The greatest amount of heart attack injury happens when the onset of ischemia occurs between 1 a.m. and 5 a.m., according to a new study at the Minneapolis Heart Institute that was published online this month in the journal Circulation Research.
Heart attack size and left-ventricular damage vary significantly by time of day, MedicalXpress reported about the findings of this first of its kind study of circadian dependence of heart attack severity in humans.
Previous research in rodents indicated oxygen deprivation, termed ischemia, and reperfusion injuries exhibited circadian dependence, varying in severity by the time of day the coronary occlusion happened within the animals' natural, inborn, approximately 24-hour-long biochemical, physiological and behavioral cycles.
But it was unknown whether infarct size in humans showed a similar circadian dependency.
Senior author and cardiologist Jay H. Traverse, MD explained in the Minneapolis Heart Institute Foundation's announcement,
"We were trying to ascertain whether the time of day of when a heart attack occurs influences the amount of damage that the heart sustains, or was this just a phenomenon exhibited in rodents.""It is important to understand that the heart's ability to protect itself against more severe damage varies over a 24-hour cycle. Identifying those protective changes may be particularly relevant for pharmaceutical manufacturers that are seeking to develop cardioprotective drugs."
The team analyzed 1,031 heart attack patients and identified 165 who presented with a first heart attack with occluded arteries and well defined ischemic times, but without evidence of pre-heart attack collateral blood circulation or angina.
Infarct size varied according to the time of day of the heart attack's onset, the researchers found: the greatest myocardial injury occurred associated with a 1 a.m. ischemia onset and a 5 a.m. reperfusion onset, with an 82 percent difference between the peak and least injury periods.
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A heart attack happens when a blood clot blocks coronary arteries, killing cardiac muscle.