scholarly journals Early Left Ventricular Dysfunction Detected by Speckle Tracking in Long-Term Hemodialysis Patients with Valvular Calcification

2018 ◽  
Vol 9 (1) ◽  
pp. 22-30 ◽  
Author(s):  
Jiahui Li ◽  
Aili Li ◽  
Jiali Wang ◽  
Yu Zhang ◽  
Ying Zhou

Purpose: Cardiac valve calcification (VC) is very common in patients on hemodialysis. However, the definite effect of VC on left ventricular (LV) geometry and function in this population is unknown, especially when LV ejection fraction (LVEF) is normal. The aim of this study was to determine the effect of VC on LV geometry and function in long-term hemodialysis patients by conventional echocardiography and two-dimensional speckle tracking echocardiography (2D-STE). Methods: A total of 47 hemodialysis patients (2–3 times weekly for 5 years or more) were enrolled in this study. Cardiac VC was defined as bright echoes of more than 1 mm on one or more cusps of the aortic valve or mitral valve or mitral annulus using echocardiography as the screening method. LV longitudinal global strain (GLS) was assessed on the apical four-chamber view and calculated as the mean strain of 6 segments. LV global circumferential strain was acquired on the LV short axis view at the level of papillary muscles. Results: Twenty-five patients with VC had higher mean values of interventricular septum thickness, LV posterior wall thickness, LV mass index, relative wall thickness, and LV mass/end-diastolic volume than 22 patients without VC (p < 0.05, respectively), indicating more obvious LV hypertrophy (LVH). VC patients had higher mitral annular E/E′ values, especially at the septal side representing increased LV filling pressure compatible with diastolic dysfunction, while only the E/E′ ratio of the septal side was significantly different between the 2 groups (16.7 ± 4.1 vs. 12.3 ± 4.4, p < 0.01). When assessed by GLS, LV longitudinal systolic function was also lower in in patients with VC compared with those without VC (–0.18 ± 0.03 vs. –0.25 ± 0.04; p < 0.01). Conclusions: Cardiac VC diagnosed by echocardiography when it occurs in long-term hemodialysis patients may indicate more severe LVH, myocardial damage, and worse heart function in comparison to those without VC. Tissue Doppler imaging and 2D-STE can detect the subtle change of heart function in this population in the early stage of LV dysfunction when LVEF is normal.

Hypertension ◽  
2021 ◽  
Vol 78 (Suppl_1) ◽  
Author(s):  
Aline M De Souza ◽  
Jonathas Almeida ◽  
Nataliia Shults ◽  
Hong Ji ◽  
Kathryn Sandberg

Severe caloric restriction (sCR) increases the risk for acute cardiovascular disease. Less understood are the long-term effects on cardiovascular disease risk after the sCR period has ended. We investigated the effects of sCR on heart structure and function months after refeeding (sCR-Refed). Female Fischer rats (3-months-old) were maintained on (CT) ad libitum or a 60% caloric restricted diet for 2 weeks. Thereafter, all rats received ad libitum chow for 3 months and they were analyzed by precision ultrasound to assess their heart function. After imaging, the animals were sacrificed and the hearts were subjected to ischemia-reperfusion (I/R) using a Langendorff preparation. After 2 weeks of sCR, rats lost 15% of their initial body weight (BW) [% (100*(Final-Initial/Initial)): CT, 1.5±0.8 vs sCR, -15.4±1.1; p<0.001;n=8]. After 3 months of refeeding, there was no detectable difference in BW between CT and sFR-Refed groups. Isolated hearts from the sCR-Refed rats exhibited worse myocardial pathology after I/R compared to CT rats. The parallel orientation of myofibers and striations normally present in cardiomyocytes was lost in sCR-Refed rats. Further analysis revealed uneven blood-filling of the microcirculatory vessels and prominent interstitial edema of the myocardium. Hearts from sCR-Refed rats had more atrophied cardiomyocytes than CT [Atrophied/Total (%): CT, 0.2±0.1 vs sCR-Refed, 50.6±1.1; p<0.001; n=5]. The number of arrhythmic events during a 30 min ischemic interval in isolated hearts doubled after 2 weeks on the sCR diet ( data not shown ) and remained doubled 3 months later [Arrhythmias (% of time): CT, 34±8 vs sCR-Refed, 68±9; p=0.02; n=8]. Ultrasound imaging showed no difference in stroke volume, coronary perfusion pressure and left ventricular mass. However, the thickness of the left ventricular posterior wall was significantly reduced in sCR-Refed rats [(mm): CT, 2.55 ±0.03 vs sCR-Refed, 2.10±0.04; p=0.002; n=4]. These findings indicate heart structure and function remained damaged months after the sCR period ended and BW was restored. These studies have adverse cardiovascular risk implications for who are subjected either voluntarily (crash diets) or involuntarily (very low food security) to periods of inadequate caloric intake.


