Related Experiment Videos
Left ventricular function in experimental volume overload hypertrophy
B A Carabello1, K Nakano, W Corin
1Department of Medicine, Medical University of South Carolina, Charleston 29425.
Insights
Severe chronic volume overload from mitral regurgitation leads to impaired left ventricular function. This study demonstrates that prolonged, significant volume overload causes left ventricular dysfunction in experimental models.
Area of Science:
- Cardiovascular Physiology
- Cardiac Remodeling
- Heart Failure Research
Background:
- The impact of volume overload hypertrophy on left ventricular function remains debated.
- Previous experimental models often involved mild or short-term overload, yielding paradoxical results of normal function.
Purpose of the Study:
- To investigate left ventricular function in a model of severe, chronic experimental volume overload.
- To clarify the effects of sustained severe volume overload on contractile function.
Main Methods:
- A model of severe chronic mitral regurgitation was created in experimental subjects.
- Left ventricular function was assessed before and 3 months after inducing mitral regurgitation.
- Measurements included end-diastolic volume, left ventricular mass, ejection fraction, and stress-volume relationships.
Main Results:
- Severe mitral regurgitation (64% overload) was maintained for 3 months.
- Significant left ventricular hypertrophy occurred (36% increase in mass).
- All measured indicators of left ventricular function, including ejection fraction, were significantly reduced.
Conclusions:
- Severe, chronic volume overload, as induced by mitral regurgitation, leads to significant left ventricular dysfunction.
- This study resolves controversy by demonstrating impaired contractile function under sustained, severe volume overload conditions.
Abstract:
Left ventricular function in volume overload hypertrophy is controversial. In humans, chronic severe volume overload eventually results in left ventricular dysfunction; paradoxically, experimental volume overload hypertrophy has nearly always been associated with normal left ventricular function. However, in most cases, experimental volume overload hypertrophy has either been mild or only present for a short duration. To help resolve the issue of contractile function in volume overload hypertrophy, we examined ventricular function in a recently described model of severe chronic experimental mitral regurgitation. Left ventricular function was measured before and 3 mo after the creation of severe mitral regurgitation (averaged regurgitant fraction 0.64 +/- 0.04). At 3 mo end-diastolic volume had increased from 78 +/- 5 to 114 +/- 7 ml (P less than 0.01). Significant left ventricular hypertrophy had occurred with an increase in the left ventricular weight-to-body weight ratio from 3.84 +/- 0.2 to 5.22 +/- 0.2 (P less than 0.01). All indicators of left ventricular function (ejection fraction, the end ejection stress-volume relationship, this relationship corrected for eccentric hypertrophy, and mean velocity of circumferential fiber shortening at a common stress) were reduced at 3 mo. Our study produced 64% volume overload which was maintained for 3 mo at which time there was a 36% increase in left ventricular mass. This amount of volume overload of this duration produced significant left ventricular dysfunction.