nearly every age group.
Interestingly, after stratifying for age, Vaccarino et al. reported that younger women, but not older women, had higher in-hospital and long- term mortality rates after myocardial infarctions (MI), relative to men at the same age.13
Background Gender Differences in Cardiac Rehabilitation
One of the goals of cardiac rehabilitation should be to improve psychological health, restore self- confidence, relieve anxiety and promote the return to ordinary daily living and work.
It is well known that depression and low per- ceived support after MI are associated with higher morbidity and mortality. There is convincing evidence that improvements in lifestyle, which include smoking cessation, diet, exercise, and
stress management, can reduce further heart problems. It is known that psychosocial interven- tion is beneficial in lowering blood pressure, improving lipid levels, and reducing negative stress and symptoms of depression. However, psy- chosocial intervention in patients with MI showed no objective evidence of improvement in anxiety, depression, morbidity or mortality in a British study.14
A large US study15with 1084 women and 1397 men with a minor or major depression were treated when indicated with an SSRI or cognitive behavioral therapy. The intervention did not increase event-free survival, but less depression and less social isolation occurred in the interven- tion group.
Despite the benefits of rehabilitation, many patients fail to participate in a rehabilitation program, especially women. Women are also less likely to be referred, are less interested, and have higher drop-out rates than men.
People with low social support do not attend cardiac rehabilitation. Social support and marital status are significantly related to attendance, espe- cially in women. Married women and women in general tend to take more care of the family and their relatives than their own health. Patients with low education level will attend cardiac rehabilita- tion to a lesser extent than patients with higher education. Practical reasons such as long distance to course location will influence participation and women are more likely to have such difficulties because of small children or other social respon- sibilities or they lack a driver’s license.16–19
Depressive disorders have a clear relationship with CHD. There is overwhelming evidence that major depressions are underdiagnosed and untreated in patients with CHD. Approximately one in five patients have a major depression at the time of a cardiac event.20 Depression will also increase the risk of new cardiac events.21 In patients with CHD, the prevalence of major depression is nearly 20% and for minor depres- sion 27%.22
Depression will reduce attendance in CR pro- grams. After an acute cardiac event women express greater shortness of breath, less activity tolerance, and more anxiety and depression.23
A randomized controlled trial with 1376 post- MI Canadian patients showed that there was no
evidence of benefit for a supportive and educa- tional home nursing intervention. The female patients had a poorer overall outcome after one year compared with the male patients. It has been speculated that one of the reasons for the negative outcome in women could be that the female patients were disturbed by the frequent visits of a nurse to their homes.24
It was concluded in a meta-analysis25that inter- vention trials designed to reduce psychosocial stress have been limited in size and number.
Accordingly we need to identify patients who will benefit most from psychosocial rehabilitation programs and probably make the programs more attractive for women.
This underlines the need for further studies in this field and consequently we have started a heart rehabilitation program with stress management especially designed for women.
The Saltsjöbaden Program: A Model of Cardiac Rehabilitation for Women
At the Saltsjöbaden rehabilitation center (Sweden) we provide a CR service designed for women. This program, aiming at promoting and maintaining lifestyle changes, commences with a 2-week inpa- tient residential course; participants then return to the center 2 months later for 5 days, and subse- quently for 2 days two times yearly over the next 5 years. The groups contain 6–10 mainly younger women with established CHD. The residential course contains theoretical lectures, discussions, and different physical activities. Relatives are invited to join over a weekend. The psychosocial rehabilitation is based on an interactive, self- instructional program called “Stress as an Op- portunity,” which involves self-assessments concerning different causes of stress, a book on measures to combat stress,“homework cards,” and a tape with information on stress and relaxation techniques.27 The program consists of three phases: a diagnostic phase, an educational phase, intervention and secondary prevention (Tables 46-1, 46-2, and 46-3).
