Can a heart truly be broken? Unfortunately many people have
suffered the emotional aspects of a broken heart, but can the heart be
physically broken as well? Consider the following scenario. A sixty-seven year
old woman presents to the emergency room (ER) with chest pain. She lives alone and earlier in the day she
learned that her faithful companion, her dog, passed away. In the ER, she is found to have a very
abnormal electrocardiogram (EKG) and her blood enzymes are suspicious for a
heart attack. She is admitted to the
hospital and undergoes a heart catherization the next day. Her cath reveals
normal heart arteries, without evidence for blockage, but her heart is severely
damaged. What is happening?
She is suffering from a condition known by various colorful names
including broken heart syndrome, apical ballooning syndrome, and stress-induced
cardiomyopathy (cardiomyopathy is a weakened or damaged heart muscle). This condition was first described in Japan
in 1991. The Japanese coined the condition Takotsubo cardiomyopathy because the
heart muscle resembles a Japanese octopus trap with a narrow neck and a wide
base. Stress-induced cardiomyopathy occurs
primarily in women (90%), the majority of whom are post-menopausal. It is often
associated with a chronic psychiatric disorder such as anxiety or depression. It is commonly triggered by an emotional
event. Stressors include learning of the death of a loved one, public speaking,
a surprise birthday party, a lightning strike, or an earthquake. Physical
triggers, such as pain or anxiety over a medical procedure can provoke an event
as well. In women, an emotional trigger
is more likely, while a physical stressor is more common in men. The vast
majority of patients present with chest pain and EKG changes; their
presentation often looks like an acute heart attack. In addition, there are
high levels of cardiac enzymes in the blood. These enzymes are typically
released when the heart is damaged, as occurs with a heart attack. Heart
catherization often shows no blockage in the heart arteries but the heart
muscle is severely damaged and not contracting. The most common area of damage
is the apex or the tip of the heart. Due to this damage, the heart’s pumping
capacity, the ejection fraction, is significantly reduced. Patients are treated with beta-blockers to
reduce the effect of adrenaline (catecholamine) on the heart and ACE inhibitors
to prevent congestive heart failure from the low ejection fraction. While death
and stroke can occur with stress-induced cardiomyopathy, the vast majority
recover. Fortunately, the heart function
also usually recovers and returns to normal after several days to several
weeks. The prognosis is usually good, although about 10% of patients have a recurrent
event, despite treatment.
The exact cause of stress-induced cardiomyopathy is not
known. There are many possible explanations but the prevailing theory is that a
trigger provokes a “fight or flight response” resulting in a rush of stress
hormones (adrenaline, catecholamines) and an exaggerated stimulation of the
nervous system. It is well known that adrenaline and nervous system stimulation
can cause severe damage to the heart.
The brain is the common factor. Adrenaline is released on command from a
part of the brain (the pituitary gland) and the nervous system is activated in
the brain. Stress-induced cardiomyopathy is felt to be part of a number of
syndromes with a brain-heart connection. For example, patients with an acute
stroke or a bleed in the brain often have EKG changes similar to those seen
with stress-induced cardiomyopathy. Activation of the “fight or flight”
response can also cause irritability of the heart leading to arrhythmias and
potentially sudden cardiac death. In fact, the brain-heart axis may contribute
to deaths associated with primarily neurologic conditions such as stroke,
seizure disorders and head trauma.
