Hyperinsulinemia: effect on cardiac mass/function, angiotensin II receptor expression, and insulin signaling pathways

To investigate the association between hyperinsulinemia and cardiac hypertrophy, we treated rats with insulin for 7 wk and assessed effects on myocardial growth, vascularization, and fibrosis in relation to the expression of angiotensin II receptors (AT-R). We also characterized insulin signaling pathways believed to promote myocyte growth and interact with proliferative responses mediated by G protein-coupled receptors, and we assessed myocardial insulin receptor substrate-1 (IRS-1) and p110α catalytic and p85 regulatory subunits of phospatidylinositol 3 kinase (PI3K), Akt, MEK, ERK1/2, and S6 kinase-1 (S6K1). Left ventricular (LV) geometry and performance were evaluated echocardiographically. Insulin decreased AT1a-R mRNA expression but increased protein levels and increased AT2-R mRNA and protein levels and phosphorylation of IRS-1 (Ser374/Tyr989), MEK1/2 (Ser218/Ser222), ERK1/2 (Thr202/Tyr204), S6K1 (Thr421/Ser424/Thr389), Akt (Thr308/Thr308), and PI3K p110α but not of p85 (Tyr508). Insulin increased LV mass and relative wall thickness and reduced stroke volume and cardiac output. Histochemical examination demonstrated myocyte hypertrophy and increases in interstitial fibrosis. Metoprolol plus insulin prevented the increase in relative wall thickness, decreased fibrosis, increased LV mass, and improved function seen with insulin alone. Thus our data demonstrate that chronic hyperinsulinemia decreases AT1a-to-AT2 ratio and increases MEK-ERK1/2 and S6K1 pathway activity related to hypertrophy. These changes might be crucial for increased cardiovascular growth and fibrosis and signs of impaired LV function.

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Abstract 4197: Does Relative Wall Thickness or Left Ventricular Mass Index Best Predict Mortality Risk in Patients With Preserved Systolic Function?

Circulation ◽

10.1161/circ.118.suppl_18.s_841 ◽

2008 ◽

Vol 118 (suppl_18) ◽

Author(s):

Dharmendrakumar A Patel ◽

Carl J Lavie ◽

Sangeeta Shah ◽

Yvonne Gilliland ◽

Richard V Milani

Keyword(s):

Wall Thickness ◽

Systolic Function ◽

Age Groups ◽

Left Ventricular ◽

Relative Wall Thickness ◽

Prognostic Impact ◽

Geometric Patterns ◽

Lv Mass ◽

Mortality Table ◽

The Impact

Background: Several studies have indicated that left ventricular (LV) geometric patterns predict cardiovascular events. However, little data is available that compares the relative prognostic impact of LV mass index (LVMI) and relative wall thickness (RWT) on mortality in a large cohort of patients with preserved systolic function. Methods: The impact of LVMI and RWT on mortality during an average follow-up of 1.7±1.0 years was examined in a sample of 47,701 patients (mean age: 61.6 ± 15.4; females=54.6 %) with preserved ejection fraction(EF), as well as in age groups of <50 yrs(n=10,864; mean age=39.9 ± 8.1; females=58.4 %), 50 –70 yrs (n=20,181; mean age=59.9 ± 5.7; females=52.2 %) and >= 70 yrs (n=16,836; mean age=77.7 ± 5.5; females=55.1 %). Results: With increasing age (<50, 50 –70, >=70 yrs), both LVMI (78.5 ± 23.4, 84.3 ± 25.4, 90.3 ± 27.6; p<0.0001) and RWT (0.37 ± 0.08, 0.41 ± 0.08, 0.43 ± 0.09; p<0.0001) as well as mortality (2.2%, 5.0%, 14.2%; p<0.0001) showed significant linear trends and were independent predictors of mortality (Table , Figure ). Conclusion: Although, both LVMI and RWT were independently associated with increased mortality in all groups, RWT was by far the strongest independent predictor of all-cause mortality, especially in younger patients.

