Stress cardiomyopathy (also known as transient left ventricular apical ballooning syndrome, takotsubo cardiomyopathy, and broken heart syndrome) is a condition that mimics an MI in the absence of significant coronary artery disease. Stress cardiomyopathy causes a temporary ballooning, or hyperexpansion, of the apical portion of the left ventricle. When that portion of the ventricle is stunned, contraction stops. The basal portion of the left ventricle continues to contract, forcefully pushing blood into the noncontracting apex of the left ventricle, causing the apex to expand outward. Stress cardiomyopathy is similar to squeezing one end of a round balloon.¹

Most reports of stress-induced cardiomyopathy focus on transient dysfunction of the left ventricle. However, evidence exists that the right ventricle may also be affected.²

This syndrome, discovered in Japan in 1991, was called octopus trap (takotsubo) cardiomyopathy because the trap’s shape is similar to a ballooning left ventricle with a round bottom and a narrow neck.¹ Because of the correlation with intense emotional stresses, stress cardiomyopathy has been called broken heart syndrome.¹

When triaging patients with cardiac symptoms, physical therapists should be aware of stress cardiomyopathy as a potential diagnosis and recognize those at risk. Stress cardiomyopathy usually affects older women who have recently had an acute intense stressful event, either physical or emotional. Examples include a sudden loss of a loved one, a domestic argument or violence, a frightening medical diagnosis, public speaking, a financial crisis, or a natural disaster.¹

No single explanation exists for stress cardiomyopathy. But with immediate recognition and appropriate care, a patient can be asymptomatic and have a normal ECG within hours. Patients who survive can recover normal ventricular function within one to four weeks.³

Unlike an MI, which stems from blockage of one or more coronary arteries, stress cardiomyopathy is thought to be caused by exaggerated sympathetic stimulation that results in a surge of catecholamines (e.g., epinephrine, norepinephrine, or dopamine) to cause myocardial stunning. The myocardial cells temporarily lose the ability to contract effectively, which causes apical ballooning. While the cause of stress cardiomyopathy is understood to be a surge of catecholamines, the mechanism of action remains unknown. Several theories have been suggested. One theory points to an epicardial coronary artery spasm from increased sympathetic activity. This spasm causes vasoconstriction of the coronary arteries and a temporary decrease in blood flow. An alternative theory involves sympathetic stimulation of the microcirculation, which leads to microvascular spasm and a decrease in blood flow. Another theory involves the direct cardiotoxic effects (from increased calcium) of excessive catecholamine release to the heart muscle.³

Stress cardiomyopathy is reversible while an MI causes permanent damage.^3,4 Of patients with symptoms similar to an MI, 1% to 2% have stress cardiomyopathy.¹ The clinical presentation of stress-induced cardiomyopathy is similar to an acute MI. Most patients present with acute substernal chest pain and shortness of breath. But patients can present with syncope, nausea/vomiting, ECG abnormalities (including bradyarrhythmias or tachyarrhythmias), pulmonary edema, and even cardiogenic shock.^2,4,5 ECG, echocardiogram, and cardiac enzymes are useful for diagnosis. The ECG usually shows some abnormalities; these vary from ST depression to mild ST elevation, T-wave inversion, a prolonged QT interval, and possibly abnormal Q waves. The echocardiogram shows apical hypokinesia or ballooning of the left ventricle and decreased EF (less than 50%). Cardiac enzymes can range from normal to significantly elevated, but are typically mildly elevated. A negative cardiac angiography is the defining test.

If a patient presents with symptoms of an acute MI with ST elevation and can undergo cardiac catheterization for a percutaneous coronary intervention, ST-elevation MI protocol should be implemented. Patients with ST elevation usually receive fibrinolytic therapy when angiography and PCI are not available. Since most patients with ST elevation have critical coronary lesions, suspicion of the diagnosis of stress-induced cardiomyopathy is not sufficient to withhold fibrinolytic therapy. Patients for whom both cardiac catheterization and thrombolytic therapy are contraindicated are problematic. Diagnosis would rely on evaluating the differences in the patterns of wall motion abnormalities from patients with stress-induced cardiomyopathy and performing an echocardiogram to determine whether there is acute obstruction of flow in one of the coronary arteries.⁶

Fact or Fable?

