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 67-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 percent), 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 percent 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.
For this upcoming Valentine’s Day, let’s keep both the heart and the brain healthy and hope that there are no broken hearts out there.