Left Ventricular Twist Mechanics Research Articles

The Effects of Exercise Intensity vs. Metabolic State on the Variability and Magnitude of Left Ventricular Twist Mechanics during Exercise.

Increased left ventricular (LV) twist and untwisting rate (LV twist mechanics) are essential responses of the heart to exercise. However, previously a large variability in LV twist mechanics during exercise has been observed, which complicates the interpretation of results. This study aimed to determine some of the physiological sources of variability in LV twist mechanics during exercise. Sixteen healthy males (age: 22 ± 4 years, O2peak: 45.5 ± 6.9 ml∙kg-1∙min-1, range of individual anaerobic threshold (IAT): 32–69% of O2peak) were assessed at rest and during exercise at: i) the same relative exercise intensity, 40%peak, ii) at 2% above IAT, and, iii) at 40%peak with hypoxia (40%peak+HYP). LV volumes were not significantly different between exercise conditions (P > 0.05). However, the mean margin of error of LV twist was significantly lower (F2,47 = 2.08, P < 0.05) during 40%peak compared with IAT (3.0 vs. 4.1 degrees). Despite the same workload and similar LV volumes, hypoxia increased LV twist and untwisting rate (P < 0.05), but the mean margin of error remained similar to that during 40%peak (3.2 degrees, P > 0.05). Overall, LV twist mechanics were linearly related to rate pressure product. During exercise, the intra-individual variability of LV twist mechanics is smaller at the same relative exercise intensity compared with IAT. However, the absolute magnitude (degrees) of LV twist mechanics appears to be associated with the prevailing rate pressure product. Exercise tests that evaluate LV twist mechanics should be standardised by relative exercise intensity and rate pressure product be taken into account when interpreting results.

Interaction between left ventricular twist mechanics and arterial haemodynamics during localised, non-metabolic hyperaemia with and without blood flow restriction.

What is the central question of this study? Left ventricular (LV) twist is reduced when afterload is increased, but the meaning of this specific heart muscle response and its impact on cardiac output are not well understood. What is the main finding and its importance? This study shows that LV twist responds even when arterial haemodynamics are altered only locally, and without apparent change in metabolic (i.e. heat-induced) demand. The concurrent decline in cardiac output and LV twist during partial arterial occlusion despite the increased peripheral demand caused by heat stress suggests that LV twist may be involved in the protective sensing of heart muscle stress that can override the provision of the required cardiac output. Whether left ventricular (LV) twist and untwisting rate (LV twist mechanics) respond to localised, peripheral, non-metabolic changes in arterial haemodynamics within an individual's normal afterload range is presently unknown. Furthermore, previous studies indicate that LV twist mechanics may override the provision of cardiac output, but this hypothesis has not been examined purposefully. Therefore, we acutely altered local peripheral arterial haemodynamics in 11 healthy humans (women/men n=3/8; age 26±5years) by bilateral arm heating (BAH). Ultrasonography was used to examine arterial haemodynamics, LV twist mechanics and the twist-to-shortening ratio (TSR). To determine the arterial function-dependent contribution of LV twist mechanics to cardiac output, partial blood flow restriction to the arms was applied during BAH (BAHBFR ). Bilateral arm heating increased arm skin temperatures [change (Δ) +6.4±0.9°C, P<0.0001] but not core temperature (Δ-0.0±0.1°C, P>0.05), concomitant to increases in brachial artery blood flow (Δ 212±77ml, P<0.0001), cardiac output (Δ 495±487lmin(-1) , P<0.05), LV twist (Δ 3.0±3.5 deg, P<0.05) and TSR (Δ 3.3±1.3, P<0.05) but maintained carotid artery blood flow (Δ 18±147ml, P>0.05). Subsequently, BAHBFR reduced all parameters to preheating levels, except for TSR and heart rate, which remained at BAH levels. In conclusion, LV twist mechanics responded to local peripheral arterial haemodynamics within the normal afterload range, in part independent of TSR and heart rate. The findings suggest that LV twist mechanics may be more closely associated with intrinsic sensing of excessive pressure stress rather than being associated with the delivery of adequate cardiac output.

