Changes In Myocardial Mechanics Research Articles

Myocardial Mechanics and Valvular and Vascular Abnormalities in Cardiac Amyloidosis.

Cardiac amyloidosis is an infiltrative disease primarily caused by extracellular tissue deposition of amyloid fibrils in the myocardial interstitium. The aim of the present review was to summarize findings regarding changes in myocardial mechanics, valvular abnormalities, and vascular remodeling detected in patients with cardiac amyloidosis.

Longitudinal Changes in Ventricular Mechanics in Adolescents After the Fontan Operation

Ventricular dysfunction is a significant clinical challenge in the long-term follow-up of patients with single-ventricle (SV) physiology. Ventricular function and myocardial mechanics can be studied using speckle-tracking echocardiography, which provides information on myocardial deformation. Limited information is available on serial changes in SV myocardial mechanics after the Fontan operation. The aim of this study was to describe serial changes in myocardial mechanics in children after the Fontan operation and the relationship of these changes with myocardial fibrosis markers as obtained by cardiac magnetic resonance and exercise performance parameters. The authors hypothesized that ventricular mechanics decline in patients with SVs over time and are associated with increased myocardial fibrosis and reduced exercise performance. A single-center retrospective cohort study including adolescents after the Fontan operation was conducted. Ventricular strain and torsion were assessed using speckle-tracking echocardiography. Cardiac magnetic resonance and cardiopulmonary exercise testing data closest to the latest echocardiographic examinations were performed. The most recent follow-up echocardiographic and cardiac magnetic resonance data were compared with those from sex- and age-matched control subjects and with individual patients' early post-Fontan data. Fifty patients with SVs (31 left ventricle, 13 right ventricle [RV], and six codominant) were included. Median time at follow-up echocardiography from the time of Fontan was 12.8years (interquartile range [IQR], 10.6 to 16.6years). Compared with early post-Fontan echocardiography, follow-up assessment showed reduced global longitudinal strain (-17.5% [IQR, -14.5% to -19.5%] vs -19.8% [IQR, -16.0% to -21.7%], P=.01], circumferential strain (-15.7% [IQR, -11.4% to -18.7%] vs -18.9% [IQR, -15.2% to -25.0%], P=.009), and torsion (1.28°/cm [IQR, 0.51°/cm to 1.74°/cm] vs 1.72°/cm [IQR, 0.92°/cm to 2.34°/cm], P=.02), with decreased apical rotation but no significant change in basal rotation. Single RVs had lower torsion compared with single left ventricles (1.04°/cm [IQR, 0.12°/cm to 2.20°/cm] vs 1.25°/cm [IQR, 0.25°/cm to 2.51°/cm], P=.01). T1 values were higher in patients with SV compared with control subjects (1,009±36 vs 958±40msec, P=.004) and in those with single RVs compared with single left ventricles (1,023±19 vs 1,006±17msec, P=.02). T1 was correlated with circumferential strain (r=0.59, P=.04) and inversely correlated with O2 saturation (r=-0.67, P<.001) and torsion (r=-0.71, P=.02). Peak oxygen consumption was correlated with torsion (r=0.52, P=.001) and untwist rates (r=0.23, P=.03). After the Fontan procedures, there is a progressive decrease in myocardial deformation parameters. The progressive decrease in SV torsion is related to a decrease in apical rotation, which is more pronounced in single RVs. Decreased torsion is associated with increased markers of myocardial fibrosis and lower maximal exercise capacity. Torsional mechanics may be an important parameter to monitor after Fontan palliation, but further prognostic information is required.

Diastolic dysfunction assessed by cardiac magnetic resonance imaging tissue tracking on normal-thickness wall segments in hypertrophic cardiomyopathy

