Impact of diabetes on cardiopulmonary function: the added value of a combined cardiopulmonary and echocardiography stress test

Epicardial adipose tissue thickness is associated with reduced peak oxygen consumption and systolic reserve in patients with type 2 diabetes and normal heart function

“…Nonetheless, the relationship between EAT thickness and cardiopulmonary performance in T2D without heart disease has never been evaluated. 9 By using an imaging-cardiopulmonary exercise test (iCPET), the current study aimed to evaluate the association of echocardiographyassessed EAT thickness with heart structure and contractility (as measured by resting and exercise 2D-echo, Doppler, and speckletracking technology) and cardiopulmonary fitness (pulmonary, metabolic, and haemodynamic variables during graded, maximal cycloergometer exercise) in T2D patients without HF and with normal biventricular systo-diastolic function. We also tested whether EAT thickness is associated with plasma biomarkers of inflammation, oxidative stress, matrix remodelling, and myocyte strain and injury in a subgroup of patients, aiming to identify the pathophysiological mechanisms at play.…”

“…Nonetheless, the relationship between EAT thickness and cardiopulmonary performance in T2D without heart disease has never been evaluated. 9 …”

“…Given its consistent prognostic power both in HF without T2D 8 and in T2D without HF, 4 EAT probably plays a key role in the progression to overt HF. Nonetheless, the relationship between EAT thickness and cardiopulmonary performance in T2D without heart disease has never been evaluated 9 …”

Epicardial Fat in Heart Failure with Preserved Ejection Fraction: Bad Actor or Just Lying Around?

“…Although EAT appears to be associated with abnormal haemodynamics that are pathognomonic of HFpEF, the presence of EAT is also associated with diabetes and greater visceral and overall adiposity, which have also been associated with HFpEF and this makes a direct determination of causality with HFpEF difficult. 9,13,14,18,20,46,47 Therefore, while there is a growing body of literature to suggest a strong association between EAT and obese HFpEF, there remains difficulty in establishing causality given the strong collinear associations between epicardial fat, visceral fat and total body fat. 11,12 In other words, it remains unclear if the presence of EAT is merely a correlate of the generalised adiposity-related inflammation that drives the obese HFpEF syndrome, or if excess EAT directly contributes to HFpEF pathogenesis independent of visceral and systemic adiposity.…”

Reply to ‘Epicardial adipose tissue: does it mediate the cardio‐protective effects of sodium–glucose co‐transporter 2 inhibitors in subjects with heart failure?’ Letter regarding the article ‘Impact of epicardial adipose tissue on cardiovascular haemodynamics, metabolic profile, and prognosis in heart failure’

“…In these patients, EAT accumulation stimulates the production of locally active proinflammatory cytokines and exerts mechanical compression on the heart. 4 On the opposite end of the HF spectrum, the role of EAT in HFrEF is less understood. We hypothesize that EAT may serve as a metabolic reservoir in HFrEF; for this reason, lower EAT thickness may be correlated to the progressive impairment of cardiac structure and function.…”