Treatment With Treprostinil and Metformin Normalizes Hyperglycemia and Improves Cardiac Function in Pulmonary Hypertension Associated With Heart Failure With Preserved Ejection Fraction

Arterioscler Thromb Vasc Biol. 2020 Jun;40(6):1543-1558. doi: 10.1161/ATVBAHA.119.313883. Epub 2020 Apr 9.

Abstract

Objective: Pulmonary hypertension (PH) due to left heart disease (group 2), especially in the setting of heart failure with preserved ejection fraction (HFpEF), is the most common cause of PH worldwide; however, at present, there is no proven effective therapy available for its treatment. PH-HFpEF is associated with insulin resistance and features of metabolic syndrome. The stable prostacyclin analog, treprostinil, is an effective and widely used Food and Drug Administration-approved drug for the treatment of pulmonary arterial hypertension. While the effect of treprostinil on metabolic syndrome is unknown, a recent study suggests that the prostacyclin analog beraprost can improve glucose intolerance and insulin sensitivity. We sought to evaluate the effectiveness of treprostinil in the treatment of metabolic syndrome-associated PH-HFpEF. Approach and Results: Treprostinil treatment was given to mice with mild metabolic syndrome-associated PH-HFpEF induced by high-fat diet and to SU5416/obese ZSF1 rats, a model created by the treatment of rats with a more profound metabolic syndrome due to double leptin receptor defect (obese ZSF1) with a vascular endothelial growth factor receptor blocker SU5416. In high-fat diet-exposed mice, chronic treatment with treprostinil reduced hyperglycemia and pulmonary hypertension. In SU5416/Obese ZSF1 rats, treprostinil improved hyperglycemia with similar efficacy to that of metformin (a first-line drug for type 2 diabetes mellitus); the glucose-lowering effect of treprostinil was further potentiated by the combined treatment with metformin. Early treatment with treprostinil in SU5416/Obese ZSF1 rats lowered pulmonary pressures, and a late treatment with treprostinil together with metformin improved pulmonary artery acceleration time to ejection time ratio and tricuspid annular plane systolic excursion with AMPK (AMP-activated protein kinase) activation in skeletal muscle and the right ventricle.

Conclusions: Our data suggest a potential use of treprostinil as an early treatment for mild metabolic syndrome-associated PH-HFpEF and that combined treatment with treprostinil and metformin may improve hyperglycemia and cardiac function in a more severe disease.

Keywords: glucose intolerance; metabolic syndrome; metformin; treprostinil.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • AMP-Activated Protein Kinases / drug effects
  • AMP-Activated Protein Kinases / physiology
  • Animals
  • Antihypertensive Agents
  • Diet, High-Fat
  • Epoprostenol / analogs & derivatives*
  • Epoprostenol / therapeutic use
  • Heart / drug effects
  • Heart / physiopathology
  • Heart Failure / complications*
  • Heart Failure / drug therapy
  • Heart Failure / physiopathology
  • Hyperglycemia / drug therapy*
  • Hypertension, Pulmonary / drug therapy*
  • Hypertension, Pulmonary / etiology
  • Hypertension, Pulmonary / physiopathology
  • Hypoglycemic Agents
  • Insulin Resistance
  • Male
  • Metabolic Syndrome
  • Metformin / therapeutic use*
  • Mice
  • Mice, Inbred C57BL
  • Obesity / etiology
  • Obesity / physiopathology
  • Rats
  • Receptors, Leptin / genetics
  • Stroke Volume / physiology*

Substances

  • Antihypertensive Agents
  • Hypoglycemic Agents
  • Receptors, Leptin
  • Metformin
  • Epoprostenol
  • AMP-Activated Protein Kinases
  • treprostinil