ObjectivesMyocardial strain is reported to be a sensitive indicator of myocardial mechanical changes in patients with hypertrophic cardiomyopathy (HCM). The changes in the mechanics of the myocardium of normal wall thickness (< 12 mm) have yet to be well studied. This study aimed to evaluate the function of myocardial segments of normal thickness in patients with HCM.MethodsSixty-three patients with HCM and 30 controls were retrospectively enrolled in this retrospective study. Cine imaging, native and post-contrast T1 maps, T2 maps, and late gadolinium enhancement were performed. In addition, regional myocardial strain was assessed by cardiac magnetic resonance-tissue tracking. Strain parameters were compared between the controls and HCM patients with segments of the myocardium of normal thickness. Subgroup analysis was conducted in obstructive and non-obstructive HCM. Lastly, p < 0.05 was considered statistically significant.ResultsIn normal-thickness myocardial segments of HCM (n = 716), diastolic peak strain rates (PSRs) were significantly lower than in the control group (n = 480) (radial, − 2.43 [− 3.36, − 1.78] vs. − 2.67 [− 3.58, − 1.96], p = 0.002; circumferential, 1.28 [1.01,1.60] vs. 1.39 [1.14, 1.78], p < 0.001; and longitudinal, 1.16 [0.75,1.51] vs. 1.28 [0.90, 1.71], p < 0.001). The normal-thickness segments showed no significant difference in systolic PSRs between HCM and the controls. In the subgroup analysis, significantly decreased diastolic PSRs were noted in both obstructive and non-obstructive HCM, compared with the controls (p < 0.05).ConclusionsDiastolic changes in myocardial mechanics were observed in normal-thickness segments of HCM, occurring before morphological remodeling and systolic dysfunction developed. This finding contributed to a better understanding of the mechanical pathophysiology of HCM with preserved left ventricular ejection fraction. It may potentially aid in predicting disease progression and risk stratification.

Myocardial deformation in athletes measured with feature tracking cardiovascular magnetic resonance

Abstract Background Morphological changes of the heart associated with exercise are well studied. However, changes in myocardial mechanics of athlete's heart are less understood. The aim of this study was to analyze myocardial deformation parameters in athletes and controls, using feature tracking cardiac magnetic resonance (FT-CMR). Methods In a cohort of 73 athletes who had been submitted to CMR at 1.5T and 3 T (mean age 31±12 years, 69% males), we used CMR-FT to measure longitudinal, circumferential and radial strain and strain rates of both ventricles. Left ventricle (LV) longitudinal, circumferential and radial dyssynchrony index (L-SDI, C-SDI and R-CDI, respectively) was calculated as the standard deviation of the calculated time to peak strain percentages of the cardiac cycle with segmental strain analysis. We also measured these parameters in 73 age-matched healthy subjects. Results In comparison to the control subjects, athletes revealed lower left and right ventricle global longitudinal strain (−14.24% vs. −13.31%, p=0.03, and −18.12% vs. −15.95% p=0.01, respectively) and right ventricular (RV) global radial strain (19.28 vs 15.74, p&amp;lt;0.05) – Figure 1. There were no significant differences in LV global radial and circumferential strain. LV longitudinal, radial and circumferential systolic strain rate were also lower in athletes compared to controls (−0.69 s–1 vs. −0.78 s–1, p=0.04; 1.35 s–1 vs. 1.50 s–1, p=0.03: −0.92 s–1 vs −0.98 s–1, p=0.05, respectively). Regarding LV dyssynchrony index, we found no significant difference for L-SDI (10.76% vs. 10.72%, p=0.956), but athletes group showed lower C-SDI and R-SDI values (5.99% vs 4.84%, p=0.006, and 5.53% vs 4.47%, p=0.002). Conclusion Our study revealed attenuation of biventricular strain values and lower circumferential and radial LV dyssynchrony indexes in athletes, compared with healthy controls. We hypothesize that these differences may be related with exercise physiologic cardiac adaptations. Funding Acknowledgement Type of funding sources: None.

Evaluation of left ventricular function by vector flow mapping in females with systemic lupus erythematosus.

