Cardiac remodeling and myocardial dysfunction in obese spontaneously hypertensive rats
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Key result
Obese spontaneously hypertensive rats exhibited impaired left ventricular ejection fraction (46.2% vs 59.6%) and increased end-diastolic pressure compared to normotensive controls.
Population
Obese spontaneously hypertensive rats, lean spontaneously hypertensive rats, and normotensive controls
Comparison
Obese spontaneously hypertensive rat model vs Lean spontaneously hypertensive rats and…
Design
Preclinical
Authors
Discussion
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Implication
Hypothesis-generating in obese hypertensive rat models; leaves open whether findings translate to human LV remodeling.
Structured PICO
P
Population
26 male rats (8 obese spontaneously hypertensive, 8 lean spontaneously hypertensive, 10 normotensive controls) evaluated at 38-39 weeks of age for cardiac remodeling and function.
E
Exposure
Obese spontaneously hypertensive rat model (SHR-ob)
C
Comparator
Lean spontaneously hypertensive rats (SHR-lean) and normotensive controls (Ctr)
O
Outcome
Left ventricular function (assessed by cardiac magnetic resonance imaging and invasive LV-pressure measurements), LV-interstitial fibrosis, and protein levels of PLB, Serca2a, GLUT1, and GLUT4surrogate
Main Result
Absolute Event Rate: 46.2% vs 59.6%
p-value: p=0.007
In a hypertensive rat model, the addition of metabolic syndrome and obesity aggravates diastolic dysfunction and promotes progression toward systolic dysfunction.
Limitations
- Sprague Dawley rats do not represent the most appropriate control for the SHR-lean rats, requiring precaution in interpreting some comparisons.
Cite This Study
Linz et al. (2012) studied Hypertension, obesity, and metabolic syndrome (animal model) (n=26). Obesity and metabolic syndrome (SHR-ob phenotype) vs. Normotensive controls (Ctr) and lean spontaneously hypertensive rats (SHR-lean) was evaluated on Left ventricular ejection fraction (p=0.007). Obese spontaneously hypertensive rats exhibited impaired left ventricular ejection fraction (46.2% vs 59.6%) and increased end-diastolic pressure compared to normotensive controls.
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