Rigid Body Rotation Is a Robust and Highly Reproducible Marker of Cardiac Dysfunction in Children and Young Adults with Heart Disease

Objective: Reversed left ventricular (LV) twist, so-called rigid body rotation (RBR), is a marker of cardiac dysfunction. Speckle tracking echocardiography (STE) is commonly used for the assessment of LV twist mechanics. Region of interest (ROI) width variability affects the reproducibility of strain measurements. The aim of this study was to investigate the effect of ROI width variability on the reproducibility of RBR patterns in children and young adults.

The impact of an experimentally induced increase in arterial blood pressure on left ventricular twist mechanics.

The effects of isometric hand-grip exercise (IHG) coupled with a period of postexercise circulatory occlusion (OCC; known to sustain exercise-induced increases in blood pressure while facilitating a decrease in heart rate) on left ventricular (LV) twist mechanics was examined. Two-dimensional speckle-tracking echocardiography was used to assess LV apical and basal rotation and LV twist in 19 healthy participants (23 ± 2 years old) at rest, during 3 min of IHG (performed at 40% maximal voluntary contraction) and 3 min of OCC immediately following IHG. The IHG elicited significant (P < 0.001) increases in mean arterial pressure (rest, 91 ± 1 mmHg; IHG, 122 ± 2 mmHg) and heart rate (rest, 65 ± 2 beats min(-1); IHG, 91 ± 4 beats min(-1)). Mean arterial pressure remained elevated during OCC (116 ± 2 mmHg; P < 0.001 versus rest), whereas heart rate returned to resting levels (68 ± 3 beats min(-1); P = 0.159 versus rest). Apical rotation decreased significantly (P < 0.01) by 10 ± 5% during IHG and 21 ± 4% during OCC, whereas basal rotation remained unchanged from rest. Left ventricular twist decreased from rest to IHG (12 ± 5%; P = 0.015) and OCC (21 ± 4%; P = 0.001), whereas a decrease in LV untwist rate was observed only during OCC. An increase in blood pressure generated by IHG, and maintained by a period of OCC, impairs aspects of LV twist mechanics. Postexercise circulatory occlusion isolated the effect of the arterial blood pressure rise (from heart rate), magnifying the impairment of LV twist mechanics when compared with IHG, whilst also negatively impacting LV relaxation. We propose that a protocol using isometric exercise followed by circulatory occlusion provides a method for studying the effects of blood pressure changes on LV twist mechanics.

Left ventricular twist mechanics and its relation with aortic stiffness in chronic kidney disease patients without overt cardiovascular disease.

BackgroundRecent studies hypothesized left ventricular (LV) twist as a potential biomarker for evaluation of sub clinical myocardial disease, however its relationship with aortic stiffness has yet to be investigated. Chronic kidney disease (CKD) has been identified as a risk factor for both myocardial and arterial disease. As such we sought to explore the relationship between aortic stiffness and LV twist in CKD patients without known cardiovascular disease (CVD).MethodsIn this prospective, observational study we enrolled 106 CKD patients (Stages 1 to 5) with normal LVEF as assessed by conventional echocardiography. Aortic stiffness was measured using aortic pulse wave velocity (aPWV). We defined increased aPWV as ≥10 m/s. LV Twist was measured using two-dimensional speckle tracking echocardiography.ResultsPatients with increased aPWV had higher LV twist (p = 0.002) but similar LVEF (p = 0.486). Aortic PWV correlated crudely with age (p < 0.001), the presence of diabetes (p < 0.001), hypertension (p < 0.001), eGFR (p < 0.001), LVMI (p = 0.01), e/e’ (p < 0.001) and LV twist (p = 0.003). In multivariable analyses after adjusting for age, gender, cardiovascular risk factors and hypertensive medication, aPWV was independently associated with LV twist (β = 0.163, p = 0.025).ConclusionsAortic stiffness independently associates with LV Twist in asymptomatic CKD patients. These findings suggest a close interaction between LV twist mechanics and arterial remodeling even before CVD becomes clinically relevant.