Compare the intraventricular hemodynamics of 60 females with systemic lupus erythematosus (SLE) and 61 healthy female controls, and determine cardiac function changes using vector flow mapping (VFM). To determine the effect of pulmonary artery pressure changes on left ventricular function, SLE patients were divided into a normal pulmonary artery pressure group (S1, n=24) and an elevated pulmonary artery pressure group (S2, n=36). The energy loss (EL) at each segment of the left ventricular chamber (total, basal, middle, and apical segments) during each period of the cardiac cycle (isovolumic contraction, rapid ejection, rapid filling, reduced filling, atrial contraction) was determined. The S1 group had significantly more vortices than the control group during the rapid ejection, rapid filling, and atrial contraction periods (p<0.01), and the maximum vortex areas in the S1 and S2 groups were smaller than in the control group during rapid filling and atrial contraction periods (p<0.05). Compared with the control group, the S2 group had greater EL during the systole and diastole periods (p<0.01). EL in the S1 group was significantly greater than in the control group during systole (p<0.01). During the rapid filling period, the EL was positively correlated with septal E' (r=0.784, p<0.01), and during the atrial contraction period, EL was positively correlated with septal E/e' (r=0.812, p<0.01) and A (r=0.715, p<0.01). VFM of patients with SLE can comprehensively, rapidly, and efficiently evaluate changes of myocardial mechanics and intracardiac hemodynamics and provide quantitative analysis of complex intracardiac blood flow. Key points • Vector flow mapping (VFM) is a new non-invasive ultrasound technique that evaluates changes of myocardial mechanics and intracardiac hemodynamics, and provides quantitative analysis of complex intracardiac blood flow. • This study showed that vortex and energy loss may provide more sensitive detection of cardiac dysfunction than conventional echocardiographic indexes in patients with systemic lupus erythematosus.

Abstract 14409: TRPA1 Channels Are a Source of Calcium-driven Cellular Mechano-arrhythmogenicity

Introduction: Pathologic changes in myocardial mechanics and hemodynamic load result in arrhythmias via mechanically-induced changes in electrophysiology or intracellular Ca 2+ (‘mechano-arrhythmogenicity’). While molecular mechanisms driving mechano-arrhythmogenicity are poorly defined, they are associated with disease-related alterations in voltage-Ca 2+ dynamics. Objective: Define mechanisms of mechano-arrhythmogenicity during alterations in voltage-Ca 2+ dynamics in rabbit ventricular myocytes. Methods: Rabbit (♀, NZW) LV myocytes were transiently stretched (8-16% change in sarcomere length, 100ms) during diastole or late repolarisation in control or during K ATP channel activation (pinacidil). Drugs were used to buffer Ca 2+ (BAPTA), stabilise RyR (dantrolene), non-selectively block stretch-activated channels (streptomycin), or specifically block (HC-030031) or activate (AITC) mechano-sensitive TRPA1 channels. Voltage-Ca 2+ dynamics were simultaneously monitored with fluorescent dyes (di-4-ANBDQPQ, Fluo-5F) and a single camera-optical splitter system and diastolic Ca 2+ was measured using Fura Red. Results: Pinacidil caused greater shortening of the AP than Ca 2+ transient (-144±17 vs -74±11ms; n =24 cells, N =7 rabbits; p &lt;0.001) with no change in cell stiffness or contractility. Stretch during pinacidil application caused arrhythmias in both diastole and late repolarisation (8 and 10% of stretches; n =46, N =5), which voltage-Ca 2+ imaging revealed were Ca 2+ -driven. Arrhythmias were reduced with BAPTA (3 and 0% of stretches; p &lt;0.05), streptomycin (4 and 2%; p &lt;0.05), and HC-030031(2 and 1%; p &lt;0.01), while dantrolene had no effect ( n =40, N =5 for each). Stretch in diastole during AITC application also caused arrhythmias (15%; p &lt;0.001), which were blocked by HC-030031 (4%; p &lt;0.001) or BAPTA (3%; p &lt;0.001; n =40, N =5 each). Both AITC and pinacidil caused an increase in diastolic Ca 2+ (112±29 and 78±29% of control; p&lt;0.05), which was reduced by HC-030031 with AITC (26±24%; p &lt;0.05), but not with pinacidil ( n =25, N =5 each). Conclusions: TRPA1 activation increases mechano-arrhythmogenicity via a Ca 2+ -driven mechanism and may represent a novel anti-arrhythmic target in pathologies involving altered cardiac mechanics.

Chronic coronary syndromes lead to reduced strain parameters compared to patients without myocardial ischemia in a propensity score-matched cohort assessed by cardiac magnetic resonance imaging