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P955 left ventricle cardiac remodeling among lithuanian football versus basketball players

European Heart Journal - Cardiovascular Imaging ◽

10.1093/ehjci/jez319.588 ◽

2020 ◽

Vol 21 (Supplement_1) ◽

Author(s):

A Aldujeli ◽

J Laukaitiene ◽

R Unikas

Keyword(s):

Left Ventricle ◽

Wall Thickness ◽

Cardiac Remodeling ◽

Interventricular Septum ◽

Posterior Wall ◽

Left Ventricular ◽

Relative Wall Thickness ◽

Football Players ◽

Basketball Players ◽

Lv Mass

Abstract Background Regular physical exercise causes a continuous gradual increase of the cardiac left ventricular (LV) mass known as physiological adaptive hypertrophy. The extent of LV remodeling depends on the type, amount, and intensity of the exercise. Purpose The aim of this study was to compare structural changes of the heart among Lithuanian football, basketball players and unathletic controls. Methods A total of 50 Lithuanian males aged between 20-29 years volunteered to participate in the study. Football players (n = 15) playing for local II league football clubs,and Basketball players (n = 15) playing for local minor league basketball teams. All athletes had been regularly engaged in their sport for at least three years. Inactive healthy volunteers (n = 20) of similar age served as controls. Routine transthoracic echocardiographic examinations to measure end-diastolic LV dimensions were performed by cardiology fellow under the supervision of a fully licensed cardiologist. Statistical analyses were performed using the SPSS 20.0 software. The value of p < 0,05 was considered as statistically significant. Results No structural or functional pathologies were evident during the echocardiographic examination in any of the subjects. Absolute interventricular septum (IVS) thickness and LV posterior wall thickness, but not LV diameter, were higher in athletes than in inactive controls (P < 0,001). Indexed LV diameter was higher in football players as compared with non-athlete controls and basketball players (P < 0,05). Left ventricular mass of all athletes were higher as compared with controls (p < 0.001). Relative wall thickness was not increased in football players but was higher in basketball players as compared with controls (p < 0.05). Conclusion Cardiac remodeling in Lithuanian football players resulted in left ventricle eccentric hypertrophy due to the LV dilation, increased LV mass and relatively normal relative wall thickness. However in Lithuanian basketball players we noticed an increase in both relative wall thickness and LV mass resulting in LV concentric hypertrophy. Echocardiographic characteristics Groups n End-diastolic LV diameter(mm) End-diastolic Interventricular septum (mm) End-diastolic LV posterior wall LV mass Football Players 15 56.9 10.8 10.8 242 Basketball players 15 53.6 11.5 11.3 254 Inactive individuals 20 53.2 9.1 9.5 182 P value 0.01 <0.001 <0.001 <0.01 Abstract P955 Figure.

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A Reduction in ADAM17 Expression Is Involved in the Protective Effect of the PPAR-α Activator Fenofibrate on Pressure Overload-Induced Cardiac Hypertrophy

PPAR Research ◽

10.1155/2018/7916953 ◽

2018 ◽

Vol 2018 ◽

pp. 1-8 ◽

Cited By ~ 2

Author(s):

Si-Yu Zeng ◽

Hui-Qin Lu ◽

Qiu-Jiang Yan ◽

Jian Zou

Keyword(s):

Body Weight ◽

Angiotensin Ii ◽

Cardiac Hypertrophy ◽

Wall Thickness ◽

Protective Action ◽

Pressure Overload ◽

Left Ventricular ◽

Heart Weight ◽

Hypertensive Rats ◽

Protein Levels

The peroxisome proliferator-activated receptor-α (PPAR-α) agonist fenofibrate ameliorates cardiac hypertrophy; however, its mechanism of action has not been completely determined. Our previous study indicated that a disintegrin and metalloproteinase-17 (ADAM17) is required for angiotensin II-induced cardiac hypertrophy. This study aimed to determine whether ADAM17 is involved in the protective action of fenofibrate against cardiac hypertrophy. Abdominal artery constriction- (AAC-) induced hypertensive rats were used to observe the effects of fenofibrate on cardiac hypertrophy and ADAM17 expression. Primary cardiomyocytes were pretreated with fenofibrate (10 μM) for 1 hour before being stimulated with angiotensin II (100 nM) for another 24 hours. Fenofibrate reduced the ratios of left ventricular weight to body weight (LVW/BW) and heart weight to body weight (HW/BW), left ventricular anterior wall thickness (LVAW), left ventricular posterior wall thickness (LVPW), and ADAM17 mRNA and protein levels in left ventricle in AAC-induced hypertensive rats. Similarly, in vitro experiments showed that fenofibrate significantly attenuated angiotensin II-induced cardiac hypertrophy and diminished ADAM17 mRNA and protein levels in primary cardiomyocytes stimulated with angiotensin II. In summary, a reduction in ADAM17 expression is associated with the protective action of PPAR-α agonists against pressure overload-induced cardiac hypertrophy.