While tales of people literally scared to death or dying of a broken heart are common throughout history,³ efforts to record this phenomenon medically have been sporadic until somewhat recently. In 1943, a U.S. scientist proposed a cause-and-effect relationship between spasm of the coronary arteries and intense emotion; he speculated that such spasms could cause tissue damage from ischemia or that a clot could result if the spasm was prolonged.⁵ In the 1950s and 1960s, a nine-year study of more than 4,000 widowers in Britain found their mortality rate was 40% higher in the first six months of bereavement than for married men of the same age and that death was most often from cardiac dysfunction.⁶ 

Heart muscle damage that results from pheochromocytoma (a usually benign adrenal medullary tumor that causes hypertension when there is excessive secretion of catecholamines) is similar to the myocardial cell degeneration from the catecholamine surge in sudden, severe emotional stress.² Analysis of pericardial fluid in victims of violence in which cardiac injury was not the cause of death showed catecholamine elevations greater than in those whose cause of death was heart attack, suggesting that catecholamine-mediated injury or stress-induced cardiomyopathy is part of the physiologic response to emotional as well as physical trauma. Catecholamine levels in patients with stress cardiomyopathy can be two to three times greater in patients with an MI, and up to 34 times greater in healthy people.

Although research in Japan as early as 1991 suggested the presence of myocardial stunning or stress-induced cardiomyopathy, the syndrome, once considered a folktale, is now recognized as a legitimate diagnosis in the U.S.² For the past decade, evidence-based data suggest that contractile abnormalities, congestive heart failure, and even death can be associated with sudden emotional stress.² Using echocardiography, one study shows that 28% of patients in an ICU demonstrated left ventricular apical ballooning with reduced EF.⁷ The phenomenon of older people who die soon after the death of a spouse focuses attention on the risk for cardiac events in this population. Physical therapists now understand that during bereavement, stress-induced cardiomyopathy is a risk, particularly in otherwise healthy people.⁹

A two-way relationship exists between the heart and the mind. Emotions and stressful experiences affect the heart through the autonomic nervous system and neuroendocrine pathways. People can experience cardiac activity and cardiac function as somatic symptoms, such as fatigue, lethargy, insomnia, and loss of appetite or as chest pain and palpitations, the more classic cardiac symptoms.⁸ Psychotropic agents can affect the heart, and drugs that treat heart disease can affect the brain. For example, some antipsychotic medications can lower blood pressure or increase heart rate, while a cardiac drug that strengthens heart contractility can result in nervousness or apprehension.

There is little evidence to support the idea that people who develop stress-induced cardiomyopathy have preexisting emotional disorders. The condition seems to be more directly related to the acuity of the stress. Even though we are aware of certain physiologic changes that occur when someone is scared to death or has a broken heart, there needs to be further study on how psychological factors contribute to stress cardiomyopathy.⁸

The physical symptoms of a panic attack can look 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.¹⁰ The physical symptoms of a panic attack can include palpitations, chest pain, diaphoresis, tremor, nervousness, and a feeling of doom. Patients, especially with a first panic attack, may present to an ED afraid that they are having a heart attack. Panic attacks are usually self-limiting and resolve 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 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. There is no link between mood or anxiety disorders and stress cardiomyopathy; but further research may reveal changes in the feedback systems between the adrenals, pituitary, thyroid, and autonomic nervous system that could apply to both acute and chronic conditions.^11,12

The myocardial ballooning that results from acute stress is most often reversible with quick identification and appropriate treatment.^1,3,11 Physical therapists can provide the following when they care for patients with stress cardiomyopathy:

Awareness: Physical therapists should be aware that while cardiac disease is the No. 1 killer of both women and men, women are more likely than men to have stress-induced cardiomyopathy. Physical therapists who also understand that there can be more than one explanation for acute cardiac symptoms or heart failure can be more effective when they evaluate people who present with chest pain, palpitations, shortness of breath, and other classic symptoms of an MI. This awareness is instrumental in accurate diagnosis and prompt treatment. Most crucial is the awareness that, like an MI, stress-induced cardiomyopathy requires urgent treatment; the symptoms should never be dismissed.

