1.
Benefits of 1-Year Lifestyle Modification Program on Exercise Capacity and Diastolic Function Among Coronary Artery Disease Men With and Without Type 2 Diabetes.
Piché, ME, Poirier, P, Marette, A, Mathieu, P, Lévesque, V, Bibeau, K, Larose, É, Després, JP
Metabolic syndrome and related disorders. 2019;(3):149-159
Abstract
BACKGROUND To assess the benefits of a 1-year lifestyle modification program on exercise capacity and diastolic function in men with left ventricular (LV) diastolic dysfunction (LVDD) and coronary artery disease (CAD), according to glucose tolerance status. METHODS Fifty-three men (62 ± 8 years; BMI: 27.3 ± 3.5 kg/m2) with LVDD and CAD were enrolled in a 1-year lifestyle modification program based on dietary management and increased physical activity. Patients were classified by using a 75 grams oral glucose tolerance test as having normal glucose tolerance (n = 16), prediabetes (n = 23), or type 2 diabetes mellitus (T2DM) (n = 14). Cardiac morphology and function, visceral fat, and cardiac fat depots were measured using magnetic resonance imaging, whereas exercise capacity [cardiorespiratory fitness (CRF)] (VO2peak) was assessed with a maximal treadmill test. RESULTS The 1-year lifestyle modification program was associated with reductions in body weight, and visceral and cardiac fat levels (all P < 0.05). CRF increased by 13% (24.9 ± 4.1 vs. 28.2 ± 4.8 mL O2/kg/min, P < 0.0001). Moreover, half of patients (53%) improved LV diastolic function in response to the lifestyle intervention. Multiple regression analyses revealed that age (partial R2 = 26.9, P < 0.0001) and presence of T2DM (partial R2 = 5.9, P = 0.04) were the stronger predictors of change in diastolic function, while favorable change in LV remodeling index was the best predictor of improvement in LV diastolic function after the lifestyle intervention (R2 = 21.9, P = 0.002). CONCLUSIONS Irrespective of glucose tolerance status, a 1-year lifestyle modification program in men with LVDD and CAD is associated with significant improvements in exercise capacity and LV diastolic function in more than half of patients.
2.
Interrelationship between diabetes mellitus and heart failure: the role of peroxisome proliferator-activated receptors in left ventricle performance.
Oikonomou, E, Mourouzis, K, Fountoulakis, P, Papamikroulis, GA, Siasos, G, Antonopoulos, A, Vogiatzi, G, Tsalamadris, S, Vavuranakis, M, Tousoulis, D
Heart failure reviews. 2018;(3):389-408
Abstract
Heart failure (HF) is a common cardiac syndrome, whose pathophysiology involves complex mechanisms, some of which remain unknown. Diabetes mellitus (DM) constitutes not only a glucose metabolic disorder accompanied by insulin resistance but also a risk factor for cardiovascular disease and HF. During the last years though emerging data set up, a bidirectional interrelationship between these two entities. In the case of DM impaired calcium homeostasis, free fatty acid metabolism, redox state, and advance glycation end products may accelerate cardiac dysfunction. On the other hand, when HF exists, hypoperfusion of the liver and pancreas, b-blocker and diuretic treatment, and autonomic nervous system dysfunction may cause impairment of glucose metabolism. These molecular pathways may be used as therapeutic targets for novel antidiabetic agents. Peroxisome proliferator-activated receptors (PPARs) not only improve insulin resistance and glucose and lipid metabolism but also manifest a diversity of actions directly or indirectly associated with systolic or diastolic performance of left ventricle and symptoms of HF. Interestingly, they may beneficially affect remodeling of the left ventricle, fibrosis, and diastolic performance but they may cause impaired water handing, sodium retention, and decompensation of HF which should be taken into consideration in the management of patients with DM. In this review article, we present the pathophysiological data linking HF with DM and we focus on the molecular mechanisms of PPARs agonists in left ventricle systolic and diastolic performance providing useful insights in the molecular mechanism of this class of metabolically active regiments.