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

(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.