Exercise reveals differential coupling between aortic haemodynamics and left ventricular twist mechanics

Exercise reveals differential coupling between aortic haemodynamics and left ventricular twist mechanics

Reproducibility of Echocardiograph‐Derived Multilevel Left Ventricular Apical Twist Mechanics

Left ventricular (LV) twist mechanics are routinely assessed via echocardiography in clinical and research trials investigating the function of obliquely oriented myocardial fibers. However, echocardiograph-derived measures of LV twist may be compromised by nonstandardized acquisition of the apical image. This study examined the reproducibility of echocardiograph-derived parameters of apical twist mechanics at multiple levels of the apical myocardium. Two sets of 2D LV parasternal short-axis images were obtained in 30 healthy subjects (24 men; 19-57 year) via echocardiography. Images were acquired immediately distal to the papillary muscles (apical image 1), immediately above the point of LV cavity obliteration at end systole (apical image 3), and midway between apical image 1 and apical image 3 (apical image 2). Repeat scans were performed within 1 hour, and twist mechanics (rotation and rotation rate) were calculated via frame-by-frame tracking of natural acoustic echocardiographic markers (speckle tracking). The magnitude of apical rotation increased progressively toward the apex (apical image 1: 4.2 ± 2.1°, apical image 2: 7.2 ± 3.9°, apical image 3: 11.8 ± 4.6°). apical images 1, 2, and 3 each had moderate to good correlations between repeat scans (ICC: 0.531-0.856). When apical images 1, 2, and 3 were averaged, rotation was 7.7 ± 2.7° and between-scan correlation was excellent (ICC: 0.910). Similar results were observed for systolic and diastolic rotation rates. Averaging multiple standardized apical images, tending progressively toward the apex, generated the most reproducible rotation indices and may be optimal for the assessment of LV twist mechanics across therapeutic, interventional, and research studies; however, care should be taken given the influence of acquisition level on the magnitude of apical rotation.

Worsening of left ventricular twist mechanics in isolated rheumatic mitral stenosis immediately after balloon mitral valvuloplasty

Abstract Background Reportedly, left ventricular (LV) mechanics are worsened in patients with mitral stenosis (MS) compared to controls. The immediate effect of balloon mitral valvuloplasty (BMV) on LV mechanics is, however, not known. Aim To assess the immediate effect of balloon mitral valvuloplasty on the left ventricular twist mechanics. Methods and results We studied 39 candidates for BMV. Pressures were measured invasively before and after BMV. Speckle tracking echocardiography (STE) was done for twist mechanics (basal rotation, apical rotation, and torsion) before and immediately after BMV. Twist mechanics were also measured by STE in 15 normal subjects as control group. Mean age was 30.4 ± 7.2 years, mean BMI was 24.7 ± 3.1 and 28 patients (72%) were females. All twist mechanics apical rotation and torsion were lower post-BMV compared to pre-BMV. Left ventricular end diastolic pressure was significantly higher post compared to pre-BMV while left atrial pressure (LAP) was similar between both groups. Importantly, patients who showed an increased LVEDP post compared to pre-BMV had worse LV twist mechanics than those whose LVEDP post-BMV was similar to or lower than pre-BMV. Conclusion LV twist mechanics are worsened in MS with a further worsening, immediately after BMV probably because of failure of the LV to adapt to the sudden increased preload.

Left Ventricular Rotational Mechanics in Preterm Infants Less Than 29 Weeks’ Gestation over the First Week after Birth