Differentiation of stress-induced cardiomyopathy from other conditions: Adequate assessment is crucial to determine whether cardiac symptoms indicate transient impairment in cardiac function or permanent damage to the heart muscle. The presenting symptoms are similar for patients with an MI or stress-induced cardiomyopathy. Defining characteristics for an MI include a significantly elevated troponin level, ST elevation with reciprocal changes, and the presence of coronary artery disease. Defining characteristics of stress-induced cardiomyopathy include a normal to significantly elevated troponin level (although it is generally a mild elevation), T-wave inversion and prolonged QT interval, and absence of coronary artery disease (see sidebar). In other words, an MI represents significant cardiovascular disease while stress-induced cardiomyopathy seldom has this underlying disease process.⁴

Support and interventions: Appropriate diagnostic tests and emotional support for the patient and family are critical regardless of the final diagnosis. Apprehension and a sense of doom, as well as distressing physical symptoms, need to be addressed immediately for patients with an MI or stress cardiomyopathy. Physical therapists can provide information and support for the level of anxiety and physical distress. A high anxiety level reduces the ability to process information. The physical therapist can listen, acknowledge feelings of distress, and provide reassurance that everything is being done to obtain adequate diagnostic information and to treat symptoms accordingly. Immediate physical discomfort can be addressed as for an MI: Loosen clothing, position for adequate respiratory effort, provide a warm blanket for comfort or towel for diaphoresis, and administer oxygen and medications as indicated by the patient’s medical condition. Above all, the physical therapist should try to stay with the patient and provide explanations to family members.

Stress cardiomyopathy is not a precursor to an MI. The myocardium is not damaged, but the heart undergoes transient physical changes that impair pump action. People with this disorder generally have no evidence of coronary artery disease. These patients can become quite ill when not treated properly because of the weakened myocardium and decreased cardiac output. As myocardial stunning continues, the patient may experience congestive heart failure; if untreated, the patient may die of pulmonary edema. When the patient with stress-induced cardiomyopathy begins to develop symptoms of congestive heart failure (shortness of breath, decreasing oxygen saturation levels, fatigue, jugular vein distension, rales, or a frothy cough), immediate treatment is essential. General treatment includes rest, oxygen, positioning the patient for greater lung expansion, and thorough assessment for worsening symptoms.⁴

Supportive measures are the mainstay of management during the acute treatment phase of stress-induced cardiomyopathy. Severe left ventricular dysfunction may warrant inotropic agents, such as dopamine or dobutamine, or even hemodynamic support with intraaortic balloon-pump counterpulsation. More commonly, treatment includes the use of aspirin, ACE inhibitors, calcium channel blockers, beta blockers, and diuretics. In consideration of the possible pathophysiological mechanism of catecholamine-mediated myocardial stunning, long-term treatment with beta blockers may be an appropriate approach.⁵ Despite its severity, stress-induced cardiomyopathy is a transient disorder managed with supportive therapy. Treatment along with the resolution of the physical or emotional stress usually results in rapid resolution (within several hours) of symptoms and physiologic changes.

Evaluation and follow-up: The rapid resolution of symptoms, the absence of coronary artery disease, and an ECG 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

The link between mind and body continues to offer new frontiers for exploration and research — and new ways for physical therapists to understand the pathophysiology that underlies phenomena such as stress-induced cardiomyopathy. We know that certain neurotransmitters, particularly serotonin and norepinephrine, modulate both physical pain and depression.¹³ A literature review 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.¹²

Broken heart syndrome is a real condition, worthy of the more contemporary diagnostic terms of transient left ventricular apical ballooning syndrome or stress-induced cardiomyopathy. Even though the incidence is unknown and the pathogenesis is not fully understood, an accurate diagnosis and appropriate medical management are possible after a clinical history and minimally invasive testing. With appropriate diagnosis, treatment is likely to succeed with no long-term complications. Recognition of the condition and immediate, appropriate care can be instrumental in the recovery of these otherwise healthy people.

Helpful Websites

• Johns Hopkins Medicine
  http://www.hopkinsmedicine.org/asc/faqs.html
• He@lthLINK
  http://www.ynhh.org/healthlink/cardiac/cardiac_5_05.html

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