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Abnormal left ventricular geometry in female collegiate swimmers

European Heart Journal ◽

10.1093/eurheartj/ehab724.2784 ◽

2021 ◽

Vol 42 (Supplement_1) ◽

Author(s):

Y K Taha ◽

C A Rambart ◽

F Reifsteck ◽

R Hamburger ◽

J R Clugston ◽

...

Keyword(s):

Wall Thickness ◽

Female Athletes ◽

Interventricular Septum ◽

Posterior Wall ◽

Left Ventricular ◽

Relative Wall Thickness ◽

Left Ventricular Geometry ◽

Ventricular Geometry ◽

Posterior Wall Thickness ◽

Lv Mass

Abstract Background There is a paucity of data describing left ventricular geometry changes in female athletes. While some studies suggest that female athletes participating in dynamic sports exhibit higher prevalence of eccentric left ventricular hypertrophy (LVH) when compared to men, a recent study suggested more concentric geometry changes in female basketball athletes. We were unable to identify studies describing the left ventricular geometry of female collegiate swimmers. Objectives To describe LV geometry changes in a cohort of female collegiate swimmers. Methods We analyzed a cohort of female collegiate swimmers who had a pre-participation cardiac evaluation by 12-lead ECG and 2-dimensional echocardiography. Left ventricular (LV) geometry was assessed based on relative wall thickness (RWT) (defined as: 2 x posterior wall thickness (PWT) divided by LV end-diastolic diameter (LVEDD)) and LV mass (LVM) (Devereux's formula: LVM = [0.8 x 1.04 [(LVEDD + interventricular septum + posterior wall thickness)3 − (LVEDD)3]] + 0.6g) and was indexed to body surface area (BSA).LVH was defined as LV mass index >95 g and was defined as concentric when associated with a relative wall thickness (RWT) >0.42 and as eccentric when RWT was ≤0.42. Concentric remodeling was defined as normal LVM index and increased RWT. Results A total of 83 female collegiate swimmers were included. Their age was 18.5±0.5 years (mean ± standard deviation, SD), 74 (89.2%) were White, BSA was 1.78±0.11 m2, height 173±6.3 cm, weight 66.2±7.2 K. Their interventricular septum diameter was 0.89±0.14 cm, PWT 0.92±0.15 cm, LVEDD 4.9±0.5 cm and LV end-systolic diameter (LVESD) 3.2±0.4 cm. Left atrium diameter ranged from 2.6 to 4.3 cm (mean 3.4 cm ± 0.4 cm). Aortic root diameter ranged from 1.9 to 3.5 cm (mean 2.7±0.3 cm) (Figure 1). LVH was present in 27 swimmers (32.5%). Eccentric LVH was present in 17 athletes (20.5%), concentric hypertrophy in 10 athletes (12%), and concentric remodeling in 12 (14.5%) (Figure 2). No athletes with LVH or concentric remodeling had borderline or abnormal ECG findings based on international criteria. Only two women with normal LV geometry had abnormal ECG findings: prolonged QT interval and abnormal T wave inversion. There was a linear correlation between BSA with LVEDD, LVESD and LV mass (r=0.40, 0.35, and 0.48 with P<0.001,0.002 and <0.001, respectively). However, there was no statistically significant difference between LV geometry groups based on BSA or blood pressure. Conclusion Our data document a high incidence of eccentric hypertrophy among female collegiate swimmers. Concentric remodeling and hypertrophy were also relatively high. Differentiating physiologic from pathologic cardiac remodeling in these athletes is critical to prevent potential complications such as sudden cardiac death, arrhythmias, and other adverse outcomes. FUNDunding Acknowledgement Type of funding sources: Foundation. Main funding source(s): This work was supported in part by the American Medical Society for Sports Medicine (AMSSM) Foundation Research Grant 2016 awarded to KE, and the University of Florida REDCap uses the NIH National Center for Advancing Translational Sciences (NCATS) grant UL1 TR001427. Figure 1 Figure 2. LV geometry in female swimmers

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Urine Albumin to Creatinine Ratio and Echocardiographic Left Ventricular Structure and Function in Patients with Essential Hypertension

The American Heart Hospital Journal ◽

10.15420/ahhj.2011.9.2.90 ◽

2011 ◽

Vol 9 (2) ◽

pp. 90 ◽

Cited By ~ 2

Author(s):

Rohola Hemmati ◽

Mojgan Gharipour ◽

Hasan Shemirani ◽

Alireza Khosravi ◽

Elham Khosravi ◽

...