There is a paucity of data on left ventricular (LV) rotational physiology, twist, and torsional mechanics in preterm infants. The principal aims of the present study were to assess the feasibility and reproducibility of measuring LV rotation, twist, and torsion in preterm infants (<29 weeks' gestation) using two-dimensional speckle-tracking echocardiography and to examine the changes in those parameters over the first week after birth. This was a prospective observational study involving preterm infants <29 weeks' gestation. Echocardiographic evaluations were performed on days 1, 2, and 5 to 7 after delivery. LV basal and apical rotation, LV twist, LV twist rate (LVTR), and LV untwist rate (LVUTR) were measured from the basal and apical short-axis parasternal views and calculated using two-dimensional speckle-tracking echocardiography. Torsion was also calculated by normalizing LV twist to LV end-diastolic length. One-way repeated-measures analysis of variance was used to compare values across the three time points. Intra- and interobserver reproducibility were assessed using Bland-Altman analysis and the intraclass correlation coefficient. Fifty-one infants with a mean ± SD gestational age of 26.8 ± 1.5 weeks and a mean birth weight of 945 ± 233 g were included. There was high intra- and interobserver reproducibility for basal and apical rotation, LV twist, and LV torsion, with intraclass correlation coefficients ranging from 0.78 to 0.96 (P < .001 for all). Intra- and interobserver intraclass correlation coefficients for LVTR and LVUTR ranged from 0.70 to 0.88 (P < .001 for all). Apical rotation remained constant over the first week of age in a positive counterclockwise fashion (11.8 ± 5.0° vs 12.1 ± 6.1° vs 11.7 ± 8.3°, P = .92). Basal rotation changed from counterclockwise on day 1 to clockwise on day 7 (median, 5.5° [interquartile range, -0.3° to 8.3°] vs 4.0 [interquartile range, -4.7° to 7.2°] vs -4.5° [interquartile range, -5.8° to -2.3°], P < .001), with resultant net increases in twist and torsion (P < .05). There was no change in LVTR (P = .60), but LVUTR increased across the same time period (P = .01). Assessment of twist, LVTR, and LVUTR is feasible in preterm infants, with acceptable reproducibility. There are increases in LV twist and torsion in addition to LVUTR, suggesting changes in LV mechanics during the first week of age.

Left Ventricular Twist Mechanics Are Impaired in Patients with Coronary Slow Flow.

Coronary slow flow (CSF) is a rare condition described as the delayed angiographic passage of a contrast agent in the absence of stenosis in epicardial coronary arteries. Left ventricular (LV) systolic and diastolic dysfunctions have been described in the presence of CSF. However, the effect of CSF on LV twist functions has not been assessed. We aimed to evaluate the effects of CSF on LV twist mechanics using speckle tracking echocardiography (STE). Twenty CSF patients (24-60years) were enrolled according to the exclusion criteria. Twenty subjects with similar demographic characteristics and normal coronary arteries were the controls. Participants were evaluated with conventional echocardiography and STE. The general characteristics of the two groups were similar. LV twist, LV torsion, and apical rotation were impaired in the CSF group (P=0.015, P=0.012, and P<0.001, respectively). Time to peak twist (TPT) and time to peak untwisting (TPU) were prolonged in CSF patients (P<0.001 and P<0.001, respectively). In the CSF group, rotation-deformation delay was shortened (P<0.001) and global longitudinal strain (GLS) was lower (P<0.001). The thrombolysis in myocardial infarction (TIMI) frame count was negatively correlated with LV twist, LV torsion and apical rotation (P=0.002, r=-0.624; P=0.002, r=-0.624; and P=0.002, r=-0.632, respectively). We demonstrated that LV twist mechanics are impaired in CSF patients. Worse LV twist parameters were associated with greater TIMI frame count.

Role of left ventricular twist mechanics in cardiomyopathies, dance of the helices.

Left ventricular twist is an essential part of left ventricular function. Nevertheless, knowledge is limited in "the cardiology community" as it comes to twist mechanics. Fortunately the development of speckle tracking echocardiography, allowing accurate, reproducible and rapid bedside assessment of left ventricular twist, has boosted the interest in this important mechanical aspect of left ventricular deformation. Although the fundamental physiological role of left ventricular twist is undisputable, the clinical relevance of assessment of left ventricular twist in cardiomyopathies still needs to be established. The fact remains; analysis of left ventricular twist mechanics has already provided substantial pathophysiological understanding on a comprehensive variety of cardiomyopathies. It has become clear that increased left ventricular twist in for example hypertrophic cardiomyopathy may be an early sign of subendocardial (microvascular) dysfunction. Furthermore, decreased left ventricular twist may be caused by left ventricular dilatation or an extensive myocardial scar. Finally, the detection of left ventricular rigid body rotation in noncompaction cardiomyopathy may provide an indispensible method to objectively confirm this difficult diagnosis. All this endorses the value of left ventricular twist in the field of cardiomyopathies and may further encourage the implementation of left ventricular twist parameters in the "diagnostic toolbox" for cardiomyopathies.

