Table 3

Therapeutic Interventions in Metabolic Heart Disease

InterventionMechanismsEffects
Surgical or behavioral with weight lossDecrease in blood volume, stroke volume, and cardiac output
Increase in systemic vascular resistance in normotensive subjects, but no change or decrease in hypertensive subjects.
Decrease in pulmonary artery, RV, and right atrial pressures
Decrease in cardiac preload
Improvement in metabolic control (decrease in HbA1c, insulin resistance, and triglyceridemia)
Decrease in neurohormonal activation
Reduced pericardial fat
Decrease in LV mass and wall thicknesses
Improvement in LV diastolic and systolic performance
Improvement in cardiorespiratory fitness
Decrease in LA size
Reduced AF burden
Behavioral without intentional weight lossImprovement in intracellular calcium handling and insulin resistance due to increase in skeletal muscle glucose uptake and metabolismImprovement in only diastolic function or both diastolic and systolic function, LV torsion in T2DM, and cardiac synchrony in obesity
Less apparent improvement in aerobic fitness
Pharmacological for glycemic controlBetter metabolic control with decrease in HbA1c and glycemiaImprovement in only diastolic function, both systolic and diastolic function, or no improvements demonstrated
Antifibrotic with spironolactoneInhibition of aldosterone effects, especially promotion of fibrosisImprovement in LV systolic and diastolic function, reduction in LV mass, and amelioration of cIB and serological fibrosis markers in metabolic syndrome and obesity
Improvements in LV filling and cIB and no changes in serological fibrosis markers and T1 mapping in T2DM

AF = atrial fibrillation; HbA1c = glycosylated hemoglobin; T2DM = type 2 diabetes mellitus; other abbreviations as in Table 2.