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Published on: August 8, 2022
Hypertrophic nonobstructive cardiomyopathy: a precise assessment of hemodynamic characteristics and clinical
Insights
Hypertrophic cardiomyopathy patients show normal systolic function despite impaired relaxation and reduced unit muscle performance. Ventricular hypertrophy may be an adaptive response to maintain cardiac output.
Area of Science:
- Cardiology
- Physiology
Background:
- Hypertrophic cardiomyopathy (HCM) is a complex cardiac condition.
- Understanding the pathophysiology of HCM is crucial for patient management.
Purpose of the Study:
- To precisely assess left ventricular (LV) function in patients with hypertrophic nonobstructive cardiomyopathy (HNOCM).
- To elucidate the basic pathophysiology of HNOCM by comparing LV function with normal subjects.
Main Methods:
- Left ventricular function was assessed in 20 HNOCM patients and 22 normal subjects.
- Key hemodynamic parameters including end-diastolic pressure, end-diastolic stress, afterload, isovolumic indexes (peak positive dP/dt, (dP/dt)/DP40), ejection phase indexes (ejection fraction), end-systolic stress-volume ratio, and LV minute work were measured.
Main Results:
- HNOCM patients had high end-diastolic pressure but normal end-diastolic stress and reduced afterload.
- Isovolumic and ejection phase indexes of contractility were normal, but end-systolic stress-volume ratio was significantly reduced.
- LV relaxation was abnormal (low peak negative dP/dt, prolonged time constant T), and LV stiffness was increased.
- Unit muscle performance was significantly reduced (49% of normal), despite a normal LV minute work index.
Conclusions:
- The study suggests impaired unit muscle contraction in HNOCM, leading to inadequate whole ventricle contraction.
- Ventricular hypertrophy in HNOCM may be an adaptive mechanism to maintain normal systolic function by increasing muscle mass and reducing afterload.
Abstract:
A precise assessment of left ventricular function was performed in 20 patients with hypertrophic nonobstructive cardiomyopathy to elucidate the basic pathophysiology, and the data were compared with those in 22 normal subjects. Whereas end-diastolic pressure was high in those with cardiomyopathy, a more accurate index of preload, end-diastolic stress, did not differ from normal value. Afterload was about half the normal value. Both isovolumic indexes [peak positive dP/dt and (dP/dt)/DP40] and ejection phase indexes of contractility (ejection fraction) were in the normal range; however, the end-systolic stress volume ratio was significantly reduced (43% of the normal value). Although the left ventricular minute work index was in the normal range, the unit muscle performance (minute work/mass) was very low (49%). An abnormality of left ventricular relaxation was demonstrated by low peak negative dP/dt (56%) and prolonged time constant T (191%), and a stiff left ventricle was demonstrated by a high diastolic elastic stiffness constant (129%). These observations suggest that the contraction of a unit muscle is inappropriate to produce an adequate contraction of the whole ventricle, and that hypertrophy might be an adaptive process to maintain normal systolic function by increasing mass and reducing afterload.
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