scholarly journals HIT Poster session 1P154Preclinical diastolic dysfunction is related to impaired endothelial function in patients with chronic kidney diseaseP155Early detection of left atrial and left ventricular abnormalities in hypertensive and obese womenP156Right ventricle preserved systolic function irrespective of right ventricular hypertrophy and disease severity in anderson fabry diseaseP157Left atrial volume and function in patients undergoing percutaneous mitral valve repairP158Impact of left ventricular dysfunction on outcomes of patients undergoing direct TAVI with a self-expanding bioprosthesisP159Anatomic Doppler spectrum – retrospective spectral tissue Doppler from ultra high frame rate tissue Doppler imaging for evaluation of tissue deformationP160Phasic dynamics of ischaemic mitral regurgitation after primary coronary intervention in acute myocardial infarction: serial echocardiographic assessment from emergency room to long-term follow-upP161Reproducibility of 3DE RV volumes - novel insights at a regional levelP162Pulmonary vascular capacitance as assessed by echocardiography in pulmonary arterial hypertensionP163Three-dimensional endocardial area strain: a novel parameter for quantitative assessment of global left ventricular systolic functionP164Role of exercise hemodynamics assessed by echocardiography on symptom reduction after MitraClipP165Early identification of ventricular dysfunction in patients with juvenile systemic sclerosisP166Heart failure with and without preserved ejection fraction - the role of biomarkers in the aspect of global longitudinal strainP167Complex systolic deformation of aortic root: insights from two dimensional speckle tracking imageP168Volumetric and deformational imaging usind 2d strain and 3d echocardiography in patients with pulmonary hypertensionP169Influence of pressure load and right ventricular morphology and function on tricuspid regurgitation in pulmonary arterial hypertensionP170Left ventricular myocardial diastolic deformation analysis by 2D speckle tracking echocardiography and relationship with conventional diastolic parameters in chronic aortic regurgitationP171Extracellular volume, and not native T1 time, distinguishes diffuse fibrosis in dilated or hypertrophic cardiomyopathy at 3TP172Left atrial strain is significantly reduced in arterial hypertensionP173Symptomatic severe secondary mitral regurgitation: LV enddiastolic diameter (LVEDD) as preferable parameter for risk stratificationP174Left ventricular mechanics in isolated left bundle branch block at rest and when exercising: exploration of the concept of conductive cardiomyopathyP175Assessment of myocardial scar by 2D contrast echocardiographyP176Chronic pericarditis - expression of a rare disease: Erdheim Chester diseaseP177Aortic arch mechanics with two-dimensional speckle tracking echocardiography to estimate the left ventricular remodelling in hypertensive patientsP178Strain analysis by tissue doppler imaging: comparison of conventional manual measurement with a semi-automated approachP179Distribution of extravascular lung water in heart failure patients assessed by lung ultrasoudP180Surrogate markers for obstructive coronary artery diseaseP181LA deformation and LV longitudinal strain by two-dimensional speckle tracking echocardiography as predictors of postoperative AF development after aortic valve replacement in ASP182Left ventricular diastolic dysfunction in type 2 diabetic patients with non alcoholic fatty liver diseaseP183Myocardial strain by speckle-tracking and evaluation of 3D ejection fraction in drug-induced cardiotoxicity's approach in breast cancer

2015 ◽  
Vol 16 (suppl 2) ◽  
pp. S4-S11 ◽  
Author(s):  
AB Gevaert ◽  
A Borizanova ◽  
F Graziani ◽  
O M Galuszka ◽  
K Stathogiannis ◽  
...  

Author(s):  
My-Le Nguyen ◽  
Vandana Sachdev ◽  
Thomas R Burklow ◽  
Wen Li ◽  
Megan Startzell ◽  
...  