Keyword(s):

Essential Hypertension ◽

Peak Velocity ◽

Left Ventricular ◽

Lv Function ◽

Creatinine Ratio ◽

Uncomplicated Hypertension ◽

Urine Albumin ◽

Lv Dysfunction ◽

Mitral Annulus Velocity ◽

Lv Mass

Background:Appearance of microalbuminuria, particularly in patients with hypertension, might be associated with a higher prevalence of left ventricular (LV) dysfunction and geometric abnormalities. This study was undertaken to determine whether high urine albumin to creatinine ratio (UACR) as a sensitive marker for microalbuminuria can be associated with LV hypertrophy (LVH) and systolic and diastolic LV dysfunction.Methods:The study population consisted of 125 consecutive patients with essential uncomplicated hypertension. Urine albumin and creatinine concentration was determined by standard methods. LVH was defined as a LV mass index >100 g/m2 of body surface area in women and >130 g/m2 in men. Echocardiographic LV systolic and diastolic parameters were measured.Results:The prevalence of microalbuminuria in patients with essential hypertension was 5.6 %. UACR was significantly no different in patients with LVH than in patients with normal LV geometry (21.26 ± 31.55 versus 17.80 ± 24.52 mg/mmol). No significant correlation was found between UACR measurement and systolic and diastolic function parameters, including early to late diastolic peak velocity (E/A) ratio (R=-0.192, p=0.038), early diastolic peak velocity to early mitral annulus velocity (E/E') ratio (R=-0.025, p=0.794), LV ejection fraction (R=0.008, p=0.929), and LV mass (R=-0.132, p=0.154). According to the receiver operator characteristic (ROC) curve analysis, UACR measurement was not an acceptable indicator of LVH with areas under the ROC curves 0.514 (95 % confidence interval 0.394–0.634). The optimal cut-off value for UACR for predicting LVH was identified at 9.4, yielding a sensitivity of 51.6 % and a specificity of 48.3 %.Conclusion:In patients with uncomplicated essential hypertension, abnormal systolic and diastolic LV function and geometry cannot be effectively predicted by the appearance of microalbuminuria.

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Natural history and disease progression of early cardiac amyloidosis evaluated by echocardiography

European Heart Journal - Cardiovascular Imaging ◽

10.1093/ehjci/jeaa356.387 ◽

2021 ◽

Vol 22 (Supplement_1) ◽

Author(s):

O Itzhaki Ben Zadok ◽

A Eisen ◽

Y Shapira ◽

D Monakier ◽

Z Iakobishvili ◽

...

Keyword(s):

Disease Progression ◽

Wall Thickness ◽

Cardiac Amyloidosis ◽

Time Course ◽

Right Ventricular Dysfunction ◽

Disease Diagnosis ◽

Left Ventricular ◽

Funding Sources ◽

Lv Mass ◽

Echocardiographic Findings

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

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Abstract 16018: Impaired Intrinsic Myocardial Shortening in Both Two Directions and Compensatory Mechanism to Maintain Left Ventricular Ejection Fraction in Patients With Hypertensive Heart Disease

Circulation ◽

10.1161/circ.130.suppl_2.16018 ◽

2014 ◽

Vol 130 (suppl_2) ◽

Author(s):

Satoshi Yamada ◽

Kazunori Okada ◽

Hisao Nishino ◽

Hiroyuki Iwano ◽

Daisuke Murai ◽

...