Abstract Background Vasodilator perfusion cardiac magnetic resonance (CMR) has evolved as gold standard in detecting myocardial perfusion deficits (MPD). Even reversible chronic MPD in chronic coronary syndromes can lead to impaired myocardial contractility similar to hibernating myocardium. Feature tracking strain analysis (FTS) provides the opportunity to detect these subclinical alterations of myocardial function before ejection fraction (EF) is impaired. It was therefore the aim of this study to investigate, if subtle changes in myocardial mechanics can be detected by FT strain analysis in patients with MPD. Methods Between April 2017 and October 2019 we identified 226 patients with MPD by vasodilator stress CMR out of 1500 patients included in our tertiary care center registry. Propensity score matching was used to identify patients without MPD with similar myocardial characteristics defined by EF, enddiastolic volume indexed by body surface area (EDVi) and native T1-mapping. Steady state free precession cine CMR sequences were analyzed by FTS retrospectively generating three global strain parameters: global longitudinal, circumferential and radial strain (GLS, GCS, GRS). Results Propensity score matching yielded 104 patients in each group (MPD mean age 63.6±12.8 years, 25 females; no MPD mean age 67.7±10.6 years, 26 females; LV-EF 51.3±16.0% vs. 52.6±15.2%, p=0.2307; EDVi 88.3±32.7 ml/m2 vs. 82.6±29.3 ml/m2, p=0.1533; native T1 values 1139±60 ms vs. 1125±63 ms, p=0.118). All global strain parameters were significantly reduced in MPD patients compared to patients with no MPD (global longitudinal strain −15.5±4.9 vs. −17.1±4.9, p=0.0046, global circumferential strain −18.0±5.4 vs. −19.4±5.6, p=0.0298; global radial strain 35.4±14.8 vs. 39.4±15.6, p=0.0127). Conclusion Chronic Coronary Syndromes cause subtle changes of myocardial mechanics, which are not reflected by EF but can be detected with FTS. Funding Acknowledgement Type of funding source: None

Left Ventricular Myocardial Deformations in Hemodialysis Children by Speckle Tracking Echocardiography.

Background:Cardiac systolic dysfunction was potentially found in adult patients with end-stage renal disease (ESRD) who have preserved left ventricular ejection fraction (EF%). In children with ESRD, little data are available on early changes in myocardial function. This study aimed to detect the early changes in myocardial mechanics in pediatric patients with ESRD using speckle tracking echocardiography (STE).Methods:Thirty ESRD children receiving hemodialysis (HD) and30 age-matched controls were prospectively studied. Patients underwent echocardiographic studies before and after HD. Left ventricular longitudinal strain (LS), circumferential strain (CS), and radial strain (RS) myocardial deformation parameters (strain, strain rate) were evaluated by STE.Results:The LS was significantly reduced in pre-HD and post-HD patients compared with controls (P = .000). Controls showed the highest global longitudinal strain. The RS measurements did not differ significantly among the studied groups except for the inferior segment that is significantly reduced after HD compared with controls (P < .05). The CS was significantly reduced in pre-HD and post-HD patients compared with controls at the lateral and posterior segments (P = .035 and P = .013, respectively).Conclusion:Speckle-tracking echocardiography might detect early changes in myocardial mechanics in children with ESRD with preserved EF%.

Evaluation of myocardial mechanical changes in patients with acute myocardial infarction before and after percutaneous coronary intervention by speckle tracking technique

Objective To evaluate the changes of myocardial mechanics before and after percutaneous coronary intervention (PCI) in patients with acute myocardial infarction(AMI) by ultrasonic speckle tracking technique, and investigate the recovery of left ventricular myocardium mechanics and the effects of common complications on the improvement of myocardial mechanics. Methods Sixty-two patients with AMI were examined by echocardiography within 12 hours, 1 week and 3 months after PCI. According to the complications the patients were divided into simple AMI group (21 cases), AMI with diabetes mellitus group (21 cases), and AMI with hypertension group (20 cases). Thirty healthy volunteers were selected as control group. Conventional echocardiographic parameters and left ventricular strain parameters were evaluated in all subjects. Results ①Left ventricular end-diastolic diameter (LVEDD), left ventricular end-systolic diameter (LVESD), left ventricular end-diastolic volume (LVEDV), and left ventricular end-systolic volume (LVESV) in each AMI group before PCI were greater than the control group (P 0.05 ). ③The degree of improvement of global longitudinal and circumferential endocardial strain in AMI with diabetes group were less than those in simple AMI group(P<0.05). The degree of improvement of global longitudinal endocardial strain in AMI with hypertension group was less than that in simple AMI group (P<0.05). Conclusions Patients with AMI have poor myocardial mechanics before PCI, especially those with diabetes mellitus; myocardial mechanics improves significantly 3 months after PCI; diabetes mellitus or hypertension affectes the improvement of myocardial mechanics in patients with AMI after PCI. Key words: Echocardiography; Acute myocardial infarction; Speckle tracking; Myocardial mechanics

