The findings raise the possibility that our biological clocks – the daily routines, or ‘circadian rhythms’ that our bodies follow – contribute to the timing of sudden cardiac death.
Circadian rhythms keep us in sync with our surroundings. (Jet lag, for example, is the result of the body getting out of sync.) And the first molecular evidence for this link could lead to new methods of diagnosis and therapy to prevent fatal heart problems.
So a team led by Mukesh Jain and Darwin Jeyaraj from Case Western Reserve University took a molecular look at 2 associations that experts have long noticed:
- The occurrence of sudden cardiac death caused by ventricular arrhythmias (abnormal heart rhythms) increases within a few hours of waking up in the morning.
- The occurrences peak again in the evening.
Turns out, a particular protein that alters susceptibility to arrhythmia in mice is regulated by components of the circadian clock. The protein – called Klf15 – is involved in controlling the heart’s electrical stability, and levels of Klf15 go up and down during the day.
In this study, genetically modified mice with too much Klf15 and those with none at all BOTH had an increased risk of developing deadly disturbances of cardiac rhythm.
And as for humans, as HealthDay explains:
For example, patients with heart failure lack KLF15 while too much KLF15 causes electrocardiography changes such as those that occur in patients with a genetic heart rhythm disorder called Brugada syndrome.
Translating the findings into medicine, BBC reports, could mean targeting the most vulnerable stage, such as slow-release blood pressure drugs that become active first thing in the morning when the risk is highest.
Image by Leonardo da Vinci via Wikimedia