The purpose of this program is to inform healthcare providers about the features and treatments for stress cardiomyopathy.
Upon completion of this self-study module, the participant will be able to:
What becomes of a broken heart? For centuries, man has immortalized the broken heart in song, poetry, art and theatre. As these poets and philosophers have written, the sudden death or departure of a loved one can cause a broken heart. Being jilted can break your heart. Potentially lethal effects of emotional stress are well known in folk wisdom as demonstrated by the phrase “scared to death." Intuitively, people have long suspected heart function and emotions were intertwined. Research has now proven that a broken heart is not just a clever play on words. The pain of heartbreak may actually cause changes in the heart muscle. Strong emotion or physical stress can trigger a severe but reversible left ventricular dysfunction in patients without coronary disease. This is caused by an exaggerated sympathetic response with symptoms very similar to those of a heart attack. Today, science is increasingly concerned with physiological stress of a broken heart and its psychological effect on the body. As a result, many have begun to explore the significance of emotional stress as it relates to reversible heart dysfunction. The purpose of this program is to inform healthcare providers about the features and treatments for stress cardiomyopathy.
Stress cardiomyopathy is a condition in which intense emotional or physical stress can cause rapid and severe heart muscle weakness, or cardiomyopathy. Exaggerated sympathetic stimulation is probably central to the cause of the syndrome. The condition goes by several medical terms including left ventricular apical ballooning syndrome and tako-tsubo syndrome. The condition has been found following a variety of emotional stressors such as grief, fear, extreme anger, and surprise. It has also occurred following physical stressors to the body such as stroke, seizure, difficulty breathing (such as a flare-up of asthma or emphysema), or significant bleeding. The identification of the clinical entity tied to emotions and the heart has sparked public interest. Media outlets quickly dubbed the newly discovered condition, “Broken Heart Syndrome," as it relates to the heart and sudden heart wrenching emotions.
Publicity surrounding “Broken Heart Syndrome" will draw women’s doctors’ attention to the general fact that heart disease in women is different than heart disease in men, and that it is no less frequent and no less fatal. Patients with this condition, also called stress cardiomyopathy, are often misdiagnosed with a massive heart attack. Misdiagnosis as heart attack accounts for a fraction of the seven million heart attacks reported in the U.S. every year. The implications for nursing practice are many. When triaging people with cardiac symptoms, nurses should be aware of stress cardiomyopathy as a potential diagnosis and recognize the profile of those at risk. Patients will need a great deal of reassurance regarding their cardiac function and the cause of their symptoms. Knowledgeable healthcare professionals can provide valuable education.
Stress cardiomyopathy has been known for ten years in Japan. There, it is called tako-tsubo cardiomyopathy, named after an octopus trapping pot with a round bottom that resembles the appearance of the left ventricle at the end of diastole of the stunned heart. Japanese physicians first described the syndrome in the 1990s. Based on 20 years of retrospective research data, they identified a type of severe left ventricular dysfunction in a group of 28 women and two men that was similar to “Broken Heart Syndrome." Other researchers in Niigata, Japan studied cardiovascular events after three strong earthquakes and 90 large aftershocks shook the region. The investigators examined the incidence of acute cardiovascular events including tako-tsubo cardiomyopathy, acute coronary syndrome and sudden death. In the eight hospitals that treated patients, cardiovascular events, including chest pain and left ventricular dysfunction, increased seven-fold in the week after the earthquake.
The disease has gone relatively unrecognized in the West until recently. Western physicians ignored this syndrome presuming it to be something unique to the Japanese race. In the February 2005 issue of New England Journal of Medicine, physicians at the famous Johns Hopkins University School of Medicine announced their findings on stress-induced cardiomyopathy. The report described 20 patients who were all hospitalized with symptoms of heart attack including chest pain, shortness of breath, fluid in the lungs, and drastically reduced ability of the heart to pump. The patients had severe left ventricular dysfunction related to emotional trauma. They found that certain patients diagnosed with heart attacks–all of whom had suffered acute emotional stress–improved more rapidly than others. They also saw the same pattern in those with intense physical stressors: emergency intubations, asthma flairs, and other sudden respiratory abnormalities. During trigger events, patients experience an immediate surge of catecholamines, hormones the body produces in periods of severe stress. The study found that the problems were just temporary, caused by a massive release of stress hormones. Sudden emotional stress led to severe but reversible heart muscle weakness, which mimicked the symptoms of heart attack. Evidence showed that this medical condition was brought on by a surge of stress-related hormones (catecholamines) that temporarily stun the heart. Mysteries surrounding matters of the physiology of a broken heart remain, and little is known about the full effect of sudden shocking news and its effect on the heart.
