Tina Myhre Pedersen has studied morphological, functional and metabolic cardiac alterations in obesity- and angiotensin II-mediated heart failure.


MAIN RESULTS:

  1. Isolated perfused working heart preparation provides unique additional information to in vivo echocardiography regarding development of cardiac dysfunction in type 2-diabetes.
  2. Obese hearts adapt to become less sensitive to an acute fat exposure.
  3. Angiotensin II does not alter cardiac substrate consumption prior to functional heart failure.

THESIS DEFENCE:

Thesis: Cardiac remodelling in obesity- and angiotensin II-mediated heart failure: Morphological, functional and metabolic alterations
Candidate: Tina Myhre Pedersen
Time: October 21, 2019 at 12:15
Place: UiT The Arctic University of Norway, MH Vest: Auditorium Cortex
Link to university website


SUMMARY:

(1) While ex vivo working hearts of mice with overt type 2-diabetes showed both systolic and diastolic dysfunction, the in vivo examination demonstrated maintained systolic function. In predabetic mice with obesity caused by a high-fat diet, ex vivo analyses suggested diastolic dysfunction, whereas both systolic and diastolic function were maintained in the in vivo analysis.

The functional changes in vivo were examined with conventional transthoracic echocardiography, and  the ex vivo methodology involved isolated heart perfusion techniques. The contrasting results could indicate a lack of sensitivity using conventional transthoracic echocardiography.

(2) Although chronic elevation of circulating fat contributes to heart failure, obese hearts also undergo adaptation making them less sensitive to an acute fat exposure.

(3) The hormone angiotensin II induces heart failure. While metabolic changes occur prior to dysfunction in obesity, Pedersens’s results describe that angiotensin II does not alter the substrate consumption prior to functional failure.


REFERENCES:

(1) Pedersen, T. M., Boardman, N. T., Hafstad, A. D., & Aasum, E. (2018). Isolated perfused working hearts provide valuable additional information during phenotypic assessment of the diabetic mouse heartPloS one13(10), e0204843.

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