Keyword(s):

Heart Disease ◽

Ejection Fraction ◽

Wall Thickness ◽

Circumferential Strain ◽

Hypertensive Heart Disease ◽

Wall Stress ◽

Left Ventricular ◽

Relative Wall Thickness ◽

Left Ventricular Ejection ◽

Compensatory Mechanism

Background: Longitudinal myocardial shortening is known to be reduced even if left ventricular (LV) ejection fraction (EF) is preserved in patients with hypertensive heart disease (HHD). However, the compensatory mechanism remains to be elucidated. Thus layer-specific longitudinal and circumferential strain as well as stress-strain relationship was observed in HHD patients. Methods: In 46 HHD patients with preserved EF (>50%) and 29 age-matched control subjects, global longitudinal strain (LS) and layer-specific circumferential strain (CS) were measured from the apical 4-chamber view and mid-ventricular short-axis view, respectively, by using speckle tracking echocardiography. LS was measured at innermost LV wall layer, and CS at innermost, midwall, and outermost layers. Layer-specific end-systolic circumferential wall stress (CWS) according to Mirsky’s formula and endocardial meridional wall stress (MWS) were calculated. Results: Systolic blood pressure (147±20 mm Hg), interventricular septal thickness (13±2 mm), and LV dimension (48±4 mm) were greater in HHD than controls, whereas EF was comparable (66±8 vs 66±5%). LS was smaller in HHD than controls (-13±3 vs -17±3%, p<0.001) in spite of reduced MWS (520±141 vs 637±164 dyn·mm -2 , p<0.01), suggesting impaired longitudinal myocardial function in HHD. Similarly, CS was smaller in HHD than controls at outer layer (-6.8±2.2 vs -8.8±2.2%, p<0.01) and at midwall (-11.3±3.4 vs -13.9±3.2%, p<0.01) in spite of reduced CWS (outer: 238±82 vs 336±110 dyn·mm -2 , p<0.001; mid: 360±107 vs 473±131 dyn·mm -2 , p<0.001). In contrast, at the innermost layer, both CS (-26±5 vs -25±5%, p=0.41) and CWS (979±153 vs 992±139 dyn·mm -2 , p=0.72) were comparable between groups. Furthermore, the difference of CS between inner and outer layers significantly correlated with relative wall thickness (r=-0.33, p<0.01). Finally, CS at inner layer significantly correlated with EF (r=-0.43, p<0.001), whereas LS did not. Conclusions: In patients with HHD, intrinsic myocardial shortening was impaired both longitudinally and circumferentially. Some compensatory mechanism associated with increased relative wall thickness might work to maintain subendocardial CS, resulting in preserved EF.

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Abstract 3435: Left Ventricular Hypertrophy is Resistant to Inhibition of Expression of the R403Q Alpha-Myosin Heavy Chain Cardiac Hypertrophy-Inducing Mutant Protein

Circulation ◽

10.1161/circ.118.suppl_18.s_423-c ◽

2008 ◽

Vol 118 (suppl_18) ◽

Author(s):

Leah Cannon ◽

Tadeusz Marciniec ◽

Bryony Mearns ◽

Robert M Graham ◽

Diane Fatkin

Keyword(s):

Left Ventricular Hypertrophy ◽

Ventricular Hypertrophy ◽

Interstitial Fibrosis ◽

Myocardial Dysfunction ◽

Left Ventricular ◽

Familial Hypertrophic Cardiomyopathy ◽

Lv Function ◽

Dependent Manner ◽

Cardiovascular Morbidity And Mortality ◽

Lv Mass

Left ventricular hypertrophy (LVH) develops as a compensatory response to myocardial dysfunction due to diverse causes, but is nonetheless a major risk factor for premature cardiovascular morbidity and mortality. It is thus unclear if regressing LVH is beneficial or may worsen patient outcome. To evaluate the effects of LVH regression, we developed a transgenic mouse model in which the expression of a familial hypertrophic cardiomyopathy (FHC)-inducing mutation (R403Q alpha-MHC) can be regulated in a temporal and dose-dependent manner. In this model, transgene expression can be shut off by feeding with a tetracycline analogue (doxycycline). Serial echocardiography and histology studies were performed in a cohort of mice expressing the FHC mutant (“gene-on”) and in wildtype (WT) littermates. A second cohort of WT and 403/+ mice was randomised to placebo or doxycycline (“gene off”) from 6 (Dox6) or 20 weeks (Dox20) and evaluated at 40 weeks of age. Compared to WT littermates, “gene on” 403/+ mice showed increased LV mass, LV end-diastolic diameter (LVDD) and left atrial diameter (LAD), and reduced fractional shortening (LVFS), with changes evident from 12 weeks of age. LV sections from 403/+ mice showed typical features of FHC: myofibre disarray and interstitial fibrosis. LV mass, LV function and myocardial histology were unchanged in both male and female placebo- vs Dox6 or Dox20 mice at 40 weeks (Table 1 ). Thus, consistent with the major LV thickening in FHC humans occurring in adolescence, overexpression of R403Q for only 6 weeks is sufficient to trigger the complete LVH phenotypic response. Moreover, switching off the genetic trigger for LVH in 403/+ mice at 6 weeks (prior to overt disease manifestation) or 20 weeks (established disease) does not induce regression of LVH or exacerbate contractile dysfunction. Interventions to induce LVH regression may, therefore, need to be directed at downstream factors in hypertrophic pathways. Table 1. Echo data for male WT and 403/+ mice aged 40 weeks