Myocardial fatigue in recreational marathon runners: A speckle-tracking echocardiography study

BackgroundProlonged aerobic exercise such as marathon running produces supraphysiological hemodynamic stress that can potentially affect the athlete's cardiac homeostasis. While cardiac structural and functional adaptations in professional athletes are well characterized, only a limited information is available for recreational runners undergoing this supraphysiological stress. MethodsPremarathon and post-marathon echocardiography was performed in 50 recreational marathon runners [age 40.8 ± 7.5 years, 44 (88%) males; running distance 42.195 km]. All the runners received 4-month training for the marathon. The baseline echocardiogram and N-terminal B-type natriuretic peptide (NT-proBNP) were obtained before training, whereas the post-marathon study was performed within 10 days (7.27 ± 0.92 days) of completion of marathon. Two-dimensional speckle-tracking echocardiography was used for characterizing the changes in myocardial mechanics. ResultsThere was a significant reduction in heart rate post-marathon, whereas the levels of NT-proBNP increased significantly (86.0 ± 9.5 pg/ml vs 106.5 ± 24.2 pg/ml, p = 0.001). The left ventricular (LV) end-diastolic volume (61.8 ± 16.5 ml vs 72.8 ± 5.1 ml, p < 0.001), LV mass (120.2 ± 30.0 gm vs 160.3 ± 43.0 gm, p < 0.001), and LV ejection fraction (64.9 ± 5.6% vs 72.0 ± 5.7%, p < 0.001) also increased significantly. However, there was a significant attenuation in LV global longitudinal (−19.3 ± 2.71% vs −16.5 ± 4.6%, p = 0.003) and circumferential strain (−17.2 ± 2.41% vs −15.2 ± 2.6%, p = 0.001) post-marathon. The LV global radial strain showed a nonsignificant reduction. ConclusionRecreational marathon runners have reduced longitudinal and circumferential shortening of the left ventricle with elevation of NT-proBNP. However, the LV ejection performance remains maintained because of an increase in the LV end-diastolic volume and mass. These changes suggest the possibility of “myocardial fatigue” occurring in response to supraphysiological hemodynamic stress of marathon running.

Cardiac mechanics and dysfunction with anthracyclines in the community: results from the PREDICT study

BackgroundOur objective was to determine the relevance of changes in myocardial mechanics in diagnosing and predicting cancer therapeutics-related cardiac dysfunction (CTRCD) in a community-based population treated with anthracyclines.MethodsQuantitative measures of...

Abstract 13501: Measures of Three-dimensional Left Ventricular Mechanics Deteriorate Acutely After Cardiotoxic Cancer Therapy

Background: Doxorubicin and trastuzumab are commonly used breast cancer therapies with established cardiotoxic effects. However, the changes in myocardial mechanics with cancer therapy cardiotoxicity remain poorly defined, and noninvasive measures are needed to identify patients at increased risk. Our objective was to define the acute changes in three-dimensional (3D) echocardiography-derived indices of cardiac mechanics in patients receiving these therapies. Methods: In a prospective, longitudinal cohort of women with breast cancer receiving doxorubicin and/or trastuzumab, we obtained 3D echocardiography images before therapy (baseline) and during therapy at 3 months and 1 year of follow-up. Images were acquired at a minimum of 22 frames per second and analyzed by two readers using a vendor-independent analysis platform (TomTec Cardiac Performance Analyses, Unterschleissheim, Germany). Left ventricular twist, torsion, and principal strain were quantitated semi-automatically using 3D speckle tracking imaging. Standard descriptive statistics were used to summarize these measures over time. Results: Eighty-seven patients (mean age at baseline 49 years, 65% Caucasian) contributed at least 1 observation to the analysis. At baseline, median twist was 10.96° (interquartile range [IQR] 6.64, 13.59), torsion was 1.41°/cm (IQR 0.86, 1.70), and principal strain was -30.40% (-33.64, -28.55). At 3 months and 1 year, there were consistent declines in twist, torsion, and principal strain as displayed in Table I. Conclusions: In a prospective cohort of women with breast cancer receiving doxorubicin and/or trastuzumab, left ventricular twist, torsion, and principal strain declined over the first year of therapy. Ongoing research is focused on determining the clinical significance of these changes over time. Table 1. Longitudinal changes in 3D twist, torsion, and principal strain; summaries presented as median (interquartile range).

