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A Rat Model of Pressure Overload Induced Moderate Remodeling and Systolic Dysfunction as Opposed to Overt Systolic Heart Failure
Published on: April 30, 2020
Does load-induced ventricular hypertrophy progress to systolic heart failure?
Kambeez Berenji1, Mark H Drazner, Beverly A Rothermel
1Div. of Cardiology, Dept. of Internal Medicine, Univ. of Texas Southwestern Medical Center, Dallas, TX 75390-9047, USA.
Insights
Ventricular hypertrophy, an enlargement of heart muscle, can signal increased risk for heart failure. This review explores if hypertrophy causes heart failure alone or requires other conditions like coronary artery disease.
Area of Science:
- Cardiology
- Pathophysiology
- Heart Failure Research
Background:
- Ventricular hypertrophy (VH) is a cardiac response to stress, initially thought compensatory.
- Studies link VH to increased risk of chronic heart failure, suggesting maladaptive aspects.
- The role of comorbid conditions in VH-associated systolic failure remains unclear.
Purpose of the Study:
- To investigate whether ventricular hypertrophy alone leads to systolic dysfunction.
- To determine the contribution of comorbid diseases, such as coronary artery disease, to heart failure progression in the presence of VH.
- To synthesize current knowledge on the relationship between VH and systolic failure.
Main Methods:
- Review of epidemiologic studies.
- Analysis of preclinical animal experiments.
- Examination of clinical trial data.
Main Results:
- Ventricular hypertrophy is a known risk marker for heart failure.
- Coronary artery disease shares risk factors with VH and can cause systolic dysfunction.
- The independent progression of VH to systolic dysfunction is not fully understood.
Conclusions:
- Further research is needed to elucidate the direct causal link between VH and systolic dysfunction.
- Understanding the interplay between VH and comorbid conditions is crucial for predicting heart failure progression.
- Clarifying the independent role of VH in heart failure is essential for targeted therapeutic strategies.
Abstract:
Ventricular hypertrophy develops in response to numerous forms of cardiac stress, including pressure or volume overload, loss of contractile mass from prior infarction, neuroendocrine activation, and mutations in genes encoding sarcomeric proteins. Hypertrophic growth is believed to have a compensatory role that diminishes wall stress and oxygen consumption, but Framingham and other studies established ventricular hypertrophy as a marker for increased risk of developing chronic heart failure, suggesting that hypertrophy may have maladaptive features. However, the relative contribution of comorbid disease to hypertrophy-associated systolic failure is unknown. For instance, coronary artery disease is induced by many of the same risk factors that cause hypertrophy and can itself lead to systolic dysfunction. It is uncertain, therefore, whether ventricular hypertrophy commonly progresses to systolic dysfunction without the contribution of intervening ischemia or infarction. In this review, we summarize findings from epidemiologic studies, preclinical experiments in animals, and clinical trials to lay out what is known-and not known-about this important question.
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