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[Progression from hypertrophic obstructive cardiomyopathy to dilated cardiomyopathy. Apropos of 4 cases]
C Bourmayan1, M Desnos, J Baragan
1Service de cardiologie, hôpital Boucicaut, Paris.
Insights
Hypertrophic obstructive cardiomyopathy can progress to dilated cardiomyopathy over years, worsening symptoms and leading to adverse outcomes. Obstruction signs resolve as the heart chambers dilate and function declines.
Area of Science:
- Cardiology
- Cardiovascular Medicine
- Clinical Medicine
Background:
- Hypertrophic obstructive cardiomyopathy (HOCM) is a complex cardiac condition.
- Understanding its natural progression is crucial for patient management.
Observation:
- This study reports on four cases of HOCM.
- The patients were monitored over extended periods, up to 20 years.
Findings:
- All four cases showed progression from HOCM to dilated cardiomyopathy.
- This transition was associated with clinical worsening, including two deaths and atrial fibrillation in three patients.
- Key signs of intraventricular obstruction, such as systolic murmurs and pressure gradients, resolved as left heart chambers dilated, ventricular wall motion decreased, and the ventricular wall thinned, without changes in myocardial mass.
Implications:
- The findings highlight a potential, severe long-term evolution of HOCM.
- This progression necessitates long-term monitoring and management strategies for affected individuals.
- Further research into the mechanisms driving this transition may reveal new therapeutic targets.
Abstract:
Four cases of hypertrophic obstructive cardiomyopathy diagnosed on clinical, phonomechanographic, echocardiographic and haemodynamic criteria progressing to dilated cardiomyopathy are reported. This evolution was observed over a number of years (up to 20 years) and was accompanied by a clinical aggravation in all cases with 2 deaths and atrial fibrillation in 3 of the 4 cases. The signs of intraventricular obstruction [systolic murmur, bulge on the carotid pulse tracing, systolic anterior motion of the mitral valve (SAM) and intraventricular pressure gradient] disappeared as the left heart chambers dilated with a reduction in ventricular wall motion and parietal thinning but no change in myocardial mass.