Quantitative Assessment of Left Ventricular Diastolic Stiffness in Man

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Abstract
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 (P1, D1) and peak (P2, D2) of left atrial mechanical systole. In addition, left ventricular volumes, V1 and V2, were calculated from D1 and D2 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.