Effect of Pacing Mode and Pacing Site on Torsional and Strain Parameters and on Coronary Flow

Right ventricular apical pacing may induce detrimental effects on left ventricular function and coronary flow. In this study, the effects of pacing site and mode on cardiac mechanics and coronary blood flow were evaluated. This prospective study included 25 patients who received dual-chamber pacemakers with the ventricular lead placed in the right ventricular apex and presented in sinus rhythm (SR) at their regularly scheduled visits at the pacemaker clinic. Patients underwent complete transthoracic echocardiographic examinations while in SR, followed by noninvasive Doppler assessment of coronary flow in the left anterior descending coronary artery (LAD) and speckle-tracking echocardiography of short-axis planes in SR, atrial pacing (AAI-P), atrioventricular (dual-chamber) pacing (DDD-P), and ventricular pacing (VVI-P). Rotation of the base was significantly decreased with VVI-P compared with AAI-P. Left ventricular twist decreased significantly with DDD-P compared with AAI-P. Circumferential strain of the base significantly decreased with DDD-P and VVI-P compared with SR. The velocity-time integral of diastolic flow in the LAD decreased significantly with DDD-P compared with SR (10.7±2.2 vs 10.2±2.2 vs 8.9±1.6 vs 8.7±2.6cm in SR and with AAI-P, DDD-P, and VVI-P, respectively, P=.003). Basal rotation and time from onset of the QRS complex to peak basal rotation as a percentage of systole were independently associated with the velocity-time integral of diastolic flow in the LAD during SR and the three pacing modes. Acute right ventricular apical pacing showed a detrimental effect on left ventricular twist and basal mechanics, with the latter being independently associated with decreased LAD diastolic flow velocity parameters.

Assessment of left ventricular twist mechanics by speckle tracking echocardiography reveals association between LV twist and myocardial fibrosis in patients with hypertrophic cardiomyopathy.

We aimed to investigate whether left ventricular (LV) twist analysis can detect the extent of myocardial fibrosis in patients with hypertrophic cardiomyopathy (HCM). This prospective case–control study recruited 81 consecutive patients with HCM examined between January 2012 and April 2013. Data of 76 patients were analyzed after excluding 5 patients whose echocardiographic images were of poor quality. Healthy volunteers (n = 46) served as controls. Both groups underwent comprehensive echocardiographic examination (i.e., Bas-Rotation, AP-Rotation, LVEF, LADs, IVST, LAVi, E/Em, LVMI, advanced LV-twist analysis by speckle tracking echocardiography) and magnetic resonance imaging. Between-group differences were analyzed by independent t test; logistic regression analysis was performed to identify effect factors. No significant differences were found between baseline characteristics of HCM and control groups (all p > 0.05). HCM patients had significantly higher Bas-Rotation, AP-Rotation, LV Twist, LVEF, LADs, IVST, LAVi, E/Em and LVMI than controls (all p < 0.0001) and significantly lower LVDd and E/A (both p < 0.001). Bas-Rotation, AP-Rotation, LV-Twist, LADs, IVST, LAVi, E/Em and LVMI were significantly higher in HCM patients with fibrosis than in those without fibrosis (p < 0.001), but no significant differences in other echocardiographic parameters were found between those with and without fibrosis. Age, Bas-Rotation, AP-Rotation, LV twist, LADs, IVST, LAVi, E/A, E/Em, and LVMI were significant effect factors for fibrosis. AUROC analysis showed that LV twist had high discriminatory power to detect extent of myocardial fibrosis (AUC 0.996, 95 % CI 0.989–1.004, p < 0.001). Left ventricular twist mechanics are associated with the extent of myocardial fibrosis. LV-twist assessment by STE may be clinically useful.Electronic supplementary materialThe online version of this article (doi:10.1007/s10554-014-0509-6) contains supplementary material, which is available to authorized users.

