Reduced First-Phase Ejection Fraction and Sustained Myocardial Wall Stress in Hypertensive Patients With Diastolic Dysfunction: A Manifestation of Impaired Shortening Deactivation That Links Systolic to Diastolic Dysfunction and Preserves Systolic Ejection Fraction

Abstract

Impaired shortening deactivation of cardiac myocytes could sustain myocardial contraction, preserving ejection fraction at the expense of diastolic dysfunction. We examined the relationship between first-phase ejection fraction (EF1), the fraction of left ventricular volume ejected from the start of systole to the time of the first peak in left ventricular pressure (corresponding to the time of maximal ventricular shortening) to the duration of myocardial contraction and diastolic function in patients with hypertension (n=163), and varying degrees of diastolic dysfunction. Left ventricular systolic pressure was estimated by carotid tonometry; time-resolved left ventricular cavity and wall volume were obtained by echocardiography with speckle wall tracking. Measurements were repeated after nitroglycerin, a drug known to influence ventricular dynamics, in a subsample (n=18) of patients. EF1 and time of onset of ventricular relaxation (as determined from the temporal pattern of myocardial wall stress) were independently correlated with diastolic relaxation as measured by tissue Doppler early diastolic mitral annular velocity (E', standardized regression coefficients 0.48 and -0.34 for EF1 and time of onset of ventricular relaxation, respectively, each P<0.001, irrespective of adjustment for age, sex, antihypertensive treatment, measures of afterload, and ventricular geometry) and with diastolic function measured by the ratio of transmitral Doppler early filling velocity (E) to E' (E/E', regression coefficients -0.34 and 0.34, respectively, each P<0.001). Nitroglycerin increased EF1, decreased time of onset of ventricular relaxation, and improved diastolic function (each P<0.05). Hypertensive patients with diastolic dysfunction exhibit reduced EF1 which may sustain myocardial contraction, preserving systolic ejection fraction at the expense of impaired diastolic function.

Keywords: blood pressure; diastole; echocardiography; hypertension; ventricular function.

Figure 1.

Endocardial volume curve (solid line) obtained by echo wall tracking, central aortic pressure waveform (dotted line) obtained by carotid tonometry, together with ejection-phase myocardial wall stress (dashed line), computed from the central aortic systolic pressure waveform and instantaneous left ventricular dimensions in a normotensive subject. Myocardial wall stress starts to fall at the first peak of central aortic pressure (T1), coinciding with peak aortic flow and maximal rate of ventricular shortening. First-phase ejection fraction (EF1) is percentage volume change between end diastole and T1. EF indicates ejection fraction; and MWS, myocardial wall stress.

Figure 2.

Total systolic ejection fraction (EF, gray bars) and first-phase ejection fraction (EF1, black bars; Figure 1) in 3 groups defined according to E/E′ (ratio of mitral valve Doppler early flow [E wave velocity] to tissue Doppler mitral annulus movement [E′ wave velocity]). Total EF was preserved and was similar between groups. EF1 was significantly lower in subjects with impaired diastolic function compared with those with preserved diastolic function.

Figure 3.

Typical myocardial wall stress traces in a subject with preserved systolic function and first-phase ejection fraction (EF1; solid line, E/E′=8.0, EF1=19.7%) and a subject with impaired diastolic function and reduced EF1 (dashed line, E/E′=16.6, EF1=14.8%) demonstrating longer time to onset of relaxation (TOR, dotted arrows) in the patient with diastolic dysfunction (TOR, 61.2% vs 22.0% of ejection duration). Both subjects had preserved ejection fraction (EF; 63.4% and 63.5%) and similar resting heart rate. E/E′ indicates ratio of mitral valve Doppler early flow (E wave velocity) to tissue Doppler mitral annulus movement (E′ wave velocity; and MWS, myocardial wall stress.