Stress cardiomyopathy, or “Broken Heart Syndrome," is not as common as a typical heart attack but occurs more frequently than doctors realize. Though this syndrome is seen in men and women, women tend to be more susceptible to the effect of sex hormones on the sympathetic nervous system activity and coronary spasm. Therefore, “Broken Heart Syndrome" is found most frequently in middle-aged and older female patients who have suffered sudden emotional stress. Researchers at Johns Hopkins University School of Medicine listed the following sequela: a clinical presentation including chest pain, severe left ventricular dysfunction, pulmonary edema, and cardiogenic shock. As common precipitating stressors, the patients had such things as hearing news of a death, suffering an accident, and armed robbery. They also list as culprit stressors such things as fear of public speaking, court appearance, or even the shock from a surprise party.
Recent reports have included similar responses to opioid withdrawal. These reports demonstrate that cocaine use and abrupt withdrawal from high-dose painkillers, such as OxyContin, can potentially trigger transient left ventricular apical ballooning in certain susceptible individuals.
According to the National Heart, Lung, and Blood Institute (NHLBI), women do not take the risk of heart disease seriously, or personally. They fail to make the connection between the risk factors and their own chance of developing heart disease. Facts regarding heart disease include:
It is important to understand what “stress" is. “Stress" refers to the body’s response to things it perceives as abnormal. These abnormalities can be physical, such as high body temperature, dehydration, or low blood sugar, or can be emotional, such as receiving news that a loved one has passed away. When the abnormalities occur, the body produces various hormones and proteins such as epinephrine and norepinephrine, which are meant to help one cope with stress.
As most couples are aware, men and women respond differently to stress. Studies of stress response conducted prior to 1995 corroborated the “fight-or-flight" model, which states that when confronted with a stressful situation, humans either will respond with aggressive behavior or will withdraw. These studies focused heavily on male subjects because researchers believed that a woman’s monthly hormonal fluctuations created stress responses that were too varied to be statistically valid, but in 1995, the federal government mandated representation of both men and women in agency-funded studies. As a result, more females were included in stress research.
A study at the University of California, Los Angeles (UCLA) published in 2000 offered clues to the biological and behavioral differences in the ways men and women cope with stress. This study found that females respond to stressful situations by protecting and nurturing their young and by seeking social contact and support from others, particularly females. It referred to this response as “tend-and-befriend." Fighting or fleeing in stressful situations was not a good option for a female who was pregnant or taking care of offspring, and women who developed and maintained social alliances were better able to care for multiple offspring in stressful times.
The hormone, oxytocin is secreted by both males and females in response to stress. People with high levels of oxytocin are calmer, more relaxed, more social, and less anxious. In males, the effects of oxytocin seem to be reduced by male hormones, but in females, oxytocin, along with other stress hormones, may be a key factor in reducing the female response to stress. Men are more likely than women to respond to stressful experiences by developing certain stress-related disorders, including hypertension, aggressive behavior, or substance abuse. The “tend-and-befriend" response may protect women against stress. In this case, the stress hormone responses work against women, making them more susceptible to serious consequences of extreme stress. Stress cardiomyopathy is most commonly seen in postmenopausal women.
A two-way relationship exists between the heart and the mind. Emotions and stressful experiences affect the heart through the autonomic nervous system and the neuroendocrine pathways. People can experience cardiac activity and function as somatic symptoms of fatigue, lethargy, insomnia, and loss of appetite, or as more classic cardiac symptoms like chest pain and palpitations. Psychotropic agents can affect the heart, and drugs used to treat heart disease can affect the brain. Some antipsychotic medications, for example, can lower blood pressure or increase heart rate, while a cardiac drug used to strengthen heart contractility can result in nervousness or apprehension. Stress cardiomyopathy reflects the important connection between the brain and the heart. Chronic stress can cause health problems, but stress cardiomyopathy seems to be directly related to the acuity of the stress.
