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Patterns of diastolic dysfunction in left ventricular hypertrophy
1National Heart Hospital, London.
Insights
Different measurements of diastolic function were assessed in patients with left ventricular hypertrophy. The study found at least four distinct abnormalities, suggesting no single underlying cause for diastolic dysfunction.
Area of Science:
- Cardiology
- Echocardiography
- Diastolic Function Assessment
Background:
- Left ventricular hypertrophy (LVH) can impact cardiac diastolic function.
- Assessing diastolic dysfunction requires understanding various physiological parameters.
Purpose of the Study:
- To compare the sensitivity and interrelations of different diastolic function measurements in LVH patients.
- To identify distinct patterns of diastolic dysfunction in LVH.
Main Methods:
- Digitized M-mode echocardiography, Doppler echocardiography, and apexcardiography were used.
- Measurements included isovolumic relaxation time, filling intervals, and velocity parameters.
- Data from 50 LVH patients were compared to 20 age-matched controls.
Main Results:
- Most diastolic function measurements were significantly different in LVH patients compared to controls.
- The 'a' wave height on apexcardiogram was the most sensitive indicator; peak dimension increase rate was least sensitive.
- Correlations between parameters were weak, suggesting independent physiological bases.
Conclusions:
- Abnormal diastolic function in LVH is not a single entity but comprises at least four discrete abnormalities.
- These include prolonged isovolumic relaxation, incoordination, reduced rapid filling, and increased 'a' wave amplitude.
- These abnormalities can occur individually or in combination.
Abstract:
The relative sensitivities of and interrelations between different measurements of diastolic function were studied in 50 patients with left ventricular hypertrophy diagnosed on anatomical grounds. Isovolumic relaxation time, the interval from minimum cavity dimension to mitral valve opening and relative dimension increase during this period, and the peak rate of dimension increase and wall thinning during rapid ventricular filling were measured by digitised M mode echocardiography. The relative heights of peak early diastolic and atrial velocities (a/E) and the time for decline of early diastolic velocity to half its peak value (velocity half time) were measured on continuous wave and pulsed Doppler and the relative height of the "a" wave was measured by apexcardiogram. All sets of values except those of the interval from minimum dimension to mitral opening were unimodally distributed, and all differed significantly from those in 20 age matched controls. The relative height of the "a" wave on the apexcardiogram (90% values were abnormal) was the most sensitive method of studying left ventricular diastolic function and peak rate of dimension increase was the least sensitive. Though none of the correlations was high, there were individual associations between peak rate of dimension increase, a/E, peak wall thinning rate, and velocity half time, and independently between delay in mitral valve opening and dimension change during this period. Other values seemed to be independent of one another, suggesting a different physiological basis. It is concluded that these various abnormal values do not reflect a single underlying disturbance of diastolic function. There are at least four possible discrete abnormalities: prolongation of isovolumic relaxation; incoordination during isovolumic relaxation; reduced rate of rapid filling; and an increase in the relative amplitude of the "a" wave probably caused by increased passive stiffness. These may be present singly or in combination in any patient.