Abstract Context Lipodystrophy syndromes are rare disorders of deficient adipose tissue, low leptin, and severe metabolic disease, affecting all adipose depots (generalized, GLD) or only some (partial, PLD). Left ventricular (LV) hypertrophy is common (especially in GLD); mechanisms may include hyperglycemia, dyslipidemia, or hyperinsulinemia. Objective Determine effects of recombinant leptin (metreleptin) on cardiac structure and function in lipodystrophy. Design/Participants/Intervention/Setting Open-label treatment study of 38 subjects (18 GLD, 20 PLD) at the National Institutes of Health before and after 1 (N=27), and 3-5y (N=23) of metreleptin. Outcome Echocardiograms, blood pressure (BP), triglycerides, A1c, HOMA-IR Results In GLD, metreleptin lowered triglycerides (median(IQR) 740(403-1239), 138(88-196), 211(136-558) mg/dL at baseline, 1y, 3-5y, P&lt;0.0001), A1c (9.5±3.0, 6.5±1.6, 6.5±1.9%, P&lt;0.001), and HOMA-IR (34.1(15.2-43.5), 8.7(2.4-16.0), 8.9(2.1-16.4), P&lt;0.001). Only HOMA-IR improved in PLD (P&lt;0.01). Systolic BP decreased in GLD but not PLD. Metreleptin improved cardiac parameters in patients with GLD, including reduced posterior wall thickness (9.8±1.7, 9.1±1.3, 8.3±1.7 mm, P&lt;0.01), and LV mass (140.7±45.9, 128.7±37.9, 110.9±29.1 g, P&lt;0.01), and increased septal e’ velocity (8.6±1.7, 10.0±2.1, 10.7±2.4 cm/s, P&lt;0.01). Changes remained significant after adjustment for BP. In GLD, multivariate models suggested that reduced posterior wall thickness and LV mass index correlated with reduced triglycerides and increased septal e’ velocity correlated with reduced A1c. No changes in echocardiographic parameters were seen in PLD. Conclusion Metreleptin attenuated cardiac hypertrophy and improved septal e’ velocity in GLD, which may be mediated by reduced lipotoxicity and glucose toxicity. The applicability of these findings to leptin-sufficient populations remains to be determined.


2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A315-A316
Author(s):  
My-Le Nguyen ◽  
Vandana Sachdev ◽  
Thomas Burklow ◽  
Wen Li ◽  
Rebecca J Brown

Abstract Lipodystrophy (LD) syndromes are rare disorders of deficient adipose tissue and severe metabolic disease, including insulin resistance, diabetes, and hypertriglyceridemia. LD may affect all adipose depots (generalized LD, GLD) or only some depots (partial LD, PLD). Low adipose mass leads to very low leptin in GLD, and variable leptin in PL. Treatment with exogenous leptin (metreleptin) improves metabolic disease in LD, particularly GLD. Left ventricular (LV) hypertrophy is frequent in LD, especially GLD. The mechanism for hypertrophy in LD is not known and may relate to glucose or lipotoxicity. We hypothesized that metreleptin would improve cardiac abnormalities in LD, and that this would be mediated by improvements in glucose and triglycerides (TG). We analyzed echocardiograms (echo), blood pressure (BP), heart rate (HR), and metabolic parameters in 38 subjects with LD (18 GLD, 20 PLD) who were treated with metreleptin in open-label clinical studies at the National Institutes of Health. 27 had repeat echo after 1y of metreleptin (mean 1.0 ± 0.2y), and 23 after 3 to 5y (mean 3.7±0.6y). In GLD, metreleptin significantly improved metabolic disease, including reduced TG (median(IQR) 740(403–1239), 138(88–196), 211(136–558) mg/dL at baseline, 1y, & 3-5y, P&lt;0.0001), hemoglobin A1c (9.5±3.0, 6.5±1.6, 6.5±1.9% at baseline, 1y, & 3-5y, P&lt;0.001), and insulin resistance by HOMA-IR (34.1 (15.2–43.5), 8.7 (2.4–16.0), 8.9 (2.1–16.4), P&lt;0.001). Only HOMA-IR improved in PLD (P&lt;0.01). Systolic BP and HR decreased after metreleptin in GLD (BP 120±11, 117±10, 109±16 mmHg, P=0.046; HR 89±9, 82±12, 80±16 bpm, P=0.018; at baseline, 1y, 3-5y, respectively) but not PLD. Metreleptin improved cardiac parameters in patients with GLD, including reduced posterior wall thickness (9.8±1.7, 9.1±1.3, 8.3±1.7 at baseline, 1y, & 3-5y, P&lt;0.01), LV mass (140.7±45.9, 128.7±37.9, 110.9±29.1 at baseline, 1y, & 3-5y, P&lt;0.01), and LV mass index (88.6±22.0, 81.6±16.9, 81.6±16.9 at baseline, 1y, & 3-5y, P&lt;0.01). Metreleptin also improved septal e’ velocity, a measure of early diastolic cardiac function, in GLD (8.6±1.7, 10.0±2.1, 10.7±2.4 at baseline, 1y, & 3-5y, P&lt;0.01). All changes remained significant after adjustment for BP. In GLD, multivariate variable selection models suggested that changes in posterior wall thickness and LV mass index related to metreleptin-induced reductions in TG, and changes in septal e’ velocity related to metreleptin-induced reductions in hemoglobin A1c. No changes in echo parameters were seen in PLD. These findings suggest that metreleptin improves cardiac hypertrophy and diastolic function in patients with GLD, and these improvements may be mediated by reduced lipotoxicity and glucose toxicity. The applicability of these findings to a broader, leptin-sufficient population with LV hypertrophy and/or diabetic cardiomyopathy remains to be determined.