Cardiomyopathy is a weakening of the heart muscle or a change in heart muscle structure. It is associated with inadequate heart pumping. Cardiomyopathy can be caused by viral infections, heart attacks, alcoholism, long-term severe high blood pressure, and now, extreme stress. Specific types of cardiomyopathy include:
Sudden emotional stress can cause left ventricular dysfunction that is brought on by a surge in adrenaline levels. This surge causes blood vessels to squeeze down and reduces blood flow to the heart. Some people respond to overwhelming stress by releasing large amounts of catecholamines (epinephrine and norepinephrine) into the blood stream along with their breakdown products and small proteins produced by an excited nervous system. When catecholamines spill into the blood stream, they can be temporarily toxic to the heart, effectively stunning the muscle and producing symptoms similar to a typical heart attack. The myocardium cells temporarily lose the ability to contract effectively as a result of the acute stress. Myocardial stunning is a reversible process, while coronary artery disease and AMI result in permanent damage. Catecholamine levels in stress cardiomyopathy patients can be up to 30 times higher than normal levels and up to five times the levels seen in someone who has had a heart attack. Catecholamine metabolites, such as metanephrine, are also elevated, as are other stress related proteins, neuropeptide Y, brain natriuretic peptide, and serotonin. Heart biopsies show injury patterns consistent with high catecholamine states and not heart attack. A majority of the patients with stress cardiomyopathy had few risk factors for heart disease.
Stress cardiomyopathy is of medical interest because of its presentation, which mimics myocardial infarction and acute coronary syndrome potentially unfavorable consequences and high likelihood of survival with appropriate medical therapy. When it occurs, the tip of the left ventricle, the heart’s main pumping chamber, balloons out and weakens. Initial clinical findings are consistent with acute coronary syndrome, including ST-segment elevation myocardial infarction, recent abrupt onset of severe substernal chest pain, marked hypotension, dyspnea, and ventricular fibrillation. Some authors recommend that differential diagnosis include coronary angiography in most cases.
Stress cardiomyopathy is different from typical heart attack in the fact that there is no blockage on angiogram. There is no increase in enzymes released from a damaged heart. Heart attack occurs when blockage to the heart interrupts blood flow. In heart attack the damaged heart releases enzymes. Heart attack is ruled out when testing finds no sign of blood clot or blockage and no evidence that the heart tissue has been irreversibly damaged, as evidenced by high level of cardiac enzymes.
The symptoms of stress cardiomyopathy are so severe that it is inconceivable that anyone who develops it will fail to seek medical help; the clinical manifestations of the condition are so obvious that no doctor that sees these patients could fail to realize that something serious is going on. It is strikingly similar to acute heart failure. Patients experience sudden chest pain and shortness of breath. Some are in profound shock with very low blood pressure. The heart pumps at about a third of the normal capacity, similar to severely ill heart failure patients. There is severe left ventricular dysfunction with normalization of cardiac function within 48 to 72 hours after the emotionally charged event. The hallmark feature of the syndrome is the heart’s unique contraction pattern as viewed by echocardiogram or ultrasound. While the base of the heart’s main pumping chamber, the left ventricle, contracts normally, there is weakened contraction in the middle and upper portion of the muscle. “Broken Heart Syndrome" has a unique electrocardiographic pattern, a surprisingly mild cardiac enzyme elevation (a heart attack usually shows a much higher elevation), the absence of significant coronary artery disease (no blockages in the arteries supplying the heart), and a very rapid improvement in heart muscle function. Symptoms include:
Differentiation of stress cardiomyopathy from other conditions is crucial in determining whether cardiac symptoms indicate transient impairment in cardiac function or permanent damage to the heart muscle. A correct diagnosis not only determines what tests and procedures physicians order, but it also influences the patient’s state of mind post-hospitalization. Initial EKGs in these patients are different, although it does evolve, and can take up to 30 hours to illustrate what have come to be two distinctive features of stress cardiomyopathy syndrome:
Initial and serial serum troponins are normal to slightly increased. Thallium scan is usually normal or shows a minimal defect in the apical region, even in the acute phase. Myocardial iodine-123-metaiodobenzylguanidine scintigraphy studies have revealed large defects and high washout rate in the apex, which might reflect impaired activity of the sympathetic nervous system. Blood flow at rest is relatively preserved, whereas fatty acid metabolism and cardiac innervations are severely impaired in the acute phase.
Another clear indication of stress cardiomyopathy is the echocardiogram, which will show a characteristic wall motion abnormality, creating a distinctive left ventricular apical ballooning. The echo is easily recognizable if you know what to look for. Angiograms of patients in the acute phase of stress cardiomyopathy exhibit left ventricular (LV) systolic dysfunction with substantially reduced ejection fraction (15 percent to 40 percent). With supportive treatment the ejection fraction will normalize to 63±6 percent. They also have large wall-motion abnormality that is confined to the distal one-half to two-thirds of the LV chamber, which creates a distinctive "atypical ballooning" appearance associated with basal hypercontractility at end systole. LV end diastolic pressures are > 15 mm Hg.
