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Histological Quantification of Chronic Myocardial Infarct in Rats
Published on: December 11, 2016
Circadian variations of infarct size in acute myocardial infarction
Aida Suárez-Barrientos1, Pedro López-Romero, David Vivas
1Coronary Care Unit, Cardiovascular Institute, Hospital Clínico San Carlos, Madrid, Spain.
Insights
The circadian clock influences heart attack (myocardial infarction) size, with larger infarcts occurring in the morning. This finding on infarct size variation may impact clinical trials for heart attack treatments.
Area of Science:
- Cardiology
- Chronobiology
- Biomedical Science
Background:
- The circadian clock regulates cardiovascular physiology, affecting conditions like acute myocardial infarction.
- Previous rodent studies suggested circadian variation in infarct size, but clinical evidence was lacking.
Purpose of the Study:
- To investigate the impact of the time of day of ST-segment elevation myocardial infarction (STEMI) onset on infarct size.
Main Methods:
- A retrospective analysis of 811 STEMI patients (2003-2009) was conducted.
- Infarct size was assessed by peak enzyme release (creatine kinase and troponin-I).
- STEMI onset times were analyzed in relation to circadian rhythms.
Main Results:
- A significant circadian variation in infarct size was observed, correlating with STEMI onset time (p=0.015 for CK, p=0.012 for TnI).
- Peak enzyme levels were highest during the 6:00 AM to noon period, indicating larger infarcts.
- STEMI onset between 6:00 AM and noon resulted in significantly larger infarcts compared to onset between 6:00 PM and midnight.
Conclusions:
- Significant circadian variations in infarct size exist in STEMI patients based on the time of day of onset.
- STEMI onset during the 6:00 AM to noon period is associated with larger infarct sizes.
- These findings may influence the interpretation of clinical trials for cardioprotective strategies in STEMI.
Background:
The circadian clock influences a number of cardiovascular (patho)physiological processes including the incidence of acute myocardial infarction. A circadian variation in infarct size has recently been shown in rodents, but there is no clinical evidence of this finding.
Objective:
To determine the impact of time-of-day onset of ST segment elevation myocardial infarction (STEMI) on infarct size.
Methods:
A retrospective single-centre analysis of 811 patients with STEMI admitted between 2003 and 2009 was performed. Infarct size was estimated by peak enzyme release. The relationship between peak enzyme concentrations and time-of-day were characterised using multivariate regression splines. Time of STEMI onset was divided into four 6-hour periods in phase with circadian rhythms.
Results:
Model comparisons based on likelihood ratio tests showed a circadian variation in infarct size across time-of-day as evaluated by peak creatine kinase (CK) and troponin-I (TnI) concentrations (p=0.015 and p=0.012, respectively). CK and TnI curves described similar patterns across time, with a global maximum in the 6:00-noon period and a local minimum in the noon-18:00 period. Infarct size was largest in patients with STEMI onset in the dark-to-light transition period (6:00-noon), with an increase in peak CK and TnI concentrations of 18.3% (p=0.031) and 24.6% (p=0.033), respectively, compared with onset of STEMI in the 18:00-midnight period. Patients with anterior wall STEMI also had significantly larger infarcts than those with STEMI in other locations.
Conclusions:
Significant circadian oscillations in infarct size were found in patients according to time-of-day of STEMI onset. The infarct size was found to be significantly larger with STEMI onset in the dark-to-light transition period (6:00-noon). If confirmed, these results may have a significant impact on the interpretation of clinical trials of cardioprotective strategies in STEMI.
