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Delayed left ventricular untwisting in hypertrophic cardiomyopathy
Bas M van Dalen1, Floris Kauer, Michelle Michels
1Department of Cardiology, Thoraxcenter, Erasmus University Medical Center, Rotterdam, The Netherlands.
Insights
Left ventricular (LV) untwisting is delayed in hypertrophic cardiomyopathy (HCM) patients, contributing to diastolic dysfunction. This study assessed LV untwisting using speckle-tracking echocardiography in HCM patients and controls.
Area of Science:
- Cardiology
- Biomedical Engineering
- Physiology
Background:
- Hypertrophic cardiomyopathy (HCM) frequently involves left ventricular (LV) diastolic dysfunction, though its mechanisms are not fully understood.
- Targeting the root causes of LV diastolic dysfunction is crucial for effective therapeutic strategies.
- Assessing LV diastolic untwisting may offer insights into the mechanisms of diastolic dysfunction.
Purpose of the Study:
- To investigate and characterize left ventricular (LV) untwisting patterns in patients with hypertrophic cardiomyopathy (HCM).
- To compare LV untwisting parameters between HCM patients and healthy control subjects.
Main Methods:
- Speckle-tracking echocardiography was employed to assess LV untwisting parameters.
- The study included 75 consecutive patients diagnosed with HCM and 75 age- and sex-matched healthy control subjects.
Main Results:
- Patients with HCM exhibited significantly lower untwisting at 5%, 10%, and 15% of diastole compared to controls (P < .001).
- Key parameters like peak diastolic untwisting velocity and untwisting rate from peak systolic twist to mitral valve opening were reduced in HCM patients (P < .05 and P < .01, respectively).
- Time-to-peak diastolic untwisting velocity was prolonged in HCM, and untwisting rates correlated with diastolic dysfunction severity.
Conclusions:
- Left ventricular (LV) untwisting is demonstrably delayed in patients with hypertrophic cardiomyopathy (HCM).
- This delay in LV untwisting is a likely significant contributor to the observed diastolic dysfunction in HCM.
Background:
Almost all patients with hypertrophic cardiomyopathy (HCM) have some degree of left ventricular (LV) diastolic dysfunction. Nevertheless, the pathophysiology remains incompletely characterized. Conceptually, an ideal therapeutic agent should target the underlying mechanisms that cause LV diastolic dysfunction. Assessment of diastolic LV untwisting could potentially be helpful to gain insight into the mechanism of diastolic dysfunction. The purpose of this study was to investigate LV untwisting in patients with HCM and control subjects.
Methods:
LV untwisting parameters were assessed using speckle-tracking echocardiography in 75 consecutive patients with HCM and compared with those from 75 healthy control subjects.
Results:
Untwisting at 5%, 10%, and 15% of diastole was lower in patients with HCM (all P values < .001) compared with control subjects. Peak diastolic untwisting velocity (-92 +/- 32 degrees/s vs -104 +/- 39 degrees/s, P < .05) and untwisting rate from peak systolic twist to mitral valve opening (MVO) (-37 +/- 20 degrees/s vs -46 +/- 22 degrees/s, P < .01) were lower, while the for diastolic duration normalized time-to-peak diastolic untwisting velocity (17 +/- 9% vs 13 +/- 9%, P < .05) was higher in patients with HCM. Untwisting rate from peak systolic twist to MVO was negatively correlated with the E/A ratio (R(2) = 0.15, P < .01). Peak diastolic untwisting velocity and untwisting rate from peak systolic twist to MVO were increased in mild but decreased in moderate and severe diastolic dysfunction compared with control subjects.
Conclusion:
LV untwisting is delayed in HCM, which probably significantly contributes to diastolic dysfunction.
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