Objective
The aim of this study was to noninvasively quantify global left ventricular (LV) contraction and relaxation, and to investigate their relationship in normal, hypertrophic, and failing myocardium.
Methods
Fifty patients with hypertensive LV hypertrophy (LVH) (LVH group), 50 patients with dilated cardiomyopathy (DCM) (DCM group), and 50 normal subjects (control group) had echocardiographic evaluations. Global LV peak systolic strain (PSS) and peak relaxation rate (PRR) during early diastole were analyzed by speckle-tracking strain and strain rate imaging in the longitudinal and circumferential directions.
Results
Both global PSS and PRR were reduced in the LVH group in the longitudinal direction. In the circumferential direction, global PSS was maintained and global PRR was reduced in the LVH group. The reductions in both global PSS and PRR were more pronounced in both directions in the DCM group compared with the other 2 groups. Global PSS correlated strongest with global PRR among the clinical and echocardiographic variables, which exhibited the best fit with exponential regressions in both the longitudinal and circumferential directions in all subjects (longitudinal: y = 0.15e −0.10x , r 2 = 0.75; circumferential: y = 0.21e −0.09x , r 2 = 0.76, P < .01, respectively). Multiple regression analysis indicated that global PSS was the most powerful determinant of global PRR in both longitudinal and circumferential directions.
Conclusion
Global LV function quantified using speckle-tracking echocardiography revealed strong coupling of LV contraction to relaxation sequentially from normal to failing myocardium, regardless of their heterogeneous pathophysiology. In addition, the extent of myocardial systolic shortening was the most powerful independent contributor of LV relaxation in both the longitudinal and circumferential directions. These results strongly indicate that LV myocardial systolic contraction directly regulates its relaxation.
Congestive heart failure is clinically classified as systolic or diastolic heart failure on the basis of left ventricular (LV) ejection fraction. It has been recognized that the cause of the initial structural abnormalities of the left ventricle contributes significantly to the development of systolic or diastolic heart failure. LV hypertrophy (LVH) can contribute to LV relaxation abnormalities even if the LV ejection fraction is preserved, whereas dilated cardiomyopathy (DCM) typically has reduced LV systolic function at initial presentation.
Conversely, prior studies have demonstrated that LV relaxation occurs in a series of energy-consuming steps and is physiologically coupled to contraction, regardless of the cause of their respective structural abnormalities. Although underlying mechanisms regulating myocardial relaxation during early diastole are complex, it has been well recognized that increased contractility produces heightened systolic shortening of elastic structures with creation of more prediastolic potential energy that is released during isovolumic relaxation. Helmes et al assessed myocyte restoring force by measuring the velocity of recoil during the early phase of diastole in isolated unloaded skinned myocytes and demonstrated that the velocity of sarcomere relengthening is tightly correlated with the amplitude of the sarcomere shortening, as expected for a simple spring obeying Hooke’s law.
Speckle-tracking echocardiography is a new approach to quantify global and segmental LV deformation and its speed (ie, strain and strain rate) separately from longitudinal and circumferential directions. Accordingly, we hypothesize that speckle-tracking strain and strain rate imaging is capable of accurately quantifying global LV myocardial systolic shortening and relaxation, and their strong coupling in normal, hypertrophic, and failing myocardium.
Materials and Methods
Study Population
Fifty patients with hypertensive LVH (LVH group), 50 patients with DCM (DCM group), and 50 age- and gender-matched normal subjects (control group) were enrolled in this study. All patients with LVH exhibited interventricular septal or posterior wall thickness ≥ 12 mm and preserved LV ejection fraction of at least 45%. None of the subjects in the LVH group had asynergic LV wall motion abnormalities by conventional visual assessment. Although 10 patients with LVH had chest symptoms, all of them had negative exercise stress test results. The DCM group was composed of 36 patients with idiopathic DCM and 14 patients with non-idiopathic DCM. All patients with DCM underwent coronary angiography to exclude the presence of coronary artery disease. Patients with mild DCM and an ejection fraction greater than 45% were excluded. Subjects with atrial flutter/fibrillation, ventricular pacing, valvular heart disease, coronary artery disease, and suboptimal images (2% of the subjects) were also excluded from this study. The control group had no history of cardiopulmonary disease, no diabetes, no hypertension, normal electrocardiography, and normal echocardiography. Written informed consent was obtained from all patients, and the protocol was approved for use by the Human Studies Subcommittee of Mie University Graduate School of Medicine.
Echocardiography
All subjects were examined with a complete transthoracic echocardiography using a Vivid 7 ultrasound system (GE-Vingmed Ultrasound AS, Horten, Norway). Arm-cuff blood pressure measurements were performed at the beginning of each echocardiographic study for all subjects. LV volume and ejection fraction were assessed by biplane Simpson’s rule. LV mass index was calculated on the basis of the area–length method. Systemic vascular resistance index (dynes per s/cm −5 ·m 2 ) was calculated as follows: systemic vascular resistance index = (mean arterial blood pressure) × 80/(stroke volume × heart rate)/(body surface area). Ratio of peak early to late diastolic transmitral flow velocity (mitral E/A) was calculated by pulsed Doppler echocardiography. Digital tissue Doppler cine loops from 3 consecutive beats were obtained from apical 4-, 2-, and long-axis for off-line analysis of averaged peak early diastole mitral annular velocity (Ea) at 6 corner sites (inferior-septum, lateral, inferior, anterior, antero-septum, and posterior site) in the mitral annulus. The E/Ea ratio was calculated as a Doppler parameter reflecting LV diastolic pressure. All Doppler values represent the average of 3 beats.
Strain and Strain Rate Imaging
Digital routine B-mode gray-scale cine-loops from 3 consecutive beats were obtained from the apical 4-, 2-, long-axis, and mid-LV short-axis views for off-line analysis of strain and strain rate using commercially available software (EchoPAC, GE-Vingmed). A frame rate of 80 ± 21 Hz was used for this study. To generate myocardial strain and strain rate data for evaluating myocardial dynamics, a line was loosely traced along the LV endocardium at the frame in which it was best defined. On the basis of this line, the myocardium was automatically tracked by the algorithm and divided into 6 segments in the apical 4-, 2-, long-axis, and mid-LV short-axis views, respectively ( Figure 1 , top ). Segmental peak systolic strain (PSS) and peak relaxation rate (PRR) during early diastole obtained from time-strain and time-strain rate curves were defined as the indices of regional LV myocardial systolic shortening and relaxation, respectively ( Figure 1 , bottom ).
Global strain and strain rate data were calculated for the entire U-shaped length of the LV myocardium from apical views for longitudinal function and circular length from parasternal short-axis views for circumferential function.
Global strain ( % ) = [ L ( end – systole ) – L ( end – diastole ) ] / L ( end – diastole ) × 100 %
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