The biannual follow-up sessions start with a group interview and each session has a specific topic including theory (e.g. burnout symptoms, type A behavior, assertiveness, how to handle
TABLE46-1. Diagnostic phase Aim:
• Identify previous and present stress factors.
• Detect stress symptoms.
• Diagnose states of depression and/or anxiety.
How:
• Workshop where women interview each other respectively, and subsequently present their companion to the group in order to create a feeling of belonging and openness in the group.
• In-depth interview with a psychologist. The interview is focused on present strains and symptoms in private life and at work, i.e. factors that are of immediate importance to deal with. Referral for individual therapy whenever needed.
TABLE46-2. Educational phase Aim:
• To increase the women’s awareness and understanding of the impact of stress and psychological strain.
• To increase ability to distinguish heart symptoms from stress and/or anxiety symptoms.
How:
• Education on mechanisms of work-related strains: high demands and low control, role conflicts, under- or overstimulation.
And on: contribution of personality factors such as low self-esteem, internal demands and stress-evoking behavior, increased strain and decreased resistance to illness and disease.
TABLE46-3. Intervention and secondary prevention Aim:
• To initiate and support improvements in lifestyle and in the psychosocial environment at home and/or at work.
How:
• Learn to use the module “Stress as an Opportunity.”
• Learn: different relaxation techniques, e.g.: mini relaxation, progressive muscle relaxation, diaphragmatic breathing, visualization, and repetition of thought or word.
• Identify individual stress factors (group discussions, the self-assessment forms).
• Make an individual “action plan” how to reduce stress and/or adverse health behaviors in daily life (under the surveillance of CR personnel).
• Staff support to maintain health-promoting abilities and behaviors.
• Five-year follow-up of the individual action plan.
Quality of life ladder (1 = low, 10 = high)
1 2 3 4 5 6 7 8
Intervention Control
baseline 1-year 2-years p < 0,003
manipulative behavior and criticism), practical exercises (e.g. role-play), group discussions and self-assessments with feedback. In the annual assessment using validated questionnaires, data are collected on lifestyle and behavior, self-rated health and symptoms, sick leave and early retire- ment, healthcare utilization, medical and psycho- logical risk factors, and personality factors (e.g.
the Life Ladder (Figure 46-1)). At present the outcome of the program is being established in a
FIGURE46-1. Quality of life measurement in patients in the intervention and control groups.
controlled study, where it appears that the typical patient is well-educated, often in administrative or other leading positions and highly devoted to their work; they are often smokers, divorced, and bringing up small children on their own with a low degree of social support and limited social network.
Conclusion
Do we need specially designed programs for the female heart patient? Risk factors and preventive actions to avoid risks differ between men and women. There is a difference in psychological and physiological reactions after a cardiac event and a gender difference in life conditions. The fact that depression and anxiety are more common in women may lead to different demands on cardiac rehabilitation.
Furthermore, women’s increasing double work and multiple roles (now a recognized risk factor for CHD in both sexes) will increase the stress burden both at work and at home. There are obvious benefits of structured cardiac rehabilita- tion programs for women with special emphasis on psychosocial risk behavior.
References
1. Healy B. The Yentl syndrome. N Engl J Med 1991;325:274–276.
2. Kannel WB, Sorlie P, McNamara P. Prognosis after myocardial infarction: The Framingham Study. Am J Cardiol 1979;44:53–59.
3. Mosca L, Appel LJ, Benjamin EJ, et al. Circulation 2004;109:672–692.
4. Schenck-Gustafsson K. Risk factors for cardiovas- cular disease in women: assessment and manage- ment. Eur Heart J 1996;17(Suppl D):2–7.
5. Rosengren A, Hawken S, Ounpuu S, et al.; INTER- HEART investigators. Association of psychosocial risk factors with risk of acute myocardial infarction in 11119 cases and 13648 controls from 52 countries (the INTERHEART study): case-control study.
Lancet 2004;364(9438):912–914.
