Depression and Stress Hit Hard on the Heart

Victoria Porter

March 05, 2003


"The damage to the heart, with its symbolic meaning as the essence of the human being, may shatter the patient's sense of wholeness and safety."[1]

Karni Ginzburg
Bob Shapell School of Social Work
Tel Aviv University, Israel

We have all heard the phrases: "my heart aches..."; "be still my beating heart"; "that's a heartfelt remark", and other similar sentiments. These words demonstrate that the human heart serves more than a physiologic function, and extends into a symbolic sense of emotions. A heart attack or other cardiac event certainly represents injury to the physiological function of the heart, but could the damage also affect the heart's symbolic meaning? Some patients and now, even researchers, would say "yes".

In fact, this damage, manifested as depression, is a common problem in the aftermath of a cardiac event, and is also associated with other illnesses such as diabetes, cancer, and chronic pain. Unfortunately, despite its prevalence, depression continues to be underdiagnosed and undertreated by primary care physicians, cardiologists, and other specialists.

Some may ask, which comes first: illness or depression? The answer...a confusing "both." The relationship between the 2 appears to be heavily intertwined, such that there is not necessarily a clear-cut cause-and-effect relationship. Depression takes its toll on other factors that extend beyond the psychological and physiological. For instance, left untreated, depression can lead to a variety of health problems that result in high costs to the depressed individual and to society as a whole. Studies have consistently demonstrated that depression and anxiety disorders cause an affected individual to spend more days in bed due to illness, lose more workdays, have increased functional impairment, and increase the use of health services.[2]

Depressive disorders also have a significant impact on the outcome of comorbid medical illnesses such as cardiac diseases (eg, the risk of heart disease is doubled in people with depression),[3] diabetes, and cancer.

The disability caused by depression and anxiety can be as extensive as that caused by other common medical conditions, such as arthritis, diabetes, and hypertension. The World Health Organization Global Burden of Disease Survey estimates that by the year 2020, major depression will be second only to ischemic heart disease in the degree of disability it confers on sufferers.[2] Despite the relatively high prevalence of depressive disorders (which typically affect more than 10% of patients), they continue to be widely unrecognized and untreated.[4] Now, more than ever, there is great need to identify the signs, symptoms, and factors that contribute to depression and its health-related consequences.

As stated above, the risk of heart disease is doubled in people with depression.[3] According to a group of UK researchers,[5] one possible explanation to account for this disturbing statistic may lie with impaired endothelial function. Broadley and colleagues from the University of Wales in Cardiff[5] evaluated arterial function in 12 patients, aged 18-55 years who were under treatment for clinical depression, and compared their results with those of 10 matched healthy controls. The patients treated for depression, who had been recruited from local community mental health clinics, general practices, and patient support groups, were all doing well at presentation (ie, their depression had been stabilized for at least 3 months and they had no major cardiovascular risk factors). The investigators found that endothelial function, as measured by flow-mediated dilatation, was impaired in the depressed patients (mean [SEM] -0.7% [1.7%]) compared with controls (5.7% [0.9%], P = .005 by non-paired t test). These investigators also tested the baroreflex system, which controls heart rate in response to changes in blood pressure. Baroreflex sensitivity did not differ significantly between the groups. The link between depression and impaired artery function -- a hallmark of coronary artery disease -- remains unclear. Further study is needed to determine whether impaired arterial function is caused by depression itself, the drugs used to treat it, or a combination of the two.

Regardless of its etiology, reactions to stressful events such as earthquakes, terrorist attacks, and explosions can trigger cardiac events. It is therefore not surprising that a group of 200 patients with implantable cardioverter defibrillators (ICDs) experienced an increased incidence of life-threatening arrhythmic episodes during the month after the September 11th attacks on the World Trade Center and the Pentagon.[6] According to a recent report presented at the 2002 American Heart Association meeting, the rate of device-delivered electrical shocks to restore normal sinus rhythm had more than doubled a month after the 9/11 disasters compared with the month preceding September 11th. The study included 200 patients with ICDs (average age 69 years) who lived within 100 miles of the World Trade Center.

Just as we cannot ignore the lingering repercussions of 9/11, we should not minimize the effects that the looming threat of war has on the collective and individual psyches. This is further exacerbated by the daily stresses of life: financial woes, problems at work, and domestic strife, to name a few. Although some people have better coping mechanisms than others, these stresses can take their toll even on the healthiest constitution. Such stress-inducing factors may not always be directly related to cardiac injury, but they also contribute to the underlying depression that can exacerbate heart disease.

