The DOI matches its Crossref record; 54 of the 54 references it cites were found in a registry or an index.
Short-Term Disruption of Diurnal Rhythms After Murine Myocardial Infarction Adversely Affects Long-Term Myocardial Structure and Function
Abstract
Rationale: Patients in intensive care units are disconnected from their natural environment. Synchrony between environmental diurnal rhythms and intracellular circadian rhythms is essential for normal organ biology; disruption causes pathology. Whether disturbing rhythms after myocardial infarction (MI) exacerbates long-term myocardial dysfunction is not known. Objective: Short-term diurnal rhythm disruption immediately after MI impairs remodeling and adversely affects long-term cardiac structure and function in a murine model. Methods and Results: Mice were infarcted by left anterior descending coronary artery ligation (MI model) within a 3-hour time window, randomized to either a normal diurnal or disrupted environment for 5 days, and then maintained under normal diurnal conditions. Initial infarct size was identical. Short-term diurnal disruption adversely affected body metabolism and altered early innate immune responses. In the first 5 days, crucial for scar formation, there were significant differences in cardiac myeloperoxidase, cytokines, neutrophil, and macrophage infiltration. Homozygous clock mutant mice exhibited altered infiltration after MI, consistent with circadian mechanisms underlying innate immune responses crucial for scar formation. In the proliferative phase, 1 week after MI, this led to significantly less blood vessel formation in the infarct region of disrupted mice; by day 14, echocardiography showed increased left ventricular dilation and infarct expansion. These differences continued to evolve with worse cardiac structure and function by 8 weeks after MI. Conclusions: Diurnal rhythm disruption immediately after MI impaired healing and exacerbated maladaptive cardiac remodeling. These preclinical findings suggest that disrupted diurnal rhythms such as found in modern intensive care unit environments may adversely affect long-term patient outcome.
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“For instance, recovery from experimentally induced myocardial ischemia is impaired in mice by rapidly shifting light/dark cycles, suggesting that sleep and circadian rhythm disruption that occurs in intensive care units may compromise recovery (145).”
From Role of the circadian system in cardiovascular disease (2018) · cites this paper as [145]
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Circadian rhythms and the molecular clock in cardiovascular biology and disease
Crnko, S., Du Pré, B. C., Sluijter, J. P. G., & Van Laake, L. W. (2019) · Nature Reviews Cardiology · doi:10.1038/s41569-019-0167-4 · Cited by 499
Role of the circadian system in cardiovascular disease
Thosar, S. S., Butler, M. P., & Shea, S. A. (2018) · Journal of Clinical Investigation · doi:10.1172/jci80590 · Cited by 443
“For instance, recovery from experimentally induced myocardial ischemia is impaired in mice by rapidly shifting light/dark cycles, suggesting that sleep and circadian rhythm disruption that occurs in intensive care units may compromise recovery (145).”
Ruben, M. D., Smith, D. F., FitzGerald, G. A., & Hogenesch, J. B. (2019) · Science · doi:10.1126/science.aax7621 · Cited by 249
Monocytes in Myocardial Infarction
Dutta, P., & Nahrendorf, M. (2015) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/atvbaha.114.304652 · Cited by 223
“Homozygous clock mutant mice exhibited similarly aggravated ventricular remodeling after MI, which accords with the idea that blood monocyte levels, regulated by circadian rhythm, may determine myocardial repair post-MI.”
InfluentialSleep Apnea and Cardiovascular Disease: An Enigmatic Risk Factor
Floras, J. S. (2018) · Circulation Research · doi:10.1161/circresaha.118.310783 · Cited by 209
“In experimental preparations, temporal misalignment of such gene expression with myocardial metabolic demand promotes left ventricular (LV) hypertrophy, insulin resistance, and reperfusion injury,(2,3) and in a model of myocardial infarction, maladaptive cardiac remodeling, involving impaired early innate immune, repa…”
Background
Metadata
- Authors
- Alibhai, F. J., Tsimakouridze, E. V., Chinnappareddy, N., Wright, D. C., Billia, F., O’Sullivan, M. L., Pyle, W. G., Sole, M. J., & Martino, T. A.
- Affiliations
- University Health Network (CA)
- ORCID
- Venue
- Circulation Research
- Published
- 2014-05-23
- Volume
- 114
- Issue
- 11
- Pages
- 1713-1722
- ISSN
- 0009-7330 (ISSN-L)
- 1524-4571
- OpenAlex
- W2129546872
- Semantic Scholar
- 52dc76bbff6a1eb6aeaa8f8ad67a1849f7a682fe
- Cited by
- 122
- References
- 54
- Citations by year
- 2026: 3 · 2025: 9 · 2024: 9 · 2023: 18 · 2022: 13 · 2021: 8 · 2020: 11 · 2019: 11 · 2018: 9 · 2017: 10 · 2016: 5 · 2015: 10 · 2014: 6
- FWCI
- 5.03
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Circulation Research (publishedVersion)
- PubMed (publishedVersion)
- IslandScholar (University of Prince Edward Island) (submittedVersion)
- Funders
- Canadian Institutes of Health Research (MOP119518)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Acute Myocardial Infarction Research
- Keywords
- myocardial infarction, circadian rhythm disruption, diurnal cycle, cardiac remodeling, myocardial fibrosis, innate immune response, macrophage infiltration, neutrophils, myeloperoxidase, infarct healing, coronary artery ligation, ICU environment, left ventricular dilatation, infarct expansion, Clock mutant mice
- MeSH terms
- Animals, Circadian Rhythm, Coronary Vessels, Disease Models, Animal, Heart, Ligation, Male, Mice, Inbred C57BL, Myocardial Infarction, Myocardium, Time Factors, Mice
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