6. Ali-Khalili F. Coronary Heart Disease in women.
Diagnostic and prognostic markers. Thesis 2000, Karolinska Institutet, Stockholm, Sweden.
7. Richey Sharrett A, Coady SA, Folsom AR, Couper DJ, Heiss G; ARIC Study. Smoking and diabetes
differ in their association with subclinical athero- sclerosis and coronary heart disease – the ARIC study. Atherosclerosis 2004;172:143–149.
8. Hulley S, Grady D, Bush T, et al., for the Heart and Estrogen/progestin Replacement Study (HERS) Research Group. Randomized trial of estrogen plus progestin for secondary prevention of coronary heart disease in postmenopausal women. JAMA 1998;288:605–613.
9. Grady D, Herrington D, Bittner V, et al., for the HERS research group. Cardiovascular disease out- comes during 6.8 years of hormone therapy: HERS II. JAMA 2002;228:49–57.
10. Writing Group for the Women’s Health Initiative Investigators. Risks and benefits of estrogen plus progestin in healthy postmenopausal women: prin- cipal results from the Women’s Health Initiative ran- domized controlled study. JAMA 2002;228:321–333.
11. Lundberg V, Wikström B, Boström S, Asplund K.
Exploring sex differences in case fatality in acute myocardial infarction or coronary death events in northern Sweden MONICA Project. J Intern Med 2002;251:235–244.
12. Thomas RJ, Houston Miller N, Lamendola C, et al.
National survey on gender differences in cardiac rehabilitation programmes. Patient characteristics and enrollment patterns, J Cardiopulmon Rehabil 1996;16:402–412.
13. Vaccarino V, Krumholz HM, Yarzebski J, Gore JM, Goldberg RJ. Sex differences in 2 years mortality after hospital discharge after myocardial infarction.
Ann Intern Med 2001;134:173–181.
14. Jones DA, West RR. Psychological rehabilitation after myocardial infarction: multicentre ran- domised controlled trial. BMJ 1996;313:1517–1521.
15. The ENRICHD Investigators. JAMA 2003;289:3106–
3116.
16. Gallagher R, McKinley S. Predictors of women’s attendance of cardiac rehabilitation programmes.
Prog Cardiovasc Nurs 2003;121–126.
17. Cooper AF,Jackson G.Factors associated with cardiac rehabilitation attendance: a systematic review of the literature. Clin Rehabil 2002;16:541–552.
18. Worcester MV, Murphy BM. Cardiac rehabilitation programmes: Predictors of non-attendance and drop out. Eur J Cardiovasc Prev Rehabil 2004;
11(4):328–335.
19. Lieberman L, Meana M, Stewart D. Cardiac rehabil- itation: Gender differences in factors influencing participation. J Womens Health 1998;7:717–723.
20. Frasure-Smith N, Lesperance F, Juneau M, Talajic M, Bourassa MG. Gender, depression, and one year prognosis after myocardial infarction. Psychosom Med 1999;61:26–37.
nursing intervention for patients recovering from myocardial infarction. Lancet 1997;350(9076):473–
479.
24. Rozanski A, Blumenthal JA, Kaplan J. Impact of psy- chological factors on the pathogenesis of cardio- vascular disease and implications for therapy.
Circulation 1999;99:2192–2217.
25. Eriksson I, Moser V, Unden A-L, Orth-Gomer K.
Prevention of stress at work. Case study no 10. Con- dition of Work digest. ILO 1992; vol 11,2.
21. Verrier RL, Dickerson LW. Central nervous system and behavioural factors in vagal control of cardiac arrhythmogenesis. In: Levy MM, Schwarz PJ, eds.
Vagal Control of the Heart. Armonk, NY: Futura;
1994;557–577.
22. Carney RM, Rich MW, Tevelde AJ, et al. Major depressive disorders in coronary artery disease. Am J Cardiol 1987;60:1273–1275.
23. Frasure-Smith N, Lesperance F, Prince RH, et al.
Randomised trial of home-based psychosocial