Cardiac illness may compound life's everyday stresses and increase the susceptibility of depression among patients with heart disease. Among other cardiac conditions, depression is also common among stroke survivors and can interfere with recovery. According to Dutch researchers,[7] stroke survivors with a high degree of pessimism are nearly 5 times more likely to develop poststroke depression. This finding was based on a study that used a 5-point scale ranging from "strongly agree" to "strongly disagree" to assess 190 people recovering from a first stroke for depressive symptoms at 1, 3, 6, 9, and 12 months after the stroke. Survivors also completed questionnaires covering the 5 main personality traits: (1) the tendency to experience negative mood states (called neuroticism), (2) extraversion, (3) openness to new experiences, (4) agreeableness, and (5) conscientiousness. Findings revealed that 38.7% of the survivors were depressed 1 year after suffering a stroke. Those with the high neuroticism scores had a 4.6 times higher risk of developing poststroke depression than those with the low scores (P = .001). This effect was stronger in men than in women. Neuroticism was the only 1 of the 5 personality traits that increased the risk of poststroke depression. The only other independent risk factor was the survivor's level of disability. The effect of negative emotions was independent of other factors such as patients' age, gender, location of the brain tissue affected, the level of disability, and a prior episode of depression.

Depression may have an impact on surgical outcomes among heart transplant patients. For instance, Zipfel and colleagues[8] studied 152 patients with ischemic (n = 57) or dilated (n = 95) cardiomyopathy who were awaiting heart transplantation, and found that patients who reported being depressed preoperatively -- especially those with ischemic heart disease -- were more likely to have an unfavorable outcome after transplantation. Of the 152 patients enrolled, 103 underwent heart transplantation and were followed for a mean of 4.4 years. The authors used proportional hazard models to assess the influence of psychosocial and somatic factors on outcome. Those with ischemic heart disease had higher depression and anxiety scores compared with patients who had dilated cardiomyopathy. Findings revealed that donor and recipient age contributed to the risk of mortality after heart transplantation, and ischemic cardiomyopathy patients who were categorized as having high levels of preoperative depression had a significantly higher mortality after transplantation. This result remained significant even after controlling for sociodemographic and somatic variables. The authors recommend screening for depression among patients with an ischemic cause of their end-stage heart disease so that treatment interventions can be undertaken.

Could age and gender after an acute myocardial infarction (AMI) predict those who may be at higher risk for depression? Researchers sought to determine the significance of age, gender, and ethnic differences in their independent assessments of depression and general distress, social support, and health-related quality of life in post-AMI patients. Standardized psychometric measures were administered to a series of 88 patients from the Enhancing Recovery in Coronary Heart Disease (ENRICHD) pilot study who had been hospitalized for AMI at 8 US clinical centers.[9] Patients were aged 62.1 ± 14.2 years and 46% were female. Findings on multivariate analysis revealed gender and age differences with regard to levels of depression/distress and social support. Female patients reported higher levels of depression and distress compared with male patients (P = .040), with the majority of reports observed among younger female patients. Older patients (P = .014) and female patients (P = .025) reported lower levels of social support compared with younger and male patients, respectively. On the other hand, ethnicity did not seem to contribute to patient differences in mental health functioning; minority and nonminority patients exhibited similar levels of mental health functioning and social support. There were no significant differences in post-AMI health-related quality of life on the basis of age, gender, or ethnicity.

Could an individual with a certain personality type be more prone to heart disease? There is considerable evidence to suggest that, yes, personality does play a major role in determining who will develop premature heart disease, particularly among those who are angry and irritable.

A long-term study of more than 1000 men found that those who had angry or irritable responses to stressful situations were 3 times more likely to be diagnosed with heart disease and 5 times more likely to suffer a heart attack before the age of 55.[10] In 1995, when the average age of the group was 65 years, about 8% had been diagnosed with premature heart disease. Men who reported that they became irritable, expressed their anger, felt angry but concealed their emotion, and/or participated in gripe sessions had a higher risk of premature heart disease and heart attack compared with men who did not report similar instances. These results were independent of cholesterol levels, body mass index, or blood pressure. Anger was also found to increase the risk of depression and anxiety. Although it is not clear exactly how anger manifests into cardiovascular problems, it has been demonstrated that the catecholamine release triggered by anger causes blood vessels to constrict and heart rate and blood pressure to rise, the authors noted.