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Cardiac Effects of Dexamethasone in Very Low Birth Weight Infants

PEDIATRICS ◽

10.1542/peds.97.6.818 ◽

1996 ◽

Vol 97 (6) ◽

pp. 818-821 ◽

Cited By ~ 2

Author(s):

Andrew S. Bensky ◽

Jamanadas M. Kothadia ◽

Wesley Covitz

Keyword(s):

Birth Weight ◽

Low Birth Weight ◽

Wall Thickness ◽

Very Low Birth Weight ◽

Systolic Function ◽

Left Ventricular ◽

Low Birth Weight Infants ◽

Cardiac Effects ◽

Significant Prolongation ◽

Lv Mass

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.

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Abstract 12952: Global Longitudinal Strain is Simple, Effective & Sensitive Assessment of Cardiac Chamber Function in Patients With Acute-phase Myocarditis

Circulation ◽

10.1161/circ.142.suppl_3.12952 ◽

2020 ◽

Vol 142 (Suppl_3) ◽

Author(s):

Shaun Khanna ◽

Aditya Bhat ◽

Henry H Chen ◽

Kennith Gu ◽

Gary Gan ◽

...

Keyword(s):

Acute Phase ◽

Longitudinal Strain ◽

Myocardial Dysfunction ◽

Global Longitudinal Strain ◽

Disease Process ◽

Left Ventricular ◽

Lv Function ◽

Lv Mass ◽

Echocardiographic Parameters ◽

Cardiac Therapy

Introduction: Myocarditis is an inflammatory disease process with growing clinical relevance in the current COVID-19 pandemic. Acute-phase myocarditis is known to result in subclinical changes in left ventricular (LV) function despite normal LV ejection fraction (LVEF), as assessed by myocardial deformation indices. The presence of right ventricular (RV) and left atrial (LA) subclinical dysfunction however has not been well described in current literature. Hypothesis: Myocarditis patients have subclinical impairment of LV, RV and LA function as assessed by global longitudinal strain (GLS) on speckle tracking echocardiography. Methods: Consecutive patients with clinical diagnosis of myocarditis admitted to our institution during 2013-2018 were assessed (n=76). Patients who did not meet appropriate diagnostic criteria (n=14), had impaired LVEF or prior cardiac disease (n=8) or poor transthoracic echocardiogram images (n=14) were excluded from analysis. Clinical and echocardiographic parameters were compared to age- , gender- and risk factor- matched controls. GLS was performed by two independent observers using vendor independent software (TomTec Arena, Germany v4.6). Results: The final cohort consisted 40 patients with myocarditis (age 44.3±16.7, 60% male) and 40 matched controls (44.5±16.6, 60% male). No significant differences in baseline clinical characteristics were observed between groups. No differences in LVEF, indexed LV mass, RV fractional area change, indexed LA volume or TR pressure gradient (p>0.05 for all) were demonstrated between the two groups. Patients with myocarditis had a lower mean LV strain (GLS%: -16.4±2.9 vs -19.7±2.7, p=0.0001), a lower mean RV Free Wall Strain (FWS) (GLS%: -22.1±4.1 vs -26.2±6.9, p=0.03) and a lower mean LA reservoir strain (GLS%: 27.5±4.6 vs. 33.7±6.3, p<0.0001) when compared to controls. Conclusions: Our results demonstrate the presence of significant subclinical global myocardial dysfunction despite normal traditional echocardiographic indices, in patients with acute-phase myocarditis. Routine assessment of GLS may identify such patients for early targeted cardiac therapy.

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