The physical symptoms of a panic attack can look very much like those of acute coronary syndrome or stress cardiomyopathy. A misfiring of the emotional center of the brain (the limbic system, most often the amygdala) causes the body to react as if it were under severe threat. The physical symptoms of a panic attack can include palpitations, chest pain, diaphoresis, tremor, nervousness, and a feeling of doom. Patients, especially those experiencing their first panic attack, may present to an emergency department afraid that they are having heart attacks. Panic attacks are usually self-limiting, resolving in an hour or less (which may seem like an eternity to the person affected). Evaluation, monitoring, and emotional support are still needed while symptoms are sorted out.
More chronic in nature than panic attacks, depression and anxiety increase cardiac risk factors and vice versa. People with depression or anxiety are at a higher risk to develop cardiac disease and experience cardiac events, while those with cardiac conditions are more prone to develop symptoms of anxiety and depression. No link has been established between mood or anxiety disorders and stress cardiomyopathy. Appropriate diagnostic tests and emotional support of the patient and family are critical regardless of final diagnosis.
The unique features of stress cardiomyopathy syndrome are:
Supportive therapy is required for a few days to allow the heart to recover. Apprehension and a sense of doom, as well as distressing physical symptoms, need to be dealt with in patients with either AMI or stress cardiomyopathy. Healthcare providers can provide information and support matched to the person’s level of anxiety and physical distress. The higher the anxiety, the less able the person is to process information. The healthcare provider can listen, acknowledge feelings of distress, and provide reassurance that everything necessary is being done to obtain adequate diagnostic information and to treat symptoms accordingly.
In an acute situation, patients should be managed according to established guidelines for ST-elevation myocardial infarction or acute coronary syndrome. This includes combinations of negative inotropic agents (Β-blockers, orally or intravenously), aspirin, nitrates (sublingual or intravenous) and heparin. Vasopressor agents (e.g. Dobutamine and dopamine) may be required for marked hypotension to sustain cardiac output and systemic blood pressure. Immediate physical discomfort can be addressed in the same way as for AMI. Loosen clothing, position for adequate respiratory effort, provide a warm blanket for comfort or towel for diaphoresis, and administer oxygen and other medications as indicated by the patient’s condition. When patient history includes a recent stressful event, emergency department staff may now be including stress hormone levels in addition to the typical cardiac enzymes.
The rapid resolution of symptoms, the absence of coronary artery disease, and an EKG pattern characteristic of acute cardiac stress cardiomyopathy point to transient, rather than permanent, damage. However, the patient still needs rest and supportive treatment while the poorly functioning myocardium and neurohormones return to normal levels.
Physical or emotional stress has long been known to have an impact on the cardiovascular system. Reversible electrocardiographic and echocardiographic changes have been reported in patients under emotional stress or physical stress including noncardiac illnesses. With increasing application of primary angioplasty for the treatment of acute coronary syndromes, patients are being identified with transient left ventricular dysfunction in the absence of obstructive epicardial coronary disease. Stress cardiomyopathy syndrome is not as common as acute coronary syndrome, but it is expected that numbers will increase as more physicians learn to recognize the syndrome’s unique clinical features.
The links between mind and body continue to offer new frontiers for exploration and research, and new ways to understand the pathophysiology underlying phenomena such as stress cardiomyopathy. Certain neurotransmitters, particularly serotonin and norepinephrine, modulate both physical pain and depression. The literature also suggests that the emotional responses of “social pain" or rejection may follow the same neural pathways as physical pain, perhaps serving similar purposes of self-preservation and self-protection.
“Broken Heart Syndrome" is a real condition. The incidence is unknown, and the pathogenesis is not completely understood. An accurate diagnosis and appropriate medical management are possible following a complete clinical history and minimally invasive testing. With appropriate diagnosis, treatment is likely to be successful with no long-term complications. Recognition of the condition and immediate, appropriate care can be instrumental to the recovery of these otherwise healthy people. While the folklore of “Broken Heart Syndrome" has been around for decades, the prevalence of the condition remains unknown. Reports exist primarily from Japan and Johns Hopkins that describe similar syndromes, but no biochemical analyses have been performed that link the condition to the elevated catecholamine levels. Future studies need to evaluate whether there is genetic vulnerability. “Broken Heart Syndrome" brings medicine one step closer to the wisdom of “old wives" over the centuries. How many times when you were growing up did you hear your grandma or an aunt tell about somebody who had a shock that nearly killed them?
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