Hostility may be a contributing factor to heart attacks or other acute cardiovascular events in those with and even without existing heart disease. In one study, researchers evaluated whether hostility among women with heart disease was a contributing factor for heart attacks. Approximately 800 postmenopausal women with heart disease who participated in the Heart and Estrogen/progestin Replacement Study were asked to respond to detailed questionnaires that posed questions regarding the women's levels of cynicism, anger, mistrust, and aggression. Results showed that women with heart disease who were hostile were more than twice as likely to have a heart attack or to die from heart problems than those women who were not hostile.[11] In fact, hostility appeared to be a greater risk factor than smoking, high blood pressure, and high cholesterol. Many of the study subjects had atherosclerosis, and the researchers suspected that this could be attributed to a response triggered by an episode of anger that caused plaque to rupture and subsequently impede blood flow. The authors of this study recommend behavior modification through exercise and counseling to control hostility levels.

These study results are supported by earlier findings indicating that anger and hostility increase the risk of a heart attack or other acute cardiovascular event, even in such populations as older men without heart disease.[12]

Although compelling, the above findings are somewhat contradicted by the results of a study published in January 2003.[13] A cohort of 23,522 male professionals aged 50-85 years without previous cardiovascular disease responded to a mailed questionnaire incorporating the Spielberger Anger-Out Expression Scale in 1996. At 2-year follow-up, men with moderate levels of anger expression had a reduced risk of nonfatal MI compared with those with lower levels of expression (relative risk [RR] = 0.56; 95% confidence interval [CI] = 0.32-0.97). Anger expression was also inversely associated with risk of stroke (RR = 0.42; 95% CI = 0.20-0.88). The study controlled for coronary risk factors, health behaviors, use of psychotropic medication, employment status, and social integration.

Another study assessing the role of personality in heart disease, this one involving young adults (aged 18-30 years), was reported at the 2002 AHA meeting.[14] Researchers examined a sample of 3138 young men and women (black, n = 1411; white, n = 1727) who participated in the Coronary Artery Risk Development In Young Adults (CARDIA) study.[15] On enrollment in 1985, participants in CARDIA were asked how traits such as "eating too quickly," "getting upset when having to wait for anything," "usually feeling pressed for time," and "often feeling time pressures at the end of a work day" described them. Responses ranged from "very well" to "not at all." After adjusting for age, race, gender, body mass index, physical activity, alcohol consumption, and systolic blood pressure, the researchers found that, after 13 years, subjects who registered the highest scores indicating a major type A behavior trait known as time urgency/impatience (TUI) were more than twice as likely to have developed hypertension as those with the lowest scores (17% incidence of hypertension among those with the highest TUI scores vs 10% for those with the lowest scores). People with higher TUI scores were more likely to be white, female, and better educated, and were less likely to have a healthy lifestyle (eg, they smoked more, drank more alcohol, and had less physical activity).

People with high blood pressure who are depressed or have signs of depression may be less likely to take their antihypertensive medications than people who are not depressed, according to a study conducted by Wang and colleagues.[16] Using a survey instrument designed to assess patients' psychosocial and behavioral characteristics, they investigated the effects of depression on compliance with blood pressure medications in 496 individuals with high blood pressure. After adjusting for the potential confounding effects of demographic, clinical, and other psychosocial variables, they found that patients who reported a high degree of depressed mood, loneliness, worthlessness, or other depressive symptoms were less likely to comply with their medications than their peers. In unadjusted analyses, however, this relationship did not reach statistical significance. Noncompliance increased with the degree of severity of depressive symptoms and neither knowledge of hypertension, health beliefs and behaviors, social supports, nor satisfaction with care had any bearing on compliance.

The link between depression and noncompliance needs further exploration, but Wang and colleagues noted that "depression could reduce patients' motivation or make them pessimistic over the effectiveness of treatments.... Furthermore, depression can have adverse effects on attention, memory and other cognitive abilities that are needed to consistently take medications over time." They also pointed out that depression can lead to self-destructive behavior, which would explain why patients did not comply with blood pressure medication regimens even when they believed in their efficacy.

and Denial: A Sensible Solution?

The depression that many heart patients experience can interfere with recovery and may increase the odds of dying. Undoubtedly, more information is needed to determine the best means of therapeutic intervention. According to 2 studies, antidepressant medication and self-denial may help to improve one's mindset.

Although an antidepressant could be the answer to the problem, some of the older antidepressants have been shown to be harmful to people with heart disease (they can disturb heart rhythms and may further weaken an already fragile pump), and the newer ones have not been well studied.