Abstract 169: Impact of Resistance to Intravenous Immune Globulin on Changes of Left Ventricular Myocardial Deformation Over Time in Children with Kawasaki Disease

Introduction: This study aimed to assess the impact of resistance to intravenous immune globulin(IVIG) on left ventricular(LV) myocardial deformation in children with Kawasaki disease(KD) during the acute and convalescent phases of illness. Few studies have elucidated the impact of resistance to IVIG on the progressive changes of myocardial mechanics over time in patients with KD. Methods: We studied 26 patients with KD and 8 normal control subjects. Of the 26 patients, 16 were IVIG non-responders. Echocardiograms were obtained during the acute and convalescent phases of KD. Standard echocardiographic data and peak systolic global LV longitudinal strain[strain(ε)] were obtained using vector velocity imaging. Results: During the acute phase of KD, peak systolic global LV longitudinal ε decreased significantly in both IVIG non-responders(-21.18 % ± 3.97) and responders(-20.94 % ± 3.15) compared to controls(-24.99 % ± 2.23). Although in the acute phase, LV ejection fraction(EF) was significantly higher in the IVIG non-responders(55.38 % ± 5.14) compared to the responders(50.2 % ± 6.53), peak systolic global LV longitudinal ε was not significantly higher in the IVIG non-responders compared to the responders. During the convalescent phase, peak systolic global LV longitudinal ε tended to increase in non-responders(-21.62% ± 3.98) and responders(-21.83% ± 2.61) compared to the acute phase, but remained significantly decreased in both groups compared to controls. The increment of peak systolic global LV longitudinal ε from acute to convalescent phase tended to be smaller in the IVIG non-responders compared to the responders. The proportion of patients with coronary dilatations in both IVIG non-responders(4 of 16) and IVIG responders(2 of 10) did not differ significantly. Conclusions: The increment of peak systolic global LV longitudinal ε over time tended to be smaller in the IVIG non-responders compared to the IVIG responders. Resistance to IVIG may delay normalization of myocardial mechanics in IVIG non-responders. Further studies with larger number of patients, as well as long-term follow-up of myocardial deformation in KD are necessary.

Echocardiographic study of left ventricular three-dimensional, radial and longitudinal displacement during base condition in vivo: a canine model

Objective To evaluate the changes of left ventricular myocardial peak 3-dimensional displacement(3D-D), radial displacement(RD) and longitudinal displacement(LD) during baseline patterns, and provide a reliable and appropriate mechanical database for myocardial structure and function. Methods Left ventricular 3D full volumetric real-time imaging in open-chest Beagle canine models(n=10) were acquired in a complete cardiac cycle. The 3D-D, RD and LD for differences and rules were calculated and analyzed by speckle tracking imaging. Results ① There were not difference between 3D-D and RD at baseline patterns with all segments(P>0.05). There were significant difference between 3D-D and LD at baseline patterns with all segments(P 0.05). There were significant difference between 3D-D and LD at baseline patterns with the global(P<0.01). There were significant difference between LD and RD at baseline patterns with the global(P<0.01). ③ There were significant correlation between 3D-D and the most segments of RD(P<0.01). There were correlation between 3D-D and the partly segments of LD (P<0.05). There were correlation between the partly segments of RD and LD(P<0.05). Conclusions Echocardiographic study of left ventricular 3D-D can actually reveal myocardial mechanics and strcture during baseline patterns. 3D-D can accurately reflect left ventricular motion condition. The changes of myocardial mechanics mainly depends on the radial motion.Left ventricular RD can be more accurately reflection on myocardial motion state than LD. Key words: Echocardiography, real-time three-dimensional; Ventricular function, left; Displacement

Cardio-Oncology: Role of Echocardiography

Current therapies for cancer have improved life expectancy of patients. Breast cancer and lymphoma survivors in up to 26% of cases can develop complications as a consequence of the chemotherapeutic and radiotherapeutic treatments. Echocardiography is a noninvasive method that can in all stages of cancer treatment perform a comprehensive evaluation and detect coronary, myocardial, valve and pericardial disease complications secondary to the therapeutic regimen used (radiotherapy and/or chemotherapy). Three-dimensional echocardiography derived left ventricular ejection fraction (LVEF) has an excellent correlation with cardiac magnetic resonance imaging and can be used to monitor LVEF; 2-dimensional speckle tracking echocardiography (2D-STE) derived strain and strain rate can detect changes in myocardial mechanics before changes in LVEF occur and can predict a future decrease in ejection fraction to less than 50% or of greater than 10% indicative of cardiotoxicity. Echocardiography should be used as the method of choice to evaluate serial changes in heart function, detect late side effects of treatment, and to identify patients at risk of a future decrease in LVEF.

