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Diltiazem reverses tissue Doppler velocity abnormalities in pre-clinical hypertrophic cardiomyopathy
1Launceston General Hospital, P.O. Box 98, Launceston, Tasmania, Australia. don.mctaggart1@bigpond.com
Insights
Diltiazem treatment improved cardiac function in pre-clinical hypertrophic cardiomyopathy patients. Early diastolic velocities normalized, and systolic velocities improved, suggesting a preventative role for diltiazem.
Area of Science:
- Cardiology
- Genetics
Background:
- Pre-clinical hypertrophic cardiomyopathy (HCM) exhibits systolic and diastolic dysfunction detectable by tissue Doppler imaging.
- These functional abnormalities worsen with left ventricular hypertrophy development.
Purpose of the Study:
- To investigate if diltiazem can reverse cardiac function abnormalities in pre-clinical HCM.
Main Methods:
- Six adults with a cardiac myosin binding protein-C gene mutation (pre-clinical HCM) received 240mg diltiazem daily.
- Tissue Doppler imaging assessed mitral annular velocities (systolic and early diastolic) before and after 8 weeks of treatment.
Main Results:
- Significant improvement in both peak systolic and early diastolic velocities was observed.
- Early diastolic velocities returned to normal, and most systolic velocities also normalized.
Conclusions:
- Diltiazem may prevent functional abnormalities and potentially left ventricular hypertrophy in pre-clinical HCM.
- This suggests a therapeutic role for diltiazem in early-stage HCM.
Background:
Abnormalities in systolic and diastolic function shown by tissue Doppler imaging have been shown to be present in patients with hypertrophic cardiomyopathy who do not yet show clinical or echocardiographic evidence of the disease. These become more marked as left ventricular hypertrophy develops. We attempted to show that these abnormalities could be reversed by treatment with diltiazem.
Methods And Results:
Six adults, who were carriers of a mutation involving the cardiac myosin binding, protein-C gene and who did not show clinical electrocardiographic or echocardiographic evidence of the disease were given a dose of 240mg of diltiazem daily. Tissue Doppler peak systolic and early diastolic velocities at the lateral mitral annulus were examined before treatment and at a mean of 8 weeks after starting treatment. Improvement in both parameters occurred with early diastolic velocities returning to normal and most systolic velocities also becoming normal.
Conclusion:
Diltiazem may have a role in helping to prevent abnormalities of function and perhaps the development of left ventricular hypertrophy in patients with pre-clinical hypertrophic cardiomyopathy.
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