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Pathological features of hypertrophic cardiomyopathy without asymmetrical septal hypertrophy
Insights
Hypertrophic cardiomyopathy without asymmetrical septal hypertrophy shows enlarged myocytes but not increased cell numbers. Myocardial disarray and fibrosis patterns are consistent across hypertrophic cardiomyopathy types.
Area of Science:
- Cardiovascular Pathology
- Cardiac Histology
Background:
- Hypertrophic cardiomyopathy (HCM) is a complex cardiac disease.
- Asymmetrical septal hypertrophy (ASH) is a common feature of HCM.
- Understanding cellular changes in HCM without ASH is crucial.
Observation:
- Hearts with HCM without ASH showed similar myocyte counts and interstitial space in the septum and posterior wall.
- In contrast, HCM with ASH exhibited more myocytes in the septum.
- Myocyte size was significantly increased in HCM without ASH compared to normal hearts.
Findings:
- HCM without ASH does not increase the number of transmural myocytes.
- Myocardial fiber disarray and fibrosis distribution were similar in HCM with and without ASH.
- Cellular hypertrophy, not hyperplasia, characterizes HCM without ASH.
Implications:
- These findings differentiate HCM subtypes based on cellular morphology.
- Clarifies the pathological mechanisms in HCM without ASH.
- May inform diagnostic criteria and therapeutic strategies for specific HCM presentations.
Abstract:
In a heart with hypertrophic cardiomyopathy without asymmetrical septal hypertrophy the number of transmural myocytes, the mean size of myocytes, and the percentage area of interstitial space were similar in the ventricular septum and left ventricular posterior wall, whereas in a reported series of 14 hearts with hypertrophic cardiomyopathy with asymmetrical septal hypertrophy the number of transmural myocytes was greater in the ventricular septum than in the left ventricular posterior wall. In hearts with hypertrophic cardiomyopathy without asymmetrical septal hypertrophy the mean size of myocytes was significantly greater than that of normal hearts, but the number of transmural myocytes was not increased. The extent and distribution pattern of myocardial fibre disarray and fibrosis in the left ventricle were similar in hearts with hypertrophic myopathy whether or not asymmetrical septal hypertrophy was present.