Three-dimensional speckle tracking echocardiography for the preclinical diagnosis of hypertrophic cardiomyopathy

The aim is to detect early changes in myocardial mechanics in hypertrophic cardiomyopathy (HCM) mutation carriers, three-dimensional speckle tracking echocardiography (3DSTE) was used for screening of family members in the HCM population. Eighty subjects were divided as: HCM mutation carriers (n = 23), manifest HCM patients (n = 28), and normal controls (n = 29). They prospectively underwent 3DSTE for left atrial (LA) and left ventricle (LV) strain analysis. HCM mutation carriers showed significantly higher LA minimum volume (ml/m(2)) (17 ± 6 vs. 14 ± 4, respectively, P = 0.03) and a significantly lower peak atrial longitudinal strain (PALS) (%), (27 ± 5 vs. 31 ± 7, respectively, P = 0.02) when compared to controls. However, no differences were found in global or regional LV systolic myocardial deformation between both groups. Manifest HCM patients, compared to carriers showed significantly higher LA minimum (27 ± 10 vs. 17 ± 6, respectively, P < 0.001) and maximum volume (42 ± 14 vs. 32 ± 8, respectively, P = 0.007) as well as lower LA ejection fraction (%) (35 ± 8 vs. 47 ± 9, respectively, P < 0.001) and PALS (17 ± 5 vs. 27 ± 5, respectively, P < 0.001). Comparing LV strain, HCM patients showed reduced global longitudinal (-11 ± 4 vs. -16 ± 3, respectively, P < 0.001) and area strain (-35 ± 6 vs. -40 ± 5, respectively, P = 0.005). HCM mutation carriers may be distinguished from healthy subjects using 3DSTE through detection of LA dysfunction that may indicate LV diastolic dysfunction. Further research in a larger study population with gene-specific analysis is warranted for potential clinical usefulness of 3DSTE in family screening for HCM.

Changes in myocardial mechanics in patients with obesity following major weight loss after bariatric surgery

The purpose of this study was to evaluate myocardial mechanics in obese subjects using 2D-speckle tracking echocardiography (2D-STE). 63 obese individuals, including 28 who underwent bariatric surgery for weight loss (BMI 51 ± 9 kg/m2) and 35 managed conservatively (BMI 43 ± 7 kg/m2 ) were included. Changes in strain (S) and strain rate (SR) measured by 2D-STE. Mean follow-up was 23 ± 10 months. The surgery group had a significant weight loss (BMI 37 ± 10 kg/m2 , P < 0.0001), but no change was noted in the nonsurgery group (BMI 42 ± 7 kg/m2 , P = 0.1). For the surgery group, S and SR in early diastole (SRe) improved significantly in the longitudinal left ventricle (LV) (S: P = 0.0004, SRe: P = 0.02) and right ventricle (RV) (S: P = 0.02, SRe: P = 0.009), whereas no changes were seen in LV ejection fraction (LVEF). In the nonsurgery group, there was no change in S, SR, or body weight. For all patients, weight changes correlated significantly with changes in LV S (r = 0.43, P = 0.0005). The improvement of S after bariatric surgery suggests that weight loss could improve myocardial performance, despite the lack of change in LVEF.

