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Updated: Nov 10, 2025

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Published on: February 23, 2020
Aortic aneurysm disease-Make room for chronobiology
Aleksandra Lopuszko1, Sven Zhen Cian Patrick Tan1, Wahaj Munir1
1Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom.
Insights
Aortic aneurysm (AA) incidence peaks in the morning and colder months, mirroring other cardiovascular events. Understanding these chronobiological patterns is key for developing new prevention strategies.
Area of Science:
- Chronobiology
- Cardiovascular Pathophysiology
- Atherosclerosis
Background:
- Aortic aneurysm (AA) is a significant cause of mortality, often resulting from atherosclerosis or genetic disorders.
- AAs are frequently asymptomatic until rupture, which has a high fatality rate.
- AA incidence may follow chronobiological patterns, similar to other cardiovascular diseases.
Purpose of the Study:
- To evaluate the association between circadian rhythms, seasonal variations, and genetic factors in AA pathogenesis.
- To review the impact of chronobiology on aortic aneurysm development and incidence.
Main Methods:
- Comprehensive literature review.
- Analysis of existing studies on chronobiology and aortic aneurysms.
Main Results:
- AA incidence peaks in the early morning (6-11 a.m.) and during colder months.
- AA incidence troughs in the evening and warmer months.
- These patterns resemble those observed in myocardial infarcts and cerebrovascular strokes.
Conclusions:
- A clear link exists between chronobiology and the incidence/pathogenesis of ruptured AA.
- The association is more pronounced in individuals with Marfan syndrome or vitamin D deficiency.
- Further research into chronotherapeutics is needed for precision medicine approaches to AA prevention.
Background:
Aortic aneurysm (AA) is a common atherosclerotic condition, accounting for nearly 6000 deaths in England and up to 175,000 deaths globally each year. The pathological outward bulging of the aorta typically results from atherosclerosis or hereditary connective tissue disorders. AAs are usually asymptomatic until spontaneous rupture or detected on incidental screening. Eight in 10 patients do not survive the rupture and die either before reaching hospital or from complications following surgery. Similar to other cardiovascular pathologies, AA is thought to be subject to chronobiological patterns of varying incidence.
Methods:
We performed a literature review of the current literature to evaluate the association between circadian rhythms, seasonal variations, and genetic factors and the pathogenesis of AA, reviewing the impact of chronobiology.
Results:
The incidence of AA is found to peak in the early morning (6-11 a.m.) and colder months, and conversely troughs towards the evening and warmer months, exhibiting a similar pattern of chronobiological rhythm as other cerebrovascular pathologies, such as myocardial infarcts, or cerebrovascular strokes.
Conclusion:
Literature suggests there exists a clear relationship between chronobiology and the incidence and pathogenesis of ruptured AA; incidence increases in the morning (6-11 a.m.), and during colder months (December-January). This is more pronounced in patients with Marfan syndrome, or vitamin D deficiency. The underlying pathophysiology and implications this has for chronotherapeutics, are also discussed. Our review shows a clear need for further research into the chronotherapeutic approach to preventing ruptured AA in the journey towards precision medicine.
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