Broken heart syndrome may actually protect the grief-stricken from dying by halting the organ being pumped with too much adrenaline, reveals a study by the Imperial College London. People who suffered intense grief after the death of loved one are often thought be at risk of dying from a broken heart after developing symptoms of cardiac arrest.
Elderly patients especially women suffer symptoms that look similar to heart attack, but various test found no blockage in the coronary arteries. Sometimes, the similar condition is seen in people who are injected with adrenaline to treat severe allergic reactions. Researchers carried out a mice study to see the affect of broken heart syndrome or Takotsubo cardiomyopathy.
Researchers replicated the condition by injecting high doses of adrenaline in anaesthetised mice; heart muscle contraction was suppressed towards the bottom of the heart, seeing that in Takotsubo patients. The study findings showed that mice were protected from a terminal overstimulation of the heart, which suggests adrenaline acts through different lane than normal.
This switch protects the heart from toxic levels of adrenaline. The study also found that some beta blockers that are used to treat high blood pressure, angina and heart failure, enhanced qualities of Takotsubo. They also found that a different type of drug known as Levosimendan, which is given in heart failure, had beneficial effect.
The researchers suggest the body alters its reaction to adrenaline by switching from its usual role in invigorating the heart to reducing its pumping power. They believe this switch might have evolved to protect the heart from being over stimulated by high doses of adrenaline that body releases during stress.
Lead researcher Prof Sian Harding, explained stimulatory effect of adrenaline on the heart is significant to help get more oxygen around the body in stressful situations, but it can be damaging if it goes on for too long. In patients with Takotsubo cardiomyopathy, adrenaline works in a different way and shuts down the heart instead. This seems to protect the heart from being over stimulated.
The study was published in the journal Circulation.