An approach to the quantitative assessment of left ventricular (LV) diastolic stiffness in man has been developed utilizing strip-chart recordings of simultaneous ultrasonic LV dimensions, LV pressure, and electrocardiogram (ECG). In 23 patients without regional abnormalities of contraction, LV pressure, and LV internal diameter (D = distance between endocardial surfaces of LV posterior wall and septum at the plane of the mitral valve) were determined at the onset (P 1 , D 1 ) and peak (P 2 , D 2 ) of left atrial mechanical systole. In addition, left ventricular volumes, V 1 and V 2 , were calculated from D 1 and D 2 using a regression formula for end-diastolic volume previously determined from biplane angiographic studies. This allowed calculation of ΔP/ΔD and ΔP/ΔV associated with the "a" wave of the LV pressure trace, and these ratios were utilized as measures of LV stiffness late in diastole. Patients with LV hypertrophy by standard ECG criteria had much greater late diastolic stiffness (11 patients, ΔP/ΔD = 6.1 ± 1.1 mm Hg/mm, ΔP/ΔV = 1.0 ± 0.2 mm Hg/cc) than those without LV hypertrophy (12 patients, ΔP/ΔD = 1.8 ± 0.2 mm Hg/mm, ΔP/ΔV = 0.29 ± 0.04 mm Hg/cc, P < 0.001 for each ratio). Comparison of the stiffness ratios showed significant variation among patients with different disease states. Thus, late diastolic stiffness was highest in patients with aortic stenosis (three patients, ΔP/ΔD = 8.9 ± 2.9 mm Hg/mm, ΔP/ΔV = 1.5 ± 0.5 mm Hg/cc), lowest in mitral stenosis (four patients, ΔP/ΔD = 1.5 ± 0.5 mm Hg/mm, ΔP/ΔV = 0.23 ± 0.06 mm Hg/cc), and intermediate in patients with aortic regurgitation (three patients, ΔP/ΔD = 4.8 ± 0.7 mm Hg/mm, ΔP/ΔV = 0.83 ± 0.12 mm Hg/cc) and mitral regurgitation (three patients, ΔP/ΔD = 3.2 ± 0.7 mm Hg/mm, ΔP/ΔV = 0.5 ± 0.1 mm Hg/cc). It is concluded that the quantitative evaluation of LV diastolic stiffness obtained by this approach correlates well with the presence or absence of LV hypertrophy and with the underlying pathophysiology.
Diastolic properties of the left ventricle (LV) are probably influenced by several factors, including completeness of ventricular relaxation, composition of the ventricular wall, and wall thickness. This study has utilized a combined ultrasonic and hemodynamic technique to examine the influence of LV posterior wall thickness at end diastole (h p ) on LV diastolic characteristics in 24 patients with various forms of heart disease. The slope of late diastolic LV pressure-diameter relations (ΔP/ΔD) was calculated and used as a measure of effective diastolic stiffness (S) late in diastole. S was normalized for average LV pressure during the interval of measurement (P) as S/P, called S N . LV end diastolic pressure (LVEDP), volume index (LVEDVI), and mass index (LVMI) were measured in each patient during the same study at which h p , S and S N were determined. The range of h p was 5.6 to 18.6 mm; it was highest in a patient with aortic stenosis, and lowest in those with mitral stenosis. Linear regression of h p against S, S N and LVEDP showed significant correlation, with r = 0.85, 0.75, and 0.74 respectively ( P < 0.001 for each regression analysis). Poor correlation was noted with LVEDVI, ΔP, and ΔD. Of 12 patients with LV hypertrophy (LVH) by ECG, four had normal h p (7.9 ± 1.0 mm) and eight had abnormal h p (13 ± 0.6 mm). Those with normal h p had nearly normal values for S (3.5 ± 0.5 mm Hg/mm) while those with abnormal h p showed significant increases in S (7.7 ± 1.5 mm Hg/mm), indicating that LVH may alter S only insofar as there is an associated increase in h p . Consistent with this was the observation that within the group of patients having increased LVMI, LVMI itself was a poor predictor of S ( r = 0.50, NS) while h p remained an excellent predictor of S ( r = 0.86, P < 0.001). In summary, this study suggests that wall thickness is an important determinant of left ventricular diastolic stiffness and pressure, and that wall thickness appears to predict diastolic stiffness independent of the presence or absence of LVH or increased LV mass.
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