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Published on: November 28, 2018
Dynamic left ventricular dyssynchrony: a potential cause of no contractile reserve in patients with low-gradient
Patrizio Lancellotti1, Catherine Szymanski, Marie Moonen
1Department of Cardiology, University Hospital of Liège, Liège B-4000, Belgium. plancellotti@chu.ulg.ac.be
Insights
Dobutamine stress echocardiography revealed increased left ventricular (LV) dyssynchrony in a patient with low-gradient aortic stenosis (AS). This dyssynchrony, alongside ischemic cardiomyopathy, impacted stroke volume response.
Area of Science:
- Cardiology
- Cardiac Imaging
- Heart Failure
Background:
- Low-gradient aortic stenosis (AS) poses challenges in risk stratification.
- The role of left ventricular (LV) dyssynchrony in AS is not well understood.
- Dobutamine stress echocardiography (DSE) is a key tool for assessing AS severity and cardiac function.
Observation:
- A case study of a patient presenting with AS and significant LV dyssynchrony.
- DSE demonstrated a lack of contractile reserve.
- An increase in LV dyssynchrony was observed during DSE.
Findings:
- Reduced aortic valve area was attributed to severe AS and inadequate forward stroke volume from ischemic cardiomyopathy.
- LV dysfunction was likely multifactorial, including intrinsic myocardial dysfunction and afterload mismatch.
- Dynamic LV dyssynchrony emerged as a potential determinant of forward stroke volume response.
Implications:
- This case highlights the importance of evaluating LV dyssynchrony in patients with low-gradient AS.
- Understanding dyssynchrony may refine prognostic assessments and treatment strategies for AS.
- Further research is warranted to explore the interplay between AS, LV dyssynchrony, and ischemic cardiomyopathy.
Abstract:
Dobutamine stress echocardiography (DSE) has the potential to stratify patients with low-gradient aortic stenosis (AS) but little is known about ventricular dyssynchrony associated with AS. We report the case of a patient who presented AS associated with left ventricular (LV) dyssynchrony. A DSE was performed, which showed no contractile reserve but an increase in LV dyssynchrony. In this patient, the reduced aortic valve area was probably because of the association of inadequate forward stroke volume due to ischaemic cardiomyopathy and fixed severe AS. The cause of LV dysfunction may include a certain degree of intrinsic myocardial dysfunction due to ischaemic cardiomyopathy and afterload mismatch associated with dynamic LV dyssynchrony, which could be a determinant of forward stroke volume response.
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