Aging with systemic hypertension impairs left ventricular twist mechanics in never treated hypertensive patients: comparison with young healthy volunteers

Aging with systemic hypertension impairs left ventricular twist mechanics in never treated hypertensive patients: comparison with young healthy volunteers

Myocardial Mechanics in Cardiomyopathies

Cardiomyopathies are a heterogeneous group of diseases that can be phenotypically recognized by specific patterns of ventricular morphology and function. The authors summarize recent clinical observations that mechanistically link the multidirectional components of left ventricular (LV) deformation with morphological phenotypes of cardiomyopathies for offering key insights into the transmural heterogeneity of myocardial function. Subendocardial dysfunction predominantly alters LV longitudinal shortening, lengthening and suction performance and contributes to the phenotypic patterns of heart failure (HF) with preserved ejection fraction (EF) seen with hypertrophic and restrictive patterns of cardiomyopathy. On the other hand, a more progressive transmural disease results in reduction of LV circumferential and twist mechanics leading to the phenotypic pattern of dilated cardiomyopathy and the clinical syndrome of HF with reduced (EF). A proper characterization of LV transmural mechanics, energetics, and space-time distributions of pressure and shear stress may allow recognition of early functional changes that can forecast progression or reversal of LV remodeling. Furthermore, the interactions between LV muscle and fluid mechanics hold the promise for offering newer mechanistic insights and tracking impact of novel therapies.

Left Ventricular and Atrial Functions in Hypertrophic Cardiomyopathy Patients with Very High LVOT Gradient: A Speckle Tracking Echocardiographic Study

Determination of myocardial deformation (strain) by two-dimensional (2D) speckle tracking echocardiography (STE) is a new method for evaluating left ventricular (LV) regional function in patients with hypertrophic cardiomyopathy (HCM). The aim of this study was to assess LV and left atrial (LA) functions with 2DSTE in HCM patients and to investigate relation between strain analysis and LV outflow tract (LVOT) gradient. Forty consecutive HCM patients (26 male, mean age: 47.7 ± 15.2 years), and 40 healthy volunteers (22 male, mean age: 46.6 ± 11.2 years) were included in the study. All subjects underwent a transthoracic echocardiography for evaluation of LV and LA functions with 2DSTE. The HCM patients were divided into 2 groups according to the presence of resting LVOT gradient >100 mmHg. Left ventricular global longitudinal strain (GLS), global radial strain (GRS), and global circumferential strain (GCS) were significantly lower in patients with HCM compared with controls (-20.3 ± 3.6% vs. -24.1 ± 3.4% P < 0.001, 38.1 ± 12.8% vs. 44.8 ± 10.2% P = 0.012, and -22.0 ± 4.4% vs. -23.9 ± 4.0% P = 0.045, respectively). Although basal and apical rotation were similar between the groups, mid-rotation was significantly clockwise in HCM patients (-1.53 ± 2.06° vs. 0.05 ± 1.7° P < 0.001). Both LA reservoir functions and LA conduit functions were significantly lower in HCM patients (21.6 ± 9.1% vs. 39.4 ± 10.6% P < 0.001, and 10.5 ± 4.3% vs. 15.7 ± 5.3%, P < 0.001). Fifteen patients had a resting LVOT gradient of >100 mmHg and they had significantly decreased GLS, twist and untwist compared to the HCM patients with lower resting LVOT gradient (-18.7 ± 2.3% vs. -21.2 ± 3.9% P = 0.016, 19.4 ± 4.3° vs. 23.5 ± 7.4° P = 0.038 and -94.0 ± 29.1°/sec vs. -134.9 ± 55.8°/sec, 0.005, respectively). Although basal and apical rotation were similar between the 2 groups, mid-rotation was significantly clockwise in HCM patients with higher LVOT gradient (-2.52 ± 1.76° vs. -0.96 ± 2.03°, P = 0.018). Correlation analysis revealed that LVOT peak velocity was associated with GLS (r = -0.358, P = 0.023), LV mid-rotation (r = -0.366, P = 0.024), and LV untwist (r = -0.401, P = 0.013). Left ventricular and LA functions are impaired in patients with HCM. 2DSTE is useful in determining patients with impaired myocardial mechanics. High LVOT gradient may be one of the responsible factors that trigger deterioration of LV longitudinal strain and twist mechanics in patients with HCM. Further studies are required to clarify the preliminary results of this study.