New hope for treating depression in patients who have suffered a cardiac event comes from the results of a small study suggesting that the antidepressant sertraline (Zoloft; Pfizer Inc, New York, NY) is safe and effective for this purpose.[17] The researchers compared the effects of sertraline and a placebo pill in 369 patients who had been hospitalized for a heart attack or unstable angina. All were diagnosed with major depression and had left the hospital in the past month. During the 24-week study, depressive symptoms improved in about 67% of patients administered sertraline compared with 53% of patients taking a placebo. Among patients with the most severe depression, those who took sertraline were more likely to improve during the study -- they reported a 72% improvement vs 51% in the placebo group.

The study results also suggest that treating depression may improve heart health. The authors pointed out that sertraline-treated patients were about 20% less likely to be rehospitalized for heart-related complications or to die from cardiovascular causes compared with placebo-treated subjects.

The authors of an accompanying editorial[18] argued that this study did not include severely ill patients and that it was too small to detect potential interactions between the antidepressant and other medications. They also pointed out that the trial tested the effects of only 1 type of selective serotonin reuptake inhibitor -- and the drug was not administered until an average of 1 month after heart attack.

Israeli researchers at Tel Aviv University conducted a study whose findings suggested that a repressive coping style -- so long as the patient does not go too far into denial -- may promote adjustment to traumatic stress, both in the short and longer term.[19] The study subjects (N = 116), all of whom had recent MI, took standardized tests for acute stress disorder -- termed posttraumatic stress disorder (PTSD) if it lasts more than a month or occurs more than a month after the event -- within a week of their MI and were retested 7 months later. Within a week of MI, self-report questionnaires were administered and hospital records were obtained to assess patients' repressive coping style, perceived threat, acute stress disorder, and severity of MI. At 7 months, PTSD was assessed. The distribution of the repressive coping style was compared with that of 72 matched control subjects. Findings revealed that patients who tended to repress their anxiety exhibited less acute stress disorder than those who did not repress their anxiety, both at 1 week and at 7 months after MI. Anxiety repressors also had lower levels of posttraumatic stress at 7 months compared with nonrepressors.

These enlightening and varied studies provide impressive evidence to support the role of anger, hostility, and stress as triggers of cardiac events. However, further studies are needed, perhaps involving younger populations or individuals without a history of heart disease, to validate the above findings and to determine whether the effects of anger and stress exertion differ by subpopulations.

Although depression affects patients of all sorts, including cardiac patients, the ideal solution to the problem has yet to be fully established. Certainly one effective form of treatment may be direct interaction and intervention with a patient who exhibits signs of depression and/or is at potential risk. Several recent studies have documented the effectiveness of combined forms of intervention for the depressed cardiac patient, including the importance of counseling caretakers of cardiac patients.

Research has shown that caregiver depression can worsen a stroke survivor's depression and can have a negative impact on rehabilitation. Since about 80% of stroke survivors return to their homes after rehabilitation, the need to support caregivers in their new role of managing the physical, emotional, and cognitive changes associated with stroke is important. In fact, caregivers who receive such support may play a role in improved stroke rehabilitation and increased likelihood that stroke survivors remain at home instead of going to nursing homes, a group of Alabama researchers reported.[20]

This finding came from a study examining "social problem-solving telephone partnerships" (SPTP) -- a program in which nurses use the telephone to help family caregivers resolve challenges of caring for stroke survivors. Previous studies have examined SPTP using face-to-face contacts with individuals or groups. Researchers classified 74 primary caregivers into 3 groups:

  1. Intervention: received the problem-solving assistance phone conversations.

  2. Sham intervention: received phone calls that did not cover solving problems but caregivers were offered information about healthcare services received by the stroke survivor.

  3. Control: received no phone calls.

In the phone intervention, nurses conducted an initial 3-hour home visit, then helped caregivers use effective problem-solving steps to manage caregiving problems during regular telephone calls. Over a 4-week period, those in the intervention group improved significantly with respect to the way they viewed caregiving problems. On average, their depression scores improved by 56% and their negative problem orientation scores improved by 50%. Participants also improved in emotional well-being, mental health, and vitality.

The authors of a small study evaluating the relationship between depression and congestive heart failure (CHF) advocate for increased physician screening and psychological assessment of CHF patients.[21] The researchers observed that psychiatric treatment for CHF patients who scored positive on the Zung Depression Inventory test resulted in a decrease of depressive symptoms compared with those depressed CHF patients who did not undergo any treatment.

Clinicians need to be aware of the risk factors for depressive disorders -- eg, traumatic life events, multiple medical problems, chronic pain -- and should inquire about positive psychiatric family history and prior depressive episodes. Among other forms of intervention a recent study[22] favors a depression management program that includes treatment with the newer antidepressants, which have typically been shown to be safe and well tolerated, and counseling patients on unhealthy behaviors that exacerbate the depression or that pose a risk for comorbid disorders.


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