2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Marianna Török ◽  
Petra Merkely ◽  
Anna Monori-Kiss ◽  
Eszter Mária Horváth ◽  
Réka Eszter Sziva ◽  
...  

Abstract Background We aimed to identify sex differences in the network properties and to recognize the geometric alteration effects of long-term swim training in a rat model of exercise-induced left ventricular (LV) hypertrophy. Methods Thirty-eight Wistar rats were divided into four groups: male sedentary, female sedentary, male exercised and female exercised. After training sessions, LV morphology and function were checked by echocardiography. The geometry of the left coronary artery system was analysed on pressure-perfused, microsurgically prepared resistance artery networks using in situ video microscopy. All segments over > 80 μm in diameter were studied using divided 50-μm-long cylindrical ring units of the networks. Oxidative-nitrative (O-N) stress markers, adenosine A2A and estrogen receptor (ER) were investigated by immunohistochemistry. Results The LV mass index, ejection fraction and fractional shortening significantly increased in exercised animals. We found substantial sex differences in the coronary network in the control groups and in the swim-trained animals. Ring frequency spectra were significantly different between male and female animals in both the sedentary and trained groups. The thickness of the wall was higher in males as a result of training. There were elevations in the populations of 200- and 400-μm vessel units in males; the thinner ones developed farther and the thicker ones closer to the orifice. In females, a new population of 200- to 250-μm vessels appeared unusually close to the orifice. Conclusions Physical activity and LV hypertrophy were accompanied by a remodelling of coronary resistance artery network geometry that was different in both sexes.


2021 ◽  
Vol 22 (Supplement_1) ◽  
Author(s):  
O Itzhaki Ben Zadok ◽  
A Eisen ◽  
Y Shapira ◽  
D Monakier ◽  
Z Iakobishvili ◽  
...  

Abstract Funding Acknowledgements Type of funding sources: None. Background Since the diagnosis of cardiac amyloidosis (CA) is often delayed, echocardiographic findings are frequently indicative of already advanced cardiomyopathy. Aims to describe early echocardiographic features in patients subsequently diagnosed with CA and to delineate disease progression. Methods Pre-amyloid diagnosis echocardiographic studies were screened for structural and functional parameters and stratified according to the pathogenetic amyloid subtype (immunoglobulin light-chain (AL) or amyloid transthyretin (ATTR)). Abnormalities were defined based on published guidelines. Results Our cohort included 75 CA patients of whom 42 (56%) were diagnosed with AL and 33 (44%) with ATTR. Forty-two patients had an earlier echocardiography exam available for review. Patients presented with increased wall thickness (1.3 (IQR 1.0, 1.5)cm) ≥3 years before the diagnosis of CA and relative wall thickness (RWT) was increased (0.47 (IQR 0.41, 0.50)) ≥7 years pre-diagnosis. Between 1 to 3 years before CA diagnosis restrictive left ventricular (LV) filling pattern was present in 19% of patients and LV ejection fraction (LVEF)≤50% was present in 21% of patients. Right ventricular dysfunction was detected concomitantly with disease diagnosis. The echocardiographic phenotype of ATTR versus AL-CA showed increased RWT (0.74 (IQR 0.62, 0.92) vs. 0.62 (IQR 0.54, 0.76), p = 0.004) and LV mass index (144 (IQR 129, 191) vs. 115 (IQR 105, 146)g/m2,p = 0.020) and reduced LVEF (50 (IQR 44, 58) vs. (60 (IQR 53, 60)%, p = 0.009) throughout the time course of CA progression, albeit survival time was similar. Conclusions Increased wall thickness and diastolic dysfunction in CA develop over a time course of several years and can be diagnosed in their earlier stages by standard echocardiography Abstract Figure. Schematic proposed timeline of CA


PEDIATRICS ◽  
1996 ◽  
Vol 97 (6) ◽  
pp. 818-821 ◽  
Author(s):  
Andrew S. Bensky ◽  
Jamanadas M. Kothadia ◽  
Wesley Covitz