Left Ventricular Rotational Deformation is Impaired in Pulmonary Hypertension: A Speckle Tracking Imaging- Based Study

OP-005 Right ventricular (RV) pressure overload influences ventricular interdependence and subsequent left ventricular (LV) geometry. In the present study, we aimed to demonstrate the impact of increased RV pressure on LV systolic deformation and LV twist mechanics in the setting of pulmonary

Effect of stellate ganglia stimulation on global and regional left ventricular function as assessed by speckle tracking echocardiography

Left ventricular (LV) twist mechanics and regional strain during cardiac sympathetic efferent activation are poorly understood. The purpose of this study was to compare the effects of left stellate ganglia (LSG) and right stellate ganglia (RSG) stimulation on cardiac twist/untiwst mechanics and regional strain. In nine pigs, echocardiographic imaging and LV pressure-volume measurements were performed before and during unilateral and bilateral stellate ganglion stimulation. LSG and RSG stimulation significantly augmented LV end-systolic pressure by 24% and 22% (P < 0.01), maximal rate of LV pressure change by 167% and 165% (P < 0.01), and time constant of LV relaxation by 20% and 12% (P < 0.01), respectively. RSG stimulation resulted in a greater chronotropic response than LSG stimulation (RSG: 68% vs. LSG: 12%, P < 0.01). Both LSG and RSG stimulation significantly increased global epicardial and endocardial LV rotation and diastolic untwisting rate and reduced the time to peak rotation (P < 0.05). However, LSG stimulation predominantly increased radial and circumferential strain in the LV inferoseptal, inferior, posterior, and lateral regions, whereas RSG stimulation primarily increased radial and circumferential strain in the anteroseptal, anterior, and lateral LV regions. Stimulation of both stellate ganglia led to a uniform increase in all LV segments. Our data suggest that LSG and RSG stimulation lead to a global increase in LV twist, driven by distinct regional strain heterogeneity that may result from myocardial innervation from the LSG and RSG. These findings provide a better understanding of the global and regional functional consequences of regional myocardial innervation from the LSG and RSG.

EVALUATION OF LEFT VENTRICULAR TORSION AFTER ARTERIAL SWITCH OPERATION FOR D-TRANSPOSITION OF THE GREAT ARTERIES WITH INTACT VENTRICULAR SEPTUM BY TWO-DIMENSIONAL SPECKLE TRACKING IMAGING

ObjectivesTo evaluate anatomic left ventricular twist and untwist mechanics in patients of transposition of the great arteries with intact ventricular septum (TGA/IVS) up to 4 years after arterial switch operation...

The impact of isometric handgrip testing on left ventricular twist mechanics

Left ventricular (LV) rotation occurs due to contraction of obliquely oriented myocardial fibres. Left ventricular twist (LVT) results from rotation of the apex and base in opposite directions. Although LVT is altered in various cardiac diseases, physiological factors that affect LVT remain incompletely understood. Isometric handgrip testing (IHGT), a well-established laboratory-based technique to increase LV afterload, was performed for 3 min at 40% maximum force generation in healthy human subjects (n = 18, mean age 29.7 ± 2.7 years). Speckle-tracking echocardiography was used to measure LV volumes, LV apical and basal rotation, peak systolic LVT and peak early diastolic untwisting rate (UTR) at rest and at peak IHGT. IHGT led to significant increase in systemic blood pressure (systolic, 120.6 ± 9.7 vs. 155.6 ± 14.5 mmHg, P < 0.001; diastolic, 67.5 ± 6.4 vs. 94.1 ± 21.1 mmHg, P < 0.001) and LV end-systolic volume (44.2 ± 7.8 vs. 50.5 ± 10.8 ml, P = 0.005), as well as a significant increase in heart rate (62.8 ± 11.7 vs. 84.7 ± 13.8 beats min−1; P < 0.001). IHGT produced a significant acute reduction in LV stroke volume (63.9 ± 12.0 vs. 49.4 ± 7.8 ml, P < 0.001). In this setting, there was a significant decrease in peak systolic apical rotation (11.9 ± 3.0 vs. 8.6 ± 2.2 deg, P < 0.001) and a resultant 25% decrease in peak systolic LVT (16.6 ± 2.8 vs. 12.5 ± 2.8 deg, P < 0.001). The magnitude of peak early diastolic UTR did not change (−114.5 ± 26.4 vs. −110.6 ± 39.8 deg s−1, P = 0.71). Peak systolic apical rotation and LVT decrease during IHGT in healthy humans. This impairment of LV twist mechanics may in part underlie the LV dysfunction that can occur in the clinical context of acute increase in afterload.