How rapidly can diastolic function alter with acute afterloading: insights from a closed chest/closed pericardium acute afterload porcine model

Cardiologia CROATICA Background: The speed and timing of changes in diastolic function parameters during acute LV loading and unloading is unknown. Methods: In a closed chest, closed pericardium porcine model, LV systolic pressure was increased by 30% using a transient descending aortic partial balloon inflation. Morphology and mechanical changes were monitored in real time by echocardiography, as were changes in left and right heart diastolic pressures by 3 Millar catheters. Simultaneous blood pool and tissue Doppler data (radial and long axis) were acquired during afterload changes. Results: In 7 animals, acute loading consistently induced LV dilatation and a rightwards ventricular septal shift due to lateral LV pericardial restraint. This reduced RV volume. Afterload increase caused an immediate decrease in early diastolic filling wave (E) and lateral wall velocity (E’). This was mirrored by an immediate increase in both early diastolic LV (LVDPmin) and LA (LADPmin) pressure (Figure 1). Pulmonary vein flow gradually reduced with decreased late flow. The rightwards septal shift induced a small but significant increase in RVDPmin and an increase in mean RA pressure, but failed to increase pulmonary artery pressure. Acute afterload release immediately returned E values to baseline, but E’ showed a transient further 3 to 5 beat increase before it normalized. Conclusion: Acute afterloading variably elevates all cardiac diastolic pressures and reduces LV relaxation. These early changes in myocardial mechanics occur simultaneously with changes in LVDPmin. Right heart diastolic pressures increase due to the septal shift which both reduced RV volume and decreased LV compliance but did not elevate pulmonary pressure. E’/E recovery differed which could be attributed to transient preload changes.

Tissue Doppler Myocardial Velocity Imaging in Infants and Children-a Window into Developmental Changes of Myocardial Mechanics

In adults, tissue Doppler myocardial velocity imaging (TDI) is a recommended component of routine echocardiography and particularly useful to assess diastolic function of the left ventricle. In contrast, color and pulsed-wave TDI velocities are less accepted in pediatrics, perhaps due to their strong age dependence in children. This review discusses the strengths and limitations of TDI velocity imaging in the pediatric age group. Myocardial velocities increase during normal childhood heart development, starting from fetal life, and these changes vary by cardiac segment. TDI velocity maturation opens an interesting window into the normal development of myocardial mechanics in childhood, but makes it difficult to interpret data in an individual child. Moreover, there is a wider range of normal for any given pediatric age than in adults. Still, TDI has been useful to monitor systolic heart function in children with cardiomyopathy or after heart transplantation. TDI studies revealed diastolic dysfunction in obese children and in cancer survivors with preclinical anthracycline cardiomyopathy. There is a growing body of studies using TDI to assess right heart function in children with congenital heart disease or pulmonary hypertension. Another potential strength of TDI velocities is the study of myocardial dyssynchrony where color TDI is well suited for rapid pediatric heart rates, even on fetal echocardiogram. Quantitative stress echocardiography with TDI is an emerging application in children that already offered insight into heart function in children with tetralogy of Fallot. Therefore, TDI velocity imaging should become part of the routine assessment of heart function in children.

Changes in Left and Right Ventricular Mechanics During the Mueller Maneuver in Healthy Adults

Background— Obstructive sleep apnea is highly prevalent in patients with cardiovascular disease and has detrimental effects on systolic and diastolic function of the ventricles. In this research, the changes in strain (S) and strain rate (SR) during the performance of the Mueller maneuver (MM) in an effort to better understand how negative intrathoracic pressures affect ventricular mechanics. Methods and Results— The MM was performed to maintain a target intrathoracic pressure of −40 mm Hg. Echocardiography was used to measure various parameters of cardiac structure and function. Myocardial deformation measurements were performed using tissue speckle tracking. Twenty-four healthy subjects (9 women; mean age, 30�6 years) were studied. Global left ventricular longitudinal S in systole and SR in early filling were significantly decreased during the MM (S: baseline, −17.0�1.6%; MM, −14.5�2.2%; P &lt;0.0001, SR: baseline, 1.09�0.20 s −1 ; MM, 0.92�0.21 s −1 ; P =0.01). Global right ventricular longitudinal S was also significantly decreased during the MM (baseline, −22.0�3.1%; MM, −17.2�2.5%; P &lt;0.0001), as was global right ventricular longitudinal systolic SR (baseline, −1.34�0.35 s −1 ; MM, −1.02�0.21 s −1 ; P =0.0006). Conclusions— Left ventricular and right ventricular longitudinal deformation are significantly reduced during the MM. These results suggest that negative intrathoracic pressure during apnea may contribute to changes in myocardial mechanics. These results could help explain the observed changes in left ventricular and right ventricular mechanics in patients with obstructive sleep apnea.