Hormones Affect Carotid Plaque Stability and Stroke Vulnerability

MedicalResearch.com Interview with:

Marija Glisic Epidemiology, Erasmus MC

Marija Glisic

Marija Glisic
Epidemiology, Erasmus MC 

MedicalResearch.com: What is the background for this study?

Response: Carotid atherosclerosis is one of most important risk factors for developing stroke. Carotid atherosclerotic plaques characterized by lipid core presence and intraplaque haemorrhage are considered to be unstable, and therefore more prone to rupture and lead to consequent stroke. Sex differences have been observed in carotid plaque composition as well as in stroke incidence. Sex hormones, particularly estrogen and testosterone actions are suggested to underlie the observed sex differences in atherosclerosis. Experimental evidence suggests a direct action of estradiol and testosterone on the vascular system, affecting various mechanisms that may impact plaque composition and subsequently stroke risk.

MedicalResearch.com: What are the main findings?

Response: It this study we investigated the association between estradiol and testosterone and carotid plaque features as well as risk of stroke in middle-aged and elderly men and postmenopausal women (on average 17 years into menopause).

We observed sex differences in the association between estradiol, carotid plaque composition and risk of stroke. While total estradiol was associated with higher prevalence of lipid core in both men and women, total estradiol was associated with higher odds of having intraplaque hemorrhage and risk of stroke in women but not in men. We did not observe consistent association between testosterone and plaque composition and risk of stroke in either sex. Therefore, we hypothesize that endogenous estradiol levels in middle-aged elderly women can lead to plaque instability by increasing lipid content and intra-plaque hemorrhage which on the other hand can increase the risk of stroke.

MedicalResearch.com: What should readers take away from your report?

Response: Endogenous estradiol might play an important role in the development of vulnerable carotid plaque composition and increases risk of stroke in postmenopausal women. As endogenous estradiol levels in postmenopausal women can be alter by using hormone therapy our results raise a concern on whether the exogenous estradiol could have similar effect in women with carotid atherosclerosis. Therefore, until future studies replicate or refute our findings, we believe hormone therapy should be taken with caution among postmenopausal women with carotid atherosclerosis.

MedicalResearch.com: What recommendations do you have for future research as a result of this study?

Response: Due to several limitations of our study and its observational nature, our results are hypothesis-generating, therefore, future studies should replicate our findings and explore mechanisms of action of estradiol in carotid artery atherosclerosis, but as well in the other blood vessels. Also, our results encourage future research investigating whether estradiol might help to predict ischemic stroke in women with subclinical atherosclerosis, and thus, whether estradiol levels might be used in stroke risk prediction models.

MedicalResearch.com: Is there anything else you would like to add?

Response: I would like to thank to my entire team from Erasmus Medical Center for being involved in this project. 

MedicalResearch.com: Thank you for your contribution to the MedicalResearch.com community.

Citation:

Associations of Endogenous Estradiol and Testosterone Levels with Plaque Composition and Risk of Stroke in Subjects with Carotid Atherosclerosis

Marija Glisic, Blerim Mujaj, Oscar L Rueda-Ochoa, Eralda Asllanaj, Joop S Laven, Maryam Kavousi, M. Kamran Ikram, Meike W Vernooij, M Arfan Ikram, Oscar H Franco, Daniel Bos, Taulant Muka
Circulation Research. 2017;CIRCRESAHA.117.311681
Originally published November 2, 2017

 

Note: Content is Not intended as medical advice. Please consult your health care provider regarding your specific medical condition and questions.

 

 

 

 

 

 

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