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Parathyroid hormone accelerates decompensation following left ventricular hypertrophy
Hyeseon Cha1, Hyeon Joo Jeong, Seung Pil Jang
1Global Research Laboratory and Department of Life Science, Gwangju Institute of Science and Technology, Gwangju, Korea.
Experimental & Molecular Medicine
|November 6, 2009
Summary
Parathyroid hormone (PTH) treatment worsened heart failure in mice with left ventricular hypertrophy (LVH) after transverse aortic banding (TAB). PTH accelerated cardiac decompensation, increasing heart failure indicators and fibrosis.
Area of Science:
- Cardiology
- Endocrinology
- Molecular Biology
Background:
- Parathyroid hormone (PTH) previously demonstrated benefits in cardiac function post-myocardial infarction.
- Left ventricular hypertrophy (LVH) is a condition of increased cardiac workload.
Purpose of the Study:
- To investigate the effects of PTH treatment on compensated LVH induced by pressure overload.
- To determine if PTH exacerbates or ameliorates heart failure progression in a mouse model.
Main Methods:
- Induction of LVH in mice via transverse aortic banding (TAB).
- Treatment with PTH or saline for 2 weeks post-TAB.
- Assessment of cardiac function using echocardiography, histology, and molecular analysis after 4 weeks.
Main Results:
- PTH treatment led to more severe heart failure phenotypes, including reduced fractional shortening and increased left ventricular dimensions.
- Increased heart and lung weight-to-body weight ratios were observed in PTH-treated mice.
- Elevated markers of heart failure, fibrosis, and angiogenesis, along with SMAD2 phosphorylation, were noted in PTH-treated hearts.
Conclusions:
- PTH treatment appears to accelerate the decompensation of the left ventricle in the context of pressure overload.
- PTH may worsen cardiac function and promote adverse cardiac remodeling, leading to heart failure.
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