UAB logoWe all know how fatal a heart attack could be. Well, it now emerges that the time of the day could also play an important part in deciding the amount of damage that may have been caused by a heart attack. University of Alabama at Birmingham (UAB) Division of Cardiovascular Disease researchers claim that the internal body clock seems to contribute to the severity of a heart attack.

The internal body clock is also called the circadian clock and it appears to indicate the clock that regulates the 24-hour cycle in human and animal biological processes. Experts associated with this research claim to have analyzed mouse models. Upon close examination, they found that the time of the day seems to be a key factor in determining the severity of the heart attack.

UAB Associate Professor of Cardiovascular Disease Martin Young, Ph.D., and colleagues who studied the mouse models observed up to a three-and-a-half-fold impact of the time of day on the amount of tissue that could die during the heart attack. This was seen mainly due to the internal body clock.

“In our mouse model, the most damage was shown to occur in the early morning, at the sleep-to-wake transition,” Young mentioned. “This is the same time of the day at which previous studies have shown more heart attacks occur in humans.”

According to Young, the time of day, week or season of the year has been widely accepted to influence cardiovascular health and disease. Heart attacks for example have been found to occur with greatest incidence early on a Monday morning in fall and winter. Apparently it is believed to occur due to fluctuations in posture, physical exertion, food consumption and body temperature during the day.

The internal body clock was being closely investigated by Young and his colleagues, including UAB Physiology and Biophysics graduate student David Durgan as a predictor of damage to the heart. They claim it to be a natural progression from this previous research.

“What has become increasingly clear is a significant contribution of intrinsic mechanisms mediating temporal-dependence of cardiovascular physiology and pathophysiology,” Young further remarked. “For instance, travelers retain time-of-day oscillations in sudden cardiac death, in such a way that the peak incidence is equivalent to the early hours of the morning in their time zone of origin, not where they have traveled to. Although circadian rhythms in heart-attack timing are well established, time-of-day oscillations in heart-attack damage have not been reported previously.”

“From this we concluded that cardiac muscle cell circadian clock mediates time-of-day-dependent changes in heart-attack tolerance,” he further explained. “Future efforts likely will focus on identifying ways to reset the heart clock as a means to improve heart-attack tolerance.”

Apparently Young along with colleagues also uncovered that the time-dependence in damage could be absent in a mouse model that showed a disrupted circadian clock. This could be true particularly if the disruption is exhibited in the cardiac muscle cells.

The research is published online in the journal Circulation Research.