Objective. To characterize the cardiac effects of dexamethasone in very low birth weight infants. Design. Prospective, randomized, placebo-controlled, double-blind trial. Enrolled subjects were randomized to receive either a 42-day tapering course of dexamethasone or a saline placebo. Echocardiographic measurements were obtained on days 0, 7, 14, 28, and 42. Subjects. Thirteen infants received dexamethasone and 13 a saline placebo. The two groups were similar in birth weight, gestational age, age at enrollment, and sex/race composition. Results. Patients receiving dexamethasone had a significantly larger increase in septal thickness on days 7, 14, and 28 and left ventricle (LV) posterior wall thickness on day 14. A significantly lower left ventricular enddiastolic dimension in the dexamethasone group was initially noted on day 7 and persisted until day 42. With the reduced left ventricular end-diastolic dimension, no significant differences in LV mass were noted, despite the increased wall thickness. No differences in LV systolic function, as assessed by area shortening, were seen. Assessment of diastolic function showed a significant increase in the atrial portion of mitral inflow in dexamethasone patients on day 14, as well as a significant prolongation in isovolumic relaxation time on days 7, 14, and 28. Conclusions. Infants receiving dexamethasone developed evidence for impaired LV filling with a larger increase in wall thickness but no increase in LV mass, asymmetric septal hypertrophy, or augmented systolic function. This suggests that alterations in left ventricular filling play an important role in the development of hypertrophy seen with dexamethasone administration.


2021 ◽  
Vol 22 (Supplement_1) ◽  
Author(s):  
F Loncaric ◽  
A Garcia-Alvarez ◽  
P Garcia-Canadilla ◽  
L Sanchiz ◽  
H Dejea ◽  
...  

Abstract Funding Acknowledgements Type of funding sources: Public grant(s) – EU funding. Main funding source(s): Horizon 2020 European Commission Project H2020-MSCA-ITN-2016 (764738) and the Clinical Research in Cardiology grant from the Spanish Cardiac Society. Background The aetiology of left ventricular hypertrophy (LVH) is a relevant clinical challenge with consequences for patient management. Phenotypes resulting from hypertensive remodelling and sarcomere mutation often overlap. Synchrotron X-ray phase-contrast imaging (X-PCI) is a technique that can provide 3-dimensional detailed information on myocardial micro-structure non-destructively. The aim is to relate macrostructural/functional, non-invasive, imaging phenotypes of hypertrophic cardiomyopathy (HCM) to the underlying myocardial microstructure assessed with X-PCI. Methods Myocardial tissue samples were obtained from three patients (P1-3) with obstructive myocardial hypertrophy undergoing septal myectomy. Medical history and the 5-year HCM risk scores were evaluated. The patients were imaged with magnetic resonance imaging and echocardiography prior to procedure. Myocardial structure was assessed with wall thickness, late gadolinium enhancement (LGE), whereas function with speckle-tracking deformation (STE) and tissue Doppler imaging (TDI). Myectomy tissue was imaged with X-PCI in the TOMCAT beamline, using a multiscale propagation-based protocol combining a low-resolution (LR) and a high-resolution (HR) setup (5.8 and 0.7 um pixel size, respectively). Results The clinical and imaging data are shown in Fig 1. On initial assessment, wall thickness, LGE distribution, global longitudinal strain and septal TDI demonstrated a similar macrostructural and functional phenotype of P1 and P2, whereas P3 stood out with more severe hypertrophy, scarring and dysfunction. Additional regional deformation analysis with STE revealed reduced deformation in the basal and mid septum in P1, paired with a hypertensive pattern of post-systolic shortening (PSS) (yellow arrows). In comparison, in P2 and P3, deformation was more heterogeneous regionally, with regions of almost complete absence of deformation (orange arrows). Upon further exploration with TDI, areas with abnormal deformation were identified on the transition from basal to mid septum in both P2 and P3, whereas deformation was normal, but reduced in P1, and paired with PSS. LR X-PCI defined regions of interest to scan with HR (yellow frame), where HR revealed extensive interstitial fibrosis (orange arrow) with normal myocyte size and organisation in P1, compatible with severe hypertensive remodelling. However, in P2 and P3, patches of fibrosis (yellow arrow) paired with enlarged myocytes organized in visible disarray, considerably more prominent in P3, were both compatible with sarcomere-mutation HCM. Conclusion The results demonstrate multiscale phenotyping of HCM - relating micro- and macrostructural findings to function, and integrating multimodality data. In-depth regional deformation analysis, validated by synchrotron-based microstructural analysis, showed potential to identify distinct imaging phenotypes in HCM, distinguishing between overlapping presentations in different aetiologies. Abstract Figure 1


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